Yawning is contagious in humans, which means that, in general, it is more likely that a person yawning after perceived (by sight, hearing, or both directions) yawning issued by another person. The frequency of infection varies throughout the day, with a peak in early morning and late evening.

A recent study conducted by Ivan Norscia and Elisabetta Palagi (University of Pisa) has provided the first evidence that the behavioral contagion of yawning is associated with the empathic bond between people. The study showed that the infection follows the same gradient of empathy: is greatest in close relatives (parents / children / grandchildren, brothers, stable couples), decreases in friends, then acquaintances in (people connected only by a third, external, ie work or a friend in common) and reaches a minimum in the unknown.

Various studies of clinical, psychological and neurobiological suggest and support the link between the yawn contagion and empathy. For example, the infection begins to occur at 4-5 years of age, when children develop the ability to identify, in a proper way, the emotions of others. In addition, the infection is reduced or absent in people who have problems related to empathy, how people with autism, and is positively related to subjective scores of empathy based on tests of psychological type. Finally, the areas of the brain related to the emotional sphere overlap, in part, with those involved in the response to yawn, with a possible involvement of mirror neurons.

Yawning has been observed among various primates. In these cases the yawn is a threat gesture, a way of maintaining order in the primates' social structure. Specific studies were conducted on chimpanzees and stumptail macaques. A group of these animals was shown a video of other conspecifics yawning; both species yawned as well. This helps to partly confirm a yawn's "contagiousness".

In animals, yawning can serve as a warning signal. For example, Charles Darwin, in his book The Expression of the Emotions in Man and Animals, mentioned that baboons yawn to threaten their enemies, possibly by displaying large canine teeth.

see yawn

autism

Gordon Gallup, who hypothesizes that yawning may be a means of keeping the brain cool, also hypothesizes that "contagious" yawning may be a survival instinct inherited from our evolutionary past. "During human evolutionary history, when we were subject to predation and attacks by other groups, if everybody yawns in response to seeing someone yawn the whole group becomes much more vigilant and much better at being able to detect danger.

Personally, I can make an observation. Cats yawn as specific means to calm people, and especially to reassure the other cats and the pups. In order, they stretch, yawn, lie down, half close theyr eyes as if they start to sleep. When the whole group repeats the gestures, the majority of them (now calm) actually falls asleep.

EDIT @kmm

Norscia & Palagi
The Pisa Group in cooperation with CNR Consiglio Nazionale delle Ricerche =
Friends and loved ones yawn together - Science Daily
The Pisa Group/ Elisabetta Palagi, Ivan Norscia, and Daniela Antonacci - University of Michigan - Dearborny
Gordon G. Gallup


How do large herbivores get enough protein?

It boils down to the anatomy.

Herbivores are very good at digesting plant matter, which us monogastrics are not particularly good at. Many herbivores (such as ruminants) have large, highly developed gastrointestinal tracts containing symbiotic bacteria to allow them to digest plant matter. Once the cellulose in the plant cell walls is digested, the animal can then access the nutrients  contained in the plant matter to a degree we cannot. Ruminants (such as cows) are even better able to absorb nutrients in this way than monograstric herbivores (such as horses). Rumen microbes are also an important source in ruminants for production of amino acids.

There's also a reason why the GI tract of these herbivores is so big. In the cow, it's an enormous rumen. In the horse, it's a massive colon for hindgut fermentation. To get all the nutrients they need - such as amino acids - these herbivores have to consume and ferment vast quantities of plant matter. A carnivore can generally get all the nutrients it needs in a much smaller meat meal, meaning it does not need such an extensive GI tract.

Different species, of course, have different metabolic demands and corresponding nutritional needs. Cows and other herbivores cannot synthesize all the amino acids they need, meaning they have to be consumed through the diet. Though it is somewhat dated, an interesting discussion on this subject is Protein and Amino Acid Requirements of Mammals (PDF) by Anthony Albanese (1950). The author goes through in great details the different protein requirements for various species, but I will bring your attention to one interesting table on p 116 as it is pertinent to your last question:

As you can see, the protein content of milk seems to correspond with the time to double birth weight. Cats with a high protein milk grow very quickly, while cows, horses, and humans grow comparitively more slowly (and thus have lower protein milk).

All animals have to get protein or amino acids through the diet, but they just have different methods to satisfy their metabolic requirements. For carnivores, they consume small protein-packed meals. For large herbivores, they have to consume and digest large quantities of plant matter to meet their needs.


Why doesn't nitrogen diffuse into blood?

I like it that nitrogen came to your mind ;)

I guess in school they didn't tell you about the nitrogen at all, for the matter of simplification, because it is of no function in the body and the $O_{2}$ and $CO_{2}$ are the important gasses for biological function of breathing.

However, all of these small gas molecules are very small and generally the biological membrane is very permeable to them. That's why the cell cannot decide to let $O_{2}$ and $CO_{2}$ in and $N_{2}$ not as you suggest.

(However, the cell is able to control the permeability of these gases to some content, based on the level of cholesterol in its membrane$^1$)

The process of gas exchange is generally passive. In alveolar membrane the gas flows from the site of its higher concentration (in case of gases we talk rather about partial pressure) to the site of lower concentration. The speed of this process depends mostly on the difference in partial pressures and if you let the blood "interact" with the air in alveoles for long enough, partial pressure of all small gas molecules would come almost to equilibrium. (This happens under physiological conditions for all of the three mentioned gases)

Khan academy is right too actually. This is because as $N_{2}$ isn't either produced or consumed in the body, its partial pressure in the venous blood is similar to that in the alveolar air, and there is no force to cause its movement between these two compartments in general.

In the table you can see, that the partial pressure of nitrogen in the blood is the same as in the alveolar gas.

Picture source


Tissue identification in vascular bundle sections

Here is a single Helianthus (sunflower) vascular bundle, complements "The" Ohio State University. The xylem in a vascular bundle is generally the easiest to discern. The phloem tissues is always exterior to the xylem and the cells are generally more uniform and smaller than most of the xylem. Picking out the phloem is also more complicated by other cell types exterior to the xylem such as the "fibers" shown here. The phloem will always be interior to the sclerenchyma or collenchyma "fibers" when they are present. That is, the phloem is always adjoining, and exterior to, the cambium.
The most difficult to precisly locate is the vascular cambium since it is very thin. Notice in the diagram below, the relatively continuous line that is being pointed to by the dashed line from the label. As you go inward toward xylem and outward toward phloem, the smoothness of trying to trace a line parallel to the vascular cambium becomes much more "bumpy" as the cells are already beginning to differentiate.

To find many more images on the web, search "vascular bundle labeled photo". You should investigate further, appearance of these bundles varies between dicots, monocots, roots, shoots and species.


I think it is Anemone hupehensis. We have this species in our garden, and the seeds and dead leaves look very similar to the ones in your picture. The leaves are large,jagged and palmate and they have beautiful flowers in the summer/autumn (I've seen red, pink and white). The fruits/seeds also look very distinctive and cotton-like. The species is originally from Asia/China.

Here is a picture of the fruits/seeds:

(Hard to find good ones, this from Instagram page http://www.ipopam.com/tag/höstanemoner)


Differentiating Antaresia (Children's Complex) Pythons using something other than color pattern

I finally got frustrated enough to dig up A Revision of the Liasis childreni species-group (Serpentes: Boidae) L.A. Smith, 1985 - the original paper that split up this species complex, and when even Smith made primary determinations off of pattern and color alone, I took matters into my own hands and dug into the his raw data.

I have compiled the mean scale counts for each species into a table, and truncated any rows that showed no useful degrees of deviation for any species, resulting in the following:

             A. Childreni  A. Maculosa  A. Stimsoni  A. Stimsoni Orientalis  A. Perthensis
Ventrals     272.8        263.5         279.5        263.8                   232
Subcaudals   47.3         42.1          46.2         42.8                    38.7
Midbody      41.3         38.3          43.4         40.3                    32.7
Loreals      7.9          4.7           12.2         7.9                     7.3
Postoculars  3.6          3.1           4.2          3.8                     3.4
Pits         4.5          4             5.6          4.8                     3.1

I am including this table in its entirety to assist future identification efforts within the complex, as the original paper did a poor job of presenting this data.

The most useful difference for my purposes - distinguishing between A. maculosa and A. childreni - appears to be loreal scale count. The loreal scales sit between the eye and nostril of the snake, and do not include scales which belong to the orbital and nasal structures (The region marked "l" in the diagram below).

Following up on this, I examined a number of close-up photos of known examples of both species, and very quickly identified a distinctive difference in not just the count but also the pattern of loreal scales. Once you're looking in the right place, the difference is obvious.

A. Childreni showing its distinctive granularly-clustered loreal scales:

A. Maculosa showing its smaller number of tightly structured loreal scales:


No.

Brain death is permanent damage to the brain. Depending on the specific definition, it may refer to either cerebral death or to failure of the brainstem to maintain functions like respiration.

It could be possible for mistakes to be made and for brain death to be declared in a patient who has not actually experienced brain death. However, this is incredibly incredibly rare: zero cases have been reported when appropriate guidelines are followed (Wijdicks et al. 2010). If someone is diagnosed as brain dead after a trauma, the medical staff involved in making that decision are stating that there is effectively no chance for recovery. Brain death is not diagnosed lightly.

Wijdicks, E. F., Varelas, P. N., Gronseth, G. S., & Greer, D. M. (2010). Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 74(23), 1911-1918.


Are male and female brains physically different from birth?

Short answer
Yes, men and women's brains are different before birth.

Background
First off, learning effects versus genetic differences is the familiar nature versus nurture issue. Several genes on the Y-chromosome, unique to males, are expressed in the pre-natal brain. In fact, about a third of the genes on the Y-chromosome are expressed in the male prenatal brain (Reinius & Jazin, 2009). Hence, there are substantial genetic differences between male and female brains.

Importantly, the male testes start producing testosterone in the developing fetus. The female hormones have opposing effects on the brain as testosterone. In neural regions with appropriate receptors, testosterone influences patterns of cell death and survival, neural connectivity and neurochemical composition. In turn, while recognizing post-natal behavior is subject to parenting influences and others, prenatal testosterone may affect play behaviors between males and females, whereas influences on sexual orientation appear to be less dramatic (Hines, 2006).

The question is quite broad and I would start with the cited review articles below, or if need be, the wikipedia page on the Neuroscience of sex differences.

References
- Hines, Eur J Endocrinol (2006); 155: S115-21
- Reinius & Jazin, Molecular Psychiatry (2009); 14: 988–9


If plants "alternate generations" between sporophytes and gametophytes, why don't we say the same of humans?

The big difference is that in humans, there is no mitosis in the haploid phase.

There are three terms that are important here:

Haplontic: Most of the life is spent in the haploid phase
Diplontic: Most of the life is spent in the diploid phase
Haplodiplontic (aka. diplohaplontic): About as much time is spent in the haploid phase than in the diploid phase

At the extreme, when there is absolutely no mitosis in one of the phase, then the organism is clearly not haplodiplontic. Haplodiplontic organisms have an alternation of generations.

Note that the term alternation of generations is also used for systems that are much more complex than haplodiplontie. Examples of such complex alternation of generation include many parasites such as the giant liver fluke


How to incorporate intraspecific variation in discrete characters in comparative analyzes?

Kostikova et al. 2016. Syst. Biol. developed an algorithm to model trait evolution with inter- and intraspecific variation. The authors use it to show

  whether a life-history trait (i.e. annual versus perennial) influences the evolution of intraspecific variation in the climatic niches of species

While they do not directly incorporate the space component as in the RLQ analysis, the approach might be informative in your case. The functions are available through dryad.


In terms of Prions is there a possibility, that other proteins apart from PRPC could be misfolded

There are many prions other than PrP; it is often helpful to e.g. read wikipedia for these cases.
For example, there are many yeast prions that are not homologous to PrP https://en.wikipedia.org/wiki/Fungal_prion.
But even in humans there are a number of other proteins that form amyloids and are described as "prion-like" even though they aren't the canonical protein: https://en.wikipedia.org/wiki/Prion#In_other_diseases


Wearing sunglasses during a solar eclipse

Your eyes can dilate behind sunglasses, especially when the main source of light (the sun) is blocked, and ambient light decreases. Regular sunglasses offer some protection against certain UV wavelengths, but not enough to protect your eyes when looking directly at the sun (or, during an eclipse, the corona). Most sunglasses are mainly designed to, first and foremost, look good. After that, there is some protection against UVA (400-315 nm) and UVB (280-315 nm) light. Some sunglasses also offer "UV400" protection, which is short-wavelength blue light longer than 400 nm. Polarized sunglasses do not protect against UV at all, only reflected light (such as shining off the water or from an automobile's body or glass) and glare. Different sunglasses tints (or colors) also do not protect against UV, but they can affect color perception.

  Surely wearing proper sunglasses at any time is safer than not?

That is true, it is safer, the question is to what degree? Sunglasses offer some protection from indirect UV and visible light that has been scattered by the atmosphere and reflected off of things around us. However, the number and energy of photons (the "particles" of light) reaching your eyes when looking directly at the sun is dramatically greater, and so much more dangerous. Eyes can be damaged quite quickly by high-energy light of many wavelengths, including UV and visible, with the magnitude of the damage correlating to the energy of the light. Damage is also cumulative, accruing over a lifetime. Even small peeks directly at the sun will contribute to your overall lifetime risk of eye damage, and may cause permanent, irreversible harm very quickly.

There are a number of much safer alternatives for watching solar eclipses, including pinhole projectors, welding goggles rated higher than 14, various solar filters for cameras, telescopes, and binoculars, and fully exposed and developed black-and-white film (good luck finding that nowadays), among others.

Above all, make sure you're safe, and if you have any doubts consult with an expert, such as a science/natural history museum or local university's astronomy department.


The words "hawk" and "eagle" are very confusing and may mean different things in different parts of the world. In fact, the nearly thirty species of raptors (not including owls) native to Taipei apparently include one called a mountain hawk-eagle (Nisaetus nipalensis).

If no one can answer your question, you might narrow the field with a process of elimination. I can't vouch for the accuracy of Wikipedia's list of birds native to Taipei, but it's a start.

There are apparently seven native raptors that are called eagles. If you can eliminate all seven eagles, then it presumably is not an eagle.

Your photographs are helpful insofar as they illustrate the bird's general outline, but it's very hard to distinguish its color pattern. However, the shape of the wings should help narrow the field.

Birds Native to Taiwan

EDIT

I don't know if you're familiar with the terminology, but many raptors are classified as buteos or accipiters. If I remember correctly, species with broader wings are generally buteos. Species commonly called "hawks" include both buteos and accipiters, but I believe most birds called "eagles" are buteos.

Anyway, here's another link...

Buteos


Is there any biological reason that professional swimming is dominated by white people?

It's not biological, it's simply an education issue, and googling would give you:

Just under 70% of African-American children surveyed said they had no or low ability to swim. Low ability merely meant they were able to splash around in the shallow end. A further 12% said they could swim but had "taught themselves".

http://www.bbc.co.uk/news/world-us-canada-11172054

Unlike the UK, where learning to swim is enshrined in the national curriculum except in Scotland, the ultimate responsibility in the US often lies with parents.


How does evolution produce complex organs

The best introduction to evolution of complex phenotypes via master control genes is Endless Forms Most Beautiful: The New Science of Evo Devo and the Making of the Animal Kingdom by Sean B. Carroll. You might also want to have a look at a more recent Evolutional developmental biology (Evo Devo) book like those you get when searching for "Evo Devo" in Google Books.

In summary, it is possible for a mutation to change a shape by changing the spatial distribution of a transcription factor during embryo development. What's more, by changing the distribution of two mutually dependent factors, formation of any shape is possible if the distributions overlap. Such transcription factors are highly conserved in evolution and the most important cause of the endless forms we see.


Cells of umbilical cord - mom's or son's?

Answer: Son's.

The interface you are looking for is in the placenta. https://en.wikipedia.org/wiki/Placenta

Formally the fetal side of the placenta is called the Chorion frondosum, which develops from the outer cells of blastocyst (trophoblast), and the maternal side of the placenta, Decidua basalis, which develops from the maternal uterine tissue.

  How is it even possible?

Immune tolerance in pregnancy or gestational/maternal immune tolerance

The placenta functions as an immunological barrier between the mother and the fetus, creating an immunologically privileged site. For this purpose, it uses several mechanisms

It secretes Neurokinin B containing phosphocholine molecules. This
is the same mechanism used by parasitic nematodes to avoid detection
by the immune system of their host.
Also, there is the presence of small lymphocytic suppressor cells in the
fetus that inhibit maternal cytotoxic T cells by inhibiting the
response to interleukin 2.
The placental trophoblast cells do not express the classical MHC
class I isotypes HLA-A and HLA-B, unlike most other cells in the
body, and this absence is assumed to prevent destruction by maternal
cytotoxic T cells, which otherwise would recognize the fetal HLA-A
and HLA-B molecules as foreign. On the other hand, they do express
the atypical MHC class I isotypes HLA-E and HLA-G, which is assumed
to prevent destruction by maternal NK cells, which otherwise destroy
cells that do not express any MHC class I. However, trophoblast
cells do express the rather typical HLA-C.
It forms a syncytium without any extracellular spaces between cells
in order to limit the exchange of migratory immune cells between the
developing embryo and the body of the mother (something an
epithelium will not do sufficiently, as certain blood cells are
specialized to be able to insert themselves between adjacent
epithelial cells). The fusion of the cells is apparently caused by
viral fusion proteins from endosymbiotic endogenous retrovirus
(ERV). An immunoevasive action was the initial normal behavior of
the viral protein, in order to avail for the virus to spread to
other cells by simply merging them with the infected one. It is
believed that the ancestors of modern viviparous mammals evolved
after an infection by this virus, enabling the fetus to better
resist the immune system of the mother.

Other mechanisms include exposure to immune modulating factors present in seminal fluid from vaginal and oral sex. https://en.wikipedia.org/wiki/Pre-eclampsia#paternal_tolerance


Do archaea undergo the same horizontal gene transfer processes as bacteria?

Wagner A, Whitaker RJ, Krause DJ, Heilers JH, van Wolferen M, van der Does C, Albers SV (2017) Mechanisms of gene flow in archaea. Nat Rev Microbiol 15: 492-501.

  The exchange of genetic material is a major driving force for genome
  evolution across the tree of life and has a role in archaeal
  speciation, adaptation and maintenance of diversity.

Soucy SM, Huang J, Gogarten JP (2015) Horizontal gene transfer: building the web of life. Nat Rev Genet 16: 472-482.

  Horizontal gene transfer (HGT) is the sharing of genetic material between organisms that are not in a parent-offspring relationship. HGT
  is a widely recognized mechanism for adaptation in bacteria and
  archaea.

Fuchsman CA, Collins RE, Rocap G, Brazelton WJ (2017) Effect of the environment on horizontal gene transfer between bacteria and archaea. PeerJ 29: e3865.

  Potential hotspots of horizontal gene transfer between archaea and
  bacteria include hot springs, marine sediments, and oil wells.


Can action potential generating ion channels only be understood as assemblies of membrane proteins (and not as single proteins)?

Wikipedia's statement

  A voltage-gated ion channel is a cluster of proteins embedded in the membrane.

is most likely referring to the fact that most ion channels (maybe all? I hate to say "all" in biology) are made up of multiple protein subunits; usually these are all considered one protein's quaternary structure, though, so wikipedia's language is not ideal.

I think you are then running with a misunderstanding of this statement to make some conclusions that are not warranted. Of course multiple ion channels come in to play when you are talking about membrane potentials at the cellular level. Of course you need to consider multiple ion channels when considering the overal membrane potential, but it is sufficient to know only a) the gating properties of a given channel and b) the membrane potential to know the contribution of that channel.

Action potentials are only roughly the same 'size' in terms of voltage amplitude - they are certainly not identical, and this size is because of the gating properties of voltage gated channels and the reversal potential for sodium. The membrane potential can never exceed the reversal potential for sodium via sodium-based conductances, so that puts an upper limit on action potential size. In addition, hyperpolarizing potassium-permeable voltage gated channels will open at depolarized potentials, further limiting the maximum amplitude of an action potential.

Ion channels don't exhibit any firing patterns: neurons exhibit firing patterns that depend on all the channels present and the physical morphology of the cell.


Cells in the brain communicate with each other through electrical (and chemical) signals. The electrical signals from millions of neurons add up, and can be detected from outside the skull. This is called electroencephalography.

The signals that are strongest when measured in this way are often periodic or oscillatory (i.e. wave-like), because similar electrical signals from many neurons support each other if they are active synchronously. In contrast, when neurons are firing in a disordered way, then their electrical signals can partially cancel each other out when measured from outside the skull.


It depends of what order and even what family of insects we are talking about. Insects may have complete or incomplete metamorphosis, being the complete more complicated. Even inside the first group (wich in fact contains most of the insects since coleoptera, diptera, lepidoptera and himenoptera have complete metamorphosis) there are important differences. However, I'll try to explain some basics.

First of all, metamorphosis is a molting-related process. It's regulated by the same hormones and they share many characteristics. In insects with uncomplete metamorphosis, this is very visible, since the "metamorphosis" is the last molt, wich usually involves growth, sexual maturity and the development of functional wings.

The choice between a regular larval molt is determined primarily by the levels of juvenil hormone, wich decays during the last larval instar (pupae and adult are instars, too). The molting is triggered by a peak of ecdysone, an steroid.

Once the insect has entered into the state of pupae, the organs start to suffer diverse changes. The formation of adult organs de novo arise from some special structures called imaginal discs, wich are clusters of stem cells that are more or less isolated in the larvae.

Position of the imaginal discs in Drosophila. Source.

Note that diptera larvae lack legs, mandibles and even head, while coleptera larvae usually have true legs, a set of mandibles and many other adult features.

A typical larva of a coleoptera of the genus Lucanus. Note the mandibles and the legs. Source.

Some other organs remain more or less the same, such as the hearts or many parts of the nervous system. On the other side, some larval organs needs to dissapear and suffer programmed cell death. The gut, many parts of the nervous system, between others, suffer modifications that may be more or less drastic. In many cases this happen by simple growth and differenciation of the tissue or degeneration by apoptosis, but in some others the whole organs suffers apoptosis and regenerates itself with adult characteristics.  For example, the innervation of the abdominal parapods (false legs) in caterpillars suffer a progressive degeneration, while the opposite happens in toracic nerves, wich will have to control legs and wings. This whole process is pretty similar to embrionic development and it shares many traits with it.

Finally, metamorphosis in other animals, such as crustaceans, vertabrates (fishes and amphibians), echinodermae, annelidae, cnidaria and many others will probably vary widely. I know for sure that amphibians metamorphosis is regulated by tiroid hormones, but I'm not even sure that many of the other examples have even been studied at a phisiological level.


definition of tempo and mode in evolution

Actually, we can go right to the source on this: George Gaylord Simpson's Tempo and Mode in Evolution (1944).

Tempo is the rate of evolution. Simpson was a paleontologist, so he was trying to answer questions like "what is the percent change in the size of this tooth per million years?" He has a chapter estimating these rates for various characters in horses, which have a very good North American fossil record.

Mode encompasses the mechanisms responsible for evolution and their patterns. Simpson was working at the time of the Modern Synthesis (the wikipedia page is decent and brief enough on the topic, about which books are written), coming from the perspective of a paleontologist trying to reconcile genetic evolution with the macroevolutionary patterns he was seeing in the fossil record.

Simpson was really the first paleontologist to look at fossils in a quantitative way, trying to understand of connections between microevolutionary processes and macroevolutionary patterns. He even co-authored one of the first quantitative and statistical methods books for "organismal" biologists: Quantitative Zoology.

Specifically, of tempo, he says (p. xvii):

  "...evolutionary rates under natural conditions, their acceleration and deceration, the conditions of exceptionally slow or rapid evolutions, and phenomena suggestive of inertia and momentum."

Of mode, he says (p. xviii)

  "...the study of the way, manner, or pattern of evolution, a study in which tempo is a basic factor, but which embraces considerably more than tempo. The purpose is to determine how populations became genetically and morphologically differentiated, to see how they passed from one way of living to another or failed to do so, to examine the figurative outline of the stream of life and the circumstances surrounding each characteristic element in that pattern."

Mode basically encompasses all the processes of evolution. Tempo is the subset of mode that concerns how fast evolution is (or is not) happening.

The great thing is that 70 years after Simpson's book, biologists are still trying to understand tempo and mode of evolution.


Is there a biological neuron that spikes in response to hyperpolarizing currents?

I was doing some more research and stumbled upon this paper here by Dr. Izhikevich that describe neurons as a system that can exhibit resonance. The author built a model that he calls the resonate and fire, which is a linear piece-wise model of a neuron.

The interesting thing, and why I bring it up, is it can respond to a "two inhibitory pulses, that if timed correctly will cause the neuron to fire. but neither inhibitory pulse alone can cause the neuron to fire.

Following some of the citations in the article (found here), apparently thalumus neurons can exhibit resonance and thus theoretically can fire in response to the right frequency of input. However it is important to note that they thalamic neurons are close to threshold, and are not receiving the double inhibitory input that Izhekivich talks about in his paper. The second paper uses a ZAP protocol.

A Zap protocol is injecting a Sine wave into a neuron and slowly change the frequency linearly in time.

$$I_{ZAP}(t) = \sin((\omega_0+\omega t) t) $$ where $\omega_0$ and $\omega_1$ are constants.


Connective tissue in animals are mostly made up of collagen

Tissue is not like a simple chemical mixture ; rather tissue means a group or assemblage of cells, obeying certain defining-characteristics.
Animal connective tissues contain collagen mostly in the extracellular matrix. There are also other cell-constituents like phospholipid(membranes), DNA, RNA, etc.  Blood is a liquid connective tissue which do not contain collagen in its matrix (plasma)

  What is the equivalent connective tissue in plants?

Connective tissue is defined as all the tissues originated from the mesoderm layer of the animal embryo.

Now plants have a different mode of development than animals (plausibly due to evolution in separate route). So no part of a plant-body is homologous with a part of animal-body. It is impossible to bring a compare.

However; plants too; have their extracellular matrix; which is more popular as plant's cell wall (that contain cellulose, hemicellulose, etc.) as well there are intercellular spaces.

Still, if you forcefully want to bring a comparison; then the ground-tissue system of plant maybe called as a rough analogy with connective tissues in animals ( Similarly epidermal tissue of plant maybe a rough analogy with epithelial tissue of animals)


The structure on the oak nut is a knopper gall.

  It is a distortion of growing acorns on pedunculate oak (Quercus robur L.) trees, caused by gall wasps(Andricus quercuscalicis), which lay eggs in buds with their ovipositor.

An Andricus quercuscalicis larva in an open gall of an acorn:
Link

Here's a video by BBC on the same you may find it interesting.


How come only a handful of animals can do photosynthesis?

It is all about energy.
It is estimated to take 5000 square meters of plants to feed the average person in the developed world, while the same source gives the lowest possible for a human under ideal conditions at 700 square meters.  In comparison, the average person covers less than 1 square meter.  While there is a lot of waste (animals are able to eat only a few percent of the energy the plant produces), the total energy available from photosynthesis is still orders of magnitude smaller than daily requirements for a typical animal.
Even in the case of the slug you linked (which you would expect would need about as little energy as possible for a mobile animal), it seems they obtain little or none of their actual energy from photosynthesis.
Hence you see photosynthesis restricted to life that has extraordinarily low energy requirements, which typically means being stationary (or moving very, very slowly as in the case some plants).  As soon as you adapt to a mobile, higher energy niche, you need access to a lot more energy than photosynthesis can provide.


Best methodology to compare computed phylogeny tree with taxonomy?

Take a look at the ape package in R. It has a function called cophyloplot which allows you to visualize two trees like so:

Which is well described in this question (also the source of the image).

There is also the dist.topo function which produces a metric which describes the topological distance between two phylogenetic trees. I don't know if this is what you mean by "divergent" but I hope it helps.


Pasteurization and Bioavailability of Antioxidants in Beet Juice

So, when they subjected "ready to drink" beetroot juice to thermal pasteurization, they found the betacyanin and betaxanthin (our major antioxidants, and pigment molecules) content to be 39.9 and 42.28% degraded, respectively (1). Their conclusion was as follows:

  Standardization of process condition and
  quality degradation of beetroot juice due to thermal
  pasteurization was studied. The standardized T2
   batch
  with total heating time (fh) of 720 s thermal in-pack
  pasteurization leads to the minimal degradation of
  color, betalain content (Betacyanin and Betaxanthin),
  antioxidant activity and complete inactivation of
  micro flora of beetroot juice. The color, betalain
  content (Betacyanin and Betaxanthin) antioxidant
  activity and sensory of the beetroot juice was
  significantly (p < 0.05) reduced during 180 days
  ambient (27-30°C) storage, but still the quality of the
  juice was adequate upto 180 days. We concluded that
  thermal pasteurization of 96 °C for a total heating time
  (fh) of 720 seconds with P-values of 11.16 would be
  a good method to produce microbiologically stable
  beetroot juice with the retention of quality attributes.

So our goal is to get a juice that retains as many "good" attributes as possible, while producing a product that isn't going to get anyone a foodborne illness. As for the net effect of pasteurization on fruit juice in general, im still coming to a conclusion there. The process shouldn't render too much of the fruit/vegetable ineffective, though I'd still expect some degradation either in storage or processing.


It is an insect of family Chrysopidae under the order Neuroptera (net-winged insects).
The insects of this family are commonly called Green lacewings.
Neuropterans have large lateral compound eyes, four wings and a generalised pattern of veins.

(Source: Wikipedia)
Identifying morphological features:

Soft-bodied insects with copper-colored eyes, long thread-like antennae, and lacy wings.
Most species are green, but some are brown, especially overwintering adults of certain species

( Reference: Bugguide )
A similar family of lacewing, Hemerobiidae also exists which are brown, have rounded smaller wings and found throughout the world.
Here's a link to wikipedia showing the phylogeny of the Neuroptera as explored using mitochondrial DNA sequences: link .


Building a PDB file from amino acid sequence of non-folded structure

So to be clear, it sounds like you want the 'coil' or unfolded structure of a protein based on the sequence?

There are plenty of programs out there to do homology modelling, which is taking a sequence of unknown structure and modelling it onto one with a known structure. On the other hand, there are many libraries for analyzing existing structures. What you want is somehow in between these two.

I'll add some links here as I find them:

There is a Lua library that might be useful : https://github.com/rob-miller/rFold
Modeller has functions for this: https://salilab.org/modeller especially this page
The Structural Bioinformatics Library : http://sbl.inria.fr/doc/index.html
The Rosetta library (as used in fold.it): https://www.rosettacommons.org/

I'm sure there are more, but it really depends on what programming language you want to use, or if you are implementing stuff yourself versus running some standalone software.


Why can I see a light flicker when it's in my peripheral vision?

Your retina contains both rods and cones. Cones are color sensitive, slow, and concentrated near the center of your field of vision. Rods are "light" sensitive, fast, and concentrated near the periphery. You want to be able to respond quickly to a threat "in the corner of your eye" without needing to see the color of the threat.

This is nicely explained by this diagram (source: http://hyperphysics.phy-astr.gsu.edu/hbase/vision/imgvis/retina.gif)

So when you see a CRT in the corner of your eye, your rods respond quickly enough that you can tell the light of the CRT is flickering. As you turn your gaze towards it, you get the higher resolution, color rendition of the cones - and lose the temporal resolution.


What does it mean when a patient suffering from malignant tumor (cancer) has been declared cured?

TL;DR - ask someone who has survived 45 years after treatment of their testicular cancer. The patient (and most doctors) would consider that a cure.

I believe the kxcd cartoon explains prognosis quite well. There is something that @Crags has overlooked, though, and that is the caveat "Once most cancers spread out into your body, they're incurable".

I would consider that sentence to be quite correct. A good prognosis is very different from a cure. Most of the surgeons, radiation therapists and oncologists I have worked with make that distinction. (Even surgeons, whose mottoes include "A chance to cut is a chance to cure." and "Nothing heals like cold hard steel." are careful not to use the word cure, unless it is a cure.)

I am not an oncologist, but oncologists do write papers. From one of them:

  METHODS: We analysed postmenopausal women with localised invasive breast cancer. The primary endpoint disease-free survival (DFS), and the secondary endpoints time to recurrence (TTR), incidence of new contralateral breast cancer (CLBC), time to distant recurrence (TTDR), overall survival (OS), and death after recurrence were assessed... FINDINGS: At a median follow-up of 100 months (range 0-126), DFS, TTR, TTDR, and CLBC were improved significantly in the ITT and hormone-receptor-positive populations.

Although this study only followed patients for 100 months (8.3 years), some studies are much longer, and a cure is what you or I would think of as a cure: disease-free survival, not of months, but for a lifetime, that is, non-recurrence of the cancer.

Your professors sound like they are using the standard approach to cure, which is to hedge one's bets:

  In medicine, a disease is considered cured when it’s been successfully treated and does not return. The concept of “cure” is difficult to apply to cancer because undetected cancer cells can sometimes remain in the body after treatment, causing the cancer to return later (referred to as a recurrence or relapse). Many cancers are considered “cured” when there is no cancer detected five years after diagnosis. However, recurrence after five years is still possible.

In the past, cure was defined as 5-years cancer free. We now know that that is survival, not cure. The same can be said of 10 years (thought that one runs more true to cure). The fact is, most studies don't follow patients indefinitely. That doesn't mean no cancer is "cured". The patients (even many of those in the xkcd comic) without recurrence are cured. Therefore it is a fallacy to say cancer can never be cured. Semantics and statistics are at play.

As I said in my comments, there are curable cancers.

Curable cancers: non-invasive basal cell carcinoma:

  Nearly every basal cell cancer can be cured, especially when the cancer is found early and treated.

(This is not a hedge. The authors are lumping aggressive BCCs in here with the less aggressive BCCs.)

Certain early prostatic cancers:

  These results suggest that a patient has a high likelihood of biochemical cure after treatment for prostate carcinoma with conventional doses of external beam RT if he has not demonstrated biochemical failure within 5 years of treatment. Patients with lower pretreatment PSA levels and lower Gleason scores may require longer follow-up than those with less favorable characteristics to achieve the same certainty of cure. Patients who achieve a PSA nadir ≤ 0.4 ng/mL and require ≥ 2.0 years to reach this nadir have the highest probability of cure.

Cervical cancer:

  Early cervical cancer can be cured by removing or destroying the precancerous or cancerous tissue.

Colorectal cancer:

  Conclusion: Patients who survive 10 years appear to be cured of their disease, whereas approximately one third of actual 5-year survivors succumb to a cancer-related death. In well-selected patients, there is at least a one in six chance of cure after hepatectomy for CLM. The presence of poor prognostic factors does not preclude the possibility of long-term survival and cure.

Childhood acute lymphocytic leukemia:

  Impressive improvements of survival rates in pediatric acute lymphoblastic leukemia (ALL) have been achieved during the last decades.1–21 Today, a long-term cure can be attained for approximately 75% of patients.

(Although good survival rates - defined by *event free survival - are defined at 6 years in this paper, there are papers which follow to 15 years with little change in the group. Like most studies, longer times mean more patients are "lost to follow-up".)

It goes on and on.

Finally, my comment was an admonition to you to be wise with your words, not an absolute.

Understanding Statistics Used to Guide Prognosis and Evaluate Treatment
The cure of cancer: A European perspective
Basal cell carcinoma: Diagnosis, treatment, and outcome
Cervical cancer
Risk-adjusted therapy of acute lymphoblastic leukemia can decrease treatment burden and improve survival: treatment results of 2169 unselected pediatric and adolescent patients enrolled in the trial ALL-BFM 95


What phase of Action Potential (AP) exactly defines the Relative Refractory Period?

Neither is an accurate definition; both are correct and not conflicting if you interpret "corresponding" to mean "typically/approximately corresponding".
The absolute refractory period is any time in which you cannot evoke another action potential no matter the strength of stimulus, due to an action potential in progress/that has just occurred.
The relative refractory period is any time in which you can trigger an action potential but need a stronger stimulus than normal.
Neither of these definitions refers to specific phases of the action potential in terms of voltage or change in voltage. Yes, typically the absolute period includes the ascending and descending phases of the AP, but there's no reason it can't last longer depending on the gating properties of the sodium channels. Similarly, the relative refractory period starts with the end of the absolute refractory period and continues through the hyperpolarization phase, but there is no reason it cannot end sooner or later, again depending on gating properties.


What is the advantage of having multiple pathways to activate complement?

There can be many reasons for this, but generally redundancy in biological systems is very important in that it makes the system more robust. If one pathway fails, due to mutation or some environmental factors, the other(s) can compensate and the function of the pathway remains. In some cases it can also be used to tune the degree of activity or speed of activation.

Article on pathway redundancy


This is due to presence of a hydrophobic chemical called as cutin present at the the aerial surfaces of plants.

  Cutin is one of two waxy polymers that are the main components of the plant cuticle, which covers all aerial surfaces of plants. The other major cuticle polymer is cutan, which is much more readily preserved in the fossil record,.[1] Cutin consists of omega hydroxy acids and their derivatives, which are interlinked via ester bonds, forming a polyester polymer of indeterminate size.

Source: https://en.wikipedia.org/wiki/Cutin


When was it discovered XY chromosomes decide the sex of a child in humans?

The discovery of genetic sex determination, and determination of sex via male gametes (in XY species, female in ZW), occurred over some time in the late 1800's and early 1900's. Advances were made with methods to stain chromosomes and, in 1891, Henking noted that wasps produced sperm with a varying number of chromosomes. However, he was unable to gather evidence that the "x-element" was determining sex. Nettie Stevens, in 1905, then used beetles and noted an odd set of chromosomes in sperm, which later became known as the sex chromosomes. This was the discovery of sex determination through male gametes.

  "In 1905, while studying the gametes of the beetle Tenebrio molitor, Stevens noted an unusual-looking pair of chromosomes that separated to form sperm cells in the male beetles. Based on her comparisons of chromosome appearance in cells from male and female beetles, Stevens proposed that these accessory chromosomes were related to the inheritance of sex." - Link

In 1905, Beecher-Williams also made the same discovery, so they are both credited with discovering sex determination by the sex chromosomes. However, Clarence Erwing McClung also contributed to theory that Henkings X-elements may determine sex in 1901.

Thomas Hunt Morgan also contributed some major work on heredity and sex chromosomes, having been initially sceptical of Stevens' discovery. He found that eye mutations in Drosophila appeared to be sex linked, and concluded that the mutations were likely carried on the sex chromosomes.

There is a paper from 1910 where Michael Guyer concludes that accessory chromosomes (the sex chromosomes) likely determined sex in humans.

  "It is probable that in man and certain other vertebrates, as in the insects, myriapods and arachnids, the accessory chromosomes are in some way associated with the determination of sex."

However, Theophilus Painter, in 1921, concluded for the first time that human sex determination was by the presence of X or Y in the sperm; Guyer had gone for an XO system. While Painter got the chromosome count wrong, being hampered by the techniques of the day (an issue that wasn't resolved until the 1950's), he got the sex determination system right.


A clutch usually refers to all the eggs for a single reproductive event or laying or location. It can mean either all those laid by one organisms in one event or all those laid in a population in a single time and place. Which is usually clear in context.

Even just for an individual it is a bit vague however and can refer to one laying or multiple layings if they happen close together in time.

There is also a usage difference by specialization, agricultural scientists tend to favor a boarder usage for instance.


Why does the body not recycle red blood cells?

They are recycled, the iron and other components are broken down and then absorbed. Adaptations of the RBC prevent the same RBC being used. They lack a nucleus to make them highly efficient oxygen carriers (pack as much haemoglobin as possible). Without a nucleus and other organelles they're unable to synthesise the stuff they'd need for renewal. There's a lot of wear and tear that occurs as they're constantly flowing in tiny blood vessels and getting damaged or affected by substances in the blood.


Are brown eyes healthier than blue eyes?

People conflate "Dominant" traits to mean "healthier" which is a huge misconception. The previous answer provided a good example of how what is adaptive in one environment can be Mal-adaptive in another. Many Disorders can be dominant for example Huntingtons disease or achondriplastic dwarfism.


What animal produces male gametes by mitosis?

In organisms which have haploid males (such as honeybees), there is a variation of meiosis during spermatogenesis. The meiosis-I is abortive i.e. the chromosomal events such as crossover and separation of homologous chromosomes, do not happen. However, some cytological changes do happen which is described by Sharma et al (1961) as "simulation of the normal meiosis I". This is followed by meiosis II (which is mechanistically same as mitosis). So, basically there is no halving of the number of chromosomes and the gametes are also haploid.

So, as far as I can guess, the question in your exam sheet probably refers to spermatogenesis in Hymenopteran haploid males.

Reference:
Sharma, G. P., Brij L. Gupta, and C. G. Kumbkarni. "CYTOLOGY OF SPERMATOGENESIS IN THE HONEY‐BEE, APIS INDICA (F.)." Journal of the Royal Microscopical Society 79.4 (1961): 337-351.


How is the antigen against which autoantibodies are formed, identified?

All of the above, basically. If it's a protein antigen, you can perform an immunoprecipitation with the auto-antibody and use any one (or more) of several methods (Western blot, various methods of sequencing, etc.) to identify the binding partner(s). DNA and RNA can be identified easily by biochemical means. You can also use ELISAs or similar methods like electrochemiluminescence which allow a greater degree of multiplexing.

Sequencing the autoantibodies' variable regions may give some information about the structure of the antigen, but not enough to actually identify the binding partner. Also, one key fact to keep in mind is that the antibody response in many autoimmune diseases is polyclonal (just as the T cell response often is), meaning there could be dozens to hundreds of different complementarity-determining regions (CDRs) to sequence, a very laborious process that may not yield much information.

Immunohistochemistry (IHC) can be useful for seeing which cell types the antibodies bind to, but it doesn't give great resolution on the subcellular level, and doesn't tell you anything about what the actual target is. Additionally, due to the amount of chemical processing a formalin-fixed paraffin-embedded (FFPE) tissue goes through, the antibody's antigen may not be exposed properly for the antibody to bind.

From what I can find, people suspected an association between ANCA and lupus due to the similarities in both diseases' clinical presentation. Here is a paper from 1996 talking about it, there are many others.


Why is it $q^2$ for the individual count in hardy weinberg?

First of, let me correct your equation: $q = \sqrt{\frac{1}{100}} = \frac{1}{10} = 0.1 ≠ 10 $.

From allele frequency to genotype frequency

Imagine you were to randomly sample an allele from a population of allele where the allele A is present at frequency $q$. What is the probability that you draw allele A? Answer: $P(A) = q$. Now, put this allele back in the pool and imagine you have to draw two alleles. What is the probability that the two alleles are A. Well it is the probability that the first allele is A times the probability that the second allele is A, it is $P(A) \cdot P(A) = q \cdot q = q^2$.

From genotype frequency to allele frequency

Therefore, under Hardy-Weinberg conditions, if the allele A is at frequency $q$, then the homozygote genotype AA is at frequency $q \cdot q = q^2$. Now let's denote the frequency of the genotype AA by $f_{AA}$. You know that $f_{AA} = q^2$ from the above though experiment. If you take the square root of both sides, you get $\sqrt{f_{AA}} = \sqrt{q^2} = q$. In words, the frequency of the allele A is the square root of the frequency of the genotype AA.

Recessivity and dominance

Btw, you'll note that those calculations tell nothing about the patterns of dominance/recessivity of alleles (Hardy-Weinberg principle assumes no selection anyway).


When happens when pollen grains land on the a part other than the stigma of a flower of the same species?

Sometimes, the morphology and the topology of the flower structure is such that the pollen grains falling on certain parts are gravitationally (or hydrostatically) drawn towards the stigma.
I remember having read that the waxy streamlined stigma of submerged hydrophytes (Vallisneria, Hydrilla)  creates mini vortices around it during steady water flow. These vortices then pull nearby pollen, (which may be sitting on nearby flower parts) towards itself. Certain hydrophyte morphologies also maximise the water flow towards stigma, which in turn gathers pollen incident elsewhere on the plant and bringing in towards the stigma.(For example, the streamlined and bladder shaped hydrophyte flowers have stigmas at their centre)

Another way to do this is via the common sloping surface of the petals or the perianth, which on gathering pollen, gravitationally push them to the centre of the flower where the stigma usually resides. The entire inflorescence stalk might be modified into specific shapes to do this. The common pyramidal arrangement of the inflorescence (broad at the base, tapering towards the apex) helps in gathering the pollen incident on non-stigma parts of the apex region at the bottom.

Apart from this, pollen falling elsewhere, may again be taken up by the agents of pollination. But I believe the formation of pollen tube never occurs at any place other than stigma. Nor does any re-absorption take place.

It is also worth mentioning that just because pollen falls on the correct stigma does not ensure fertilization. Absence of stigma maturity/receptivity, synergid abnormality, inviable pollen etc could still hinder fertilization.

[I am not perfectly aware about studies on whether any chemical reaction occurs if pollen lands on places other than stigma. But I doubt it, since the chemical specificity required to begin the pollen tube formation is very high in most species.]


A graph is generally meant to be interpreted as y being a response to a change in x. This graph highlights that as the partial pressure of oxygen $P_{O2}$ increases, so does the percentage of hemoglobin that are saturated in oxygen. The relationship is not linear (unlike you seem to suggest) but is logistic.

The graph also highlights how three different level of affinity would affect the relationship between $P_{O2}$ and the fraction of hemoglobin that is saturated and highlights side consequences of such affinity variation.

Finally, with vertical dotted lines, the graph indicates what the $P_{O2}$ is in the lungs and in the other tissues.

  why a decreased affinity is a shift to the right and an increased affinity is a shift to the left?

Consider a single point in the x axis such as $P_{O2} = 40$ for example. If affinity is increased you would expect that the percent saturation of Hb would increase, right? This causes a shift of the left.


How to determine if this blood disorder is recessive or dominant?

Given that this is a text book question about classical genetics, you can safely disregard any reality about the disorder.

I'd argue that the two alleles show incomplete dominance. The mild anemia, which is intermediate between healthy individuals and those with severe anemia, can be attributed to heterozygous individuals. In this case, the expression of the functional allele is not enough to compensate for the nonfunctional allele, producing the mutant phenotype.


Are CN3, CN7, CN9 and CN10 the only Parasympathetic Cranial Nerves?

Yes, only III, VII, IX, and X are cranial nerves that carry parasympathetic autonomic neurons. The key phrase is "cranial." Pelvic splanchnic nerves also carry parasympathetics, but they arise from the pelvis, not the brain.


Is it correct that the body only responds to the most painful stimulus?

Your question statement is a little bit incorrect or, better say, imprecise.

First of all it is not clear what you mean by the "body response" here? Pain is sensed by peripherial receptors (several types of receptors, mostly purinergic, are assumed to play role in pain preception) and then this sensation is propagated into CNS. So, the local "response to pain" (like swelling, increase of the blood perfusion) is not the response to the pain stimulus, but rather a methabolic response to the cell injures and release of many humoral factors like interleukins, "wound hormones" etc.

And this is true that out of many different pain inputs the one with highest intensity seems to "outshine" all other inputs and ultimately the pain perception is constrained to a single body part. However, if you consciously focus your perception on other parts of your body you may be able to percieve the pain originating from these parts even if this pain is lower.

This principle is known as a smaller particular case of a more general principle known as "the dominance principle of Ukhtomsky". Wikipedia has only the Russian language version about this principle (as well as about Ukhtomsky, a prominent Russian physiologist) and it seems to be not really known outside of the Russian scientific community (this is the only page I found about him in English).

The more general principle of Ukhtomsky postulates the following: one certain input may lead to the formation of the dominance center in the cortex. The domaninace center is characterized by the higher level of nerve cell excitation, whereas the rest of the cortex undergoes an inhibition so that different, even unrelated inputs converge here, helping this center to exist for longer time. The only way how this center can be ceased is to form another dominance center by a extremely high stimulus (for example a startle sound). Here the most insensive pain leads to the formation of such a center and all substantial pain stimuli just contribute to the persistence of this center: the pain is however percieved to originate from the place where the first stimulus, responsible for dominance center formation, originated from.


Well, the oldest intact DNA found is actually 419 million years old, and it belongs to (not surprisingly) bacteria. Samples were extracted from surface-sterilized salt of different geological ages (23, 121, 419 million years of age, MYA).

But as you mentioned, these are fragments. Studies on the half-life of DNA suggest that even under ideal circumstances, DNA sequences older than 1.5 million years will be too short to be readable.

The oldest genome known to date, though, is 700,000 years old, and was recovered from samples from a horse leg bone. You were correct, the leg was in permafrost. That's a considerable jump from mastodon and polar bear fossils which were about 50,000 and 110,000 years old.


Are SLC52A2 and GPR172A really the same?

This isn't a case of gene splicing causing different protein variants.  In the studies that identified these two functions (GHB sensitivity and riboflavin transport), they were using DNA derived from mRNA (cDNA), which means what was being expressed in their experiments did not have introns, so there was no chance for alternative splicing.

This gene has a weird history, here is the summary:

Takeda et al. 2002: Identification of G protein-coupled receptor genes from the human genome sequence

Takeda and co. download a copy of the human genome and translate it looking for GPCRs.  They look at all the ORF that DIDNT have introns: "We collected intronless open reading frames (ORFs), which were long enough to cover GPCRs from the human genome". They also only look at things with 6-8 transmembrane helices as determined by the prediction program SOSUI.  One of the GPCRs they found was named hGCRP41 (hypothetical protein similar to GPCR) accession number: AB083623.  They report it probably has 8 transmembrane helices, and 418aa.  This protein probably doesn't exist because they read straight through two introns in their analysis.  The protein also terminates in the middle of a frame-shifted exon.

Ericsson et al. 2003: Identification of receptors for pig endogenous retrovirus

Next, Ericsson et al come along looking for receptors for the pig endogenous retrovirus and find this gene.  They used cDNA to make a bunch of transduced cell lines that had difference human cDNAs expressed.  They found two related proteins that could serve as receptors to the pig endogenous retrovirus.  They named the first one HuPAR-1, which is 445aa long and has 11 transmembrane helices.  This is the length of one of the proper splice variants of this gene.

Andriamampandry et al. 2007: Cloning and functional characterization of a gammahydroxybutyrate receptor identiﬁed in the human brain

Andriamampandry is looking for gammahydroxtbutyrate (GHB) receptors by using cDNA and seeing which cDNA-transduced cells become sensitive to GHB.  They find two nice proteins that are sensitive to GHB, GHBh1 and C12K32.  GHBh1 is identical to HuPAR-1, it has 445aa and 11 transmembrane helices.  C12K32 is a frameshifted version of GHBh1 that is slightly longer, but has the same number of helices. They had previously found a 512aa ortholog in rats, in 2013.

Yao et al. 2010: Identification and Comparative Functional Characterization of a New Human Riboflavin Transporter hRFT3 Expressed in the Brain.

Finally, we have Yao et al, who searched for homologs to their Riboflavin transporters.  They found one in a cDNA library, and it was 445aa long.  But they noticed upon BLASTing it that people had been calling it a GPCR.  They point out that this is weird since it has 11 transmembrane helices, and go on to show that it is a Riboflavin transporter, concluding: "The molecular function of GPR172A has yet to be determined. We designated it hRFT3 (GenBank accession no. AB522904) based on its functional characterization as shown below."  This paper is in pretty poor form, because somehow they don't address the Andriamampandry paper which presented data supporting its function as a GPCR.

So this protein, in this specific spliced formation, has been shown to be a virus receptor, a GHB G protein-coupled receptor, and a riboflavin transporter.  It is very weird that it is a GPCR with 11 transmembrane domains... they very rarely have more or less than 7.  I'd wait for more studies to confirm both of these findings before I'd accept that this protein is an XXL GPCR moonlighting as a riboflavin transporter.


Help in understanding a sentence about TCR-MHC interaction and immune synapse formation

Does it mean that after a TCR binds to a peptide-MHC complex, other TCRs present on the cell gather around that TCR?

Yes. Other TCRs bind other MHC/antigen complexes and they all cluster together, forming an immunological synapse.

Does it mean that one TCR can bind more than one peptide-MHC complex (which, as far as I understand, isn't true)?

No. TCR:MHC bind 1:1.
Your final paraphrase is correct.


What does completing the course of antibiotics accomplish?

As anongoodnurse has mentioned in the comments, an incomplete course can allow weakly resistant stains to expand their population. As you mentioned, the antibiotic does not cause the bacteria to mutate but it kills all strains that do not carry the mutation that provides the resistance. This mutation arises randomly (in certain cases it can be acquired by other mechanisms such as lateral gene transfer).

Many antibiotics may not kill the resistant strains but may still impose some burden on their growth. Now, with a complete course you would have eradicated a lot of strains and only a few resistant strains would be left. The probability of extinction/eradication depends on how many individuals are present in a population. When you do a complete course, then the chances of extinction of the resistant strains due to random birth-death process (and attack by the immune system) would be high because of their low numbers. However, with an incomplete course these bacteria would quickly expand their population once the antibiotic is gone. Now, with the next round of antibiotic treatment you would have more number of resistant cells to kill. As again pointed out by anongoodnurse, this will lead to further selection of resistant strains.

There are additional factors:

Microbial community (colony) is more than just a bunch of cells. They can protect each other.
There are some cells called persisters which are not really genetically resistant strains but tolerate the drug because of adaptive phenotypes. Again, the microbial community plays some role here.


Why is oxygen needed for the electron transfer phosphorylation?

Aren't there any other alternatives for this acceptor?

Not that we're aware of. Every other alternative requires an anaerobic environment - which means small, and often less efficient.

  Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?

When we're talking about a molecule's fit there are many things to consider. Primarily its electronegativity, as that determines its stability, ability to accept and donate electrons, protons, and its ease of acquisition given plentiful amounts in the environment.

Molecular Oxygen is comparatively stable to a lot of di-atomic molecules, and comparatively reactive to others. It's in the butter zone for the act of being the terminal acceptor.

Let's think about Fluoride: Almost all of it is bound up in rocks with other elements. It's not available everywhere. It might be an alright candidate if we could eat rocks, but it also replaces minerals in our bones and teeth. Yes, you're familiar with this - but too much leads to fluorosis - where too much of the calcium compound is replaced, and it ends up making the bones and teeth much weaker.

Alright, let's think about Nitrogen - Very stable, pretty good electronegativity, abundant... but a little too stable. Yup, it's a gas, it's everywhere, and we can't use a lick of it. It's so stable that it's basically inert. The only reason rhizomes and other beneficial bacteria can use it is because they're in a controlled environment away from oxygen with significantly different biochemical processes which produce much less energy (and probably wouldn't be able to support large multicellular organisms that are as active as we are). So, Nitrogen is out.

Carbon? Nope, as an ion it's dangerously reactive, and as anything else it's too stable. Plus, we're carbon-based! If we used carbon as the terminal acceptor then the proteins handling the electrons would have to be even more exotic and filled with other elements to prevent them accidentally gobbling up the electron and becoming useless.

Sulfur? Not electronegative enough for human purposes, unfortunately. It wouldn't act as a terminal acceptor unless our bodies seriously oxidized it; and any oxidized molecules floating around would be more dangerous than molecular oxygen floating around. Plus most sulfur is bound to minerals as well - not abundant unless you're in the ocean.

Oxygen is both incredibly abundant and easy to perform the chemistry with. More reactive molecules are usually not abundant and tied up in the Earth's crust and could be more dangerous.

Less reactive molecules tend to be so non-reactive that we can't do anything with them, and if we could force them into a state where they would be reactive they tend to be violently reactive or require very specific environments that we can't reproduce on a scale necessary to be as mobile as we are.

Oxygen is not perfect, but it's a good fit.

  Why does it even require an "acceptor" to accept the electrons and hydrogen ions? What would happen if they were left alone?

Same thing that would happen if you clogged a pipe or hose. Once all of the electron acceptors on the transport chain are full, movement stops. The electrons won't be magically absorbed by other parts of the proteins making up the chains, and while there might be errant reactions with other molecules, you'd be lucky to get a whole ATP molecule out in a day - assuming you could magically stay alive.

In reality, Cyanide poisoning is precisely what you're asking, and will kill you very quickly.


In vitro translation is not as efficient as other chemical polymer reactions. For example, when proteins are synthesized using in vitro translation systems, many researchers have been using radio-labeling to see the products because the yield is too low to detect them by other methods, although few small proteins have been successfully produced at a microgram level. It should be noted that it is also difficult to produce exogenous long peptides at sizes more than 100kDa in E coli in vivo expression system.


What strange jelly-like thing is shown in the photo?

I agree with @Gerardo-Furtado's comment that what you most likely have here is a colonial tunicate (or sea squirt) from the genus Botrylloides.

According to images and information available via the Taxanomic Toolkit for Marine Life of Port Phillip Bay$^2$, it appears as though you have a specimen of Botrylloides perspicuus (aka B. perspicuum).

[Photo credit: Mark Norman / Museum Victoria]

[Photo credit: Mark Norman / Museum Victoria]

Background

See here for a good general description of colonial tunicates (using the example of a related Botrylloides species).

In general, colonial tunicates are composed of numerous zooids embedded in a firm matrix called a tunic (or test).

Description

B. perspicuus is a colonial ascidian that can persist in tropical and subtropical waters at depths ranging from 1-170 m.
From The Australian Ascidiacea$^1$ (my emphasis):

  External Appearance: The colonies are always robust, but very variable. Some are large, flat, stalked or sessile lobes up to about 4cm long, while others are thick, investing colonies, sometimes growing around wees or other debris. Occasionally ,the lobes are constricted along their length, and sometimes a stalked lobe grows out from a sessile cushion.

  The test is always firm, translucent and smooth....

  Zooids are sometimes in circular systems, arranged in rows along the length of the colony.

  As with other species in the subfamily, the colours of the living colony are very variable.... [including] orange zooids.

The Australian Ascidiacea$^1$ also provides remarks about similarities/differences between B. perspicuus and closely related B. leachi (mentioned in the question's comments):

One difference to note is that B. perspicuus has a firmer tunic, which might explain the retained shape of the OP's specimen even out of water.

Range

This species lives primarily around Australia, with specimens ID'd from waters off Western Australia, South Australia, Victoria , and New South Wales$^1$. The specimen is found in Port Phillip Bay$^2$, which is where the OP's location (Queenscliff) is located.

  [Source: Atlas of Living Australia]

Other Info

Another similar looking species is B. violaceus, but this species is typically found elsewhere in the world.
Like many tunicates, B. perspicuus has been known to invade non-native waters, including those of the eastern Pacific and the Caribbean.

Transport of adult colonies on boat hulls, sea chests and aquaculture equipment is the most likely cause of anthropogenic introduction.
Though ID'd as a different related species, photos showing specimens very similar looking to that of B. perspicuus were documented around the United States.

Citations

Kott, P. (1985). The Australian Ascidiacea part 1, Phlebobranchia and Stolidobranchia. Mem Qd Mus. 23: pp 278-279., available online at http://biostor.org/reference/109626/page/279
Patullo, B., 2011, Ascidian, Botrylloides perspicuum, in Taxonomic Toolkit for marine life of Port Phillip Bay, Museum Victoria, accessed 27 Feb 2017, http://portphillipmarinelife.net.au:8098/species/10656

Note: The remaining info is supported by the above linked websites without formal citations.


How to combine gene set enrichment analysis with hierarchical clustering?

You can try Enrichr for enrichment analysis. On 'Results' page you can use Clustergram view.
Or you can upload your results to Clustergrammer itself.


Why do stomata close in low intensity light?

The primary function of open stomata is to promote gas exchange in leaf tissue: atmospheric carbon dioxide is a substrate for photosynthesis. A side effect of opening the stomata is an increase of water loss through transpiration. If light intensity is low then photosynthesis will be depressed: under these conditions it makes sense to close the stomata to conserve water.


Is there a difference between visual sensation and imagination in the brain?

Short answer
Visual perception and visual imagery draw on much of the same neural machinery.

Background
I have interpreted your question as: What are the common neural circuitries between visual sensation and the imagination of sensation?

In neuroimaging, mental imagery of visual images is a big deal. For example, there is a large body of literature on cross-modal activation of visual areas in the brain in blind people. It is known that visual deprivation results in neural plasticity and the recruitment of visual areas in the brain for other sensory systems. For example, blind Braille readers show activation of the primary visual cortex when reading Braille (reviewed in Stronks et al., 2015). However, interpretation of these findings is difficult in late-blind individuals, because they have experienced visual input earlier in life. Hence, while Braille reading they can be mentally reproducing the visual representation of the Braille cells using visual neural circuitry.

Indeed, it has been shown with fMRI that visual imagery and visual perception draw on most of the same neural machinery (Ganis et al., 2004). However, the spatial overlap of the activated regions is neither complete nor uniform. The overlap in this study was more pronounced in frontal and parietal regions than in temporal and occipital regions, indicating that cognitive control processes function comparably in both imagery and perception, but not identically.

Various studies reveal different results, however. In another imaging study, 'just' two-thirds of brain regions overlapped in visual sensation and imagery (Kosslyn et al., 1997). Indeed, the experimental task used may have important effects on study outcomes.

Most notably in this regard is that approximately half of the studies done have found activation of the primary visual cortex during imagery (Kosslyn et al., 1999). This is interesting, because the primary visual cortex is generally thought to be an early, low-level area in the visual system that depends on thalamic input that relays information from the optic nerve to the brain. I.e., it is generally believed to depend on sensory stimulation. Generally, only the higher-level associative visual areas are associated with higher cognitive processes.

References
- Ganis et al., Cognitive Brain Res (2004); 20: 226–41
- Kosslyn et al., Neuriomage (1997); 6; 320–34
- Kosslyn et al., Science (1999); 284; 167–70
- Stronks et al. Brain Res (2015); 1624: 140–52


That is a rare condition that can only occur when taking too much doses of vitamin D. It has nothing to do with sun exposure.

High levels of vitamin D stimulate hypercalcemia and all its negative consequences. It can also exacerbate liver and kidney chronic diseases.

Reference: Katherine Zeratsky, What is vitamin D toxicity, and should I worry about it since I take supplements?


Average number of gene products in (a) eukaryote(s)

One answer can be found in the UniProt FAQ:

  What is the human complete proteome?

  In 2008, a draft of the complete human proteome was released from
  UniProtKB/Swiss-Prot: the approximately 20,000 putative human
  protein-coding genes were represented by one UniProtKB/Swiss-Prot
  entry, tagged with the keyword 'Complete proteome'. This
  UniProtKB/Swiss-Prot complete H. sapiens proteome (manually reviewed)
  can be considered as complete in the sense that it contains one
  representative (canonical) sequence for each currently known human
  gene. Close to 40% of these 20'000 entries contain manually annotated
  alternative isoforms representing over 15'000 additional sequences ...

http://www.uniprot.org/faq/48

So, we have 20,000 genes and 35,000 products yielding about 1.75 gene products per gene. Alternatively, the 8,000 genes undergoing alternative splicing give about 2.88 proteins per gene.


If you didn't have an utricule or saccule would you still know if you are accelerating and going up or down?

Your semicircular canals are concerned with balance (or spatial orientation). Proprioception, on the other hand, deals with where the body parts are with respect to each other and the physical world. (Some people lump the two; it's easier to think of them independently, because they really do quite different things.)

Proprioception (and closely associated kinesthetics) is possible because of nerve signals from skin, tendons, muscles, and joints. This gives us the senses of limb position and movement, the sense of tension or force, the sense of effort, the sense of gravity.[1] Propioception alone cannot compensate for serious balance problems.

The vestibular system exists through input from three semicircular canals located in the inner ear on each side. The canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).

  Three sensory systems, vestibular, visual, and somatosensory/proprioceptive, serve our sense of balance. Each of these systems provides unique sensory information to the brain where it is integrated (often in complex ways) to produce a final motor output to muscle groups for maintaining gaze, head and body posture, and controlling static and dynamic balance.[3]

Without these systems, we would be completely unable to get or stay in a standing position. We certainly could not walk.

An analogy would be to get strapped into one of those spinning seats, in this case, one that rapidly spins inverting you, alternating between forwards and backwards (which would kind of include up and down) but not sideways. You would be unable to focus your eyes on anything. You would see your world spinning, and you would have lost your sense of balance. You would immediately go to the ground, even though your proprioceptors were working perfectly.

However, once you did "go to ground", say, in an elevator, you probably could tell if you were accelerating upwards or downwards. Closing your eyes would help to drown out the more unpleasant 'noise' (input).

So, long story short, the answer is yes. Likewise, you would probably still be able to touch your nose, etc. But it would not be possible to do more complex things, like walk, or even sit unless your back and sides were supported.

[1] Proprioception From a Spinocerebellar Perspective
[2] mpairments of reaching movements in patients without proprioception. I. Spatial errors
[3] Anatomical and Physiological Considerations in Vestibular Dysfunction and Compensation


A good book for history of biology/biotechnology for lay people

Some that just come to mind, in random order:

One cannot skip reading:

Richard Dawkins - The selfish gene

And, obviously:

Charles Darwin - The Origin of Species

And, for those interested in the evolution of the brain (and its quirks):

David J Linden - The Accidental Mind
Oliver Sacks - The Man Who Mistook His Wife for a Hat

Not very DNA/evolution-oriented, but wonderful science books nonetheless:

Primo Levi - The Periodic table
And the neveraging must-read:
Isaac Asimov - A Short History of Chemistry


There have been several Turing machines constructed using DNA computing. One of these machines has been used to solve the boolean satisfiability problem, another was used to solve the bounded post correspondence problem, both NP-hard combinatorial problems which are difficult for conventional computers to solve.
Also, a DNA computer was constructed that plays the optimal strategy in tic-tac-toe.

DNA computers store information in DNA sequences and perform calculations by DNA baseparing and other molecular biology strategies. In principle, DNA stores Information much denser than any modern hard drive and uses orders of magnitude less energy per calculation than a conventional computer ($10^{-22}$ vs $10^{-10} \frac{J}{operation}$) however, so far i/o is slow and calculations are comparatively error prone, limiting the practical use of DNA computing.

Also, a recent article has demonstrated that molecular motors can perform basic addition and solve the NP-complete subset sum problem by exploring nanolithographically fabricated networks. This could also, in principle, be used to construct a turing machine.


This is not so easy to answer, since alpha-tubulin has at 10 known genes in this family (data from Ensembl):

TUBA1A   tubulin, alpha 1a
TUBA1B   tubulin, alpha 1b
TUBA3E   tubulin, alpha 3e
TUBA3D   tubulin, alpha 3d
TUBA4A   tubulin, alpha 4a
TUBAL3   tubulin, alpha-like 3
TUBA1C   tubulin, alpha 1c
TUBA3C   tubulin, alpha 3c
TUBA8    tubulin, alpha 8
TUBAL3   tubulin, alpha-like 3

You can go on the site linked above and choose any of the proteins. I checked TUBA1A, and get a length of 451 amino acids and a weight of approximately 50,1 kDa.


Where to put the gene after eukaryotic promoter for best expression levels?

I used pEYFP-N1 (stock vector) where the spacing between the CMV promoter and the EYFP start codon is ~88 nt, and the expression is high.

I also cloned a protein 5' of the EYFP, only 4 nt after the CMV promoter. The expression of this fusion was also high. Because I was only using the chimeric protein in experiments, I did not try to assess differences in EYFP expression.

If you look here: https://synbiota.com/projects/19/sequences you'll see the basic pEYFP-N1 vector and the separation between the CMV promoter and the EYFP coding sequence.

On wiki: "The TATA element and BRE typically are located close to the transcriptional start site (typically within 30 to 40 base pairs)."


This is the nest of a cicada killer wasp, Sphecius speciosus.

  Harmless, solitary and  Cicada-killer wasp holes are ½ half to 1-inch around with thinly scattered loose soil, usually where there is no grass. Cicada-killer burrows have a U-shaped mound of soil at the entrance. Adults emerge June/July.

Source: All the Dirt on Gardening blog

According to the Wikipedia article linked above:

  this species occurs in the eastern and midwest U.S. and southwards into Mexico and Central America.

so being in Michigan, you are certainly within the region in which the insect is found.

Parenthetically, also according to the blog from above:

  Crayfish holes are 1-inch wide, 2-inches high and made of mud balls.

and the texture of that hole looks more even.

Related Bio.SE question:  Cicada Killer Behavior


What happened to the gypsy moth epidemics in the Northeast US?

It appears that the gypsy moths were controlled by pesticide spraying by the US Forestry Service.

The defoliation areas measured peaked at 12 million acres in 1981 and again at 7 million acres in 1990.

In response, there was significant spraying of various insecticides starting from 1982 through 1996, peaking in 1990. This spraying managed to keep gypsy moth defoliation areas under 2 million acres since 1993.


How does natural selection explain how organisms that are poisonous evolved?

There is a lot to say on this question. I will try to keep it short, to the risk of oversimplifying the problem. I can think of three main reasons:

1. Predation does not necessarily means death of the prey

Most of predation does not directly kill the prey. Typically herbivory, will often damage the prey but a single individual won't kill the prey entirely. In such systems, being poisonous may eventually either directly stop the predator (because the predator quickly sense it is poisonous or because the predator immediately dies) or will ensure that the predator remembers not to attack this same individual.

2. Kin selection

kin selection (aka. Group selection although there are a few authors who do not equate them), is selection above the level of the population of individuals (see also unit of selection; see this recent answer for some book recommendation on the subject).

In very short, under kin selection, an individual who dies of predation but can either cause suffering to the predator or just kill it, will protect its close relatives that live nearby from the same predator (who is iether dead or who may have learned to avoid these particular plants). As close relatives share of lot of DNA in common, a gene for toxicity - even if it fails to protect the individual being preyed upon - can protect the copies of itself present in the siblings of this individual.

3. Side effect

Let's not make the mistake of assuming that a trait has necessarily come to high frequency because it was selected for the specific purpose we associate this trait with. A plant may happen to become toxic for reasons that are unrelated to predation. While toxicity is often costly to the plant, it may sometimes eventually just be a by-product. Unfortunately, I would not be able to cite an example where toxicity is simply a side effect.


Is it true that newborn babies don't produce tears while crying? Why?

It is not completely true.  Babies develop the lacrimal system at 42 days, in utero.  The canals and ducts for tears are formed at 60 days [2].

At birth, tear production by the lacrimal gland is minimal. Normal tearing develops several days to 2 weeks after birth.[1]

Some 6% of newborns are born with a tear duct obstruction (in some online articles it stated up to 10%, but I think my source is more reliable).  The child still produces tears, but they can well up on the eyelid [2].
Other more serious abnormalities can cause this problem.  Duct cysts or hemangiomas can also cause tear duct blockages in more severe cases.  Various factors, such as anatomical abnormalities and problems with pumping tears increase the propensity for the disorder in children with Trisomy-21 [2].  As nico has alluded to in the comments, there may be a lag in the development of the physiology of tear production even in non-Trisomy-21 children.

[1] Thomas K. McInerny, MD, FAAP, ed. 2009. American Academy of Pediatrics Textbook of Pediatric Care. Elk Grove Village, IL. American Academy of Pediatrics, p1706.
[2]M. E. Wilson et al. (eds.), Pediatric Ophthalmology, 2009, pp. 276-284.  DOI 10.1007/978-3-540-68632-3_1.


Why are vaccines for polio taken orally while vaccines for TB need to be injected?

There are different polio vaccines - one live (attenuated) vaccine which is given orally and one inactivated, which is injected. The main reason for using the live orally vaccine is that it provides excellent immunity (better than the inactivated) since it uses the natural infection route (oral-faecal) in the body where it enters through cells in the intestine. Besides that, it is also much less expensive than the inactivated form, which is a big thing when doing mass immunisations in developing countries.

The live vaccine, however, may mutate back into a more infectious form as you shed live (attenuated) viruses after the immunisation, so these are not used anymore. Now we are very close to the eradication of the poliovirus. The risk of getting new infections is viewed as being too high these days. See this paper for more information: "Vaccine-derived polioviruses and the endgame strategy for global polio eradication."


If a dead animal is electrified, will it decay?

Environemental factors would degrade it (wind-water etc.).

But from what I know, electricity will follow a certain shortest path inside the body to close the circuit. The rest shouldnt be electrified and bacteria will be alive.

Bacteria are indeed not resistant to high levels of electricity and would die of it. The current would need to traverse the Entirety of the animal to kill every single bacteria which is highly improbable. Leave one alone, it will reproduce fast.

From what I researched, a constant electrical current of the power of an electric line would cook the animal in a short time. The flying fox you saw probably didnt have live current traversing him anymore and died from a quick jolt (this is a guess only).

Even in the extreme case that 100% of the bacteria would die, the dead animal would be recolonized by bacteria really fast. Even in the wires, wind or animals would carry bacteria.

Power lines are probably protected from arcing this way through anything that could touch them. Imagine if they werent, trees touching them would burn, shoes you throw and hang on them would be calcinated etc.

Off-topic: Are you sure he wasn't only sleeping on his improvised power-line hammock ? :P

Sources:

Conduction of Electrical Current to and Through the Human Body: A Review

Effects of high electric fields on microorganisms I. Killing of bacteria and yeasts


Why is pericardium muscle repolarizated earlier than endocardium?

I'm just going to link you to another post here, which I believe answers the same question. It's because the facilitation of the transient outward current if much more prominent in epicardial regions than in endocardial regions.

And the following citation, "Transient outward potassium current, ‘Ito’, phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms," provides some mechanistic insight.

To answer the rest of the question:

So in an ECG you have leads that record whether a charge is moving toward, or away from the lead. These net charges are reflected on the ECG as either positive or negative deflections. You have a signal from the sinoatrial node that causes a depolarization in the right atrium, then the left atrium (biphasic p wave). In each case, however, we see the positive p wave because in this depolarization the net charge is moving toward the electrodes. Studies on atrial repolarization note that yes, the atrial repolarization is generally obscured by the QRS complex but occurs with polarity opposite that of the p wave.

With the ventricles, and the T wave you end up with a special case. The endocardial regions and the interventricular septum are the first to depolarize, and you get the QRS complex. These regions have a longer period of contraction than the epicardial regions, however. The outside of the ventricles begin to repolarize quickly (transient outward current, surface becomes more positive), and this repolarization begins at the apex and propagates toward the base of the heart. Where you'd get a negative T wave with the change in charge, the direction that the repolarization travels causes you to get a positive reading.


Why do humans suffer anxiety when they view "Trypophobia trigger images"?

Trypophobia is not a recognised specific anxiety disorder (Washington Post). It is worth mentioning that anyone can have a phobia to anything, this is merely a question of whether many people associate these spatial patterns with anxiety. Nevertheless, the response of individuals to these images can be quantified (Le et al., 2015). Ultimately the findings show that a response of trypophobia is not correlative with anxiety. Note that here we are discussing anxiety in a phobia response test. Typically anxiety manifests as sweating, dizziness, headaches, racing heartbeats, nausea, fidgeting, uncontrollable crying or laughing and drumming on a desk. This is not merely feeling uncomfortable.

One hypothesis was that these images had irregular spatial patterns that cause revulsion. A study found that in nature some animals and plants may use this patterning as a warning mechanism and that it is associated with poisonous animals  (spatial pattern quantification of 10 poisonous animals versus 10 control animals p=0.03), and indeed spiders were among those that use irregular patterns (Cole & Wilkins, 2013). Note that this hypothesis was presented in a psychology journal so the evolutionary mechanisms remain, in my opinion, not fully explored and scrutinised.

Hover over the below yellow box to view a lotus seed head, which has typical irregular spatial patterning presented in the 2013 study.

This image is often reported as inducing trypophobia.

Answer: In summary, humans do not reliably feel anxious when viewing these images. It also remains unclear why some people do get anxious or uncomfortable when viewing these images. It is perhaps to do with an aversion to some potentially harmful animals, but evidence remains scarce.


Healthy plant growth depends on a microbial community that lives around and inside the roots of plants (Bais et al. 2001). Roots secrete from the roots a number of chemical compounds that influences the microbial community around but outside of the roots. The microbial community can include bacteria, fungi, and single-celled parasites, as well as larger organisms like insect larvae and even roots from other plants. Some chemicals attract certain organisms while other chemicals repel organisms. This community of organisms around the roots is called the rhizosphere (Walker et al. 2003). The paper by Walker (open access) describes some of the many types of symbiotic relationships that occur in the rhizosphere.
Endorhiza refers to the internal environment of the root system. The endorhiza contains another microbial community of bacteria and fungi (Backman and Sikora 2008). The organisms of this endorhizal community are collectively called endophytes. Like the rhizosphere, the organisms in the endorhiza are important symbiotic species that benefit the health of the plant.
Similar communities have been identified for other regions of the plant, such as the phyllosphere, the organisms that live on the leaves, stems and other plant parts above the ground (Backman and Sikora 2008).

Citations
Backman, P.A. and R.A. Sikora. 2008. Endophytes: An emerging tool for biological control. Biological Control 46: 1-3.
Bais, H.P. et al. 2001. Root specific metabolism: The biology and biochemistry of underground organs. In Vitro Cellular & Developmental Biology - Plant 37: 730-741.
Walker, T.S. et al. 2003. Root exudation and rhizosphere biology. Plant Physiology 132: 44-51.


Thanks to @S-Pr I found the answer on wikipedia. On the Supersedure section of the article it is written the following:
If a queen suddenly dies, the workers will attempt to create an "emergency queen" by selecting several brood cells where a larva has just emerged which are then flooded with royal jelly. The worker bees then build larger queen cells over the normal-sized worker cells which protrude vertically from the face of the brood comb. Emergency queens are usually smaller and less prolific than normal queens.
Although, There is no reference to a source. Maybe one of the citations at the end of the page has the answer.