Is it possible for parsimony to estimate more state changes than stochastic character mapping

If the number of taxa is large enough, an exhaustive search is not possible, and parsimony methods use heuristics to explore the tree space. It is therefore not guaranteed that the most parsimonious tree will be encountered.

This might explain your observation if your tree has a high number of taxa (> 20).

According to wikipedia:

  However, although it is easy to score a phylogenetic tree (by counting the number of character-state changes), there is no algorithm to quickly generate the most-parsimonious tree. Instead, the most-parsimonious tree must be found in "tree space" (i.e., amongst all possible trees). For a small number of taxa (i.e., fewer than nine) it is possible to do an exhaustive search, in which every possible tree is scored, and the best one is selected. For nine to twenty taxa, it will generally be preferable to use branch-and-bound, which is also guaranteed to return the best tree. For greater numbers of taxa, a heuristic search must be performed.

How many taxa do you have?


If a fully functional lab grown pancreas can exist, can it be used as a cure for type 2 diabetes?

Since the consensus is that the underlying initial problem in t2dm is the development of insulin insensitivity in the presence of a normally functioning pancreas, then replacing that pancreas at a more advanced stage of the disease will not cause normalisation of glucose levels.

http://journal.diabetes.org/clinicaldiabetes/v18n22000/pg80.htm


How does one determine the sex ratio of a ZZ and ZW cross?

Let $Z$ be the chromosome carrying the non-lethal dominant allele, and $Z_l$ the chromosome carrying the lethal recessive allele.
The Punnett square goes:

$Z_lW$ is not viable, so there are two possible male genotypes ($ZZ$ and $ZZ_l$) and only one possible female ($ZW$). So the correct answer is A. indeed.


What’s this bug? Sign of an infestation? Found crawling up the side of my washing machine. [WA]

Don't worry, it is definitely not a roach. It is a true bug, Hemiptera. Not a household pest.


To a good first approximation $\overline{\Delta f} = 0$. Where $\overline{\Delta f}$ is the mean change in fitness down to any point or indel mutation. The reasons for this are as follows:

In the genome of higher organisms, most of the genome is non-functional ("junk") so most mutations will not have any effect regardless of the change made.
A substantial proportion of in-frame point mutations will be synonymous mutations that result in the same amino acid being coded for (actually this can have an effect on protein expression but I don't believe anyone has - yet - shown a fitness difference?)
Even where a mutation does alter an amino acid many amino acid changes have no measurable effect on the protein produced. Especially where the new amino acid has similar properties to the one it has replaced.
Even when a mutation does alter the protein function, or render the product non-functional, in many cases this will not impact fitness since fitness is conditional on the environment in which it is measured and not all genes impact all environments.

So the distribution, whatever it is, will have a large spike at 0. Probably this spike is several orders of magnitude higher than the next highest value. Further, we can be reasonably certain that $\overline{\Delta f} < 0$ since there are more possible ways to break a Gene through a point or indel mutation than there are to improve it. If this is the case, so that there is a large excess of mutations with a negative effect on fitness, we can conclude that the distribution of mutational changes in fitness will be non-normal (negative skew and spike at zero), and that the normal distribution will be a poor approximation.


What happens when seeds are refrigerated before planting?

That might be a good experiment.

I know that before planting bulbs you want to put them in the refrigerator or even the freezer sometimes.

In fact this process of cold treating seeds has a name: Stratification.

To paraphrase: some seeds become inactivated at higher temperatures like lettuce and delphinium.  You can place the seeds in medium and put them in the fridge or freezer for a day or two.

You can see how this makes sense.  The seeds have adapted to start growing when they are freezing because the timing results in the plants breaking ground as early as possible when the temperature is warm enough in the spring.

A quick search doesn't seem to imply that silverbeet needs to be stratified before planting.  The result might be negative, but there is definitely some good expectation that it makes a difference to some plants.


Can neurons divide if somehow centrioles are introduced in nerve cells?

Induced Pluripotent Cells
https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell?wprov=sfla1

You should probably look into this. This introduces what is called iPSCs, which are stem cells derived from adult cells.

What it is is that  they use signals that are found in embryonic cells, and the adult cells revert from their differentiated form into cells that can become virtually anything.


Do mosquitoes need to pump blood out of the host?

Take a look at Ramasubramanian et al.[1] The authors have some great SEM images of the proboscis and fascicle tip and derive a mathematical model for the "bite" itself.

They mention that there are two types of feeding: pool feeding, where the mosquito creates a hemmorrhage and feeds slowly via capillary action, and capillary feeding, wherein the mosquito taps into a capillary and the feeding process is much faster, as the blood is driven under pressure.

Another source to check, one that the authors above cite, is by Kashin[2]. This only links to the abstract, however.  You'd have to hit the stacks to get the article, I'd imagine.

Edit

This source[3] indicates that:

  "The blood is imbibed by action of the cibarial and pharyngeal pump muscles via the food canal formed by the labrum and hypopharynx. Blood then passes into the midgut."

For @Luke, and others:

All images are from Ramasubramanian et al.[1]

Ramasubramanian MK, Barham OM, Swaminathan V. 2008. Mechanics of a mosquito bite with applications to microneedle design. Bioinspiration & Biomimetics, 3: 046001, doi:10.1088/1748-3182/3/4/046001.
Kashin P. 1966. Electronic recording of the mosquito bite. Journal of Insect Physiology, 12(3): 281-286, doi:10.1016/0022-1910(66)90143-0.
Robert V, Brey PT. 1998. Biting physiology of Anopholes affecting Plasmodium transmission. Research and Reviews in Parasitology, 58 (3-4): 203-208.


The carapace shows the distinctive lines of Chiromantes dehaani (Kurobenkei-gani in Japanese). This species can be found quite far away from the ocean, commonly in brackish streams and rivers. The size fits your description, the width of the carapace is approximately 3-4 cm, giving the entire body roughly the same size as you observed. These crabs are also most active at night.

I have seen these crabs in sheltered areas slightly inland from the sea. Here is a photo of C. dehaani that I took in Tokyo:

While there is a slight possibility that this is Chiromantes haematocheir (Akategani in Japanese), your photo does not show the distinctive red claws and this species is less common in Tokyo Bay due to development and loss of its natural environment of mudflats. Therefore, I think it is save to identify this as C. dehanni.


The correct name of the coating is "pollenkitt", not "pollen kit" (I edited your question accordingly).

From the book "Biology of pollen" (Shukla, Vijayaraghavan and Chaudhry, 1998):

  The term pollenkitt is used for the oily, pigmented and sticky coating deposited on the pollen grain surface during the final stages of maturation. (emphasis mine)

That may explain why you and others struggled to find an answer in Google/Google Scholar.

Back to your question: there are two types of adhesive coats in pollen grains:

Pollenkitt
Tryphine

Pollenkit is the most common one and, as tryphine, it is secreted by the tapetum.

According to Pacini and Hesse (2005):

  Two types of sticky pollen coat material exist in angiosperms, both produced by the anther tapetum. Pollenkitt is the most common adhesive material present around pollen grains of almost all angiosperms pollinated by animals, whereas tryphine seems to be restricted only to Brassicaceae. (emphasis mine)

Sources:

Pacini, E. and Hesse, M. (2005). Pollenkitt – its composition, forms and functions. Flora - Morphology, Distribution, Functional Ecology of Plants, 200(5), pp.399-415.
Shukla, A., Vijayaraghavan, M. and Chaudhry, B. (1998). Biology of pollen. New Dehli: APH Publ. Corp.


Why do polyneuropathies affect the extremities first?

Polyneuropathy is actually not a very specific term, so the reasons will no doubt vary depending on which specific class you are talking about.

That said, here are two reasons that longer neurons are preferentially affected:

Some polyneuropathies involve conduction problems that include "failures" where action potentials aren't propagated down the full length. It doesn't matter where along an axon the failure occurs, and longer axons therefore have more "chances" to fail.
Axons are somewhat isolated from the soma where most proteins are created, and it is common in certain neuropathies for degradation to begin furthest from the soma, presumably because the neuron has less capability to deal with problems or repair damage in those areas far from the soma. Neurons with longer axons by definition will have some part of their axons that are further from the soma than neurons with shorter axons. This is the answer that is most relevant to your question, see for example this source that reviews the causes of diabetic neuropathy.

References:

Yagihashi, S., Mizukami, H., & Sugimoto, K. (2011). Mechanism of diabetic neuropathy: where are we now and where to go?. Journal of diabetes investigation, 2(1), 18-32.


Phylogeny and evolution of ferns (monilophytes) with a focus on the early leptosporangiate divergences:

  The monilophytes (= Infradivision Moniliformopses, sensu Kenrick and Crane, 1997⇓) share a distinctive vasculature, having protoxylem confined to lobes of the xylem strand (Stein, 1993⇓), therefore the Latin moniliformis appellation for “necklace-like.”


What are these stars in my microscopic image?

Despite low resolution, I'd say those are trichomes. Jasminum is genera that produce essential oils, so it have glandular hairs and other trichomes wich help to rettain the oil layer.

Source: http://cms.herbalgram.org/herbalgram/issue53/article2207.html?ts=1376643526&signature=b4349f7f3ca6f6a47823f4754237eaac

The image displayed above shows glandular and non-glandular trichomes in lavander shown by scanning electron microscopy. I'm afraid I couldn't find anything about Jasminum in particular, but I think it must be the same kind of structure.


How is it possible for a new species to evolve?

Suppose a new species is created from a random mutation that happened
  during an instance of reproduction in an existing species.

No honest informed person would define species in this manner.

This is a better analogy


Does catching a cold give you an "effective" advantage against future colds?

Short answer: no.

The "cold" is a common term for symptoms caused by dozens of different viruses. Even the canonical "cold" virus (rhinovirus) has large numbers of strains.

Exception to the short answer: Getting a cold might be effective against similar strains of the same virus.

Most of the time, future colds will be due to a different strain or a different virus. Best protection is to block unused/vulnerable receptors in the nose.


What kind of fish is this? I don't remember the full name but it started with Tiger

It's probably a juvenile tiger loach, or tiger botia.

Adult Tiger Loach

Younger individual of another species

These fish are from the genus Syncrossus and the family Botiidae which include many common aquarium fishes. This genus comes from India, Myanmar, and Southern Asia.

These fish can grow up to 20-25cm (~10in).

Syncrossus species can be told appart using appropriate litterature. This specie sheet from seriously-fish is well documented and provide interesting links from further reading and a quick explanation of its taxonomy easily accessible for the average guy,


Cytoplasmic determinants - protostomes and deuterostomes

The two distinct types you have mentioned in your question (determinate/indeterminate cleavage) are actually called autonomous specification and conditional specification, respectively.

In the case of the former one, if we were to remove a blastomere, it would still produce the previously determined type of cells, while in the case of conditional specification the cells, which are going to be produced, depend entirely on the neighbouring ones. The latter's ability to alter their fate is called regulation.

As for answering your questions, cytoplasmic determinants are spread unevenly in deuterostomes as well, as otherwise no axis could be developed.

You might be interested about this answer as well.

I've used the following book as source: Gilbert, S. (2000). Developmental Biology [ online version ]


Acrosomal enzymes and the female reproductive tract

The acrosome reaction does not take place till the sperm reaches the zone pellucida of the ovum, which causes the acrosome to rupture. Thus the female reproductive tract does not get exposed to the enzymes.

Links:
https://en.wikipedia.org/wiki/Acrosome_reaction


Check this online book on NCBI: An Introduction to Genetic Analysis. 7th edition

  Let’s examine each of these components and see how they fit together to produce our current picture of DNA synthesis in E. coli, the best-studied cellular replication system

I used it a bunch while studying E. coli for my master degree, lots of really usefull information.


According to the (non peer reviewed) scientific experiment found here, simply placing a piece of kiwi onto gelatin that has set will cause the gelatin to be hydrolysed by actinidain.

  This experiment aims to show the effects of Proteolytic enzymes on proteins and, subsequently, the effects of extreme temperatures on the proteins themselves. Petri dishes filled with gelatin, a derivative of collagen, were acted upon by kiwifruit samples overnight. Some samples were fresh and used as controls; others had been frozen or boiled for two, four, six, eight or ten minutes. The mass of digested gelatin was taken the next day. The results ultimately reflect the effectiveness of the actinidin, the kiwi’s Proteolytic enzyme, under normal conditions and after exposure to extreme temperatures.


Why does a distraction cause a longer reaction time?

I am not sure which sort of answer is expected. The minimal answer to that would be that the more distracted you are the longer it needs to sample the stimulus space of interest as you are sampling another distracting stimulus simultaneously with your limited sensory capabilities.

Cognitive tasks get just more complex with distraction as the brain cannot know which features (of the full stimulus space from all the sensory modalities) to take into account and therefore needs to sample more data to find out which of the inputs matter for the specific task.  In most of natural situations the inputs match together in terms of experienced stimulus combinations (visual field and sound while walking for example) except for surprising situations that require to alter ones attention (a sound that does not match to the visual scenery is unexpected and might be important to check for danger). To decide whether the system can ignore such parts of the input requires computation and computation takes time. I don't think it is useful to tackle the question in terms of delayed signaling along specific neurons or pathways. The signaling itself is more or less of constant speed and not directly altered by distraction. Of course on a very basic level an increased adrenaline level or similar due to distraction might affect the "weights" of certain basic pathways as one is pushed into another state. In such cases therefore it requires the system to compensate those changes with respect to the actual task of interest as it might be biased to different reaction scheme that is not useful for the specific task.

Actually our brains are very good in focusing on specific parts of the inputs that are important for a task (i.e. cocktail party problem) but still it needs more time to correct the erroneous parts in the presence of distraction. In terms of a simple Hopfield network that does pattern completion distraction would be like an increase of the noise level which leads to a higher number of iterations required for convergence while the speed of signal transmission from neuron to neuron was not altered.


How to wash the column during protein purification with GST tag?

The standard when purifying GST with Glutathione agarose beads is to use STE buffer (10 mM Tris-HCl (pH 7-7.5), 150 mM NaCl and 1 mM EDTA) for washes and we have had no problem with this in our lab!


Fetal development, gastrulation and embryonic disc

Human embryogenesis is much more complicated than the more general and simplified picture given in your 1st figure.
For details, please study http://en.wikipedia.org/wiki/Human_embryogenesis

To point out the most distinctive features which might have led to your confusion:

Before gastrulation, the blastocyst cavity is formed.
Only the inner cell mass undergoes gastrulation.
Mesoderm forms quiet late and spreads, thereby also forming the chorion as well as the amnion.
The embryo itself is formed from a subset of all embryogenetic cells. This is shown in your 2nd figure, part C and D. Yet, tissues are still going to spread such that the final ectoderm as well as mouth and anus will be formed.


Tabanus nigrovittatus as my initial guess. "Greenhead horse fly."

Source

This is probably the biggest give-away for the genus Tabanus (namely the features of the veins at the wing tip, denoted R4 and R5, versus other Diptera orders), still searching out a good identification key to solidify the ID. Furthermore, also known as the salt marsh greenhead, a swamp is a good candidate to find these (1).

So what's particular is entomologists have gone through and collected many specimens, and data about their wing venation, and based on the Comstock-Needham system, you can pin presence/absence of major veins, and branching of said veins to specific types on insects. In this case, R refers to the Radius or 3rd longitudinal vein, and the number refers part of the branching that reaches the margin of the wing. Pg 156 here helps us ID Tabanus vs other orders.

Problematic with identifying these spp. is you need to get a good look at the sternites on the under side as well, if you look at how they ID Tabanus sudeticus here, but the photos tend to match nicely with those of T. nigrovittatus you can widely find.


How would you model the evolution of two genotypes across generations?

So, what’s a way of modeling how resultant mutations might occur, such that B has a chance of producing some offspring that are fitter than A’s offspring?

Here's one possible solution that fits your criteria. You could have something like this (with "d" being the distance between "x" and "y", i.e. d=x-y and "n" being the n-th offspring, so it varies between 1 and x for A and 1 and y for B) :

A: n -> x + r(n), where r(n) is a random number between x-d and x+d
B: n -> y + r(n), where r(n) is a random number between y-d and y+d

(I write r(n) not because r is a function n, but because a different number is drawn for each n. I also didn't specify r's distribution, that would also need to be decided when making an actual model)

This is your situation where some offspring of B have a chance of being fitter than offspring of A, and the least-fit offspring of B can even be fitter than the fittest offspring of A. I think it fits your criteria and thus answers your question. The sum of the grandoffspring is basically the basic x or y squared (that you would get if each offspring had the same fitness as their parent) + the sum of all the "r"s.


Why is it so hard to find the amount of biotin in food?

Apparently, it's really hard to measure biotin levels in food accurately.

From "Determination of the biotin content of select foods using accurate
and sensitive HPLC/avidin binding" (2004, emphasis added):

  Total biotin content of 87 foods was determined using acid
  hydrolysis and the HPLC/avidin-binding assay. These values are consistent with published values
  in that meat, fish, poultry, egg, dairy, and some vegetables are relatively rich sources of biotin.
  However, these biotin values disagreed substantially with published values for many foods. Assay
  values varied between 247 times greater than published values for a given food to as much as 36%
  less than the published biotin value. Among 51 foods assayed for which published values were
  available, only seven agreed within analytical variability (720%). We conclude that published values
  for biotin content of foods are likely to be inaccurate.


Recombination frequency, linked genes, and independent assortment

The comments pretty much answer the main concern here. But just to sum up:-

  "....T and X assort independently, so they should be on different
  chromosome...."

Not necessarily. They can be on the same chromosome at such a distance that there is usually atleast one chiasma formation between them, and will undergo independent assortment, i.e.  segregation of one gene among the gametes will be independent of the other. They will pretty much act and segregate like mendelian factors. Specifically, if the recombination frequency is 0.5 (50cM or map units' distance on the chromosome), they will assort independently.

  "....And then due to recombination, X gene crosses over so that it's also
  on the same chromosome as T and R...."

This part is a little bit unclear. I assume (correct me if I am wrong) is that you are assuming X,T,R to be alleles, which can be present on only one chromatid and hence recombination might change their distribution and positions relative to one another. But as the question states, they are genes (or specifically gene loci) which are present on both chromatids and their relative position is fixed. The recombination frequencies refer to the recombination of different alleles at this locus.


What is this plant with white-spotted thorny leaves from Morocco?

The distinctive leaves identify the plant as Silybum marianum. It is a member of the plant family Asteraceae. It is commonly called "milk thistle". Originating in the Mediterranean region, it has now spread to many places around the world.  The plant in your photo is immature at ground level. These links will give a better idea of the mature plant.

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

https://www.google.com/search?q=silybum+marianum&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiG46Kj6L7aAhWvpFkKHfYjA0AQ_AUICigB&biw=1097&bih=642


Microtubules polymerise from and depolymerise into alpha-beta-tubulin dimers.

Both happen on both ends, see this question: At which end does polymerization of microtubules occur?.


What is the purpose of measuring both VS (volatile solid) and TS (total solid)?

Total solids (TS): The part of the sludge that remain after drying at 105$^{\circ}$C for 20 hours:

$$ TS(\%) = \frac{\textrm{weight dried at } 105^{\circ}C}{\textrm{wet weight} }\times 100 $$

Volatile solids (VS): The part of the sludge that is combusted at 550$^{\circ}$C after 2 hours:

$$ VS(\% \textrm{ of TS}) = \frac{\textrm{dried weight at }105^{\circ}C -
 \textrm{dried weight at }550^{\circ}C}{\textrm{dried weight at }105^{\circ}C}\times100$$


Identifying an insect looking like a crumle

Looks like the nymph of a masked hunter.
They carmouflage in dust and sand.


This plant is a bellflower. Either a Campanula Takesimana or a Campanula Alliariifolia


Q1: Partially. T cells are important for the immune response through pathways other than cytokine release. Being activated by contact with another immune cell presenting their corresponding antigen, T cells proliferate and themselves activate their compatible B cell counterpart. These then produce antibodies specific to that antigen, the basis of the adaptive immune response (see figure below, from Wikipedia). The important part here is that this mechanism requires cell-to-cell contact, not simply cytokines. Without it, any pathogen for which memory B cells do not exist yet will not produce an adaptive immune response - and will persist if the infection is not cleared by the innate immune response.

Q2: I expect because merely injecting T cell cytokines would not be sufficient in order to replace the essential function of T cells. Aside from that, WYSIWYG's point about the general response is probably also true: the side effects would be horrendous.


What does a typical, perfectly healthy vaccinium corymbosum (highbush blueberry) leaf look like?

Vaccinium species are ericaceous plants (acid soil loving) so they will not do well in alkaline soils, and/or being watered with hard water. In fact they have a narrow optimum pH range 4.8 - 5.2 (Source http://www.westernfarmpress.com/management/blueberry-iron-chlorosis-has-multiple-causes)

The pH of the soil will effect the plants ability to access the minerals in needs from the soil, and mineral deficiencies will indeed show themselves in the leaves first.

Here is a photo of a healthy Highbush Blueberry leaves


What can myelination tell you about the evolution of sensory receptors?

Interesting question. I will dissect your question into its assumptions before giving my view on the overall question.

1) ..that nerves became larger.. : Why should there be a general tendency for nerves to increase in size during the course of evolution when there is no need to?

2) ...that nerves became more myelinated...: A general tendency towards more myelination is not the case. Myelination is definitely a trait that has been acquired later in evolution, but "the more the better" does not apply. Imagine an electrical conductor - to insulate it a bit of plastic is enough. Adding more after that doesn't make a substantial difference.

3) ...the order in which these receptors evolved...: myleine sheaths are made up of glial cells that wrap themselves around axons of neurons. Myeline makes neural transduction more efficient and faster. Hence, the amount of myelination tells you something about the efficiency and speed of transduction of the nerve (Hartline (2007)). For example, longer axons tend to be myelinated, short ones not. That, in turn, will have certain evolutionary benefits for the host, as more efficient communications means less energy required, lesser loss of information, and increased processing speeds. The amount of myelin hence tells you something about the importance of efficient communication of that sensory system. However, it does not tell you anything about when this receptor evolved.

Hence, the relation between myelination and receptor evolution is remote at best. In terms of evolution, amounts of myelination may tell you something about the evolutionary pressure placed on faster and more efficient workings of the receptor systems.


Short answer
Myopes may have some benefit in terms of identifying small objects due to their ability to focus objects nearer to their retina than emmetropes, but only marginally so.

Background
The more myopic you are, the more blurred your distance vision, but the closer up you can see clearly. Hence, myopes have a range of clear vision that is closer to their eyes than emmetropes (normally sighted people) (Triad Publishing).

A young emmetropic adult can focus at an object some 10 cm away, which is defined as an amplitude of accommodation (lens adjustment) of 10 diopters.

A severely myopic eye can be up to minus 6 diopters, bringing the tally from 10 to 16 diopters, meaning you can view something up to 6 cm instead of 10 cm.

Bringing objects closer increases retinal image size and hence increases spatial detail. Going from 10 to 6 cm increases the retinal angle by 10/6 = ~1.7 x, so not even a doubling of the angle.

A random search for a magnifying glass for the visually impaired that aids in reading small print (newspapers etc.) yielded one that magnified 4x (16 diopters):

Clip on reading aid. Source: Eschenbach

Microscopes typically have lenses with magnification factors from 4x to 100x.

So in all, myopes do not have microscopic superpowers. A standard magnifying glass for the visually impaired magnifies several times more than a severely myopic eye.


How fast does activity affect synaptogenesis?

Synaptogenesis at such a fine temporal resolution is currently still best studied in animal models and reduced preparations where the activity levels can be more precisely controlled and advanced imaging methods can be used to monitor morphological changes. A series of studies with relatively high temporal and spatial resolution have been carried out in vitro and in vivo with two-photon microscopy on dendritic spines, which are considered as a proxy for the existence of synapses, since ~98% of them contain one.

The fastest effect after stimulation is the enlargement of pre-existing  or newly-formed spines and their synapses, as fast as ~2 min (Matsuzaki et al. 2004, Harvey et al. 2007, Hill and Zito 2013). Next, immature structures (often called filopodia) are starting to form within the first ~15 min (Maletic-Savatic et al. 1999). It is not yet clear what percentage of those structures bear an actual synapse, however they certainly have the potential to obtain one. A more gradual increase in the number of spines that persist for several hours and are very likely to contain a synapse occurs in later stages, ~30 min after stimulation (Engert and Bonhoeffer, 1999; Nägerl et al., 2004, 2007). However, note that the overall spine density is almost never affected in vivo (Holtmaat and Svoboda 2009), which indicates that compensating mechanisms counter-balance any synaptogenesis, so you should not expect to see an overall increased number of synapses.

References
- Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. R., & Kasai, H. (2004). Structural basis of long-term potentiation in single dendritic spines. Nature, 429(6993), 761–766. https://doi.org/10.1038/nature02617
- Harvey, C. D., & Svoboda, K. (2007). Locally dynamic synaptic learning rules in pyramidal neuron dendrites. Nature, 450(7173), 1195–1200. https://doi.org/10.1038/nature06416
- Hill, T. C., & Zito, K. (2013). LTP-Induced Long-Term Stabilization of Individual Nascent Dendritic Spines. Journal of Neuroscience, 33(2), 678–686. https://doi.org/10.1523/JNEUROSCI.1404-12.2013
- Maletic-Savatic, M., Malinow, R., & Svoboda, K. (1999). Rapid dendritic morphogenesis in CA1 hippocampal dendrites induced by synaptic activity. Science (New York, N.Y.), 283(5409), 1923–1927. https://doi.org/10.1126/science.283.5409.1923
- Engert, F., & Bonhoeffer, T. (1999). Dendritic spine changes associated with hippocampal long-term synaptic plasticity. Nature, 399(6731), 66–70. https://doi.org/10.1038/19978
- Nägerl, U. V., Eberhorn, N., Cambridge, S. B., & Bonhoeffer, T. (2004). Bidirectional Activity-Dependent Morphological Plasticity in Hippocampal Neurons. Neuron, 44(5), 759–767. https://doi.org/10.1016/j.neuron.2004.11.016
- Nagerl, U. V., Kostinger, G., Anderson, J. C., Martin, K. A. C., & Bonhoeffer, T. (2007). Protracted Synaptogenesis after Activity-Dependent Spinogenesis in Hippocampal Neurons. Journal of Neuroscience, 27(30), 8149–8156. https://doi.org/10.1523/JNEUROSCI.0511-07.2007
- Holtmaat, A., & Svoboda, K. (2009). Experience-dependent structural synaptic plasticity in the mammalian brain. Nature Reviews Neuroscience, 10(9), 647–658. https://doi.org/10.1038/nrn2699


That's a barklouse, order Psocoptera. https://en.wikipedia.org/wiki/Psocoptera
It's very hard to identify those to species in a picture.


This may be Clitocyte odora commonly known as aniseed toadstool.

They can be found growing in small groups along the side of tree roots.

it is widespread in the temperate zones, occurring in Asia, Europe, and North America

Young specimens have a light blue texture on the cap which fades to grey in age. The gills and stem are white with no ring.

Reference


Just googling, they are SSLPs.  You do PCR, and the different alleles make different length amplicons.  Looks like there is some kind of artifact that causes some of the amplicons to have peaks that look 2, or 4, or 6 letters shorter than the true length.

So for the top marker, the 211 bp long allele is linked to the disease, and for the other one, the 118 bp allele is linked to the disease.


How does Genetic drift and selection affect fixation of an allele?

It would take a lot of writing to fully answer your question. Below I give an answer without spending too much time on the underlying math assuming you are confortable with probability theory and Taylor series. If you really want to understand more of all of that you would just need to consider reading a book in population genetics (see end of the post for recommendation).
Probability of fixation under drift only
In absence of selection, mutation and migration, drift only may yield an allele to eventually reach fixation (or loss). The probability of an allele to get fixed is then just equal to its frequency $P_{fix}=p$. When the neutral mutation has just arisen, this probability is therefore $P_{fix}=p=\frac{1}{2N}$ for a diploid population of size $N$.
See this post for more information.
Drift and population size - Intuition
For some intuition about the effect of population size on drift you might want to have a look at Why is the strength of genetic drift inversely proportional to the population size?.
Drift and population size - Effective population size
To go a little further than the linked post, note that the the strength of genetic drift is defined by what we call the effective population size $Ne$. But before talking about that let's talk about the variance in possible allele frequencies in the next generation (which we'll call $var(p')$).
The number of alleles $A$ in the next generation follows a binomial distribution (if we follow Wright-Fisher model). The variance of this binomial distribution is $2 p N (1-p)$, where $p$ is the frequency of the allele $A$ in the previous generation. Dividing this variance by $(2N)^2$ (the square is caused by the fact that $var(k X) = k^2 var(X)$, where $X$ is a random variable), to get the variance in allele frequency in the next generation
$$var(p') = \frac{p(1-p)}{2N}$$
We define the strength of genetic drift as $var(p')$ and for intuition, we usually refers to it as the value of $N$ that corresponds and to avoid confusion with the actual population size we call this new measure $Ne$. Therefore,
$$var(p') = \frac{p(1-p)}{2Ne}$$
Solving for $Ne$ yields to
$$Ne = \frac{p(1-p)}{2var(p')}$$
and this effective population size $Ne$ is what we use to talk about strength of genetic drift.
Probability of not reproducing
As I will refer to this statistic later, I will introduce it here. What is the probability of a given individual to not reproduce? Let's call this quantity $P(k=0)$ as the probability that the number of offspring $k$ is $0$.
Imagine you sample $2N$ haplotypes (with replacement) to form the next generation and each of them has a probability $1-\frac{1}{2N}$ to be chosen, the the probability of not reproducing is $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N}$. Taking the Taylor series of this expression for large values of $N$ yield to the approximation $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N} ≈ e^{-1} ≈ 0.37$. So, any individual has a probability greater than a third to leave any offspring in the following generation.
Probability of fixation under both drift and selection
If an allele if beneficial, then its probability of fixation is greater than its frequency $p$ (and vice-versa if deleterious).
Approximation
There are a number of ways to derive such probability and they all end up with some complicated form. An easy approximation (which I am not going to make any demonstration) for this probability is
$$P_{fix}≈\frac{1-e^{-4Ns} }{1-e^{-4Nsp}}$$
Just to give you some intuition about the form of the above approximation (but without doing a full demonstration that would be quite long), consider that the number of offspring an individual have follows a Poisson distribution with fitness as the rate. The fitness of the mutant individual is $1+s$, and therefore the probability of this individual of having $k$ offspring is
$$P(k) = \frac{(1+s)^k e^{-1-s}}{k!}$$
Think of the generation where the mutation just arised and only one individual has this mutation. The probability of this mutation to disappear immediately is therefore
$$P(0) = e^{-1-s}$$
, which for reasonable values of $s$ is not very different from the probability of not reproducing when $s=0$ and the probability become $e^{-1}$ (as already shown above via an other mean).
A less accurate approximation (but with a very easy form) for the probability of fixation is
$$P_{fix} = 2Ns$$
Some more calculations about the interplay of drift and selection can be found in this post.
Source of information
The post Book recommendation on population/evolutionary genetics? will give you great sources of information to learn more on the subject. It will also re-explain what I just said with a lower pace. I particularly recommend Population Genetics: A Concise Guide


Are the chemical constituents of human bodily fluids similar to sea water?

Let's just consider mineral salts, since obviously sea water does not contain animal proteins or cells, and (fortunately) our bodies don't contain phages, micro-algae etc.

Sea water is very salty; on average about 0.5mol/L of NaCl (the main salt dissolved in sea water).

On the other hand, human biological fluids like plasma and the intracellular space are at least 2-3 times more dilute.

Unless some other human bodily fluids are exceptionally salty, it seems that there is a pretty big difference and it is not very accurate to say that bodily fluids and sea water have close chemical compositions.

There are not many fluids that are very close from bodily fluids in term of composition. Popular culture tells the tale of emergency transfusions of coconut water during WWII, but that's not supported by medical literature; even though more recently, in exceptional emergency cases, it has been reported to be possible as a short term solution because of the similarity of osmolarity between plasma and coconut water.


How do prokaryotes perform cellular respiration without membrane-bound organelles?

Mitochondria are very similar to bacteria and are thought to have originated from bacteria. This points you to the answer: bacteria produce ATPs the same way mitochondria do, with the oxidation machinery place in their plasma membrane (analogous to the mitochondrial membrane).


How might IVF (and related technologies) alter epigenetic marks?

I was at a talk last year where some geneticists were starting to look at the effect of IVF techniques on genetic issues.  Because of the work being done and the inclinations of the clients involved, this has not been studied very much.  One presumes that since zygotes are still used, there will not be much epigenetic effects due to methylation patterns - its the same cell stocks being used in vitro and in vivo.

There may be an effect on genetics because the natural selection process.  Spermatogenesis and oogenesis is a highly selective process; only a small fraction of the ova generated by the ovaries ever mature and a large percentage of sperm generated are not motile or have other irregularities.  During fertilization, sperm competition obviously throws out all but one in 250 million.  It also appears that there are processes in the fallopian tubes that can store the sperm for several (up to 5) days before fertilization.

So while its not strongly established one can see how various IVF processes vary from in vivo fertilization.  This could have an impact on epigenetic factors, although different sperm vary genetically due to Meiosis and this would be a big source of genetic variation in the outcome.


How did our bodies decide on the right enzymes and where did we get them?

I can understand why your asked this sort of question so I will clear your doubts one by one.

First of all Enzymes are not scattered inside our body, every enzyme is localised in a particular orgenelle or compartment of protoplasm in the cell, where they play their specific role.

Such as the enzymes of glycolysis ( the process by which you create ATP and breakdown glucose to pyruvate) are present in cytoplasm where as the enzymes for TCA ( Oxidative-decarboxylation of AcetylCoA) are present in mitochondria.

Enzymes are very specific.(1) If you have heard of lock and key hypothesis which states that an enzyme binds to the substrate that is complementary to its active site. Enzymes have very high specificity for their substrates the active site where reactions happen are somewhat complementary to the Enzyme substrate complex and thereby it provides the binding energy that lower downs the activation energy of that particular reactions that enzyme is going to catalyse.

I hope that helps!

References: (1) please refer to lehninger principles of biochemistry for further information!


Are Zebras white with black stripes, or black with white stripes?

It is not like someone painted a zebra one color (say white) and then painted lines of the other color (say black) on top. But it does not mean we can't give some thoughts on the question.

What causes these patterns?

The colors are caused by pigments. Melanocytes either produce black pigments or do not and this cause the alternation of white and black stripes. The exact developmental pathway for producing these stripes is still very much unknown. All we know is that several environmental variables seem to affect this pattern. The most important correlate found so far is temperature, where higher temperature lead to darker and better defined stripes (Larison et al. 2015). This pattern can also be observed geographically (although there might have other important covariate driving this pattern, such as genetic typically)

So, are zebras black or white?

According to the Brevard Zoo, under their white or black fur, the skin is always black. This, I suppose, might lead others to rather claim zebras are black with white stripes.

From @iayork's answer, it appears that embryos are first black and then white tripes appear. This an extra reason to claim that zebras are black with white stripes. Note however, that I am not sure whether the skin of zebras are not first white, then turn black and then black fur and then white fur. Under such circumstance, one might want to argue that zebras are white with black stripes.

So if we take your question as phrased

  [A]re zebras black or white below the surface?

If by "below the surface" you are referring to their skin, then they are black (according to the Brevard Zoo)!


ExAC Browser: What does a "dubious variant annotation" mean?

Briefly speaking you expect more or less uniform coverage for reads. So if you see a systematic difference in quality scores or coverage for minor and major alleles or for forward and reverse strand, it could be an SNV, but most likely it is a technical issue. That's a 'dubious variant'.

A lot of such biases are described in "Genotype and SNP calling from next-generation sequencing data":

  Other types of filtering based on deviations from the HWE — generally
  low-quality scores, systematic differences in quality scores for major
  and minor alleles, aberrant LD patterns, extreme read depths, strand
  bias, and so on — can also help to improve the accuracy of genotype
  and SNP calling. The appropriate filters depend on the sequencing
  protocol and the upstream analyses. For example, a site with strand
  bias (where a disproportional number of plus and minus strands are
  observed) could be an indication of a problematic site that is more
  error prone and should be filtered out. However, if the sequencing has
  been performed on captured sequences, such as those used for exome
  capturing, then the bias might not be an indication of a problematic
  site but rather an artefact of the capture array.

Update
I've just received an answer from ExAC:

  The "LC LoF” means that the variant was marked as a low confidence
  loss of function variant. If you click on the “Transcripts” dropdown
  on the variant page it will show the reason why the variant is of low
  confidence for that transcript. In this case it was flagged as
  “END_TRUNC”. An explanation of the LoF filters can be found here:
  https://github.com/konradjk/loftee


Yes, bacteria will produce human (or any organism's) proteins if you introduce their genetic material but there are a few things to consider.

First, the introns must be removed from the human genetic sequence. Bacteria do not have the machinery to splice out introns after transcription. This is typically done by using a viral protein to reverse transcribe mRNA, which already have the introns removed, into DNA which you can use to transform bacteria.

Second, you need to insert a Shine-Dalgarno sequence. This allows the bacterial ribosomes to bind to the mRNA they will produce, and translate the protein you desire. This sequence is not found in eukaryotic genes, so you have to make sure it was included either in the vector or in the PCR primers you used to amplify the gene sequence.


I'd say that isnt a worm but a nonvenomous blind snake specie named Indotyphlops braminus
(Indotyphlops braminus)  .(Brahminy Worm Snake )


Does urea at different concentrations (5 or 0.5M) have different effects on proteins?

What you need to do is compare the relative amounts of the protein in the insoluble (pellet) fraction to the soluble (supernatant) one. This way you can determine how soluble the RMAS has become through the effect of the indicated compound.

DTT breaks disulfide bonds, but does nothing else to solublize the protein, so it's all in the pellet, with none detectable in the supe. NaCl is a salt that increases the ionic "strength" of the lysis buffer, but doesn't really do anything to solublize the protein, so again all of the target stays in the pellet. On the other hand, detergents like Triton and SDS free the protein from the insoluble fraction and move most of it into the supernatant, leading to the pattern you see for them. Depending on the exact subcellular localization of the protein of interest, and the amount and combination of detergent(s) used, you may see essentially no protein at all in the pellet, as it has all been solublized.

Urea and guanidinium hydrochloride are chaotropic agents, disrupting hydrogen bonding, van der Waals forces, and weakening hydrophobic associations, causing the protein to denature and separate from other proteins in the pellet, thereby putting it into the supe. This effect is generally seen at relatively high molarities (e.g. GuHCl is often used in the 6-8 M range), which explains the difference in effect seen with 0.5 and 5 M urea. At low concentrations, there is just not enough urea present to effectively denature the protein. I am a little surprised that nothing showed up in the 0.5 M lane, however, this is just a simulated Western showing ideal results - in real life things are almost never quite this cut-and-dried.


Do Pthirus gorillae remain in gorilla leaf nests after gorillas migrate and abandon them?

From the Wikipedia page on Pthirus gorillae: "Researchers theorize that humans acquired the parasite while butchering or scavenging on gorilla corpses, or sleeping in the abandoned sleeping nests of gorillas".

So yes, they are believed to remain.


Can the human brain be reduced to a binary system?

First of all, I would like to point out that making analogy between digital computers and the brain is often very misleading.

That being said, my answer is, some scientists believe so, some don't.

Several things to consider:

Some neural systems are not spiking. C. elegans for example has a nervous system that is entirely analogue. Human nervous system also contains neurons with graded responses (mostly in the sensory front-end though).
Spiking neurons may be binary at each time point, but time itself is continuous. Firing at 0.003 seconds later can represent something different. (in contrast to the usual synchronous digital architecture of computers)
The neuron doctrine is sometimes challenged. Glial cells that do not fire may have important functions for information processing. See:

Bullock, T. H., Bennett, M. V. L., Johnston, D., Josephson, R., Marder, E., and Fields, R. D. (2005). The neuron doctrine, redux. Science, 310(5749):791-793.


What large "package" is carried by this large spider underneath itself?

It's a Huntsman spider. The genus is  Heteropoda but not sure of the species (pingtungensis?) Yes, it is an egg case she is carrying.
Ask a local if it is the white barred spider, LaYa 喇犽, Mandarin is 白額高腳蛛. If so then it may be veratorias as in below article.
Wikipedia article on one species at
https://en.wikipedia.org/wiki/Heteropoda_venatoria
If you get more good photos, put them on wikipedia or somewhere. Until then, here's Heteropoda venatoria (Fam. Sparassidae) from here:
 click for full size


Can we make a rough estimate of the number of generations since the origin of life?

If you're willing to accept many orders of magnitude and define life as the Last Universal Common Ancestor.

For the rest of this answer, life begins 3.5 Gya with cyanobacterial mats and stromatolites and so on. Genetically the LUCA is dated to around this time, which matches the fossil record and everything's great. The LUCA can't have sprung from nothingness, so there may(will) have been (many)generations before the LUCA of things we would recognize as life, but I'm ignoring them. If they wanted to be considered they should have left descendants.

The fastest doubling times for modern bacteria are about 7-9 minutes but most are longer. E. coli takes about 20 minutes, and yeast takes hours. Given the 3.5 billion year clock, that gives an upper bound of about 1x10^14 generations. (Green sea turtles take 20-30 years to reach sexual maturity, or 1.1x10^9 generations). Something a bit representative is probably Pelagobacter ubique, which is vastly successful and takes about 29 hours to divide. Averaging out ice ages and so on and skipping the slowing of generations multicellularity probably implies(the Cambrian explosion is 82% of the way to the present day, being only 543 million years ago. We could account for it, but our guesses on generation time are way more inaccurate than any possible effect that could have) would estimate about 1x10^12 generations.


I can't leave a comment at the time of writing this (since I don't have enough reputation right now), so I'll leave this as an answer.

Your question is a bit confusing. It's titled "How to get taxonomic data", but at the end of the post, you mention "Basically, from this, you can construct the full taxonomic tree. When looking at the pubmed taxonomy data I don't see how to reconstruct the tree. Please show me how."

I'll try to address both your questions here.

Acquiring the lineage data:

Are you perhaps looking for something like this?

NCBI taxonomy itself is also accessible programmatically via E-Utilities.

Constructing an evolutionary tree:

You could perhaps use something like the data.tree R package to construct your tree using the lineage data.

Your question is a bit too vague, so I apologize if my answer is of no assistance here.


To me, it looks like a Lepidoptera from the Sphingidae family (Hawk moths). It is similar to species in Hemaris and might belong to this genus.

One similar species from this genus (found in India) is Hemaris tityus, but the moth in your picture doesn't look exactly like this particular species. Another similar species is Hemaris saundersii, which is found in and around India.

(Hemaris tityus, pic from wikipedia)


It is natural to be confused because the consensus has changed over the years and is still not settled.  In part this is because knowledge has been gained but remains incomplete, and in part it is a matter of opinion and aesthetics about what is best for usefulness at various levels of detail and understanding.

The system put forth in the textbook seems to best match the system Whittaker put forward in 1969.  His Monera is the text's Prokaryota, and his Protista corresponds to the text's Ursprungliche Eukaryoten.  Essentially Protista/Ursprungliche Eukaryoten is a catch-all for all Eukaryotes not included among the Plants, Animals, and Fungi.  There may be some variations in which of the eukaryotic algae are included among the Plants versus the Protista/Ursprungliche Eukaryoten.

It should be noted that in most or all systems of "Kingdoms", at least some of the kingdom groups are not monophyletic, that is, do not include all descendants of a common ancestor, and so do not exactly reflect a true tree of descent.  The Wikipedia Kingdom article notes:

  Some recent classifications based on modern cladistics have explicitly abandoned the term "kingdom", noting that the traditional kingdoms are not monophyletic, i.e., do not consist of all the descendants of a common ancestor.


Thymine must make contact in two places on HIV-RT before being added to nucleotide strand. First contact is made with the fingers region then contact is made at the N-Site.
Allosteric Regulation of HIV-1 Reverse Transcriptase by ATP for Nucleotide Selection


What percentage of human body's cells are contained in blood?

The human body has about $3.72 × 10^{13}$ cells according to Bianconi et al. 2013, although this is disputed.

It also has about 5 liters of blood, which is made approximately 40-45% of erythrocytes. Let's assume 2.5 liters = 2500 $cm^3$ of red blood cells (RBC). Assuming a mean value of 5 millions RBC per $mm^3$ there should be in total $5 \cdot 10^6 \cdot 10^3 \cdot 2500 = 7.5 \cdot 10^{12}$ RBC.

By completely taking out white blood cells and thrombocytes out of the equation, a number of ${7.5 \over {3.72 \cdot 10}} \cdot 100 = 20 \%$ of number of cells are contained in the blood (approximately).


Why is uracil, rather than thymine, used in RNA?

Regardless of the question† of which came first*, RNA or DNA, it is possible to rationalize the absence of thymine in RNA by a cost–benefit analysis. There is a cost to using thymine, so there must be sufficient benefits to make this worth while.

Cost of using thymine rather than uracil

The most obvious cost of using thymine is the energy requirement for its synthesis (in terms of reducing power — NADPH).

An analogous conversion of rUMP to rTMP (if it existed) would incur similar costs. (There may be additional costs, but they may be contentious and this is indisputable, so it will suffice.)

Benefit of using thymine rather than uracil

For DNA the benefit is clear and stated in the question. By not using uracil as the complement to adenine, uracil produced by spontaneous deamination of cytosine can be recognized as abberant and removed by the DNA proof-reading repair systems. This presumably gives the organism an advantage (benefit) by reducing harmful mutations to DNA — the genetic material.

RNA is not the genetic material of contemporary autonomous organisms. Hence unrepaired C to U deaminations will not affect that aspect of the viability of an organism. How serious will they be for the cell, though? The largest and most long-lived RNAs are the structural ribosomal RNAs. Such mutations in the cells rRNA might have no effect on ribosome function as much of the RNA is thought to be structural. However, even if they did, the inactivation of a small percentage of the ribosomes of a cell would have little impact on protein synthesis. Likewise for the small tRNA molecules.

Messenger RNA poses a different problem as we can conclude that abberant proteins made from mutant mRNA are dangerous to the cell from the fact that a proof-reading mechanism exists to correct errors in the charging (aminoacylation) of tRNAs. I would argue that the relatively short half-life of mRNA compared with the frequency of deamination of cytosine means that the latter process is not responsible for a significant amount of mutant mRNA.

Conclusion

The benefits of using thymine — together with a repair system — in RNA would be marginal, and hence not worth the energetic cost this would entail.

†Footnote: We don’t need to argue about which nucleic acid came first

The current metabolic pathways for formation of dTTP from dUTP and the reduction of ribose to deoxyribose are strongly suggestive to me that RNA preceeded DNA in evolution. (They suggest nothing about whether RNA preceeded protein.) However, the rationalization presented here does not require this assumption. If DNA came first and RNA initially had T instead of U, the rationale could be used to argue why RNA changed bases from T to U. Indeed, the rationale can be employed by those who do not even believe in evolution — they could argue (and probably do) that some deity created things that way because it was more efficient in terms of cost–benefit.


Why do gram-negative bacteria attack the digestive system more than gram-positive ones?

Gastrointestinal infections can be caused by Gram positive and negative bacteria:

Gram-positive:

Staphylococcus aureus
Clostridium difficile, botulinum and perfringens
Listeria monocytogenes
Bacillus cereus

Gram-negative:

Salmonella enteritidis and typhi
Campylobacter jejuni
Shigella
Escherichia coli
Vibrio cholerae and parahaemolyticus
Helicobacter pylori
Yersinia enterocolitica

Any part of the GIT can be infected by G+ or G- bacteria:

Stomach: S. aureus (G+), H. pylori (G-)
Small intestine: Bacillus cereus (G+), Salmonella enteritidis (G-)
Colon: Clostridium difficile (G+), Shigella (G-)

Certain bacteria typically affect only certain parts of GIT: H. pylori and S. aureus affect mainly the stomach; C. difficile affects mainly the colon.

Anyway, infections of the gastrointestinal tract are much more commonly caused by Gram negative than positive bacteria (Stat Pearls, 2019).

From the pathogenicity viewpoint, the main difference between Gram-positive and negative bacteria is that G+ bacteria produce exotoxins (which are proteins that bacteria secrete into their environment), while G- bacteria produce endotoxins (which are lipopolysaccharides as parts of bacterial walls). The differences between endo- and exotoxins (microbiologyinfo.com):

Endotoxins are heat stable, so they are not destroyed by cooking, they don't need specific receptors, they don't trigger antibodies and there are no vaccines against them.
Exotoxins are heat unstable, they trigger antibody response and have specific receptors in the GIT.

More than 80% of skin infections is caused by Gram positive bacteria, such as Staphylococci and Streptococci (Clinical Infectious Diseases).

75-95% of uncomplicated urinary infections (Microbiology Spectrum) and most sexually transmitted infections (Clinical Laboratory Science) are caused by Gram-negative bacteria.

Respiratory infections are caused by both Gram-positive and negative bacteria (Lumenlearning).

So, the only pattern I see is that in dry/air-exposed areas (skin, respiratory tract), most infections are caused by Gram-positive bacteria, and in wet areas (gastrointestinal and genitourinary tract) by Gram-negative bacteria. This doesn't mean that there is any actual biological mechanism behind this pattern, though.


Why Lungs can't work in water and gills can't work in air?

Misleading sentences in your question

  fishes can breathe in water (at least for few-hours)

Fishes can breathe for much longer than a few hours under water as they spend their whole life underwater.

  Animals-with-lungs (such as most terrestrial mammals)

All mammals, whether terrestrial (like a cow) or not (like a dolphin) have lungs. While all mammals have lungs, most fish (but not all) have gills.

Lungs vs Gills

To understand the answer, you need to understand two key organs involved in gathering oxygen from the environment: gills and lungs.

Lungs are organs that allow the transfer of oxygen into the blood when inhaling air, while gills are organs that allow the transfer of oxygen into blood when inhaling water. Lungs don't do their job properly in water and gills don't do their job properly in the air. You should have a look at the following wikipedia entries to further your understanding of these organs:

Lung
Gill

Energy consumption

You say

  does fishes require much-much less-amount of oxygen than lunged terrestrial-animals, though they stay in physical activities including predation?

I am not sure I understand the meaning of this sentence but anyway.

Making generalization about fish metabolic rate can only be misleading as there are an immense diversity of fishes. For example some fishes are endotherm (see here to understand the definition of this term) while some are not and this will vastly affect the metabolic rate.

Although eventually too advanced for the OP, Chabot et al. (2016) is an interesting reading to get an general overview of the Metabolic rate in fishes.


How fast the brain recover itself at sleep? What can be done to accelerate this process?

You should see some talks from TED about deep sleep.

One researcher summarized that adults generally need 8 hours every night to be at optimum strength. What is most important though is the Delta-wave sleep that occurs during very deep sleep.  To accelerate the process: It's pretty fringe research, what he said is early days... Alledgedly, playing a certain kind of noise triggered near the delta wave phase promotes Delta wave activity in the brain as measured with electrodes. it's essentially slow delta-synchronised seashore kinds of of grey noise played in sleep at the right moment. He said they were working on a device for it.

here's the talk.
https://www.ted.com/talks/dan_gartenberg_the_brain_benefits_of_deep_sleep_and_how_to_get_more_of_it

My own method to have amazing sleep is lots of nights at my girlfriends and to change mattress every few days mat my house, because my unconscious breathing is forced to exercise different muscles of the chest based on whether I am on a swimming pool matress, a futon, a cozy matress, covers similar to sleeping on a lawn. Physiology and muscles benefit from varied exercise, including the 8 hours of chest muscles during sleep. another matress for example I feel all the breathing in the lower belly. I just got out a pool matress for the last 2 nights on boards and rugs, and I dreamed that I was flying around the mountains and cities for about 3 hours and that other people were flying too, which is always nice. I swear I was sleeping a bit rough 3 days earlier on a normal mattres. other factor for me optimum warmth and lots of water for me:) i'm weird though because I had liver damage from a pesticide and following doctor care when I was 18 and I need drink more and sleep hot in order to sleep well.


Can mammals and/or birds see / detect infra-red light?

Infrared is a fairly large part of the electromagnetic spectrum, so to get an answer best suited to your specific case, you should specify the wavelength of your LED. There is at least one study showing that ferrets (not sure if it's the best predator to worry about for what I assume is a suspended bird's nest) can see up to 920nm.

So to answer your question, yes, at least some can, but the further into the spectrum you go, the fewer there will be.

I am much less certain, however, that this would attract danger. Nocturnal predators in biomes inhabited by humans generally evolve to avoid rather than seek out artificial light sources.


How large might a paper wasp nest become?

According to multiple reports (here, here and here), a 7m (22ft) paper wasp nest was found in an abandoned home in San Sebastian de La Gomera on the island of Tenerife (~100km off the shore from Morocco)!! The nest was estimated to be home to over 22,000 wasps! The picture is included below:

This nest broke the previous world record, a nest discovered in Waimaukau in New Zealand in April 1963 that was an impressive 3.7metres, or 12ft 2ins long, more than 5ft in diameter and 18ft in circumference!

Other big nests? ...

According to this site a 10 ft x 7ft x 2ft nest buzzing with about 400,000 yellow jackets was found in a camper in SC, U.S.
Here is a video of an apparent giant (6.5ft x 8ft) yellow jacket nest found in Florida, U.S. in 2013. A Picture of the nest is below:


It is certainly a very difficult question to answer.

There are some genetic disorders that can predispose individuals for becoming obese: https://www.ncbi.nlm.nih.gov/pubmed/18230893

There are also evidence of epigenetic influences on obesity: http://www.nature.com/nrendo/journal/v12/n3/full/nrendo.2016.18.html

Typically each case of obesity is caused a combination of both genetics, epigenetics and lifestyle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873060/

However also keep in mind that obesity is a fairly recent problem and as such the genetic changes are likely minimal between the 1980 and 2008 populations sampled by WHO: http://www.who.int/gho/ncd/risk_factors/obesity_text/en/
A doubling in the prevalence of obesity in the two populations are most likely caused by changes in lifestyle and the availability of food, rather than genetic changes as the time frame is so short.

So to sum up: Morbid obesity caused by currently unfavorable genetics exists but is very rare. People can be genetically and epigenetically predisposed for developing obesity, which when combined with certain lifestyles can further increase the risk of becoming obese.


How does activation of adenylcyclase lead to increased cAMP and diarrhea?

The crypt cells of the gut can actively secrete electrolytes (ions) via special channel which finally leads to water secretion. This is usually tightly controlled, since uncontrolled loss of water is obviously not good for the cells.
Have a look at this schematic figure, (from this webpage):

Sodium, Potassium and Chloride ions are co-transported into the cell,
sodium and potassium are transported back out via other channels.
If the adenyl cyclase is activated (for example by bacterial toxins,
cholera does this), then cAMP is made.
cAMP aktivates Protein Kinase A (PKA) which in turn phosphorylates the the Cystic fibrosis transmembrane conductance regulator
(CFTR)(this channel is also important for cystic fibrosis) which leads
to the secretion of chloride ions from the cell. This builds up a
negative potential across the membrane (positively charged ions are
missing).
This leads to the secretion of sodium ions through the tight
junctions, resulting in the netto secretion of NaCl.
The secretion of salt builds up and osmotic gradient across the
membrane, which leads to water secretion and can also lead to hyponatraemia.

To overcome this problems, the so called "oral rehydration therapy" is used. The solution contains of an isotonic solution of sodium chloride and glucose. This is taken up by the sodium-glucose symporter (a special class of transporter, that transports two molecules in the same direction) and builds up a gradient which is directed in the opposite direction of the diarrhoea, helping to fight dehydration.


Effect of the health of the male parent at the time of conceiving

It can matter, though at this point we are just starting to understand how much.

Men can typically have children much later in life than women, but there are costs as time goes on.

Epigenetics has shown us that what happens to the parents in their lifetime can affect his offspring.  Obesity especially has been shown to affect the offspring, producing a higher risk of diabetes for two generations.

It is thought that this is not going to affect fathers who develop diabetes at a later age, but primarily those who are obese around 9-12 y.o. when the spermatogenic cells are produced in the testes.

What happens to men as they get older though is that their ability to produce healthy sperm starts to degrade.  They can lose fertility and produce more birth defects typically as early as age 35.  Given this there are probably a lot of habits or events that can adversely affect fertility.

Lifestyle choices as simple as tight underwear which might block blood flow to the testes is sometimes cited.

Given all this DNA or cellular damage from chemicals or diet or poor health certainly would also affect male fertility.


What is this insect wing, based on its vein pattern?

There is a way to classify insect wings: the Comstock-Needham system.
From Wikipedia:

The Comstock–Needham system is a naming system for insect wing veins, devised by John Comstock and George Needham in 1898. It was an important step in showing the homology of all insect wings. This system was based on Needham's pretracheation theory that was later discredited by Frederic Charles Fraser in 1938.

The system assigns names to the enlarged longitudinal veins of the wings and provides subnumbering for different branches of those veins. The system also names cross-veins and cells (transparent areas between veins) relative to the major longitudinal veins.
Again, according to Wikipedia:

the major longitudinal veins are named:
> - costa C, meaning rib
> - subcosta Sc, meaning below the rib
> - radius R, in analogy with a bone in the forearm, the radius
> - media M, meaning middle
> - cubitus Cu, meaning elbow
> - anal veins A, in reference to its posterior location

The cells are named after the vein on the anterior side


Why is the ratio between action potential and threshold value called the 'safety factor'?

Action potentials propagate by depolarization of one section of the membrane causing depolarization of an adjacent section.

It is necessary that this depolarization be greater than threshold. If the amplitude of the action potential were to drop below threshold, it would fail to propagate. Additionally, it would be quite slow and inefficient.

Therefore, the action potential amplitude is far greater than the threshold. This helps speed and builds in a "safety factor" to ensure the action potential propagates - that's what your book is saying.


How do animals handle light refraction in different media?

It is more complicated than this, but... I don't think it has as much to do with the refractive index of water but rather the shape of our corneas and the loss of this shape advantage under water, for if the eyes are protected by goggles, one can see quite clearly underwater (much the same as a camera can, as the shape of it's lenses are not affected). Any change in the shape of the cornea changes the way light passes through the eye, and results in a change in vision. The following is from Ch. 9 Optics of the eyes of marine animals, from Light and Life in the Sea:

This is different for penguins (and turtles): the surface of their eyes, the cornea, is not as much vaulted as for humans (it's much flatter), and the lens is much rounder (meaning the shape can change more than our relatively flat lenses can), so the difference between air and water is not so big and the light isn't refracted too strongly. Also, the ciliary muscles (not to be confused with the pupillary muscles) holding the eye's lens (behind the pupil) are stronger, increasing their accommodation, so a penguin has a sharp sight in the water. Or as stated in A Survey of Vertebrate Strategies for Vision in Air and Water

  Whereas the cornea is usually the major refractive element of the terrestrial eye, it is of little or no refractive consequence to an aquatic vertebrate.

See the difference in these four vertebrae groups (the first is man, the second is fish, the third is whales (similar to penguins) and the fourth is sirenians - manatees and dugongs)1:

Penguins.info
[1] Comparative anatomy and physiology of vision in aquatic tetrapods


What makes the electrical charge inside the neuron more positive at the end of action potential and returns it to resting potential?

The issue is the permeability of the membrane to Potassium and how membrane potential is created in the first place. The resting membrane potential of the neuron is very close to the equilibrium potential of Potassium. Large fixed anions (proteins) in the cytosol are represented in the image below by [An-]:

If Potassium and cytosolic proteins were the only thing inside the cell and the outside were water (ignoring osmotic effects), then in Figure 1 there is an outward K+ concentration gradient.
In Figure 2, we allow the membrane to become permeable to Potassium (as it is in the cell). The Potassium begins to leave [green arrow], but as it does, it begins to create a charge separation that sets up a negative voltage in the cell that pulls the Potassium cation back in [red arrow].
In Figure 3, we see that enough K+ has left the cell to the point that the membrane potential has grown negative enough that the rates of K+ leaving and entering are equal, so no net change in K+ concentration occurs. This is the definition of chemical equilibrium, and so we call this voltage the equilibrium potential of this single-ion system (~-80mV for biologic concentrations of K+).

We could do a similar experiment with Na+ starting high outside in Figure 1, with the arrows reversed, and the equilibrium potential of the Sodium-only system would be ~+60mV.

So, if a real cell has both K+ and Na+ concentration gradients in opposite directions, why don't they just cancel each other out? Why is the resting membrane potential negative, and in fact, much closer to the equilibrium potential for Potassium alone? The answer is: permeability. Imagine if you had Figure 1 again, with [K+] high inside, and [Na+] high outside, as it is in the cell, but in Figure 2 you ONLY made the membrane permeable to K+. Would the Na+ gradient change at all? No, because there would be no pathway for it to move. Thus, if ALL the permeability is for K+, then K+ has all the influence on the membrane potential. If both are equally permeable, it would be their average (-10 mV, or about neutral).

However, the permeability for K+ AT REST is about 20 times the permeability for Na+, so we'd expect the cell's resting potential to be 1/20th of the 140mV "distance" between the equilibrium potentials for K+-only and Na+-only systems, or: -80mV + 1/20(140mV) = -73mV. The fact that it's not exactly -73mV is explained by the existence of a small amount of Cl- and other ion permeability. But, in essence, Potassium determines the resting potential, with a little offset due to sodium permeability.

Now that you understand that, understanding the action potential graph should be easy:

Rising Phase: major increase in Na+ permeability, voltage rises almost to the equilibrium potential of Sodium.
Falling Phase/Undershoot: Na+ permeability shuts down, major increase in K+ permeability, voltage drops back down to equilibrium potential of K+.
Restoration: K+ permeability drops back to normal (not completely shut down), and the Na+/K+ pump just restores the concentration gradients that allow the resting potential in the first place.

So, really, your initial confusion about the electrical work done by the Na+/K+ pump existed because you didn't take it in context with the permeability. Yes, the pump by itself makes the voltage more negative, but some of the potassium it stuffs back into the cell immediately turns around and leaks right back out until it's 95% of the way to its own equilibrium point again, as determined by the membrane permeability.


One of the easiest answers to the question; "Why do we have ____?" is "Because our ancestors did". This is not trivial or flippant, as it is a significantly important answer that is so often overlooked. Humans are members of Bilataria; a deep branch of the animal tree that is characterized by bilateral symmetry. Humans are typical of other vertebrates in having two kidneys. Selective pressure to reduce to one of two organs is typical in snakes, whose body form favors reduction. But even snakes have two kidneys. Natural selection does not reduce features we don't need unless such a reduction would increase fitness.


What is the brain's preferred energy source? Glucose or ketones?

First of all, for those readers with less knowledge of the general principles of biology, I want to state an important, even if obvious, point: The brain doesn't
"prefer" anything. Despite being the smartest organ in the body, it is subjected (like any other biological system) to changes in the concentrations of the substances in question, that is, glucose and ketone bodies.
According to a study in rats from 2010, it seems that ketone bodies suppress glucose metabolism in order to conserve glucose when its concentration is too low for the body to be used regularly. Therefore, the ketone bodies are regarded as neuroprotective, since their metabolism prevents the brain cells from starving.
Another study in rats from 2013 emphasizes this point further. Please note the following excerpt from the discussion section:
The brain's ability to switch from glucose oxidation towards ketone bodies requires a type of ‘cerebral metabolic adaptation'. This process is not well understood but is thought to be highly associated with the duration and level of ketosis. Ketones are considered to supply up to 70% of the total energy demands once maximal metabolic adaptation occurs. Blood ketones become elevated during prolonged fasting or with a ketogenic diet reaching a state [of] ketosis and glucose sparing. During this process, monoca[r]boxylic transporters upregulate at the blood–brain barrier with increasing demand for ketone utilization by brain. Recently, investigators have recognized additional therapeutic properties of ketosis, such as neuroprotection after stroke or injury. What remains unclear is whether the neuroprotective or therapeutic properties of ketosis is as a result of changes in the regulation of metabolic signaling pathways...
This means that when the balance of concentrations shifts toward the ketone bodies, they will have precedence over glucose in order to conserve the latter. The mechanism is probably upregulation of ketone bodies receptors and transporters that increase its transport into the brain, as stated above.
Therefore, when the brain is given both ketone bodies and glucose (which actually happens in the fasted state - ketone bodies transport and metabolism in the brain begins when blood glucose is low, not zero), there will be "preference" for the ketone bodies, but this depends on the glucose concentration. If it shifts back, above a certain glucose concentration glucose metabolism is supposed to be renewed.


How can an albatross stay airborne for months?

I'm not really inside the field but few weeks ago I noticed a Plos One article that was dealing with this. Indeed albatross can fly for thousands of miles and this is possible at no mechanical cost, because they use a dynamic way of flight that takes the energy from wind (dynamic soaring) (ref-1). Their muscle-skeletal system further evolved so that no energy is required to keep open the wing.

In addition, when foraging, they minimize diving and landing activities because they follow Killer Whales, so that food is always in proximity. (ref-2) Very smart birds.

ref-1 Sachs et al., Plos One 2012

ref-2 Sakamato et al., Plos One 2009 both references are open access.


In almost all metazoa, the pro-germline cells get segregated from other stem cells at an early stage of development and they thrive and differentiate in their neighborhood. This is important in order to preserve the germline. This post provides some basic explanation.

However, even drosophila have adult multipotent stem cells and help in the formation of midgut as reported by this study.


The process of genetically modifying crops is performed in a lab. Genes would not leak into planted organic crops from compost any more than they would move from decomposing soil nematodes, earthworms, or manure. So no, organic plants would not be genetically modified. However, the labeling of a crop as "organic" is not always standardized, so it could be a cause of concern for some people who do not understand the process.


What are the biological and nutritional benefits of having numerous smaller meals a day?

One rationale is that smaller meals will cause less insulin secretion compared to a larger meal. With less circulating insulin over the time, insulin will be under the threshold required to activate the adipogenic program in the white adipose tissue. So, you will burn ingested carbohydrates instead of converting them in fat despite the same caloric intake. See for instance Munster and Saris, Plos One 2012.


Was it an inchworm? It fits the description, as well as the 2nd picture.


Confusion regarding photosynthesis and respiration in plants

You haven't directed us to any evidence for your assertion, so it is difficult to evaluate.

I'm not a plant physiologist, so I will argue from first principles:

photosynthesis consumes CO2 and produces O2:

6CO2 +6H2O -> C6H12O6 + 6O2

respiration consumes O2 and produces CO2:

C6H12O6 + 6O2 -> 6CO2 +6H2O

Plants do both of these things at the same time for at least part of the day. During the day, in a growing plant, photosynthesis will exceed respiration: a lot of the fixed carbon is fed into anabolic processes to produce "plant stuff"; polysaccharides, proteins, nucleic acids. This means that the plant will be a net producer of O2 and a net consumer of CO2. At night there is, of course, no photosynthesis and respiration will dominate and the plant will be a net producer of CO2 and a net consumer of O2.

At certain times of the day, twilight for example, there will be a transition between these two states, and the plant will pass through a state where there will be no net flux in either of the gases.


What is the name of this plant has dazzling look like leaves?

It is Jatropha podagrica also known as Buddha Belly.

It comes under succulent plants.

Source: flowersofindia.net


Why does the kidney of a cow have lobules, why the kidney of a human hasn't any?

It appears that the invagination of the renal kidney is vestigial from development and unlike human and other mammals, the bovine kidney does not form a smooth outer cortex.

  The kidneys of the bovine do not lose their foetal lobulation.

-Renal Anatomy - Anatomy & Physiology en.wikivet.net

However this is not related to its function.

  Despite what it’s externally lobulated appearance may suggest, the cortex of the bovine kidney is continuous and the kidney is of multipyramidal type.

-Renal Anatomy - Anatomy & Physiology en.wikivet.net

If you want further information on the subject, The bovine kidney as an experimental model in urology: external gross anatomy; Carvalho, et. al. Cells Tissues Organs. 2009;190(1):53-8. doi: 10.1159/000159370 made measurements of the bovine kidneys and compared then to human measurements. This article is unfortunately behind a pay wall, so you will need academic access to Medline to access.

One observation that they do make is that

  There are few publications about bovine kidney anatomy. The available information is general, contains little detail and is limited to the classical texts [Bossi et al., 1909; Nickel et al., 1979; Sisson, 1981; Dyce et al., 2004].


If evolution is a gradual and continuous process, how can we say humans came about 200k years ago? What is so special about that point in time?

You're right that evolution is largely a gradual progression, but we don't have the luxury of having that gradual progression in the fossil record. We'll have a fossil from, for example, 350 KYA and another from 190 KYA. The older one is clearly not modern human and the more recent one is. So the age of modern humans is set at approximately 200 KYA, especially since genetic calculations confirm that age.

Now, if we find a 400 KYA fossil that is clearly modern human, then there'll be some 'splaining to do, but so far, nothing like that has happened.


If you have simple 1:1 connections or can list your data in that manner, you can try Cytoscape (freely available). There are numerous plug-ins to customize what you have in mind in terms of visualization.


The average domesticated dairy cow produces far more milk than would be required to feed their calf. All cows, wild and domesticated, will only lactate in the period between their calf's birth and weaning. Milk is calf-food, and when there's no calf, there's no evolutionary advantage in producing milk.

On dairy farms, cows are milked twice daily, from spring (when they give birth) until late autumn. This mechanical milking 'fools' the cow into continuing to lactate. When a cow has stopped lactating, they will only start again after giving birth. This means that you can't just start milking a cow and expect to get milk.

Generally farmers milk their cows from spring (birth) until late autumn. The reason for stopping in autumn is simply because the grass grows much slower in winter, so there isn't enough food to support lactating cows. However, it is entirely possible to milk longer than a year; I know of farmers who milk their cows continuously for two years. These farmers will have to purchase a lot of supplimental food (like hay or silage) during winter. The advantage of milking for longer than one season is that the cows do not have to give birth every spring, but instead only every second spring.

I believe (but can't guarantee) that in winter, most milk purchased in a shop comes from the opposite hemisphere. I do know that here in New Zealand, we export a lot of milk to northern-hemisphere countries.

If you were to suddenly stop milking a cow, they might get sick but generally they will survive. It's still something to avoid!
Although if the calf is left with their mother then the cow would be relieved.

I do not have an 'official' source for these facts. However, I grew up on a dairy farm, so this was my life.


How much energy is in a human brain's electromagnetic activity?

EEGs pick up about 0.5 to 100 µV on the scalp and about and about 1-2 mV when measured on the surface of the brain, it's about 100 times lower than ECG (heart) signals.

Brain waves have been categorized into four basic groups

beta (>13 Hz),
alpha (8-13 Hz),
theta (4-8 Hz),
delta (0.5-4 Hz).

Votage times current = power. In this case, the amount of current would be/is hypothetical as it would be based on a "salt water" bridge; neurons contain Na+, K+, Ca++, and Cl- ions which are the basis of the current.

EEG measurements must be amplified simply to be seen. An amplifier has to provide a gain of 100 - 100,000 in order to move a delicate needle (and draw the EEG). So, using the amplifier gain as a indication of the amount of current, let's suppose you need as much force to move a pen back and forth as would be required to accelerate a feather one inch in one second.

A feather weighs 0.0082 grams and an inch is 2.54cm. That's about 2 newtons or 2 watts. So, since the current from the brain is amplified 100 - 10,000 times then the wattage picted up by an EEG would be between 0.2 to 20 milliwatts. Supposing that an EEG was only 1% efficient at absorbing the power, then the wattage could be on the order of 20 milliwatts and 2 watts. Altogether brain power might possibly enough to accelerate a feather one inch per second... at around 100% harvesting efficiency.


I'm afraid your science teacher is wrong. Handedness is a complex trait. It is not determined by a single gene, and can't be described as being dominant or recessive. Handedness does apparently have a genetic component, but many other factors are involved as well. See the Wikipedia article on handedness:

  Handedness displays a complex inheritance pattern. For example, if
  both parents of a child are left-handed, there is a 26% chance of that
  child being left-handed. A large study of twins from 25,732
  families by Medland et al. (2006) has indicated that the heritability
  of handedness is roughly 24%.

  To date, two theoretical single gene models have been proposed to
  explain the patterns of inheritance of handedness, the first by Marian
  Annett of the University of Leicester and the second by Professor
  Chris McManus of UCL.

  However, the growing weight of evidence from linkage and genome-wide
  association studies suggests that genetic variance in handedness
  cannot be explained by a single genetic
  locus. From these studies McManus et
  al. now conclude that handedness is polygenic and estimate that at
  least 40 loci contribute to determining this trait.

What may be confusing is that the preferred hand is often called the dominant hand, but that usage of the work 'dominant' is unconnected to the concept of dominance in genetics.


Why does atheroma contain thromplastin/tissue factor?

Tissue factor is present in subendothelial tissue and leukocytes - in this case this would be within the atheroma since the atheroma consists of damaged endothelium.

Tissue factor's presence in the subendotheilum in general implies that whenever the endothelium is damaged, tissue factor is released which promotes clotting at that site. Clotting starts after an atheroma ruptures because up until that point all the tissue factor is encased within the atheroma, protected from direct contact with the bloodstream - there is still no superficial injury to the endothelium to expose the underlying tissue factor that would signal the clotting cascade to begin. Therefore, clotting only starts after the atheroma ruptures and all the tissue factor stored within the atheroma is released into the blood vessel.

It is worth noting here that in homeostasis without any injury, the coagulation cascade and fibrinolytic pathways (the clot-lysis or pathways) are both active, but they balance out each other's effects. Disruption of this balance due to pathology, injury, or other insult causes an imbalance between the two pathways which the body seeks to rectify. The imbalance is what leads to clot lysis (in the case of wound healing - after the wound has healed) and clot formation (in the case of a new injury).

Sources:

https://www.ahajournals.org/doi/full/10.1161/01.CIR.94.6.1226
https://www.ahajournals.org/doi/full/10.1161/01.CIR.96.2.396
https://ascpt.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1752-8062.2011.00351.x


Maintaining purebred pedigrees and how to lessen chance of getting disease?

Many races of dogs are relatively new with most of them appearing (were bred) in the last few hundred years. These variations are caused by small mutations in certain genes and this is also the problem. To keep a race pure, it has to be interbred to maintain the special set of mutations. And this makes the dogs vulnerable to collect more damaging mutations, especially when the number of animals used for breeding are too small. This is the same problem, that animal conservation projects face in zoos.

A good example for that is the Dalmatian dog. Its characteristic spotted pattern is caused by genes, that can also cause sensineural deafness. To avoid this, deaf dogs are excluded from the breeding and a backcross project was started.


How does being afraid or nervous affect mental performance?

I will try using logic, but that might only just get you on a lead:

Concentration means being focused on a specific task.
Consciously, you want to focus on a specific task, but there are other process that may want to claim ressources and that you cannot repress.
Anxiety, but also fear or worriness are symptoms that basically translate an unconscious (or conscious) proccess that requires your attention.
Therefore, two concurrent psychological process require focus from your conscious mind. Ergo, you cannot concentrate on either on them. Usually, the emotional part will win since it involves brain structure (such as the amygdala) that are specialized in shunting more evolved brain structures. That is when you are afraid of something, it is very hard to repress that feeling with logical thinking.
In psychoanalysis, Freud introduced something called as "The pleasure principle" (I hope that's a good translation). This principle is one of the few basic principles that rule human behavior. Now, anxiety is an indicator of displeasure. Your mind will try its best to settle that issue before settling anything else. That is why usually you cannot isolate anxiety.

Here's an example:
You hate spiders. You need to measure the surface of an old mannor. You've seen some spider webs. Odds are you will have much trouble to concentrate on measuring any room's surface, because one task your brain will perform for you is checking in every corner whether a spider can be seen, so you'll be able to identify a potential threath as soon as possible and react appropriatly (usually, get the hell out of there if you're really affraid of spiders.

Here's another example that doesn't use fear:
Your girlfriend texted you before an exam, and she said "We need to talk". Since you are emotionnaly bound to your girlfriend, you might get anxious: what does she want to talk about ? Your mind will begin scanning for every possibility, emphasizing on the worse ones (the ones that will disturb the "Pleasure principle" the most for instance). Now that you identified that she might break up with you, this thought will just keep popping up, even if you manage to think for a minute about the exam you should be thinking about right now.

Fact is this is a matter of autoconservation for your psychee. A breakup will certainly harm you more than a failed exam. Your brain is very smart about processing important stuff before, and any attempt from your conscious mind to shunt this will most probably fail.

By the way, there is a psychology stackoverflow. I guess you should have posted this question there.

Hope this helped !


One of the cornerstones of research ethics worldwide is the Nuremberg code, which was formulated shortly after the Second World War and set off by the cruelties performed by the Nazi Doctors. The Declaration of Helsinki, which is currently widely used as the guiding principle of research ethics, was directly inspired by the Nuremberg code.

Interestingly, article 5 in the Nuremberg code reads, and I quote:

  No experiment should be conducted where there is an a priori reason to believe that death or disabling injury will occur; except, perhaps, in those experiments where the experimental physicians also serve as subjects.

Basically what this tells you is that when you are a physician, you are not only ethically allowed to experiment on yourself, even when you can reasonably expect death may follow, you are even allowed to put others at that risk(!) Admittedly, it does not specifically talk about non-physicians. Nonetheless, with regard to your question, this Nuremberg article implies that self-experimentation is allowed, regardless the risks.

Annas (2010), rightfully argues that, even where risks are minimal, prior ethics committee review of research should always be sought, if only to confirm the reasonableness of the risk assessment and regardless whether investigators are subjects.

The problem then becomes whether self-experimentation (an experiment done by the investigator on himself or herself only) must be reviewed and approved by an ethics committee before it is conducted. Here Annas (2010) concludes that:

  [...] When an investigator proposes to experiment only on him or herself, that activity is not properly categorized as research at all, but as self indulgence (or, some may say, self abuse). Trivial interventions masquerading as research studies are primarily a source of amusement.

Although I do not necessarily share the concluding accusations against self-experimentation, I do share her view that self-experimentation should not be regarded as proper scientific research, and therefore should not be subject to ethical review.

Reference
Annas, BMJ (2010); 341: c7103


A question involving immunoprecipitation to identify interacting proteins?

First: You are right with your reasoning that Protein X (X) and Dcr-2 interact directly. Lets go through the blots: In the input you check for the proteins loaded into the setting and stain unspecifically with Coomassie.
This part of the blot shows you no unspecific input, and both proteins of interest present. This also shows that Dcr-2 is much bigger than X which allows an easy identification of band patterns.

In the eluate you will only see proteins which are bound directly in the reaction or which interact with bound proteins. Dcr-2 is Flag-tagged so it will directly bind to the beads and can be eluated from them. This is shown in the coomassie part of the blot. Dcr-2 alone binds and can be eluated, while X alone does not bind and therefore gives no signal. Dcr-2 and X together give two bands, sind Dcr-2 binds to the beads and X is interacting with Dcr-2.

This binding is also shown with the anti-His antibody which only recognizes Protein X. The protein shows up in the input where X is added. It also shows up in the elution lane (where Dcr-2 is also present) showing that X is an interaction partner for Dcr-2.