What is this flying animal that hovers like a hummingbird?

That's a lepidopteran insect called hummingbird moth.

There are several species of hummingbird moths. Their more distinctive feature, as the name implies, is that they hover just like a hummingbird.

Your photo is not the best one for identification, but it seems to be a hummingbird hawk-moth, from the Genus Macroglossum, specially because the rear feather like tufts (which are just elongated setae).

Here is a better photo, for comparison:

Macroglossum stellatarum

However, according to the colors you described, your species is probably different from that in the photo above.

Here is one flying (from a different species):


These two papers[1] [2] argue that bcd is a direct activator of hb, although be aware that this does not rule out downstream events feeding back to further activate  hb. (In fact, given the complexity of the embryonic gene network, it is likely that both mechanisms have a role.)

Struhl G, Struhl K, Macdonald PM. 1989. The gradient morphogen bicoid is a concentration-dependent transcriptional activator. Cell, 57(7): 1259-1273, doi:10.1016/0092-8674(89)90062-7.
Driever W, Nüsslein-Volhard C. 1989. The bicoid protin is a positive regulator of hunchback transcription in the early Drosophila embryo. Nature, 337: 138-143.


Is there any study to find the plant with the absolute minimum light need?

Let's at first take a set of SHORT DAY PLANTS which are distinguished from the other plants using the photoperiodism parameters. Taking one plant at a time and performing starch detection test by keeping the plant under sunlight may be the only possible way to determine which plant is the most efficient at producing maximum amount of food when kept under sunlight for a particular time.
If we go deeper into the molecular level, maybe a cross section of the chloroplasts could provide us with the data of number of Photosystem 2 that are present which get activated at 680nm of light and also the number of electron carries like Ubiquinone. Their abundance can determine the quickness of carrying out photosynthesis.
There are even a separate variety of C4 plants that undergo Crassulacean Acid Metabolism also known as CAM plants found in deserts that undergo photosynthesis at night.

Thus such an experiment would require diverse plants with several parameters to keep in mind and is quite difficult.


Why have ground beetles never evolved the ability to get back up?

By "floor", I'm assuming you mean a smooth floor like that inside a house or building.  I imagine that these beetles are actually quite good at flipping themselves over when they have something to grab onto -- e.g. a blade of grass, a fallen leaf, etc.  The detritus-free environment that is the modern indoor floor (or smooth path, or paved road) is not part of the natural niche of these organisms, and encountering such surfaces was uncommon in their evolutionary history.  Rare encounters are weak selective forces.


A double strand is a helix, as the basepairs move with a horizontal angle with each step to the next basepair. Identifying the sides is important for DNA-replication and RNA synthesis as the way DNA is read is from 3' to 5' so that the complementary bases can be ''glued'' together from 5' to 3' in which the phosphate groups bind to the OH groups of the other molecule by a polymerase reaction.
Disregard first answer.

There.


How is Glyceraldehyde 3-phosphate converted into glucose?

Advice to students of biochemistry

This site is concerned with biology, not with biological entries in Wikipedia. Wikipedia is a voluntary effort to which anyone may contribute, and is full of errors and omissions. It’s structure means that it is focussed on individual small topics, rather than presenting an integrated account of various areas of science. The student who wishes a balanced integrated account of a topic that has been subjected to editorial review should consult a text book. Those whose resources do not permit this should try searching on NCBI Bookshelf, which provides free on-line search-only access to old editions of texts. For biochemistry, Berg et al. is recommended.

The generation of glucose from triose produced in the dark reaction is well understood

The answer to the question can be found in e.g. Berg et al. 20.1.3:

  The 3-phosphoglycerate product of rubisco is next converted into three forms of hexose phosphate: glucose 1-phosphate, glucose 6-phosphate, and fructose 6-phosphate... The steps in this conversion (Figure 20.9) are like those of the gluconeogenic pathway (Section 16.3.1), except that glyceraldehyde 3-phosphate dehydrogenase in chloroplasts, which generates glyceraldehyde 3-phosphate (GAP), is specific for NADPH rather than NADH. Alternatively, the glyceraldehyde 3-phosphate can be transported to the cytosol for glucose synthesis.

Berg et al. Fig. 20.9

The Section 16.3.1 referred to is a general treatment of gluconeogenesis, which is the same in all organisms or cells that possess the enzymes to catalyse its unique steps. (Some cells may not have — or need to have — the initial steps from pyruvate. In fact, Fig. 20.9 shows the steps to G 6-P — the only step missing is the phosphatase step that generates glucose.) There is therefore no reason to expect an account specific for plants.


Deviation from Hardy Weinberg equilibrium (HWE)

A significance test (i.e., p-value) allows us to reject the null hypothesis, but not to confirm it. In other words, when $p<0.05$ one can say that the conditions for HWE are not met, however $p>0.05$ does not mean that HWE holds - the conditions might still not be met, but we cannot prove it. Thus, by making statements such as All of the SNPs didn't deviate from HWE and the rest of the SNPs met the HWE one may be committing Type II statistical error.
As @MaximilianPress correctly pointed out, in this case one should not be making any statements about the SNPs with $p<0.05$ either, due to the high possibility of False discovery. Indeed, a p-value gives us the probability that the data would be at least as extreme as was observed, even though the null hypothesis is true. Given $N=150$ SNPs one expects about $$N\times\alpha = 150 \times 0.05= 7.5$$ statistically significant outcomes to occur by chance, even if the HWE holds. That is, one could be also committing the Type I error of rejecting the null hypothesis, when it is true. To exclude this error one needs to use a more stringent test, e.g., Bonferroni correction, i.e., testing against the significance level $N$ times smaller than the current $\alpha=0.05$:
$$
\alpha\longrightarrow\frac{\alpha}{N}=\frac{0.05}{150}\approx 0.0003
$$


Are there any online resources for finding the signaling pathways that two proteins both belong to?

I would try "gsk3" AND "AMPK" at WikiPathways .
Here are some pathways where both GSK3 and AMPK are participants, such as:

And


What data / tools exist for mapping of disease trends?

You can use official sources such as hospital admissions, prescriptions for drugs fighting the disease you are tracking, sales of over-the-counter medicines.
CDC (cdc.gov/flu/weekly/, cdc.gov/outbreaknet/outbreaks.html, etc), WHO, EuroFlu Weekly Electronic Bulletin map official clinical data, Aurametrix uses these sources.

Several scientific studies have compared GFT, twitter, even facebook with official sources.  Johns Hopkins study (pubmed/22230244) used data from local hospitals in addition to CDC.
My sampling studies too showed that social trends are surprisingly good, despite all the noise, but provide good estimates only for highly populated areas.

You might also want to check Sickweather's algorithm, healthmap, usgs disease maps and industry databases providing coverage of pharmaceutical companies and product sales.


Why does hypertension occur in obstructive sleep apnea?

From Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control:

  OSAS directly induces negative intrathoracic pressure and decreases pulmonary stretch receptor stimulation, chemoreceptor stimulation, hypoxemia, hypercapnia and microarousal. These changes potentiate various risk factors, including the sympathetic nervous system, renin-angiotensin-aldosterone system and inflammation.

Summary:

Low oxygen levels at night increase oxidative stress to the body inducing inflammatory reactions and damage to the interior of blood vessels
Nitrogen monoxide production is decreased, decreasing flow-mediated dilation of blood vessels
Frequent night-time awakenings bring elevated sympathetic nervous system activity
During episodes of hypoxia, blood pressure and heart rate increase
"Increased sympathetic nervous activity may also cause coronary spasm and induce vasospastic angina pectoris."
"[P]eriodic negative intrathoracic pressure (−80 mm Hg, at most), together with a midnight surge of BP, exerts mechanical stress on the ventricular and atrial walls, resulting in the development of left ventricular hypertrophy and left atrial remodeling and, consequently, an elevated risk of heart failure and atrial fibrillation"


Origin of the double membrane of mitochondria and chloroplasts

The answer lies in the protein composition of mitochondrial membranes, which undoubtedly prove that the outer membrane (OM) is of alphaproteobacterial origin, and the phagosomal membrane (if there was any) is lost. Though the endosymbiotic origin is without question, bear in mind that the phagocytotic origin is still debated (cf. López-García & Moreira 2015). And if the symbiont has entered the host some other ways than phagocytosis (cf. papers of Tom Cavalier-Smith) or syntrophic engulfment (cf. papers by Bill Martin; Searcy; López-García & Moreira) (e.g. puncturing the plasma membrane as a pathogen), then there never was a third membrane.

From Symbiogenesis Wikipedia:

  Porins (transport proteins) are found in the OM of mitochondria and
  chloroplasts, are also found in bacterial cell membrane (Fischer et
  al. 1994Zeth & Thein 2010Fairman et al. 2011). The
  membrane lipid cardiolipin is exclusively found in the inner membrane
  of mitochondria and bacterial cell membrane Mleykovskaya & Dowhan
  2009.

According to many (Cavalier-Smith 2002, Cavalier-Smith 2006, Zeth 2010), the presence of β-barrel transport proteins proves that the OM evolved from the bacterial OM, not from the host food vacuole membrane. Both mitochondria and plastids contain in their OM β-barrel proteins (e.g. Tom40, Sam50 and porins in mitochondria, Toc75 homologue of Sam50 and their joint negibacterial ancestor Omp85 in chloroplasts) and these are only present in the OMs of gram-negative bacteria (cf. Schleiff & Soll 2005). All Alphaproteobacteria are gram-negative, hence the ancestor of mitochondria originating from the Rickettsiales or very close was also.

Note, that many secondary and tertiary plastids still retain their third, outermoest phagosomal membrane originating from the host's plasma membrane (cf. Keeling 2010).


Have proteins been observed to come into existence through mutations and natural selection?

How about EWS-FLI1 and other oncofusion proteins?

One could argue that cancer progression is as close to viewing "evolution in real time" (as you say) as possible.


It's probably a dugong, based on the location, lack of a dorsal fin, split tail, lack of a blowhole, and narrowing of the snout.

The prominent vertebral column looks unusual, but that might come from the strange posture it is being held in or from malnutrition.

This publication from the Australian government shows necropsy of several dugongs (note, this PDF contains graphic necropsy photographs), including one that was malnourished (see page 53). This individual shows some of the characteristics of the OP, including pronounced vertebral column and a clearly visible neck. The text notes the presence of these features as well.

  Adult dugongs showing signs of malnutrition: a) with neck becoming visible
  and prominent backbone

Sadly, the other dugong pictures I found that look most like this specimen are also ones from news sources that are often dead or injured or needing some other human assistance. Some other examples:

Queensland couple come to rescue of beached dugong
Dugong dies from propeller wounds
Trang fishermen asked to help slow-moving male dugong
Rare Dugong saved in Maliangin Community Marine Sanctuary

Some pictures do show a prominent vertebral column near the tail in animals that seem otherwise healthy, but those images don't show the rest of the animal well (thanks to @theforestecologist):

http://www.oceanwideimages.com/images/11147/large/dugong-58M1444-20D.jpg
http://www.oceanwideimages.com/images/11144/large/dugong-58M1444-17D.jpg

As an extra piece of trivia, dugongs and their manatee cousins have been closely associated with mermaid legends.

Of course, a better picture of the animal's head, especially in profile, would make identification much more clear.


Have there been any measurements on the genomic differences between cancer cell DNA and healthy cell DNA?

Yes, there are two genome projects, which aim to identify the critical mutations (and by looking for them, they discover all the mutations in a given cancer) by sequencing DNA from the cancer cells and healthy cells from the same patient.

These are "The Cancer Genome Atlas" (TCGA) and "The Cancer Genome Project (TCGP)". Both project publish their complete data and ways to browse them. The data from the TCGP can be found in the "Catalogue of somatic mutations in cancer" (COSMIC), the data from the TCGA on their project site.


Thoughts precede neuron firing or vise-verse?

I think the only way to interpret these kinds of questions biologically is to assume that "thought" means "the perception of a thought occurring." The perception of a thought, like all perception, arises from neuronal firing.

The interesting biological (rather than philosophical) questions arise when we look at the relationship between the neural firing that gives rise to the perception of intent to act and neural firing that carries out the "intended" actions.

This paper is relevant. The authors are trying to argue that the initiation of a motor action comes before the perception of intent for that action. I'm not a cognitive neuroscience person, though, so I'm not very familiar with their techniques and personally have a hard time determining if they draw valid conclusions.


Does the leaves of papaya plant help in increasing platelets in a case of dengue?

So With some digging, I found some articles/presentations that provide evidence that fresh papaya leaf extract does increase platelet counts. The first link tested this in a rodent model and found that in the test group treated with the leaf extract, there were significant increase in platelet count and red blood cells (RBCs) from the control group. Here is the summary of their results trend from the paper:

Additionally, I found a Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study and a meta-analyses that supports the observation that papaya leaf extract does in fact show statistically significant increase in platelet count than that of the control groups. (Dengue fever causes platelet counts to plummet). [#2-3]
Below is the image of platelet counts from the Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study (2):

Fig. 1: Comparison of platelet count between two groups during different
timepoint

A good criticism of the meta-analyses on Papaya leaf extract is that something being statistically significant does not equate to clinically significant. But, the placebo-controlled, double-blind prospective clinical trial provides some evidence that in this case, it is actually clinically significant.

However, the mechanism by which this occurs is not well understood. According to the 4th article, "The secondary metabolite of plants origin makes up a vast repository of compounds with a wide range of biological activities". The presentation (5) states some possible mechanisms by which the extract can inhibit the Dengue virus/vector.

Does Carica papaya leaf-extract increase the platelet count? An experimental study in a murine model
Efficacy and safety of Carica papaya leaf extract in the dengue: A systematic review and meta-analysis
A Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study to Evaluate the Efficacy and Safety of Carica papaya Leaf Extract, as Empirical Therapy for Thrombocytopenia associated with Dengue Fever.
Dengue fever treatment with Carica papaya leaves extracts
Role of Papaya in Dengue fever, an evidence based Answer


Can anyone tell me what type of worm this is?

I can't see the head clearly but based on

1: it is a big worm cruising around on land
and
2: you have never seen one before

I bet on this

From linked article.

  The flatworm (Platydemus manokwari) has few natural predators outside
  of New Guinea, and it likely will have no predators in the United
  States, Justine says. It gobbles up soil-dwelling invertebrates like
  snails, which could have a big impact on the environment.


What is this abbreviation CT in female reproductive system

I think CT is an abbreviation for connective tissue. Some examples of its use in that fashion:

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

https://web.archive.org/web/20151024041339/http://www.vetmed.vt.edu/education/curriculum/vm8054/Labs/Lab5/Lab5.htm

http://www.pitt.edu/~sshostak/biosci1450/hislec03.html


Why do ribosomes associate with rough endoplasmic reticulum but not other membranes?

Peptides that are destined to be either secreted or included in the cell membrane have a signal sequence that binds a protein called Signal Recognition Particle (SRP). The SRP will in turn bind to translocons--basically peptide tunnels in the RER membrane. You need to have this interaction between the translocon and the SRP in order to have stable ribosome attachment. That's why you won't have ribosomes attaching to other membranes. After attachment the ribosome will continue translating mRNA through the translocon into the RER lumen.

Now here's where things get a bit dicey. If the resulting structure in the RER lumen is largely hydrophilic then it will stay in the RER lumen where it will later be targeted to wherever it needs to go based on other signal sequences.

However, if there are large stretches of hydrophobic residues, then those don't like to be in the aqueous environment of the ER lumen. Ergo they will incorporate into the RER membrane. Thus they become transmembrane proteins. A good rule of thumb is that if you have 10 hydrophobic residues in a row, then there's a good chance that is going to get incorporated into a membrane.

Once protein transcription is complete the ribosome will no longer be associated with the RER and will re-enter the pool of free ribsomes (ready to pick up a new mRNA).

EDIT: In response to question in comments about why translocons are found in RER and not in other membranes

You can certainly ask the question, but you're getting close to falling into that beautiful genesis of basic science research: something I call the 'why-hole'. I searched around, and I don't think we have a full understanding of membrane organization throughout the cell, though I would defer to any cell biologists who have a better understanding. We do have some idea of the mechanisms. What follows is a stitching together of hypothesis and some facts I was able to find.

It stands to reason that since the translocon is a complex of transmembrane proteins, its parts were at some point synthesized by a ribosome through a previous translocon. That would get it into the RER membrane. Now in order for a piece of membrane (or anything within the ER lumen, for that matter) to get to its final destination it has to have another signal sequence. This signal sequence will be recognized by unique signal recognition protein. This will localize the protein to a part of the RER that has several proteins that will form a vesicle (one of which being clathrin) and a protein attached to it called a v(esicle)-SNARE. Once the vesicle buds off it will go through the cell until its v-SNARE runs into a t(arget)-SNARE. This interaction will ultimately lead to fusion of the vesicle into the target membrane (e.g. lysosome, plasma membrane, etc). I double checked all of my facts here, where you can read more about it.

All of this is to say that if a transmembrane protein doesn't have a signal sequence it won't get targeted for transport through this system and should stay in the endoplasmic reticulum.

At this point it would be good to remind everyone that the ER--both rough and smooth--is a continuous structure with the RER located closer to the nucleus and the SER closer to the cell membrane. So it would be reasonable to ask why translocons stay in the RER and doesn't diffuse into the SER. That's where we get into more emerging science. From what I gather there are many proteins that are involved in the strutrue and organization of the ER. You can look into "the ability of NDPK-B to form microdomains at the membrane level" or reticulon2, but I think there's still a fair amount of work to do in this field. I encourage you to look into these resources, and if this is something that you're interested in consider doing some research. There is some evidence that membrane dysfunction is associated with neuronal disease, so any advances would be well received.

As always, keep asking questions!


Are there any proven ways to increase the rate of bone remodeling in humans?

The main factors affecting bone remodelling are the person's age, and the load applied on the bone. It is known that in relation to fracture healing, younger children remodel much faster and more effectively. This allows surgeons to accept very displaced fractures in young children without having to restore original anatomy as remodelling will take care of that naturally. Here is an example:

http://www.brokenarmanswers.com/arm-still-crooked-cast-comes-off/arm-fracture-remodeling-children/

The reason is that bone absorbs in areas under less loading, and forms along load lines. The shape of bones therefore follows the shape and alignment of surrounding muscles, which apply some form of load even at rest due to muscle tone. The process of bone absorption and formation is much more efficient and faster in younger people and becomes slower with age. This also explains why bones become osteoporotic in people who can't weight-bear for a lengthy period of time, or in astronauts who spend long periods in zero gravity.

A well known method to accelerate fracture healing is to load the fracture as early as possible. This is the main principle of the dynamic compression plates where the holes of the plate are designed as oval rather than circular, so that when an off-centred screw is tightened, it pulls the plate in a direction that results in compressing the fracture to promote bone healing. Here is an illustration to demonstrate this technique:

https://www2.med.wayne.edu/diagRadiology/RSNA2003/Compression_Plates_Overview.htm


Production of plant derivatives using genetic engineered micro-organisms

In principle, any biological product should be able to be developed through microbial synthesis, with the appropriate choice of chassis. Indeed, this was the goal of the DARPA "1000 Molecules" program, which did indeed demonstrate it was possible to rapidly engineer new pathways for production of new biomolecules.
In practice, however, some products are far more difficult to achieve than others.
A (very) rough sorting from easiest to hardest:

Small-molecule chemicals that are "near" to an existing metabolite already being produced by the organism, requiring only small number of modifications to the organism.
Proteins, polymers, and small molecules requiring more extensive or difficult synthesis
Materials with a homogeneous structure
Materials with a highly heterogeneous structure

Basically, the more you have to manipulate the cells, the harder it is, and if you need the cells to coordinate with each other to make a material it gets much harder yet. Even some simple everyday materials, such as cotton, are actually fantastically complex and would be extremely difficult to synthetically generate, since even a single cotton fiber has a carefully controlled multilayer structure far larger than any microbe.
Finally, just because something can be produced doesn't mean it will be produced efficiently. Getting from a proof-of-principle to something that operated effectively at industrial scale is a massive challenge, and while this is likely to become easier in the future we just aren't there yet.
Something to keep an eye on, however, is BioMADE, a major government funded venture just kicking off with the aim of making such production much more feasible.
In short: in the near term, expect to see mostly high-value products with relatively simple routes to synthesis, but over the long term a much broader range of materials can in principle be produced.


Has there ever been a published experiment to take a viral "census" of a human subject's blood?

You wouldn’t try to isolate viruses, this being the 21st century.  You’d perform metagenomics analysis, which is much more sensitive.

That’s been done several times.  Two examples:

  Anellovirus and pegivirus C (GBV‐C) were detected among these donors. None of them were found solely in donors with abnormal liver enzyme. Anellovirus was highly prevalent (93.3%) and the co‐infection with multiple genera (alpha, beta, and gammatorquevirus) were more common in the donors with normal ALT values in comparison to those with elevated ALT ...

—-Full annotation of serum virome in Chinese blood donors with elevated alanine aminotransferase levels

  Anelloviruses were detected in each of the 10 plasma pools. Human pegivirus A (HPgV; GB virus type C) sequences were identified in eight of the 10 pools, more than 90% of which belong to Genotype 2. The recently described human HPgV2 in Flaviviridae was not detected. A small number of sequence reads of human papillomavirus were also detected in three pools. In one pool, two different gemycircularvirus genomes were identified and fully sequenced.

—-Viral nucleic acids in human plasma pools


What do the column labels in this table mean?

F(1,22) is the result of an F-test with degrees of freedom 1 and 22, in this context most likely this is an F-test in the context of ANOVA; for the meaning of those degrees of freedom I would suggest further reading on ANOVA. Specifically, in this table it looks like we have a 2x2 ANOVA: with stimulus songs or tones and treatment E2 or none, and the interaction between them.

P is the P-value associated with that F-test; it is the probability of observing a result as extreme or more extreme than the F-test gave in this circumstance, given the null hypothesis was true (typically the null hypothesis is something like "the groups don't differ"), and assuming all of the assumptions of the statistical test hold true.

η2 is read as "eta-squared" - it is a measure of effect size, meaning it describes the magnitude of an effect controlled for some other characteristics of the measure, typically the variance. Many statisticians prefer presentation of effect sizes rather than p-values. A large value of η2 means that lots of variance in the outcome variable is explained by the parameter of interest.


Difference between sequential and conformational epitope

Yes, the difference is "only" in the 3D structure. This makes some differences when proteins change their shape; antibodies which recognize conformational epitopes are usually not well suited for lab work, as proteins are often denatured here.

The different epitopes are also called linear epitopes (for the sequential) and discontinous epitope (for the conformational). Schematically this look like this:


I found a bug on my bedroom floor. Is this a bedbug?

To answer your question this is very likely NOT a bedbug.

See this answer for a positive ID of (and more info for) a bedbug.

However, based on the size and body shape of your specimen, it appears you've found another blood sucking paristic pest: a flea.

 Sources: Here, here and here.

 General Info:

Fleas are small flightless parasitic insects (order Siphonaptera) that consume the blood of mammals (including humans) and birds.
Over 2,500 species of fleas have been described worldwide.
Adults are 1.5-3.3mm long, narrower than wide and brown (or reddish brown). [1,2]
Flea larvae are worm-like (vermiform) in shape with a sparse covering of bristles.  They rarely live on the body of their host.  Instead, they are usually found in its nest or bedding where they feed as scavengers on organic debris (including adult feces).

 Likely Species:

I'm assuming you have a pet (cat or dog perhaps). If that is the case, you're likely looking at a cat flea or dog flea (depending on your locaiton). From UF IFAS:

  The most common [American] flea is the cat flea, Ctenocephalides felis  (Bouché). The adult cat flea, unlike many other fleas, remains on the host. Adults require a fresh blood meal in order to reproduce.

  The dog flea, Ctenocephalides canis (Curtis), appears similar to the cat flea, but is rarely found in the United States. Cat fleas are commonly found on both cats and dogs in North America, while dog fleas are found in Europe.

  The two species are distinguished by a slight morphological difference which is detectable only under high magnification.

 Cat flea (Ctenocephalides felis) from University of florida IFAS

Note: both species will parasitize multiple species (including both cats and dogs as well as humans), and their distinction (as mentioned above) is more dictated by geographic location. However, both can be found worldwide.

Linardi & Santos (2012)1 have an excellent publication for correctly identifying between the dog and cat flea.

For More General Information See:

  Wikipedia
 - Terminix
 - Orkin
 - Univ. of Evansville
 - Purdue University
 - UFL IFAS (cat fleas or dog fleas)

 Fleas vs. Bed Bugs

See this Terminix page for "What is the difference between bed bugs and fleas?"

Your specimen is almost certainly a flea because:

The body of the insect in your picture is thin but vertically "tall" (or "laterally flattened"). In other words, it appears to be narrow like a flea.

A bed bug, on the other hand, is wide and vertically very flat.

Though, an engorged adult can appear to be more narrowly long when engorged on blood. See here.

Fleas are narrow so that they can easily maneuver through a host's fur/hair/feathers; while a bedbug is flat to be able to effectively hide in crevices.

The size (3-4 mm) is more appropriate for a flea.

Although some larval stages of bed bugs can range between 2.5 - 4 mm, these larval stages still retain the relatively flat appearance of the adult (except when engorged).

Notice the reflection toward the posterior end of the specimen in your photo. This is not present on bed bugs. This light is reflecting off the flea's pygidium (or sensilium).

Some fleas have bristles on the posterior end of their body. Bed bugs do not. The insect in your picture has these posterior "hairs."
Fleas have powerful hind legs for jumping that stay relatively close to the body, while bed bugs have very skinny legs that spread laterally from the body.

When bedbugs become engorged and appear more like the insect in the question picture (i.e., not flat), their abdomen grows posteriorly but their legs do not extend very far back.
Notice when I brighten the OP's picture from the question you can see the light reflecting on the wide posterior femur that is both close to the body and extends relatively posteriorly as compared to the overall abdomen:

Location & Behavior: Although both fleas and bedbugs are generally nocturnal, both can be found during the day. However, they would generally be found in different places:

Bed bugs are likely to be digesting meals on the piping of your mattress, in and around the bed frame or box spring, along the baseboards and creeping around in other well-hidden cracks and crevices
Fleas, however, (like your specimen) are more likely to be found making themselves at home in animal sleeping areas or lurking around in your upholstery or carpeting, waiting to hop on for a bite. [Source]

Should You Still be Concerned?

Some fleas are well known to transmit diseases (e.g., plague, murine typhus, etc., and a host of issues for your pets) unlike bedbugs. So really, fleas could potentially be more harmful.

Unlike bedbugs, however, vacuuming goes a long way for managing fleas on bedding, carpets, and furniture.
However, one flea can lay between 150 and 300 eggs every week, so do not wait!

 Works Cited:

1  Linardi, P.M. and Santos, J.L.C., 2012. Ctenocephalides felis felis vs. Ctenocephalides canis (Siphonaptera: Pulicidae): some issues in correctly identify these species. Revista brasileira de parasitologia veterinária, 21(4), pp.345-354.


Do drugs' levo isomers have a better interaction with the receptors in our body than dextro isomers?

This is purely coincidental. The term levo simply means the direction that the pure enantiomer of the compound rotates plane polarized light at a specific wavelength and has no direct bearing on the interactions with biological systems. A quick search of the Dictionary of Drugs database gave 6845 compounds with optical rotation >0 (dextro-compounds) and 8406 compounds with optical rotation <0 (levo-compounds). So there are plenty of chiral drugs that rotate plane polarized light each direction.

The inclusion of 'levo' (or 'dextro' for that matter) into the name of the compound was done to distinguish enantiomers of chiral compounds. This naming convention as fallen out of favor due to the improved ability of chemists to know the absolute stereochemistry (e.g., R/S) and distinguish enantiomers based on their structure.

Dextroamphetamine (Adderall) and dextromethorphan (Robitussin) are a couple of examples of drugs with 'dextro' in their names.

With respect to the stereochemical nature of HTS and fragment libraries, most compounds are achiral (do not rotate plane polarized light). I'm not aware of any library biased toward optical rotation, and I'm not aware of any chemist making any selection of compound based solely on an optical rotation measurement. In fact, chiral compounds are often studied first as the racemate. If there is activity, the individual enantiomers are tested.


Is working with (nitrile) gloves around a bunsen burner safe?

new microbiology lab

What're the entry requirements for your lab? If you're working in BSL-2 or greater, the appropriate PPE ensemble is listed and required at all times while you're in there. Likewise, gloves are required whenever you're in contact with potentially infectious materials (OSHA 29CFR1910.1030). There shouldn't be leeway to decide when and when not to wear your PPE ensemble.

As bunsen burners do present a burn hazard, your work with a bunsen burner should be preceded by general lab safety training, and subject to work practice controls. It's safe to wear nitrile gloves working with an open flame, and your gloves are not readily combustible. Burns will typically result from a failure to exercise universal precaution and/or use the burner properly.

If you're working dangerously close to an open flame or with heated materials, consider controlling for injury with thermal gloves, tongs, or engineer out the burner with a biosafety cabinet.


The structure you are relating to is a seam (suture). This seam is formed during development of a carpel.

The indentation of the seam varies and depends on the climate and environment: for example, water stress will give a very deep suture -


There's still white blood cells with DNA.

Some forensic blood tests are:

Conventional serological analysis:

Analysis of the proteins, enzymes, and antigens present in the blood, for general doctor tests: (black/white/drunk/stoned/heroin addict/polio vaccinated/hiv pos...)

Restriction Fragment Length Polymorphism (RFLP) DNA :

Direct analysis of certain DNA sequences present in the white blood cells. This method also usually requires a "large" sample size to obtain significant results.

Polymerase Chain Reaction (PCR) DNA :

Analysis of certain DNA sequences that have been copied multiple times to a detectable level.


Does natural selection still increase biological complexity?

There are multiple definitions of complexity, ranging from algorithmic complexity to computational complexity.  In biology, I'd say that algorithmic complexity (Kolmogorov complexity) is most relevant.  Unfortunately, we don't yet know enough about genetic circuits and all the other things that go on at the subcellular level even to make plausible estimates of an organism's complexity.

If the complexity of a human being were analyzed all the way from physiology down to the subcellular & molecular level, I think it would be apparent that most of the complexity is present at the subcellular & molecular level.  In fact, essentially all of the complexity of a multicellular organism is encoded at the subcellular level, so it's appropriate to say that's where the complexity resides.
It is not entirely clear that a human being, whose genome contains ~3 billion base pairs, is more complex than a protozoan Amoeba Proteus whose genome is ~34-43 billion base pairs.

All of the processes that have been active in evolution since the beginning are still active, and changes in complexity - regardless of the definition of complexity - are still going on.

The closest things there is to a "plateau" is a relatively static distribution of genotypes that can last only as long as the adaptive landscape is unchanged.  However, the adaptive landscape is always changing because of climate changes, plate tectonics, invasive species, disease, intra-species iteractions, and even because of chance fluctuations in the distribution of genotypes.


How much energy does a neuron use for information processing as opposed to just surviving?

http://quantum-mind.co.uk/anaesthetics-and-brain-energy/

About 80% of the brain’s energy consumption is devoted to neuronal firing with only 20% involved in maintenance activity.

The energy for firing is mainly supplied by glia and astrocytes, the maintenance of the neuron itself is done mainly by the cellular machinery in the neuron.


Is there a favoured mathematical model of bacterial growth?

Some clarifications:
Commonly used models for bacterial isothermal growth curves (which represent the growth curve directly) are for example:

Exponential

Logistic

Generalized logistic

The Monod equation expresses how the growth rate changes with the availability of substrate see a related question here.
The Monod equation can be incorporated into an exponential growth model (differential equation) like this:
$$
\frac{dX}{dt}=\mu X
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X$ is the biomass concentration and $[S]$ is the substrate concentration. Or into a logistic growth model:
$$
\frac{dX}{dt}=\mu X \left(1 - \frac{X}{X_{max}} \right)
$$
with
$$
\mu = \mu_{max} \frac{[S]}{K_M+[S]}
$$
where $X_{max}$ is the carrying capacity.
Other growth-substrate relations like Haldane which takes into account growth inhibition by the substrate can be used instead of Monod one.
Regarding this:

Is there something holding the synthetic biology community back from regularly reporting growth characteristics of their cells?

It depends on what branch of synthetic biology you are looking into. Model-based design engineering biology interpretation of synthetic biology goes around the DBTL cycle. In the DBTL cycle, there are always (at least) models of both growth and gene expression.


What mechanisms do animals living in groups (herds, packs, swarms) have against spreading contagious diseases?

Three proposed mechanisms:

altruistic self-removal (i.e., diseased individuals leave the group to prevent transmission to kin) has been documented in eusocial insects (ants and bees); Rueppell et al 2010 J. Evol. Biol. say:

  altruistic self‐removal by sick social insect workers to prevent disease transmission is expected under most biologically plausible conditions. The combined theoretical and empirical support for altruistic self‐removal suggests that it may be another important kin‐selected behaviour and a potentially widespread mechanism of social immunity.

social distancing/avoidance: This is a commonly used term in human infectious disease epidemiology for the practice of avoiding contact with infected people. I don't know of any great references, but Loehle 1995 Ecology "Social Barriers to Pathogen Transmission in Wild Animal Populations" says:

  Data on animal behavior in this regard [social avoidance] are sketchy. Sick individuals in cattle herds do seem to be isolated somewhat from the group (L. R. Rittenhouse, Department of Range Science, Colorado State University, and Ray Strickland, University of Maryland, personal communication 1988), though whether by chance (failing to keep up with the group due to listlessness), by voluntary isolation, or by avoidance on the part of others is not clear. Edwards (1988) found a higher degree of investigatory behaviors but a lower degree of touching between other group members and mice infected with Trichinella spiralis, though this disease is not transmissible by contact. This example would fit the proposed behaviors perfectly. More study is needed.

seasonal migration has been proposed as a way for group-living organisms to temporarily leave their habitat, allowing the built-up parasite burden in the environment to diminish before they return; it may also have a group-level effect of filtering out diseased individuals.

Folstad et al. 1991 Can. J. Zool. Parasite avoidance: the cause of post-calving migrations in Rangifer?

  Intensities of warble fly larvae, Hypoderma tarandi (L.), were examined in slaughtered reindeer (Rangifer tarandus tarandus L.) from different summer grazing areas of Finnmark County, northern Norway. To test the hypothesis that larval abundance decreases with increase in post-calving migration distance (i.e., distance from calving grounds), herds with differing migration distances were sampled. The prevalence of infection in the total sample of 1168 animals was 99.9%. The study revealed significant differences in larval abundance among herds from different summer grazing areas. Herds with post-calving migrations have significantly lower larval abundances than herds remaining on or near the calving grounds for the whole summer. Between-herds variation in abundance of H. tarandi larvae is assumed to reflect differing densities of the infective stage (adult flies) on the herds' summer ranges. Larval abundance in a herd is in turn negatively correlated with the distance between the main larval shedding areas (i.e., calving grounds) and the areas of greatest transmission (i.e., summer pastures). These results are discussed in relation to transmission of other parasites common to Rangifer and suggest that this host's post-calving migration may be a behavioural adaptation that reduces levels of parasitic infections.

Loehle 1995 also discusses this (qualitatively/speculatively):

  A more subtle effect results from migration. Consider a species that migrates seasonally some large distance. An area that becomes fouled and unsanitary during one season will become largely clean again by the following year. In between, nest and skin parasites such as ticks and fleas will have nothing to eat and will be greatly reduced in number. For example, wide spacing in rabbits results in reduced flea numbers (Mohr 1963) for these same reasons. Excrement piles will decompose between seasons and wash away. Significant benefits could thus accrue to migratory species, even though long distance migratory behavior is not likely to have arisen from this cause alone. (It may result from predator avoidance [Fryxell et al. 1988], or more commonly be due to weather and food supply factors.) Abandonment of rookeries during the non-mating season might, however, be the result of disease avoidance. Another consequence of migratory behavior is the effect on internal parasites ...  Consideration of epidemiology thus leads to some unexpected benefits of migratory behavior.

Hall et al. 2014 J. Anim. Ecol. "Greater migratory propensity in hosts lowers pathogen transmission and impacts" explore a theoretical model of migration effects.


What are the advantages and disadvantages of using beta-galactosidase compared to luciferase as a reporter gene?

Beta-galactosidase (B-gal for short) is an enzyme that will process the substrate lactose. In applications using B-gal as a reporter (lacZ gene), two lactose analogues are commonly used: X-gal or ONPG (as pointed out by @Alan Boyd). Both substrates are colourless, becoming coloured once hydrolyzed by B-gal. The formation of this colour allows B-gal to be assayed by means of either visual inspection, or more accurate means by using a spectrophotometer or camera.

When X-Gal is hydrolyzed, an insoluble blue dye is formed. Evolution of blue colour is intensified as more substrate is hyrolyzed, allowing for quick blue/white screening by visual inspection in common applications of cloning and gene expression. Using the X-gal substrate, B-gal assays are more sensitive to gene expression (the dye precipitates out and retains colour very well), however X-gal is not quantitative (Möckli & Auerbach. BioTechniques 36:872-876 (May 2004)). In contrast, ONPG hydrolysis evolves a soluble yellow dye. This colour developement is quantitative, however is less senstive than X-gal because the linear relationship betwen light absorption (at 420 nm) and substrate concentration is small. Using ONPG as a B-gal substrate allows for quantitative measurement of B-gal activity (and therefore promoter activity). (Note that ONPG itself is not capable of inducing the lac promotor, unlike X-gal.)

Luciferase reporters (there are actually a few different luc genes) operate in a similar fashion. The enzyme cleaves its substrate, however instead of yielding an insoluble blue dye, emits a characteristic photon. Luciferase activity must be measured using specialized camera hardware to detect and count photons emitted from your yeast clones. This assay will still answer yes/no reporter questions, but can also be quantified to look at how much the reporter was activated. Luciferase activity is a quantitative reporter while also yielding spatiotemporal information.

The choice of reporters depends largely on the question you wish to answer. If promoter induction is relevant (eg, the stress-response promoter was activated), then luciferase or B-gal with X-gal are best suited for their higher sensitivity. Given that luciferase requires a special camera and optical filter (such as a gel documentation system), X-gal is ideal because it may be screened by eye. If promoter activity is being assayed, then B-gal+ONPG or luciferase will yield quantitative measurements of reporter gene activity, and require at least a spectrophotometer.

Given these are university labs, I assume that materials costs are to be minimized and ease of experimental protocol to be maximized, B-gal is the ideal reporter. Luciferase requires: more costly substrate; specialized equipment; careful handling of materials, and more time (as screening necessarily takes longer, therefore lower throughput for a lab demo setting).


Why in the Electron Transport Chain does PS2 go before PS1?

If your question is related to numbering, the photosystems were named in the order of their discoveries not participation.
In cyclic ETS PS-II doesn't participate at all.

PS-I would have gone first if PS-II was named PS-I.


What are the risks of elevating the legs too regularly and when tired?

To answer your questions, one needs to address certain issues one at a time.

Veins do have valves, but they function to hold blood from settling in the legs. When you flex muscles, the blood flows towards the heart. Valve failure occurs when people stand (especially if they stand relatively still) for long periods of time every day over many years, dilating veins. You can see this on the surface of the legs as varicose veins. One way to treat varicose veins is with elevation. So, elevation does not harm vein valves.

Lymph is made at the arterial end of capillaries and is part of the interstitial fluid of tissues. It bathes cells, and returns to the circulation via the lymphatic system (which also has one-way valves), goes through lymph nodes, and returns to the blood via connections with the subclavian veins. The treatment for too much lymph in the lower extremities (also known as edema) is to elevate the legs. So, elevation does not harm the lymphatics system.

The heart was made to pump all day, every day, for many, many years. It doesn't get "tired" during a tiring day, and doesn't need to rest like we do. But it can get weak and pump inefficiently if injured (e.g. myocarditis, myocardial infarct), or if it pumps against high arterial pressure (hypertension).

As long as you have healthy arteries to the legs, I can't see how your legs can suffer by elevation.

The main effect that I can think of is on baroreceptors. The increased volume of blood in your upper body will cause an increased stroke volume from the heart, sensed by baroreceptors, and may cause smooth muscle dilation of the vascular system. In the short term, that means you will experience more pronounced orthostatic hypotension on standing (you will be dizzier). The long-term effect from elevation for a couple of hours a day are basically nil.

Since you asked about these parameters only, I won't elucidate on other possible effects.


From what kind of insect might these eggs be

Those are likely moth eggs... moths have a tendency to attach their eggs on metal screens that you might have in your windows or doors.
Here is a video of a moth laying eggs on glass:
https://www.youtube.com/watch?v=L2zf1J8CZdg
Here is a video of a moth laying eggs on a metal screen:
https://www.youtube.com/watch?v=qKHReVNAMYw
Here are photos of eggs on a wire fence, believed to be moth eggs:
https://www.whatsthatbug.com/2013/09/19/possibly-moth-eggs-deer-fence/
And another example of moth eggs on a metal wire:
https://hardtocomebylifestyle.wordpress.com/2014/08/31/moth-eggs/


it does not, really. unless we're talking about things like frostbite or severe hypothermia.
it's a myth that it does.
the virus is more stable in colder air, however.
see more here:
Study Shows Why the Flu Likes Winter
Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature

Innate responses proved to be comparable between animals housed at 5 °C and 20 °C, suggesting that cold temperature (5 °C) does not impair the innate immune response in this system.


What is the use of having a surrogate mother in animal cloning?

It would make the result at least a little ambiguous. How would you establish with high confidence that the offspring was the results of your implanted cloned ovum and not a naturally fertilized one? DNA testing would have to be quite extensive to establish that offspring was a clone and not the result of an ordinary pregnancy. If you use a surrogate mother, the offspring will have DNA quite distinct from the surrogate.


What is the purpose of the brown louver-like structure on the underside of a mushroom?

These thin, closely-spaced structures are commonly called gills (in more formal contexts a gill is called a lamella).  Our most familiar mushrooms have gills, but there are other species that do not have structures of this form.

Photo by Jason Hollinger via WikiMedia.org

The gills exist for reproduction. Mushrooms spread by producing tiny spores that disperse on air currents.  (In fact the entire mushroom structure exists for this purpose; the main part of the organism, a fungus, is a diffuse web under the ground or other substrate.)

Mushroom spores develop on surface tissues so that they can be released into the air.  The gills evolved to provide more surface area so that more spores can be produced and released (up to twenty times the area of the supporting surface).  The gill spacing is important because the spores are shot out of the surface, are slowed by air resistance, and then fall downwards from between the gills. (Source: Why mushrooms form gills: efficiency of the lamellate morphology)


Biological meaning/interpretation of clustering coefficience

First of all, I find this an interesting question.

In short:

Clustering coefficience is widely used
It is widely accepted that hub genes are more essential than poorly connected genes
but research is not always interested in the hub genes / proteins / molecules (for example most metabolic pathways involve water)

Answering your question, why people would want to use this kind of method:
If you would take a random model (pathway) most of the lines will be equally distributed between the nodes. This is not the case for most biological networks. Because of this, the global clustering coeffiecence can be used to see if a network could be biological. Clustering coeffiecence can also be used to find out about more specific nodes. For example if a protein has a relationship with two other proteins (binding, regulation, etc.), the two other proteins are also more likely to have a relationship with each other (similar to a social network).

References:

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

http://www.biomedcentral.com/1752-0509/6/34

http://www.pnas.org/content/99/12/7821.full.pdf+html


Exercise vs stimulants, which is more effective for promoting concentration?

exercise stimulates brain regions that are involved in memory function to release a chemical called brain-derived neurotrophic factor (BDNF) which is a protein that helps in the survival of neurons and promotes the growth of new neurons. BDNF rewires memory circuits so they work better.

Memory enhancers or smart drugs or Nootropics as they are called help in improving the efficiency of neurotransmitters and its associated receptors in cognitive function. Three systems that are stimulated by these drugs which I could find are:

1) Cholineric System

2) Glutamatergic System

3) Dopaminergic & Serotonergic Systems

You can read about about them here along with links to published articles on their effects. Details of different nootropic drugs are mentioned in this article along with their effects.

Of course naturally improving concentration would be the way to go considering the hazards of long term use of drugs. Some links to the side effects are this and this


A quite safe way of shipping plasmids is to put them on filter paper (see protocol and send a letter. Much cheaper.


Which Hawaii bird makes this call at night?

Thanks to the magic of Reddit I was able to figure out that this is the Coqui frog rather than a bird. Apparently its an invasive species on Big Island and attempts are underway to eradicate them.


Is water vapour a product of fossil fuel oxidation?

Althugh water vapor contributes to greenhouse warming of the atmosphere, changes in atmospheric water vapor tend to follow rather than drive changes in temperature. Also, in the form of clouds, atmospheric water can have a cooling effect on earth temperature.

Clouds illustrate why water vapor, unlike carbon dioxide and methane, is not thought of as a driver of recent changes in earth temperature but rather is more of a follower. Unlike those other two gases, if you keep trying to put water vapor gas into the atmosphere it will convert to liquid water at some point, leaving only a constant level of water in the form of gas. That's what happens when a cloud forms; what you see and what can shield you from the sun is a collection of water droplets or ice crystals. Large amounts of water vapor are also regularly put into the atmosphere by evaporation of water from the earth's surface, dwarfing the contribution from human respiration. Eventually the atmosphere gets locally saturated with water vapor and it falls back to earth as rain or snow in the hydrologic cycle.

In principle methane and carbon dioxide could similarly condense out of the gas phase, but not at temperatures that occur in our atmosphere. You need to go far out into cold reaches of the Solar System to find naturally occurring methane lakes or solid carbon dioxide. There is no equivalent of rain to remove excess of those gases from our atmosphere. Carbon dioxide can dissolve in water to leave the atmosphere, but at the cost of acidifying the water. Ocean acidification is another serious result of adding carbon dioxide to the atmosphere.

The amount of vapor you can add before conversion to liquid water increases with the temperature. So as land temperature increases the rate of evaporation of water into the atmosphere can increase, and as atmospheric temperatures increases the amount of water vapor that the atmosphere can hold also increases. So in principle water vapor might thus serve to amplify the greenhouse warming from other gases, although its transition to liquid or ice in the atmosphere might tend to counteract that. This is a major issue being investigated in attempts to understand the interplay of factors that determine earth temperature.

A focus on carbon dioxide has an important practical aspect. If you control the excess release of carbon dioxide due to fuel combustion, you necessarily also control the associated excess release of water vapor.

In summary, human activity ends up having much less direct influence on changes in atmospheric water vapor than it does on changes in carbon dioxide or methane. That's why the latter two gases rightfully receive more attention as controllable greenhouse gases.

The American Chemical Society also discusses this issue.


What is the difference between xDNA and yDNA?

yDNA came first:

  Lee & Kool (2005) A New Four-Base Genetic Helix, yDNA, Composed of Widened Benzopyrimidine−Purine Pairs. J Am Chem. Soc. 127: 3332-3338

As seen in this Figure from the paper it is a DNA consisting of T and C substituted with yT and yC, widened analogues.

xDNA came next (also from the Kool lab.):

  Lynch et al. (2006) Toward a Designed, Functioning Genetic System with Expanded-Size Base Pairs: Solution Structure of the Eight-Base xDNA Double Helix. J Am Chem. Soc. 128: 14704-14711

As seen in this Figure from the paper, xDNA consists of an 8 base system A,C,G,T,xA,xC,xG,xT.

This field is reviewed in:

  The XNA world: progress towards replication and evolution of synthetic genetic polymers
  Pinheiro & Holliger (2012) The XNA world: progress towards replication and evolution of synthetic genetic polymers. Current Opinion in Chemical Biology 16:245-252


I can highly recommend Kandel's "Principles of neural science". I have not had any biology courses since highschool, but I was able to understand it well. It is really a book meant to teach. The style is beginner friendly, and not tedious/boring at all.

It is an expensive buy and a very long read (I think the paper version is close to 2000 pages), but given the complexity of the subject matter, I find it reasonable.

If you decide to go for it (or for any other neurobiology work, actually) get the newest edition. Getting an older one is a false economy here - our understanding of how this stuff works gets better by the year, and there is lots of missing (or sometimes even not-valid-any-longer) information in the older editions.

A few examples of what might make the book hard to understand for beginners

"Principals of neural science" does not require much preexisting biology knowledge. It is sufficient to roughly know that a cell has a nucleus, plasma with organelles swimming inside, and a membrane. But you have to be comfortable with a bit of biochemistry. This is an example passage concerning the behavior of ions in solution. I found this perfectly understandable with my prior knowledge, I don't know if you need brushing up on chemistry or not.

  The cell membrane is selectively permeable to K+ because the otherwise impermeable membrane contains proteins that form pores called ion channels. The channels that are active when the cell is at rest are highly permeable to K+ but considerably less permeable to Na+. The K+ ions tend to leak out of these open channels, down the ion's concentration gradient. As K+ ions exit the cell, they leave behind a cloud of unneutralized negative charge on the inner surface of the membrane, so that the net charge inside the membrane is more negative than that outside.

And then there are examples like this one:

  Isoprenylation is another post-translational modification important for anchoring proteins to the cytosolic side of membranes. It occurs shortly after the synthesis of the protein is completed and involves a series of enzymatic steps that result in thioacylation by one of the two long-chain hydrophobic polyisoprenyl moieties (farnesyl, with 15 carbons, or geranyl-geranyl, with 20) of the dulfhydril group of a cysteine at the C-terminus of proteins.

Here, my own chemistry is bad enough that I could only understand that a protein is modified by attaching some molecular structure to it, and this makes it possible to attach the protein to the cell membrane. The lack of understanding of the details (what is a geranyl-geranyl?) did not stop me from understanding the rest of the section, so I don't mind, but I know that there are readers who'd have a problem with that. Sadly, I don't know of a source which does not require such knowledge, and if you feel the need to know every single word, you might need to use a reference while reading, or start with a course in biochemistry first before switching to the neurobiology.

Finally, if you don't have a life science background, there might be words outside of the chemistry you might have to look up, or understand from context, but they will be unfamiliar at first. For example, I was surprised to see the word "process" used in the meaning of a physical protrusion from the cell body. But this is not such a high hurdle, you have to either read ahead and puzzle such words out, or use a dictionary. They are not so frequent to prevent comfortable reading.


Are molecular machines encoded in the DNA?

Yes.

The "molecular machines" you are referring to are particular proteins.

The specific one you are referring to, kinesin, is involved in movement along microtubules, part of the structure of the skeleton of a cell, but other proteins act as their own kind of machine to do their own tasks: sometimes catalyzing a biochemical reaction, or responding to a type of stimulus, or forming a shape or structure, or combinations of all of the above.

Protein-coding sections of DNA are well-studied, and there are substantial databases of known proteins. If you go to wikipedia you will see a whole list of different kinesins, if you click on one, for example, KIF1A, on the right hand side it shows you it is found on chromosome 2 in a human, starting at 240,713,764 base pairs and ending at 240,820,308 base pairs. Information for the mouse is also located there.

Proteins in DNA-based life are all synthesized by first producing an RNA transcript from the DNA, which is effectively an RNA copy of a short stretch of DNA, which is then translated into protein. Other RNA molecules are involved in this process, too, as the rRNA part of the ribosome (sort of a 'protein factory') as well as tRNA which carries the amino acid components of proteins as they are being built. Transcription and translation are central to understanding biology at the molecular and cellular level.

Not only can all proteins, from kinesin to collagen, evolve, they all have evolved through natural selection and other evolutionary mechanisms, and they continue to evolve today in all living organisms. Without evolution, no biology would exist. RNA-based biology (today, mostly some of the viruses) is also subject to evolutionary mechanisms, so that isn't something unique to DNA, but rather to heredity and biology in general.


What is the difference between a paralog and an isoform?

I think the confusing thing here is that the two terms come from different fields of biology. While describing something similar, they emphasise different aspects.
The term paralog is mostly used in evolutionary biology, when one wants to find out how genes developed. Paralogs are, as you correctly found out, genes that originate from the same ancestral gene which duplicated. Thus, you would use this word when you want to emphasise the evolutionary relationship.
The term isoform on the other hand is not interested in evolutionary origin, and in fact it is not perfectly defined. This word is used when people studying the molecular biology of an organism discover that there are proteins in this organism that have a very similar amino acid sequence. Here, the interesting question is what differences in function these similar, but slightly different proteins might have. The evolutionary origin is not asked for, and thus there are two different definitions of isoforms:

Some people define isoforms only as variants of the same gene that underwent different post-transcriptional modifications (e.g. English Wikipedia), thus, paralogs would not be isoforms.

Other people also allow paralogs in addition (e.g. German Wikipedia).

In your paper, I guess that the author wants to emphasise that the proteins are not the results of different splicing but encoded by two different genes.


The current working theory (note this is still an open question, but there are many leads being followed):

Sensory systems receive a combination of signals from an event, which are initially bound to the hippocampus (this is called episodic memory).  Then, typically during sleep, the memories are consolidated.

A simplified view is that consolidation basically consists of communication between the neocortex and the hippocampus, and the memories are thought to be "saved" in the neocortex.  Thus, amnesia patients with hippocampal damage still have all their long-term memories, they just can't create new memories (because their old memories were already consolidated to neocortex).

Your neocortex has many subregions with many functions.  One is the temporal lobe, where semantic memory seems to be stored.  So your episodic memory may record several interactions apples and, over time, your semantic memory will be updated (as memory consolidation occurs) to "consolidate" your concept of "apple".

The temporal lobe is highly connected with the occipital lobe (where visual information is processed) and the two likely work together to identify objects using the consolidated information.

On the molecular level, how the memories are actually stored.  The most well known concept is connectionism: different connection strengths between neurons carry different information.  But there's also genetic expression going on, and there was recently some research on prion-like proteins contributing to memory as well as astrocytes.

Realize, of course, that a lot of this is cutting edge research... and therefore could be wrong or contain numerous oversights and simplifications.


Use of beta-2 microglobulin staining to assess frozen tissue sample integrity

I'd say it is not common practice to look for B2M, although I guess there will be heavy users would would disagree.

Without seeing the paper I cannot be sure, but I guess they are using B2M as a housekeeping gene, that is, a molecule whose presence and quantity is largely unregulated in living cells, and which is commonly used in labs as reference. Biological samples vary greatly in their content. It is hard to tell if a molecule is made or destroyed in response to a treatment, by merely measuring, and finding more or less of it. But if the ratio between the aforementioned molecule to an unregulated molecule goes up, you can be more sure it responded to the treatment. That is called an internal control. You may be familiar with "normalization to actin" or to GAPDH in immunoblot and qRT-PCR.

The use you are describing is diverging from the typical use of housekeeping genes in a lab, and not optimal for what they were trying to show. Since it's there in pretty much any tissue measured by immunoblot, B2M is expected to be present in any tissue assayed by microscopy. If a tissue slide lacks B2M, it is likely spoilt. But if it has B2M, it doesn't make it 100% certain that other, scarcer, more unstable molecules have been preserved as well. It would be ideal if they looked for the specific molecule they were studying; but if many of their samples were supposedly devoid of the latter, they had to replace the ideal with something more practical.

Note that I am using "molecule" in an ambiguous manner. With antigens in the referenced paper, it's obvious B2M is used as a reference protein. But housekeeping genes, including B2M, are also used as internal control for mRNA measurements ("gene expression").


What is the best way from remove background signal from a band when doing Western blot image analysis?

I haven't done immunoblots for years, and didn't do much quantitative analysis of them even then, so caveat emptor. However:
1) "Are there any ways to determine how wide you want the band for your background to be?"
I would say that the central limit theorem is a good place to start. Basically, as the size of your background increases, the precision of your estimate of mean background intensity will also increase (asymptotically). So you want your background sample to be as big as possible.
This does have some assumptions:

Little regional fluctuation of mean background signal

(related) Absence of gel artifacts

So, you want your background sample to be as big as it can be without including any artifacts and as long as it is representative of the blot in the general region of your band. In practice, I imagine that taking a selection the size of your protein band is probably fine in most cases, and probably easier to explain. You just have to pick a representative piece of background to measure.
2) how can you know if you have made the rectangular band for the background too wide?
Wider than the blot is too wide. On an infinitely large blot, I think you can't make it too wide. For practical purposes, you want it to be as wide as you can get it and not overlap obvious artifacts or the edge of the blot. But again, it's probably easier to explain just selecting a piece of background as big as the protein band that is roughly near the protein band, to account for local background variation.


It is definitely a Siricidae and looks like a Urocerus gigas (sometimes called Greater horntail), which is also found in the UK.

In the Nordic countries this is one of the more common species of sawflies, and I suspect the same is true for the UK. The picture below and some info on their biology can be found at species.nbnatlas.org:


The evolutionary process in bird wings, especially with regard to winglets

I looked up winglets so I had context for this answer. I'm interpreting winglets as the vertical tips at the end of airplane wings. If so, then you are correct. The spread primary feathers of soaring birds like eagles function as winglets (Tucker 1993). Airbus has a biomimicry web page devoted to some of the biological designs, including winglets, they incorporated into their airplane designs. Some studies suggest airplant winglets do increase efficiency (e.g., Hossain et al. 2011), but there is still some debate.
From the aviation.se answer:

Look at birds: They use two different wingtip designs. I guess we will both agree that those designs are mature after millions of years of evolution. And still there are two distinct wing tip shapes: One is the "fingered" wingtip with large, spread-out feathers, and one is the pointed tip you find from seagulls to albatrosses. Why is there not one, mature design?
This has to do with the environment they are used in. Seabirds fly in an unobstructed environment with steady winds and need to stay aloft for longer duration. All other birds have to cope with trees obstructing a straight flight path and gusts from hills, or those trees. They need to maneuver quickly and cope with gusty winds. This is helped by a reduced span and the possibility to fold the outer wing in or fan it out in an instance. Hence the fingered wingtip.

Although bird wings do tend to match his descriptions, he is not correct that these correspond entirely to ocean-going birds vs all other birds. Many inland birds have pointed wings, including swallows, nightjars, swifts, and falcons.  Some seagoing birds have winglets, such as pelicans and cormorants.  While wing type is shaped by natural selection in a given environment, it also reflects the evolutionary history of the birds.
There is not "one, mature design" because wings many different shapes and sizeshave evolved under varying selective pressures. For example, the long pointed wings of ocean-going albatrosses are excellent for gliding with little energy expenditure but they are lousy for taking flight or for landing. Other wings are shorter and broader, providing greater maneuverability in the woods. In this sense, there is no perfect wing. Each has evolved for different evolutionary reasons.
The main question
From the aviation.SE thread:

the fact that no random mutation has produced a winglet* in birds is in no way a demonstration that airplanes do not benefit from them, there is no logical relationship. [*even though the "fanned" design you refer, such as the eagle's, can be considered a form of optimum winglet] –  Federico

followed by this response:

So you consider evolved wings as not mature. The winglet modification is just waiting to happen? Nature never tried it, in >100 million years of biological flight? Could be, yes. But is extremely unlikely. That settles it for me...

Federico is correct. The basic wing type was set long ago as birds evolved from non-avian dinosaurs. Comparisons of modern bird wings with fossils suggest that the basic structure of bird wings has not changed very much since then. The current structure may be the best that has evolved by natural selection so far but that does not mean the wing cannot be improved further. As you noted, mutations could occur in existing genes that lead to further improvements of the structure and function of the wings. If those mutations never occur, then the improvements won't occur. This is one constraint of the evolutionary process (Hoffman 2014). Natural selection can only work with existing traits, using existing genes and genetic variation.
Another consideration is that wings for powered flight have evolved independently at least four times (birds, bats, insects, pterosaurs). Each time, a different type of wing evolved. Is one better than another? Bat wings have aerodynamic properties very different from birds but function very well for bats (Hedenstrom et al. 2009). Along the lines of your argument above, each wing type perhaps is (or was for pterosaurs) optimum given the environmental circumstances and evolutionary constraints. That doesn't mean they could not be improved.  If a wing evolves again in some organismal group in the distant evolutionary future, odds are very good that the structure will be different from those that have evolved so far. Perhaps that wing will be even more efficient than current wings.
Spandrels

Another user cited the "Spandrels" in comparison to the above debate, could someone explain what could have been the meaning of the comparison?

The use of "spandrels" in evolutionary biology stems back to a well-known paper by Stephen Jay Gould and Richard C. Lewontin called "The spandrels of San Marco and the Panglossian paradigm: a critique of the adaptionist programme", published in 1979 (Gould and Lewontin 1979). A spandrel is the space that forms between two adjacent arches or between an arch and a rectangular shape.  The spandrel emerges as a result of putting two arches next to each other and filling the space. It results from the joining of two arches. It was not specifically designed as part of the arch. Gould and Lewontin claim that evolutionary biologists are too quick to assign adaptive value to every trait on an organism, and argue that not every trait results directly from adaptation. Instead, they say, the trait may be a "spandrel" that emerged as a by-product of other traits. The "spandrel trait" has no adaptive value in and of itself.
The use of spandrels in the comments of the aviation discussion is not clear to me. Clearly, the person intended the evolutionary meaning, mentioning the paper by name. But I cannot tell at all the person's intent.
Edits: Incorporated comments by @Federico and @Andrew - thanks. I corrected horrendous typos and attempted to add clarity.
Citations
Hedenstrom, A. et al. 2009. Bird or bat: comparing airframe design and flight performance. Bioinspiration & Biomimetics 4 015001. doi:10.1088/1748-3182/4/1/015001
Hoffmann, A.A. 2014. Evolutionary limits and constraints. Pp. 247-252. In: The Princeton Guide to Evolution, Princeton University Press, USA.
Hossain et al. 2011. Drag analysis of an aircraft wing model with and without bird feather like winglet. International Journal of Mechanical, Aerospace, Industrial and Mechatronics Engineering 5: 30-35.
Tucker, V.A. 1993. Gliding birds: Reducion of induced drag by wing tip slots between the primary feathers. Journal of Experimental Biology 180: 285-310.


You are correct that hydrophobia is often considered pathognomonic of rabies. However, I offer for your consideration:

Hydrophobia as a rare presentation of Cotard's syndrome: a case report.1

Cotard's syndrome itself is a bizarre psychiatric condition that the authors of the above paper define well:

  Cotard’s syndrome is a rare condition where the central symptom is a nihilistic delusion, which, in its complete form, leads the patient to deny his own existence and that of the external world.

The patient described in this case report harbored delusions that his internal organs were shrinking. He asserted that his abdomen would rupture if he internalized anything. The hydrophobia was secondary to this concern. When given a glass of water he showed a panic reaction and attempted to keep away. Orientation and memory remained intact.

The authors go to length to point out that this was not, in fact, a case of rabies (as thought that were in question at this point!). Also, the patient himself was not aware of symptoms of rabies, ruling out "rabies hysteria" (a hypochondriacal delusion that one has rabies).

Hydrophobia, then, is a rare manifestation of a rare psychiatric disease in addition to the more frequent and well-known association with rabies.

1. Nejad AG. Acta Psychiatr Scand. 2002 Aug;106(2):156-8; discussion 158.


To what extent is it possible to understand if a bacteria can produce a protein? (in silico only!)

Your problem will finally boil down to searching your sequence in the Blast databases. Performing Blast seems to be probably the best way to find out if your bacteria has that specific protein expressed or not. If you could not find it in the nearest species using Blast, then try running PSI-BLAST, which would return you distant homologs, by which you can see if your protein is expressed in the other bacterial species.


How to selectively download 3 fields from every record in UniProtKB?

Use BioMart. It retrieves UniProt information and you can select the features that you want. These files wont be that huge. So  you can download it in your PC and SFTP to wherever you are doing your analysis. A better way is to install BioMart in your workstation. See the BioMart documentation.


How to get Bacteria to attach to an Object?

You're thinking in terms of making them attach to your cloth, but they want to be attached - there are more nutrients and it is safer.  Make sure they have enough light, but not too much, and their nutrients.  They may be attaching and growing, but just not as fast as you expect.
It is also possible that your strain of Cyanobacteria has lost the ability to attach.  If it has been maintained in liquid culture for many generations, any bacteria attached to the wall of the container were selected against.


meaning of the "reads" keyword in terms of RNA-seq or next generation sequencing

In RNA sequencing, the RNA is fragmented, DNA is synthesized complementary to the RNA fragments, which is  followed by a complementary strand synthesis. Fragmentation can be done after the cDNA synthesis too.
This DNA is then amplified to form a cluster that is sequenced. Most Next-Gen sequencing approaches sequence a short segment of the DNA (it has improved with experimental and technical optimization).
A read refers to the sequence of a cluster that is obtained after the end of the sequencing process which is ultimately the sequence of a section of a unique fragment. If an RNA is expressed in high copies then there will be more reads coming from it; reads can be redundant as well.

Courtesy


For a full understanding I refer you to the KEGG pathway map which is fairly comprehensive in showing all the metabolic processes that CAN produce Adenosine.
It's a bit daunting but if you find it on the map here it is interactive and you can see the enzymes and pathways involved. If you drill down it brings you to a host of papers and references in primary literature to back things up.

However the dominant process is as follows:

   2 ADP <=> ATP + AMP

enacted by an adenylate kinase then:

   AMP + H2O <=> Adenosine + phosphate

enacted by adenosine 5'-monophosphate phosphohydrolase (a 5'-Nucleotidases )


What is the advantage of circular DNA in bacteria?

Vibrio cholerae is known to have two circular chromosomes.

Bacteria cell division is a lot simpler and efficient as compared to eukaryotic cell division, partly due in part to the nature of their chromosomes. They don't have to undergo mitosis -- condensation of chromosomes, segregation, spindle fibre formation, attachment et al aren't involved in bacterial cell division.

Circular DNA also circumvents the Hayflick limit (thus allowing it to be "immortal"), which is the number of times a cell population can divide before it stops, presumably due to the shortening of telomeres, the sequences at the end of the chromosomes. Since circular DNA lacks telomeres, it does not get shorter with each replication cycle.

Circular DNA can also facilitate horizontal gene transfer such as Hfr mediated conjugation. Remember, conjugation is analogous to a "rolling-circle" type replication which is of course, only possible on circular pieces of DNA.


Will wiping a phone down with isopropyl alcohol daily breed bacteria resistant to disinfectants?

It is possible to select bacteria in vitro, with some help, to withstand 50 g/L (5% v/v) of isopropanol.   According to this paper, bacteria at hospitals in Peru have a variable but increased resistance to isopropanol.  (That study was preliminary, however)  Since bacteria can produce isopropanol themselves, some degree of resistance is very plausible.  Even so, the fundamental nature of 70% isopropanol's attack on the membrane makes it hard to defeat.  Anything is possible in biology, but the more proper the application of disinfectant in terms of exposure time and concentration, the less plausible the selection of resistant species or strains from the bacterial community will become.


Getting PCR amplification at annealing higher than Tm!

It is very common to get annealing at higher than predicted Tm.  If it's a problem in your case, especially if you're getting mis-annealing at lower temperatures, consider using touchdown PCR to find an optimal temperature.  Or, pragmatically, if you have any flexibility in primer design, simply order a set of primers and try them all.  Primers are cheap today, and you'll often find a set that work even where the design programs claim they won't.


What are the roles of cadherins in epithelial mesenchymal transitions?

So let's just quickly define what cadherins are, using general information from wikipedia,

Source: Wikipedia
Cells express E-cadherin (epithelial), N-cadherin (neuronal, or P-cadherin (placental). These generally interact with ß-catenins to modulate cell adhesion. There are pathways intrinsic to cancer which downregulate the expression of cadherins,

Source: Epithelial–mesenchymal transition in development and cancer: role of phosphatidylinositol 3' kinase/AKT pathways
We see in the above pathway described in a study of PI3K/Akt signaling in cancer, some of the ways E-cadherin (encoded by CDH1) becomes downregulated. We also see that ß-catenin may be sequestered by E-cadherin at the plasma membrane, and cytosolic ß-catenin actually interacts within the nucleus as a transcription factor for SLUG (or snail2) where Snail2 is an essential mediator of Twist1-induced epithelial mesenchymal transition and metastasis. In the above figure this modulates reduced cell-cell adhesion, but we also see there's a number of other pathways which modulate the entirety of the EMT process.
What I found interesting, maybe unrelated
An interesting concept currently being investigated involves many of the shown membrane receptors, most of which are involved in some sort of crosstalk in aggressive cancer types. ROR1 was identified as a critical component for modulating EMT, and was shown to participate in Wnt signaling through it's frizzled domain, as well as crosstalk with Met tyrosine kinase, EGFR, and TGFß in some way. These interactions were able to increase expression of snail1/2, vimentin, etc. i.e. characteristics of EMT in breast adenocarcinoma (The linked article provides most of this background, but some may be missing, I'm unsure), and decrease expression of epithelial biomarkers like E-cadherin. When they used a ROR1 Ab to target ROR1, they found cadherin levels could be rescued, and morphological components returned to a more epithelial phenotype. Other articles showed this targeting could induce apoptosis in CLL and this occurs through interaction with PI3K/Akt.


Why haven't environmentally-reactive bodies developed as an evolutionary advantage?

As Jamesqf pointed out, food supply was likely a big contributor. As a general expansion onto that, I believe a sufficiently reasonable answer could be that animals likely found solutions (I.e. migration and hibernation) to deal could with seasonal factors out of their control (like lack of resources) before natural selection leading to more defined adaption could/would've taken place. Their behavior dealt with the problem- which leads to another interesting idea that it could have been an early sign of organisms using their intelligence to survive and change the course of natural selection.


Rhesus antigen (Rh-D) is inherited in an autosomal dominant pattern.  Therefore you are correct in your reasoning.

Simple problems like this are often best worked out using Punnet Squares, shown below for the scenarios you have considered.

Because the inheritance pattern is dominant, if either parent was homozygous (DD) for Rh-D then 100% of their offspring will be Rh+ve.

In order to have a rhesus negative child, neither parent must be homozygous for the D allele.  You are correct that one possible scenario is a matching pair of heterozygotes:

In this situation 3/4 of the children are rhesus positive and 1/4 rhesus negative.

There is an alternative where one parent is Rhesus negative and the other positive.  In this case there is one heterozygous parent and one homozygous negative parent:

In this scenario, half of the children are rhesus positive and half rhesus negative.


What is the mechanisms responsible for downregulation or loss of MHC-1 expression on the surface of cancer cells？

There is no single mechanism (as you'd expect, since there is no evolutionary relationship between different individuals' cancers).  The most common mechanisms are various forms of mutations, ranging from point mutations in single MHC molecules to large deletions of the MHC locus. Mutations in genes involved in antigen processing, that are not themselves part of the the MHC locus (e.g. TAP, b2-microglobulin), are also fairly common.  Epigenetic changes are also not uncommon.  There are several reasonably recent reviews, including

MHC Class I Antigen Processing and Presenting Machinery: Organization, Function, and Defects in Tumor Cells
Different regulation of MHC Class I antigen processing components in human tumors
The escape of cancer from T lymphocytes: immunoselection of MHC class I loss variants harboring structural-irreversible “hard” lesions


You don't get energy from breaking chemical bonds, you only get energy from making chemical bonds, while breaking chemical bonds requires the input of energy.  However, in practice chemical bonds are always broken as others are formed, and the net number of bonds is generally constant.  Otherwise you would end up with free radicals, which are highly reactive and looking to form a chemical bond with the next thing it touches.

For example, the burning of glucose in respiration involves the breaking of C-C, C-H, C-O and O-H bonds in glucose and O=O bonds in oxygen, with the simultaneous formation of C=O bonds in CO2 and O-H bonds in water.  But the C=O bonds in CO2 and O-H bonds in water contain much less energy than the bonds we break within in glucose.  So the key is that the bonds formed contain less energy than the bonds broken, and energy is released overall.

And actually it's a bit more complicated than that, because you also have to consider entropy, which is how disordered the system is.  Generally the more molecules in a system, the more entropy, so breaking a few big molecules down into lots of small molecules tends to release energy by increasing entropy.

So to answer your question, "food" is what we can draw useful energy from in the process of turning it into something else as we make and break chemical bonds.  We can't do this with water, or indeed with rocks, because their chemical bonds would require more energy to break than the energy we'd get back out by forming alternative bonds with anything else.


What are some examples of scaling laws in biology?

Here are some off the top of my head.

The height an animal can jump depends on the muscle cross-sectional area ($l^2$) and its mass ($l^3$). Mass grows faster with body size ($l$) so small animals can therefore jump higher relative to their body size ($l$) than large  animals. Very similar scaling exists for strength of limbs vs. mass, ability to fly vs. mass, etc.
In pinhole eyes (as found in clams and nautilus) sensitivity to light depends on the size of the pupil ($l^2$), the bigger the hole the more light gets in. However the ability to focus depends on the reciprocal of the size of the hole (but I don't know the scaling, so $l^{-n}$). Therefore there is a trade off between sensitivity and  ability to focus.
There are some recent models about foraging behaviour in a 2D terrestrial environment (with the front of the animal being a length  $l$) vs. foraging in a 3D marine environment (with the front of the animal being a surface $l^2$). The model predicts different behaviours for the size of prey animals should aim for.
The rate at which sound attenuates scales with the frequency of the sound as $1/f^2$. The frequency of a resonator scales with the reciprocal of volume $1/l^3$. So small animals make high pitched sounds which attenuate quickly and don't travel very far.
Finally, the properties of fluids change with size. The Reynolds number describes viscosity and is dependent on linear scale $l$. Therefore small animals experience fluids as viscous and can "crawl" through water whereas large animals have to "swim" through water.

However, any directly physical or chemical-physical property of biology will experience scaling laws.


Can anyone help identify which insect is this?

I think this is some species of mayfly (order Ephemeroptera). There are some 3000 species in the world so I can't be more precise than that. It looks very pale and it's got a bit of a strange posture, so I'm guessing it just emerged from it's larval skin (in that case the skin should be left behind close by).


Coalescent Theory - Probability for $k$ alleles that of one coalescence event occured $t+1$ generations ago

Is this the exact text from the book? The left side seems to represent the probability for

  "No coalescence in $k$ lines in $t$ generations (i.e. the $Pr(k)^t$ term), and at least one coalescence among those lines in generation $t+1$ (the $1-Pr(k)$ term)"

which is the same event as

  "First coalescence event in $k$ lines is exactly in generation $t+1$".

The right hand side is derived analogous to the second equation, with $1-\frac{1}{2N}$ ("no coalescence in two lines") replaced by $1-\frac{k\choose2}{2N}$ (approximation for "no coalescence in $k$ lines):

$$
\begin{align}
Pr(k)^t \left[ 1-Pr(k) \right] &≈ \left( 1-\frac{k\choose2}{2N} \right)^t \left [1 - 1 +  \frac{k\choose2}{2N} \right] \\
&\approx \exp\left( - \frac{k\choose2}{2N} t \right) \frac{k\choose2}{2N}
\end{align}
$$

were is first approximation is due to your first calculation. The second one seems to use a first order Tailor approximation of $\exp(x)$:

$$
\exp(-xt) = exp(-x)^t \approx (1-x)^t
$$


How do we know that mild forms of rabies are nonexistent?

There are many people worldwide who are exposed to rabies and don't die (they get treatment), but there are very few of these cases where people don't die after rabies has entered the central nervous system, and even fewer who didn't receive post exposure prophylaxis before the virus reached the central nervous system. Rabies isn't as rare as many would like to believe, unfortunately, with approximately 15 million exposures and 59,000 deaths a year, so data is available.

"Once symptoms have presented" in the Wikipedia article should probably be edited to "once central nervous system symptoms have presented". As discussed in this review rabies entry to the central nervous system is typically the "point of no return". One of the main challenges of rabies is that the virus hides from the immune system inside cells, making its way from muscle to peripheral nerves to the central nervous system before the immune system can mount a response. Once in the central nervous system, it has special protection from immune surveillance. The goal of post exposure prophylaxis is to allow the body to generate an immune response clear the virus before it gets to the central nervous system.

Generally, we say that central nervous system rabies is almost uniformly fatal without treatment because that is what has been observed and reported. *I'm not aware of any published epidemiologic survey looking for anti rabies antibody in healthy non-immunized adults. I know it's not very satisfying, but I would strongly suspect that someone has done a seroepidemiologic study and not published these results, since they're exactly what physicians have been taught since before Hippocrates: a dog bite followed by the characteristic illness leads (almost inevitably) to death. Other illnesses, on the other hand are observed to produce an antibody response in individuals' with mild disease. It is possible that there are unknown cases of mild non-encephalitic rabies that are self limited, but given the 150 years of intense study, I don't think it is likely there is a major aspect of the disease's natural history that hasn't been observed and reported.

Re: your idea about dilution of the vaccine suggesting you could dilute the virus, I think you may have a misconception about what that method actually involves. A killed virus vaccine cannot replicate, and so cannot cause rabies (though some forms of rabies vaccines used in the developing world have fairly high rates of nasty side effects).

Pasteur's risky rabies vaccine trial in 1885 may have involved a live vaccine, but he was notorious for incomplete documentation on his methods. It was essentially, a specimen of air dried rabbit spinal cord that didn't cause rabies in dogs. Here, his method was reported as drying spinal cord segments for longer and longer periods of time until the specimen did not produce rabies in dogs. This isn't a method that "dilutes the virus", but rather a method that attenuates the virus, making it less virulent. Pasteur didn't have methods for detecting what exactly that meant, other than that it didn't cause rabies, but did prevent the animal (or human child) from developing rabies after exposure to a virulent sample.

You can read more about rabies in Murray Medical Microbiology, Ch. 60

*Please see the link in @iayork's comment for a very interesting example of rabies serology in members of two communities in the Peruvian Amazon.


Does common X-like picture represent one doubled chromosome or two homologous chromosomes?

The "X" you see is a chromosome. The two strands that forms the X-shaped chromosome are called chromatids. As they are bound together (by the centromer), they are called sister chromatids. Note that chromosomes look like that only during the metaphase. Note also, that not all chromosomes have a centromer that is in the middle of the chromosome as it is obvious from the picture in your question.
Many species (including humans) have two sets of each chromosome. If you add the other chromosome in the picture, you would see a pair of chromosome. One chromosome of the pair is said to be homologous to the other one. Below is a cladogram during the metaphase of a human (I let you figure out the sex) showing each pair of chromosome.

Sister chromatids are identical (except for mutation during the last chromosomal replication). Homologous chromosomes are similar but not identical. Crossover occurs in between chromatids of homologous chromosomes.
Further comment on your figure
There are 23 pairs of chromosomes, that is 46 chromosomes. Your picture shows only one chromosome per pair, that is your picture shows only 23 chromosomes. In other words, your picture shows the haploid genome and not the diploid genome.