What happens to human dopaminergic reward system once a teenager becomes adult?

This may shed light on why the teenagers response to dopamine changes. Quote from reuniting website

  There's much still to learn, but it looks like a number of reward
  circuitry events occur after climax that have the potential to
  desensitize us for a time. First, androgen receptors decline after
  ejaculation, and take up to seven days to normalize. (That means the
  effects of testosterone on the reward circuitry are probably blunted
  for a while, quite possibly affecting outlook.) In addition, opioids
  released during copulation hang around for a while, apparently causing
  lingering declines in oxytocin, which hamper sexual responsiveness. As
  noted above, there is also likely a drop in responsiveness to a
  neurochemical vital to our sense of well-being: dopamine. In effect,
  the brain has changed. It now requires more stimulation to get the
  same pleasure response as before, and sometimes no amount of
  stimulation will truly satisfy—until it recovers. Anecdotal evidence
  suggests that such changes affect both sexes.

The author further suggests that orgasm and ejaculation increase prolactin levels for up to 14 days, during which the brain is less responsive to pleasure and requires novel entertainment or partners to produce pleasure.

From the info on that site, it seems that the 14 day dopamine-affecting cycle following orgasm continues for as long as a person is sexually active (with orgasms). With this in mind, it appears that the adult response to dopamine release is the same as teenagers who are sexually active.


Help me find out what this bird is (description, no picture)

You're describing a Ring Species: "a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" population".

The classic ring species is the Herring Gull complex, and that's probably what you read about:

  The classical example of the ring species model was originally based upon the herring gull complex (Mayr 1942). This group comprises more than 20 taxa of large gulls (Haffer 1982) which together occupy a circumpolar breeding range in the northern hemisphere. ... Mayr envisioned all taxa of the circumpolar chain to be connected by gene flow, while herring and lesser black-backed gulls in Europe, the hypothetical endpoints of the ring, have reached full reproductive isolation and now coexist as distinct species.

--The Herring Gull Complex (Larus argentatus - fuscus - cachinnans) as a Model Group for Recent Holarctic Vertebrate Radiations

However, recent genetic work shows that the situation is even more complicated than this, and it's questionable whether they really are "ring species":

  Contrary to the ring-species model, we find no genetic evidence for a closure of the circumpolar ring through colonization of Europe by North American herring gulls. However, closure of the ring in the opposite direction may be imminent, with lesser black-backed gulls about to colonize North America.

--The herring gull complex is not a ring species.


Yes differentiation is primarily about using only a portion of the genome as you pointed out. However, differentiated cells possess a kind of "memory" which enables the daughter cells to continue the usage of the same set of genes. This "memory" is enabled by epigenetic mechanisms which leave inheritable "marks" on the DNA such as methylation (I won't explain further as this would take an entire book).

About the place: each part of the body can produce cells locally (except for some tissues). For example the epithelial cells in your lips will arise from your lips. What signals the division of cells in response to a signal such as lets say injury is again a broad question. One simple mechanism is this (not an independent mode but just one aspect of a complex process): cells generally divide but stop dividing if there is no free space i.e. the cell is surrounded by other cells. This is called lateral inhibition of growth.

I would suggest that you pick up some good cell biology and molecular genetics books to understand these processes.

Cell Biology:

Molecular Biology of the Cell - Bruce Alberts et al.
Molecular Cell Biology - Lodish and Baltimore

Molecular Genetics:

Molecular Biology of the Gene - James Watson et al.
Genes - Benjamin Lewin


Can turkeys run around when their head is cut off like chickens do?

The brain does not control all bodily movements. Some movements are to a great extent controlled by neural networks in the spinal cord. The spine contains a network which is pre-programmed to control the muscles in frequently-used movements such as running or swimming in chickens. This is why a chicken can run away after you chop its head off. Likewise, turtles swim using their a spinal neural network. As long as a signal is received somewhere in this network, the network will activate the swimming movements. Such a system is coined an ‘attractor network’ (source: Science Nordic). A similar system has been shown to occur in a sea slug. I couldn't find similar information in the turkey though. Happy Thanksgiving :)

Note that walking and running in higher animals (mammals) is controlled by the motor cortex higher up in the brain, involving a more complex system including the pyramidal system. Reflexes, however are controlled by quick, short spinal relay circuits in higher animals as well.


Identify a small spider from southern Poland / eastern Europe

It is a Barn Funnel Weaver (Tegenaria domestica), In Europe it is known as the domestic house spider.
Here's some photos of this species to prove the similarities:

What caught my eye in particular that made it more clear that it was this species was the color patterns on the abdomen and cephalothorax, the size you mentioned, the shape of the feelers as well as the location.
The slight difference in shade of color may be due to being a different variety of the species or simply because of the weather and habitat that the spider is in.


With respect to at least two sources I could find, tRNA is commonly reported as encompassing 15% total RNA in both rapidly-dividing mammalian cells such as HeLa, and in S. cerevisiae (1, 2). To give you an interesting tool to look it up in the same way I did, I used Harvards' Bionumbers webpage to search tRNA.

As for the function of the variable loop, it would seem that it serves to stabilize the tRNA overall structure through three-base interactions, and somehow interfaces with the type II tRNA synthetase (3). I'll try to find more on this interaction.


Hebbian theory "fire together" clarification

Strictly stated, Hebb's rule applies only to existing synapses, and not to the formation of new synapses. (This answer applies to biological neurons, not to ANNs).

Synapse formation is a topic of active research. During development (and in fact continuously even during adulthood), many synapses are created and destroyed. It is not unreasonable to suspect that a similar form of rule is used to decide which synapses are removed and which should remain.

Synaptic connections between neurons show a good deal of specificity -- for example, in the projection from the retina to the optic tectum, synaptic connections are made only with target neurons at an appropriate retinotopic location. This happens because growing axons follow molecular gradients.

Within a cortical column, some possible connection pathways seem to be actively sought -- for example, axo-axonal cells connect specifically to the axon initial segments of target neurons. Neurons certainly have membrane molecules that could be used to identify target cell classes.

So there are probably a number of rules used to determine when a new synapse is made. However, I am not aware of a mechanism for a pre-synaptic neuron to detect how a putative post-synaptic parter is firing, without a synapse already being present. So it seems likely that some form of random process is involved to form new synapses with reasonable post-synaptic partners, after which some activity-dependent rule (like Hebb's) could be applied.


Why do I feel funny in my tummy when riding a virtual roller coaster?

Why can I feel this, when no forces are actually being applied to my
  stomach?

Acceleration sensors are in the ears and are part of the vestibular system. The vestibular nuclei in the brain uses acceleration- and visual signals to decide what happens to your body. It can be fooled by visual signals without the presence of acceleration signals. The role of the vestibulo-autonomic reflex - you feel in your stomach - is probably to protect your inner organs from the damage they can possibly suffer by acceleration.

The same can happen by watching films with fast camera movements on a monoscopic display (e.g. normal films in the cinema or video games on an average LCD monitor, etc...), however not so often than by stereoscopic displays (e.g. 3d films in the cinema, stereoscopic video games on a head-mounted display like Oculus Rift, etc...). This is because stereoscopic displays create the perfect illusion of depth (e.g. they can even be used by a therapy to overcome acrophobia), while monoscopic displays don't. So your vestibular nuclei is fooled much easier by stereoscopic displays.

References:

  These data show that a subset of PBN/KF neurons, whose activity is
  altered by a nauseogenic stimulus also respond to body motion and that
  irritation of the stomach lining can either cause an amplification or
  reduction in the sensitivity of the units to vestibular inputs. The
  findings imply that nausea and affective responses to vestibular
  stimuli may be modified by the presence of emetic signals from the GI
  system.

2011 - Integrative responses of neurons in parabrachial nuclei to a nauseogenic gastrointestinal stimulus and vestibular stimulation in vertical planes
1995 - Study on vomiting related to the vestibulo-autonomic reflex.

  This study describes the relation between the vection produced by
  optical flow and that created by galvanic vestibular stimulation.
  Vection is the illusion of self motion and is most often experienced
  when an observer views a large screen display containing a translating
  pattern. This illusion has only limited fidelity and duration unless
  it is reinforced by confirming vestibular information. Galvanic
  vestibular stimulation (GVS) can directly produce the sensation of
  vection.

2005 - Virtual acceleration with galvanic vestibular stimulation in a virtual reality environment

  Neurons in the vestibular nuclei are not only activated by vestibular
  signals, but also by visual information. Consequently, the sensations
  of body motion derived from visual and vestibular signals are
  indistinguishable.

  Sensations of body movement can also be generated by visual signals
  arriving at the vestibular nuclei. During unnatural movements of the
  body, conflict between visual and vestibular information leads to
  disorientation and nausea, as in the oculogyral illusion, the Coriolis
  effect, and vection.

Foundations of Perception - The body senses - The vestibular system

  Three-dimensional movies presented via stereoscopic displays have
  become more popular in recent years aiming at a more engaging viewing
  experience. However, neurocognitive processes associated with the
  perception of stereoscopic depth in complex and dynamic visual stimuli
  remain understudied. Here, we investigate the influence of
  stereoscopic depth on both neurophysiology and subjective experience.
  Using multivariate statistical learning methods, we compare the brain
  activity of subjects when freely watching the same movies in 2D and in
  3D. Subjective reports indicate that 3D movies are more strongly
  experienced than 2D movies. On the neural level, we observe
  significantly higher intersubject correlations of cortical networks
  when subjects are watching 3D movies relative to the same movies in
  2D. We demonstrate that increases in intersubject correlations of
  brain networks can serve as neurophysiological marker for stereoscopic
  depth and for the strength of the viewing experience.

2014 - Stereoscopic depth increases intersubject correlations of brain networks

  Statistical differences in theta activity showed that the real and 3D
  environments caused similar cognitive processes, while the 2D caused
  an increase of anxiety indicating that perhaps participants were
  looking for the third dimension. Beta and gamma activity showed that
  participants perceived the third dimension of the stereoscopic
  environment as in the real one, something that did not happen in the
  2D environment. Our findings indicate that stereoscopic 3D virtual
  environments seem to approximate the real ones as far as it regards
  the cognitive processes they cause. Three dimensional stereoscopic
  environments increase users’ attention over the 2D and cause less
  mental effort.

2013 - Stereoscopic perception of women in real and virtual environments: A study towards educational neuroscience
2001 - Human Cortical Activity Correlates With Stereoscopic Depth Perception

  In this study the effects of virtual reality exposure therapy (VRET)
  were investigated in patients with acrophobia. Feelings of presence in
  VRET were systematically varied by using either a head-mounted display
  (HMD) (low presence) or a computer automatic virtual environment
  (CAVE) (high presence). VRET in general was found to be more effective
  than no treatment. No differences were found in effectiveness between
  VRET using an HMD or CAVE. Results were maintained at 6 months
  follow-up. Results of VRET were comparable with those of exposure in
  vivo (Cyberpsychology and Behavior 4 (2001) 335). In treatment
  completers no relationship was found between presence and anxiety.
  Early drop-outs experienced less acrophobic complaints and
  psychopathology in general at pre-test. They also experienced less
  presence and anxiety in the virtual environment used in session one as
  compared to patients that completed VRET.

2004 - Treatment of acrophobia in virtual reality: The role of immersion and presence

  Despite the increasing use of virtual reality, the impact on cerebral
  representation of topographical knowledge of learning by virtual
  reality rather than by actual locomotion has never been investigated.
  To tackle this challenging issue, we conducted an experiment wherein
  participants learned an immersive virtual environment using a
  joystick. The following day, participants' brain activity was
  monitored by functional magnetic resonance imaging while they mentally
  estimated distances in this environment. Results were compared with
  that of participants performing the same task but having learned the
  real version of the environment by actual walking. We detected a large
  set of areas shared by both groups including the parieto-frontal areas
  and the parahippocampal gyrus. More importantly, although participants
  of both groups performed the same mental task and exhibited similar
  behavioral performances, they differed at the brain activity level.
  Unlike real learners, virtual learners activated a left-lateralized
  network associated with tool manipulation and action semantics. This
  demonstrated that a neural fingerprint distinguishing virtual from
  real learning persists when subjects use a mental representation of
  the learnt environment with equivalent performances.

2009 - Impact of the virtual reality on the neural representation of an environment

  Our main results are (1) stereoscopy in games increased experienced
  immersion, spatial presence, and simulator sickness; (2) the eff ects
  strongly differed across the three games and for both ge nders,
  indicating more affect on male users and with games involving depth
  animations; (3) results related to attention and cognitive involvement
  indicate more direct and less thoughtful interactions with
  stereoscopic games, pointing towards a more natural experience through
  stereoscopy.

2012 - Understanding User Experience in Stereoscopic 3D Games

  The results indicate that in a 2D movie viewers tended to look at the
  actors, as most of the eye movements were clustered there. The
  significance of the actors started at the beginning of a shot, as the
  eyes of the viewer focused almost immediately to them. In S3D movie
  the eye movement patterns were more widely distributed to other
  targets. For example, complex stereoscopic structures and objects
  nearer than the actor captured the interest and eye movements of the
  participants. Also, the tendency to first look at the actors was
  diminished in the S3D shots.

2014 - What do people look at when they watch stereoscopic movies?

  For the correlation between anxiety and presence, the results show
  very low correlation between anxiety and presence.

2009 - Using augmented and virtual reality for the development of acrophobic scenarios. Comparison of the levels of presence and anxiety

  Stereoscopic visualization in cinematography and VR creates an
  illusion of depth by means of two bidimensional images corresponding
  to different views of a scene. This perceptual “trick” is used to
  enhance the emotional response and the sense of presence and
  immersivity of the observers. An interesting question is if and how is
  possible to measure and analyze the level of emotional involvment of
  the observers during a stereoscopic visualization of a movie or of a
  virtual environment. The final goal of this research is a challenge,
  due to the large number of sensorial, physiological and cognitive
  stimuli involved. In this paper we begin this research by analyzing
  eventual differences in the brain activity of subjects during the
  observation of monoscopic or stereoscopic contents. To this aim, we
  have performed some experiments collecting EEG data using a
  Brain-Computer Interface device from two groups of users, during the
  observation of stereoscopic and monoscopic short movies inside the
  Virtual Theater of the University of Milan. From the analysis of the
  collected data, it seems that interesting differences are present in
  the average brain activity among the observers in the two groups, with
  a significative effect of stereoscopic visualization.

2012 - Analysis of brain activity and response during monoscopic and stereoscopic visualization


Phylogenetic Independent Contrasts with discrete traits

Assuming that by "discrete", you mean "discrete and ordinal" (like 2, 21, 7, 12) and not "discrete and nominal" (like red, blue, yellow, green), then it is really easy. It just mean you can just use your numbers. The contrast between lineage with average trait 6 and lineage with average trait 9, the contrast is therefore 3.

If your data are nominal, then there is no way to calculate a contrast.

Not however, that typically you might violate assumptions of the PIC model. Make sure to know those assumptions and have a feel of whether you seem to respect them.


The rounded carapace of the cephalothorax, and the relatively slim, banded legs indicate that this is one of the terrestrial Dolomedes fishing spiders.  The 'w' stripes on the abdominal pattern have white markings on the margins, but are not 'underlined' completely across in white, which rules out Dolomedes scriptus, in my experience.  Also (although I think this can be somewhat variable in these particular Dolomedes), this spider does not have the familiar white rim to the cephalothorax and abdomen.  Accordingly, I'll go with a rather light-colored individual of the fairly variable Dolomedes tenebrosus.

The links I enclose allow you to explore images of these spiders for your own interest:

https://bugguide.net/node/view/38828

https://bugguide.net/node/view/2011

Oh, yes - almost forgot.  Although these spiders can give a noticeable bite, the venom is less trouble than the standard Polistes paper wasp sting.  I have been bitten only once despite handling numerous females, and had almost no effects beyond a bit of pain and a small red bump.  Like most spiders, these can control the amount of venom they inject, so mine might have been a 'dry bite', but I've heard nothing about bad effects from bites by this very common spider.  I think it's safe to assume that this is a harmless spider - to us.  They love beetles and other large arthropods.


How did mitochondria make energy long ago?

You are asking a very interesting question.

As you correctly mention, the substrates of mitochondrial metabolism (TCA or Krebs Cycle) are pyruvate and NADH, and, through oxidative reactions, ATP is produced. Indeed, it seems unrealistic that when the "mitochondria" were by themselves there was pyruvate and NADH in the environment. Let's take a step back.

In the 1970s, Dr. Lynn Margulis proposed the extracellular origin of mitochondria. What does this mean? Margulis suggested that, due to the bacteria-like characteristics of mitochondria (e.g. circular DNA), it is plausible that the first mitochondrion was in fact a bacterial cell that had been introduced into another cell by endocytosis. Therefore, we cannot really describe mitochondria as having been "by themselves", since originally they were (most likely) bacteria. (I am emphasizing this because in your statement it seems like perhaps there is some misunderstanding with this point.)

Where were we? Ah, yes, so we have a bacterium (pre-mitochondrion) inside another (host) bacterium. Consider that the combination of one bacterium inside another works and, voilà!, we have symbiosis and, more precisely, endosymbiosis. This means that the two bacteria collaborate to survive, they benefit from interacting with each other (symbiosis) and one of them is inside another (endo-).

But, of course, the combination is not optimal: the two bacteria have common steps in their metabolism and this is a waste of energy. And evolution does not like that. Evolution encourages organisms to minimize their energy expenditure through natural selection: those organisms that manage to make the most out of their energy supplies will survive and thrive. This means that the pairs of endosymbiont bacteria that manage to use less energy to carry out the same actions will be positively selected for.

Indeed, what this possibly lead to was the host bacterium keeping its basic glucose metabolism (glycolysis), and the "inside"-bacterium exclusively keeping its TCA metabolism, effectively becoming a mitochondrion. Hence, the current arrangement of glycolysis in the cytosol and respiration in the mitochondria.

In short, it is important to look at the bigger picture: were there ever really "free" mitochondria? No, according to Margulis' Endosymbiosis Theory there mitochondria-precursors, which were bacteria. Once these bacteria were introduced into the cytoplasm of another cell, their metabolism degenerated and was reduced to the minimum necessary. This is a success story: the mitochondria are evolved bacteria that have managed to survive and thrive, and have made themselves fundamental for survival of many lifeforms, including humans.

I hope this is a useful answer to your question. Feel free to ask for clarifications in case I did not describe something well enough :)


Is the term 'allele' specific to sexual populations?

No, it's fine to use for asexuals too. There's an ambiguity in the term "locus" for asexuals, but "allele" is fine, and "gene" is not much more ambiguous than it is for sexuals (which isn't saying much).

Your final paragraph seems confused though, and I think it's related to your main question. When recombination is sufficiently frequent to keep the population in linkage equilibrium, it allows us to represent the population simply as a point in allele frequency space, rather than in the full, exponentially-larger genotype space. So Watson and Szathmary are using different terms for the two cases not because they can't use "allele" in an asexual context, but because alleles are not sufficient to describe an asexual population.

In general sexual populations are not in linkage equilibrium and cannot be simply described by allele frequencies either, as W&S note later in that paragraph.


Creative ways to deactivate alpha-amylase taken from fungi

Amylase inhibitors have attracted much attention because of their potential in treating type 2 diabetes.

You can inactivate most enzymes by using a specific inhibitor. One class of inhibitors consists of molecules that resemble the substrate molecules but are not acted upon in the same way. These will bind to the active site and will prevent the substrate from binding. An inhibitor of many amylases is acarbose. This is a competitive inhibitor which means that inhibition is overcome by high concentrations of substrate.

And if that isn't enough to get you started here is an entire thesis on the topic of amylase inhibitors.

If you want to permanently block activity the ideal compound would be one which binds to and covalently modifies the active site, destroying enzyme activity. This would be an irreversible inhibitor. I haven't been able to find a reference to such a compound however.


Most of the time, I have heard this differentiation in context of Humerus bone only. In that context, have a look at the wiki pages on the anatomical and the surgical necks.

From this, and what I remember from anatomy class, this distinction is more a functional; practical distinction rather than that based on strictly defined criteria. Surgical neck denotes the most commonly fractured region of the bone, and also the region most likely to damage the axillary nerve passing nearby, and hence would have the greatest representation in an orthopedic clinic. The anatomical neck, on the other end, is the classical distinction based on the centers of ossification and the insertion of the capsular ligament of the adjacent shoulder joint, which gives a greater weightage to its origin and to the anatomical relations (insertions, etc).


Fat released from food will form macroscopic lipid droplets in the aqueous environment of the gut. In the small intestine, bile synthesised by the liver is secreted into the lumen via the bile duct. Bile contains bile salts which act as detergents to disperse the lipid droplets by forming micelles. I think this dispersion of micelles could be described as a colloid.

I have no idea what the reference to protein digestion could mean, although some hydrophobic proteins might become associated with the micelles that I've already described, and I imagine that bile salts might help to solubilise protein aggregates in the gut lumen by direct interaction - they, or their derivatives, are sometimes used by protein biochemists as detergents for protein solubilisation (e.g sodium deoxycholate.


Using PGAL10 promoter to overexpress specific yeast genes: How to?

You're right about them being promoters, although it would be useful if you posted the link to the source of the sentence that you cite, so that we can read exactly how they are being used.

A fairly common way to study genes that aren't consistently highly expressed is to place them under the control of a strong promoter; that is, a promoter that is recognized by transcription factors in such a way that its linked gene is almost always expressed.

This is exactly what this group did in this paper, to study some features of yeast metabolism. In this case, the genes that they were interested in studying were cloned into a vector that was then inserted into yeast cells that lacked that gene. This way, the researchers knew that any expression of their gene of interest came from the vector and was driven by the pGAL1 promoter.

Similarly, if ERG10 was your gene of interest, this might be a strategy that you could adopt to study it.


First genomic survey of human skin fungal diversity

The link is given at bottom of the article that you linked to. It's a Nature paper so you need to have access rights.


Why is elevated homocysteine considered a risk factor for angina?

Homocysteine:

Causes endothelial dysfunction and damage
Accelerates thrombin formation
Inhibits native thrombolysis
Promotes lipid peroxidation through free radical formation
Induces vascular smooth muscle proliferation
Promotes monocyte chemotaxis

Many observational epidemiological studies indicate that individuals with higher Homocysteine levels have increased risks of cardiovascular disease.


From encyclopedia britannica

  Territorial behaviour, in zoology, the methods by which an animal, or group of animals, protects its territory from incursions by others of its species.

Following, this definition, yes territorial behaviour exists in humans. Here are three simple examples drawn from different (western) cultures

You seem to be confusing territorial behaviour with general, aggressive behaviour. Whether or not the behaviours you describe qualify as territorial behaviour requires one to make a psychological study to determine whether the individuals had a notion of territory that they wish to defend.


Not all "wear and tear" is bad. I will provide only one example. Trust me, I can provide many more, but I think one is sufficient to answer your question.

Exercise (against resistance, e.g. even gravity) is known to strengthen bones, for example. The stronger your bones, the less likely they will break as a result of a fall. While that sounds kinda "meh", it's incredibly important in the elderly, because once they sustain a fracture, their activity level falls dramatically for fear of sustaining another fall/fracture. Because of this, they have a decrease in muscle mass, a decrease in lung capacity, a decrease in cardiac fitness and an overall acceleration in decline of motor function, as well as a decreased quality of life.

  Low-impact fractures, commonly called fragility fractures, have even higher mortality. Older patients with injuries from a fall have five times the mortality that their same age colleagues have from injuries from MVCs (motor vehicle accidents.) Five-year survival after an osteoporotic hip fracture is similar to that of patients with breast or other cancer. Almost one in 13 (7.5%) of those with fragility fractures will die within 90 days of fracture.* ...A fracture can be a devastating blow to an older adult’s health and independence, decreasing functional status and quality of life permanently. While some may recover their independence, half of older adults will require home health care in the 6 months following a fracture, and many will have long-term functional decline.

"Wear and tear" is good for muscles, bones, the heart, the lungs, balance, proprioception, and a number of other systems which help to prolong life, as well as the quality of life.

*Mortality is mainly with regards to hip fracture.

Fractures in Older Adults


Does Sansevieria trifasciata really absorb Carbon Dioxide at night?

This is an interesting topic!

Crassulacean acid metabolism is a second CO₂ fixation pathway where CO₂ is absorbed at night.  The CO₂ is fixed into maleic acid HOOC-CH₂CH(OH)-COOH which stores some of the CO₂ in the form of carboxyl groups.  During the day carboxylases release the CO₂ for fixation during the day.

This is an adaptation where the stomata open at night to take in the CO₂ and are closed during the day - the plants sort of 'hold their breath'.  The energy for this process is derived for glycolysis which were stored during the day (nice detailed review here).

The paper says that about 6% of plants (including Mother-in-Laws Tongue) do this and you can imagine with night breathing how closing the stomata during the day would really help with dehydration.  Its interesting to note that this is found in a wide variety of plants "CAM is found in five taxonomic classes, comprising monocots and dicots, encompassing 33 families and 328 genera".  That says that CAM is a pretty old development in plant evolution and not so expensive that it is easily lost.


Do immature fruits perform photosynthesis?

The green pigment is indeed chlorophyll, and the fruits do perform photosynthesis.   It's not just "fruiting" plants that do this either.  Some shading experiments i saw estimated that  up to 30% of the sugars assimilated into the barley ears (basically the grain) can come from photosynthesis occurring in those organs.


How does the intracellular accumulation of cyclic AMP cause edema in case of anthrax?

Edema factor is a high efficiency adenylyl cyclase, an enzyme that converts ATP to cyclic AMP (cAMP). cAMP is an important second messenger in many pathways, which you can read about in Albert's Molecular Biology of the Cell. In order to be an effective second messenger, it must be tightly regulated. Several bacterial toxins disrupt this regulation, by creating an excessive amount of cAMP directly (B. anthracis EF), forcing the local activator of adenylyl cyclase to stay on (V. cholerae CT), or preventing the local inactivator of adenylyl cyclase from turning it off (B. pertussis). Some of these pathways are well understood. The pathway between cholera toxin and lethal loss of intestinal fluid, as mediated by elevated cAMP, is particularly well understood. The pathway between edema factor, edema toxin, cAMP, and tissue/organ edema is not well understood, as illustrated by this lovely figure, from this review:

Note the nice question mark between Edema Toxin and Edema

It could be mediated by protein kinase A (PKA), and probably is at least partially. It could also be mediated by EPAC and the small G-proteins Rap-1 and Rap-2 (and probably is, at least partially). It could even be mediated by the loss of ATP, since the anthrax ET is so efficient at catalyzing the conversion of ATP to cAMP.


Book on yeast reproduction, evolution and on the use of yeast as model organism

Here is my list, in no particular order.

Methods in Yeast Genetics

Some other yeast books at CSHL

Fred Sherman's primer, available free at various sites including here.

The Freiburg manual here

The timeless classics (link to volume 3 but see all volumes)

The YeastBook is an attempt to build a current encyclopaedia to replace the previous item on my list.

The Saccharomyces genome database, probably the best organism-specific resource ever.


Recalling memories by electrical impulses?

There have been quite a few studies on stimulating the brain with electrical pulses and it has been found to be successful too. Three papers of particular interest I found were:

1) In a study titled "Explaining How Brain Stimulation Can Evoke Memories", it was found that electrical stimulation in the temporal neocortex can cause neurosurgical patients to spontaneously experience memory retrieval. The subject's brain in the study when stimulated enabled him to recollect memories from the time that he was in high school. They concluded that there are patches of neurons encoding memories for differnt periods (in this case the high school). (reference)

2) In the second study titled "Memory Enhancement and Deep-Brain Stimulation of the Entorhinal Area", it was observed that

  entorhinal stimulation applied while subjects learned the locations of
  landmarks enhanced their subsequent memory of these locations: and the
  subjects reached these landmarks more quickly and by shorter routes,
  as compared with locations learned without stimulation. (reference)

3) In a third study titled "Stimulation of Entorhinal Cortex Promotes Adult Neurogenesis and Facilitates Spatial Memory", it was found that stimulating a specific region of the brain leads to the production of new brain cells that enhance memory. (reference)

In two on these studies, memory is enhanced by stimulation to the entorhinal cortex and in the first study the neocortex was stimulated. So, in a broad sense the  cerebral cortex is generally used for these studies.

This is a continuous field of research as a treatment to diseases like Alzheimers (reference).

Gray-Brodman-Entorhinal Cortex (Wikipedia)

Neocortex location (reference)


Can the mutation rate vary for individuals of the same species, growing in similar environments?

Yes.

between individuals: https://academic.oup.com/mbe/article/34/2/419/2528250
between individuals: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4617969/
hypermutation (transient): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1087688/


Is this a soldier beetle? Bug identification

It looks very much like Arhopalus rusticus, a species of long-horned beetle (Cerambycidae) that is found in England. https://en.wikipedia.org/wiki/Arhopalus_rusticus


How would our circadian rhythm change over time if we had no sunlight whatsoever?

Say we can live for 10,000 years, how would our circadian rhythm be different 10,000 years from now after zero exposure to sunlight?

Probably almost the same.

A circadian rhythm has - by definition - a free running period of more or less 24h. Of course this might change over time, but 10,000 years are not very much on an evolutionary time scale.

As an example there are some studies about the circadian clocks of fish that have lived in underground caves for over 1 million years: They still have a circadian rhythm (even though its doesn't react to light anymore), but even after 1million years the free running rhythm only changed from 24h to 47h. Interestingly it can also still be 'entrained' (synchronised) to other regular cues like feeding time (this is also the case for normal circadian rhythms).


Virus-to-virus gene transfer via "sequences integrated into a common host organism"

Does it mean that a viral gene or other DNA sequence gets integrated
  into the host's genome and then some other virus (that chanced to be
  in the same organism) manages to obtain this sequence and package it
  into its own DNA?

Yup, that's what it means (although not all viral genomes are DNA-based).

A lot of genomes contain extensive content that is thought to arrive from viral transfer. Here's a reference to get you started:

Endogenous Viral Elements in Animal Genomes (by Aris Katzourakis , Robert J. Gifford; 2010; PLoS Genetics)

If much of an organism's genome originally derives from viral transfer, then any subsequent viral transduction represents a virus-to-virus transfer of genetic information.


It is a rove beetle (Coleoptera, family Staphilinidae). These are among the most specious of beetles. You can recognize them because the elytra (forwings) are much shorter than the abdomen.https://en.wikipedia.org/wiki/Rove_beetle


Will a sandwich assay work with a GST 26 antibody/protein?

This is completely dependent on the type of antibody you are using and the epitope specificity of that antibody (or antibodies). Because you haven't given any more detail, it's very hard to give you a definitive answer.

GST is known to dimerise, so even a monoclonal antibody might work in your sandwich assay, as long as the (identical) epitopes are far enough apart in the dimeric structure to allow two antibodies to bind.

If you're dealing with a polyclonal antibody mixture, then your chances are better. But even still, you won't know until you try it.


How does the sticky ends of foreign gene bind with its counterpart in the plasmid DNA if positions are not matching?

In the Google search engine I entered "ligation of sticky ends"; then I selected the "Images" tab. Here is the first result, which addresses your question exactly:

This originates from this website:
AddGene

Based on your question it sounds like you understand the basic rules of forming Watson-Crick base pairs; but your diagram and question omits the innate polarity of the sugar-phosphate backbone in DNA and RNA. The convention in depicting double-stranded DNA is that the "top" strand (sometimes referred to as "Watson") is written in the 5'-to-3' direction, reading from left to right. Since the two DNA strands are anti-parallel, it follows that the "bottom" strand (maybe nobody refers to it as "Crick" any longer?) is written in the 3'-to-5' direction -- if you are reading from left to right.  If you want to decode the biological information encoded in the bottom strand then you need to read it from right to left.

This is a long-winded way of saying that I usually note the 5' and 3'-ends on a drawing of DNA to emphasize this, and if I can figure out how to do so I will update the image.

Here is a slightly better version from Google:

Which is from this site: A WordPress Blog


Does the body lose energy or gain energy relatively when drinking or eating hot things?

Gains heat; humans are not particularly well-adapted to make use of heat as an energy source.  In a simple matter, if something you eat is hot when it goes in then the average temperature of the body has increased.  More relevantly (and to get this more on-topic for biology), eating anything will generally increase your body temperature, as in order to digest the food your rate of metabolism will rise.  Metabolism produces a lot of heat, and that's what you feel after eating, especially a big meal.

Something like cold water, however, that doesn't require a whole lot of metabolism, will cool you down.  In fact, even drinking hot water might cool you down.  The paper cited there claims that drinking a hot drink on a hot day will disproportionally increase your sweat response such that you actually cool down.


What are the (correct) terms for these flagella-arrangements?

A good source on this subject is Tortora's Microbiology. Unfortunately, it uses a different terminology.
Have a look at this image (click on it for a bigger size), chapter 4, page 81:

As you can see, the lophotrichous arrangement is the one with the flagella at one end of the bacterium (which agrees with the arrangement at the Wikipedia page).
However, the opposite arrangement (flagella at both ends) is called amphitrichous (which, by the way, makes more sense), not cephalotrichous.
The text below that image says:

Lophotrichous: a tuft of flagella coming from one pole;
Amphitrichous: flagella at both poles of the cell;

If you assume that "amphitrichous" is synonym of "cephalotrichous", then the correct book would be your second one, which says:

A - Lophotrichous (tuft of flagella on one end)
B - Cephalotrichous (tufts of flagella on both ends)

However, there is no evidence that one should consider "amphitrichous" and "cephalotrichous" as synonyms. Besides that, things seem to be way more complicated: if you search those terms at Google Books, you'll see that most books say that amphitrichous bacteria have only two flagella, one at each end. And, indeed, some have completely opposite definitions.

Source: Tortora, G., Funke, B. and Case, C. (2010). Microbiology. San Francisco, California: Pearson Benjamin Cummings.


What studies are there showing the effectiveness of any substance on canine hypertension?

Check out this consensus statement (PMID 17552466):

J Vet Intern Med. 2007 May-Jun;21(3):542-58.
Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats.
Brown S1, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, Egner B, Elliott J, Henik R, Labato M, Littman M, Polzin D, Ross L, Snyder P, Stepien R; American College of Veterinary Internal Medicine.

It includes 185 references, at least a dozen of which are related to your question. Also, if you look to the right of the article on PubMed, there are links to other relevant articles.

FYI: I located this article using search string

(canine hypertension) NOT pulmonary Filters: Review

There are quite a few others. (Canine pulmonary hypertension is apparently a popular research topic, so I found it useful to exclude those.)


Can cirrhosis be caused by physical compression of the body?

There is the term “corset liver”. It describes changes (“grooves”) on the liver’s surface following external compression and subsequent local atrophy, e.g. from wearing a corset for a long time. (see Dancygier: Clinical Hepatology)

A paper from the 1980s describes some abnormality in the histological findings of liver tissue of dogs after chronic abdominal compression but without providing any details in the abstract (I don’t have access to the full version). They measured an increased pressure in the Vena cava and the portal vein. (Ueyoshi, Shima: Studies on spinal braces. With special reference to the effects of increased abdominal pressure. PMID 4093227.)

A (chronic) Budd–Chiari syndrome can also cause liver necrosis and consequently cirrhosis and can be the result of venous compression from e.g. tumors.

I doubt that a comparable chronic compression is possible from wearing clothing. Corsets are still used in orthopedic conditions. I have never heard about long-term side effects on liver tissue. The explanation for cirrhosis seems unlikely to me.


What triggers the release of gonadotrophin-releasing hormone with the onset of puberty?

GnRH-secreting neurons are not fully independent. To date, their most studied regulators are kisspeptin-secreting neurons. During childhood, kisspeptin-secreting neurons are off, due to GABAergic higher level structures and to lack of free leptin. So both brain and body fat have a word on it.

Caveat: most of the evidence is circumstantial (for example, higher circulating kisspeptin in naturally occurring precocious puberty) and I am oversimplifying, so the picture is more complex and will become even more so.


Epidermal layer and muscle wall of colon?

Good question. The colon is lined by epithelial cells (as are all hollow organs). These particular epithelial cells are different from epidermal cells, which are another particular type of epithelial cells found in skin.

Epithelial cells are distinguished by the way they connect with each other using tight junctions to form a permeability layer between compartments.

In the colon, the purpose of the epithelial cells is to both to absorb water and to form a barrier between the luminal contents and the body.  They form the layer facing the lumen. The muscular layers of the colon, both the circular and the longitudinal, are further out from the lumen. You can see them in this histology slide:


How are fMRI responses to auditory stimuli measured?

I could have found this article earlier, but as things go, I didn't. But possibly it contains most of what can be said to this question:

Jonathan E. Peellej, Methodological challenges and solutions in auditory functional magnetic resonance imaging, Front Neurosci. 2014; 8: 253


Why do typical acetylcholinesterase inhibitors (like carbamates) have a greater parasympathetic effect than a sympathetic effect?

We were taught that ganglionic receptors have very high thresholds. So we need a very high concentration of the drug to produce the sympathetic effects. We even solved a hypothetical problem in class, where a patient presented with a pinpoint pupil (typical insecticide poisoning) and increased secretions but an increased heart rate (usually they present with bradycardia). We would still treat the patient with atropine since the combo of pinpoint pupil and increased secretions would be exclusively explained by insecticide poisoning (either organophosphate or carbamate). The increased heart rate could be explained by ganglionic action leading to sympathetic activation of the heart.

But as said this was only a hypothetical case and patients of organophosphate or carbamate poisoning always present with bradycardia. To elicit ganglionic responses the person has to consume a dose way higher which would certainly lead to sudden death.

Hope that helps :)


aspartame in relation to generating methanol

Aspartame is the methyl ester of the aspartic acid phenylalanine dipeptide. Esters are very easily hydrolyzed by esterase enzymes in the body. This will create an acid and an alcohol. In this case the alcohol is methanol, because it was generated from the methyl group. I'm not familiar with why thermonuclear pharmaceuticals would be concerned with aspartame, generally thermoncuclear refers to nuclear fusion, and even radioactive drugs don't undergo fusion.

Anyway, some people are afraid that aspartame is toxic because the methanol it generates is toxic. This fear is unrealistic because the amount of methanol it takes to cause blindness is about 10mL, and the smallest amount needed to kill someone is about 30mL 2. To generate this much pure methanol from aspartame would require you to eat an impossible amount of aspartame.


Emergence of novel protein interactions by mutation of amino acids

The polymorphism in the gene product of the human ABO locus seems
  to provide an example of what the question demands. It does not
  involve a gene duplication or recovery from loss of function; rather it involves changes that cause
  interactions with a different ligand, and the mutations that produce
  these changes have been identified and examined at a molecular level.

I have described the biochemistry of the human blood group system in an answer I gave to a previous question, so the cartoons of the reactions are reproduced from that answer. The diagrams of the molecular interactions and the gene cluster are new.

Human AB polymorphism

The products of the A and B alleles of the human ABO locus are glycosyltransferases:

One of the enzymes recognizes the sugar, galactose (activated by UTP), whereas the other recognizes N-acetylgalactosamine. There is no doubt that they are the products of different alleles of the same gene, even though this is a member of a gene cluster (see below).

The structures of both these enzymes have been determined and the differences of the interaction with their substrates at the active site modelled as shown below:

There are four residues that differ critically between the two enzymes, three of which are shown. Two of these (Met/Leu 266 and Ala/Gly 268) make contact with the UDP-glucosyl substrates. The third (Ser/Gly 235) appears to affect the conformation of the H-antigen co-substrate.

How is a change in function possible without gene duplication?

The poster expresses the opinion (my rewording):

  “I imagine that such mutations would be extremely rare, and that
  duplication is almost always necessary to have them fixed in a
  lineage.”

Why, then, is gene duplication not necessary in this case? The reason is that the enzymes involved are not indispensable: the product is an elaborated branched cell-surface polysaccharide, the function of which can be served by a range of variants. Indeed, the polysaccharide is functional without elaboration, as in the case of blood group ‘O’, where the enzyme is inactive. However, as discussed in my answer to the previous question, there may be a ‘hidden’ function that has driven the evolution of the polymorphism in humans. It has been suggested that the blood cell surface antigens were used by parasites such as the malarial parasite to enter the cells, and that variation provide resistance (albeit temporary, i.e. until the parasite evolved in response).

Footnote: Gene Clusters of Glucosylating enzymes

The question specifically asks for examples that do not come from a recent gene duplication. However I feel it important to mention the gene duplications that have produced such changes in the gene cluster to which the ABO locus belongs. This is to make it clear that the polymorphism is distinct from such examples.

Animals have the ability to vary the sugars on their cells by selecting from a large repertoire of genes with the potential to specify different glycosylating enzymes. An example is the GT6 gene family (glycosyltransferase family 6):

There are about seven members of this family, not all of which are present in every species. A paper by Turcot-Dubois et al. gives a detailed comparison of the genes in human, rat, toad and zebrafish. I just reproduce the gene map for the human cluster in which the four members of the family are indicated by solid triangles:

The enzymes specified by some of these gene have been characterized by X-ray crystallography, e.g. in this paper by Gastinel et al..


How can paternal chromosomes be present in an egg cell during meiosis I or crossing over, if fertilisation has not yet occurred?

when they say paternal chromosome, they mean chromosome of the father of the organism. Not the father of the offspring of the specific organism. During meiosis ,in order to form the gametes, the chromosomes of the mother and the father of a specific organism interact, because homologous chromosome pairs consists of a pair of the organism's fathers chromosomes, and the mother's.
please tell if you still don't get it.


Is iodised salt harmful to the lactofermentation process?

This study found no difference in the outcome of sauerkraut fermentation with or without iodized salt:

  There was no clear influence of iodized salt on microbial populations.
  Stable fermentations were achieved using iodized as well as non-iodized salt.


Do the four cells produced by meiosis each divide into four cells again?

No, meiosis is not a cycle like mitosis. In mitosis, haploid or diploid cells divide to create two genetically identical cells, and this process can go on and on. On the other hand, meiosis results in 4 genetically unique daughter cells which are also haploid. If a haploid cell was to try to undergo meiosis, there would not be enough genetic material and you would end up with half-chromatids.


Are there proteins with multiple motifs?

Most large proteins contain multiple motifs; if you search online for pictures of protein structures, this should be immediately evident. Here's an example from something I was working on the other day: the WD40 repeat motif. It appears in many proteins, but those proteins are certainly much more than a bunch of WD40 units. If you investigate some of the proteins listed at the bottom of that Wikipedia page, you should be able to confirm that they are complex and made of many different sorts of domains, shapes, and parts.

You also mention zinc fingers; those are a DNA-binding motif that show up in many, many different DNA-binding proteins. Those different DNA-binding proteins have many different functions, and their specificity is handled by a vast array of different sorts of motifs and domains that sit on top of/outside of the zinc finger itself. The Wikipedia article on zinc fingers shows many different structures in which zinc fingers can be embedded, and even those structures are only small parts of the actual functional proteins that perform work in a cell.


determining horizontal gene transfer between two genomes?

Since the parametric model is applied to only a single genome to see if there is evidence of recent HGT via a change in the average content in coding regions, it will not tell you from where the HGT came from, just that a HGT likely occurred in an area of the genome. Since you are trying to specifically see if there was a HGT between L. lactis and L. helveticus you would have to run a parametric analysis on both, find a HGT candidate on one of the genomes and then find that sequence as a non-HGT candidate on the other genome and via BLAST.

These papers give a good argument to why to use genome signatures instead of GC content as a parametric method of detecting HGT.

Review from where most of the Wiki figures came from

Genome signature paper

Newer Genome signature paper


The answer depends on (at least):

whether the woman is affected by the condition
whether the allele is autosomal dominant or autosomal recessive (excluding X-linked recession)
the frequency of the diseased alleles in the population
the presence or not of inbreeding

Below I assume no inbreeding.

The woman is affected and the inheritance is autosomal recessive. This means that the woman carries two disieased alleles and with certainty passes one of them to her children (i.e., with probability $1$). Whether the children will be affected by the condition depends on whether they get a second diseased allele from the other parent. Assuming that the frequency of the diseased allele in the population is $p$, this means that the probability of a child inheriting the disease is $p$.
The woman is not affected and the inheritance is autosomal recessive. The woman carries only one diseased allele, and passes it with probability $1/2$ to her child. The probability that a child is affected, i.e. that s/he has two diseased alleles is $p/2$.
The woman is not affected and the inheritance is autosomal dominant. In this case the woman carries no diseased allele, so the children are not affected.
The woman is affected and the inheritance is autosomal dominant. The woman carries at least one diseased allele, and could be carrying the second with probability $p$. In the former case she passes it to her child with probability $1/2$, in the latter with probability $1$, so the probability that the child inherits the diseased allele is $1/2 + p$. This is also the probability that the child is affected by the condition, since they will be affected regardless of the allele passed by the other parent.

Assuming very small probability $p$, case 4 gives us the probability $50%$, whereas the probabily in cases 1 and 2 is much lower. The numbers given in the question are calculated assuming Mendelian experiments, which are a heavy case of inbreeding (and even then not quite correct).
John H.Gellespie, Population genetics
Matthew Hamilton, Population genetics


I think this looks a lot like a pale variety of Solanum Muricatum or Pepino dulce/melon/pear.

It's native to South America, but I think that it would be able to be cultivated in India as well.


Zoology - Help identify the kind of spider

Not too sure but it seems like the european garden spider- Araenus diadematus

[ Image source ]


I think its still called Chyme:

  After hours of mechanical and chemical digestion, food has been
  reduced into chyme. As particles of food become small enough, they are
  passed out of the stomach at regular intervals into the small
  intestine, which stimulates the pancreas to release fluid containing a
  high concentration of bicarbonate. This fluid neutralizes the gastric
  juices, which can damage the lining of the intestine, resulting in
  duodenal ulcer. Other secretions from the pancreas, gallbladder,
  liver, and glands in the intestinal wall help in digestion.

  When food particles are sufficiently reduced in size and composition,
  they are absorbed by the intestinal wall and transported to the
  bloodstream. Some food material is passed from the small intestine to
  the large intestine. In the large intestine, bacteria break down
  proteins and starches in chyme that were not digested fully in the
  small intestine.

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


Increase rate of change in coding regions?

Generally speaking, there are sequences that are under purifying selection (where new mutations are often deleterious) and there are sequences that are neutral. Sequences under constant positive selection do not really exist. So, when you ask

  If a sequence is under selection will it acquire more changes over time because of faster fixation than if changes were neutral?

No! If a sequence is under selection, then it is under purifying selection. As such the rate of fixation will be lower than for a neutral sequence.

If you have a sequence, where most mutations are beneficial, then it the sequence would fix new mutations at a higher rate then a neutral sequence. However such sequence don't really exist! If it were to exist, then mutations would quickly fix such that new mutations would then be deleterious again.

Of course, a single beneficial mutation has a higher chance of fixation than a neutral mutation. Also, when a mutation is under selection (whether purifying or not), the expected change in heterozygosity in the population is higher than if the mutation is neutral (the expected change in allele frequency is equal to the additive genetic variance for fitness at this locus). But those are not details you are asking about.


Does protein consist of repeating units of amino acids?

They are repeating units in the sense that all of the units are amino acids. The R group is different in different amino acids (it is not just different theoretically). The different R groups contribute to the different shape, structure, function of proteins, and if all were the same, then we would have a very limited range of proteins.You will still say it is composed of repeating units, since all units are amino acids, and there are no foreign groups between them.

Similarly, all repeating units of DNA/RNA are nucleotides, even if they aren't the same nucleotides.


How interrelated are computational biology and biophysics?

Computational Biology is just the application of computers to solve problems in biology. It may mean using machine learning to identify regulatory regions in DNA or it may be solving a complex system of differential equations to model chemical reactions in some metabolic pathway. Whether a background in physics, chemistry, biology, math, or computer science is more central depends on the exact problem you want to work on,  and in fact which aspect of the problem you want to work on.

  Also, what field do my research interests actually fall under? I find
  it often depends on the university and specific department,

Bingo! Your interests are clearly cross-disciplinary, so for any given research question, different researchers in different fields will all be working on different aspects of the problem. Academic disciplines don't get to declare monopolies on research problems!

You Ph.D. is going to require you to spend 4-6 years working on a VERY specific problem. It would be wonderful if you could figure out exactly which research problem you wanted to dedicate the next 6 years to, and then choose the Ph.D. program based on their research program on that problem. This is rare though. More typically Ph.D. students have to spend a year or two doing rotations and talking to potential mentors before picking a research problem. In that case you are going to have to decide which academic discipline attracts you more, and then find a department in that discipline that seems to have a lot of collaborations with the other disciplines that attract you. See Buridan's Ass;


Tardigrades can be found in almost every habitat! The easiest way to find them is probably to look in lichens or mosses (although it depends where you live).

serc.careton.edu website suggests a procedure:

  Collect a clump of moss or lichen (dry or wet) and place in a shallow dish, such as a Petri dish.
  Soak in water (preferably rainwater or distilled water) for 3-24 hours.
  Remove and discard excess water from the dish.
  Shake or squeeze the moss/lichen clumps over another transparent dish to collect trapped water.
  Starting on a low obejctive lens, examine the water using a stereo microscope.
  Use a micropipette to transfer tardigrades to a slide, which can be observed with a higher power under a compound microscope.

Just FYI, the tardigrades are a sister clade to the Arthropoda (insects, spiders and others). You can find them there on tolweb.org


When you take a very cold or hot bath how is that influencing your breath?

There is an adaptation to being submerged in cold water in mammals called the Mammalian diving reflex.  Have you ever noticed when you jump into cold water, or enter a really cold shower you take a big breath?  While not exactly correlated with the dive reflex, it shows that there is a neurological reflex of entering cold water.  Here is a brief overview of what can happen when you submerge yourself in cold water:

Lower heart rate - aka Bradycardia, slowing down the rate of blood pumped will decrease the oxygen requirement of red blood cells, which in turn allow organs like the brain to use oxygen.
Smaller veins - aka Vasoconstriction, the blood flow in your fingers and toes is reduced, allowing more blood to be used in the more important organs.  Eventually the vasoconstriction will apply to hands and feet.
Blood shift - this adaptation allows the submerged animal to dive without having their thorax to collapse due to increased pressure.  Not necessarily attributing to breathing patterns though, so I left the boring stuff out and paraphrased.

In hot water, the opposite happens with respect to #'s 1 and 2.  Increased heart rate, like when you go running, tends to increase breathing frequency.  Vasodilation allows blood to flow more easily and is primarily for heat exchange.  Have the warmer blood in your fingers exchange heat to the environment will cool it for the return to systemic circulation.  Surface area is a large factor with heat exchange.  Hope this provided some insight.


What happens to the enzymes produced by the digestive system?

The answer is autodigestion fascilitated by denaturation of the digestive enzymes.
EVIDENCES OF AUTODIGESTION OF THE DIGESTIVE ENZYMES
1.The concentration of digestive enzymes is found to decrease from the small intestinal ileum to the large intestine.

There is a general trend to a decrease in the enzyme concentration the furthur down in the intestine the samples have been collected inspite of a concentration of the intestinal content in the same direction (see Figure1).This fact must indicate that the enzymes are partly inactivated or autodigested in the lumen of the small intestine.[pg 1529].

2.Essential amino acids have been found in the small intestinal lumen even if the food ingested didnot contain them which suggests that their source was the hydrolysed digestive enzymes which would eventually be re-absorbed in the small intestine to prevent their loss from the body.

Amino acids from dietary digestion are not alone, because the ingestion of food-even non-nitrogenous food-stimulates the digestive tract to secrete endogenous protein, derived from the sloughing of intestinal cells and used up digestive enzymes. These recycled proteins are a rich source of essential amino acids.Studies by Nasset show that regardless of the amino acid mix of the meal, the intestinal tract maintains a remarkably similar ratio of essential amino acids.[source]


The picture is unclear but this ant looks like a Solenopsis queen. Maybe a Solenopsis invicta! Sorry if I'm wrong, I've only ever kept Camponotus and Lasius queens. I hope this is helpful though


Does the oxygen concentration equilibrate between red blood cells in the liver sinusoids?

The oxygen saturation (in lungs) and desaturation (in target organs) takes place via diffusion along the concentration gradient (i.e. partial pressure for gases). Therefore as long as RBCs from two different sources and having different partial pressure of oxygen mix up, the oxygen level starts to equilibrate between these cells.

But diffusion as a passive mechanism is not very fast and can take some time. So the only possibility for the second variant (there is a mixture of two types of RBCs) is if the mixture exists for very short time in liver sinusoids, so that the blood leaves them without really mixing completely up.

This is not true, at least in some animal models the blood within the liver seems to reach equilibrium very quickly and its resulting partial pressure can be influenced by adjusting the blood flow from different sources (using vasoactive substances injected directly, as in the referenced paper).


The very simple answer is that the causal factor or trigger hasn't disappeared after the first sneeze. Sneezing is a reflex, partially autonomous, to clear the nasal cavity of particles that don't belong there. As long as the trigger is not removed, the reflex is repeated.

This is also one of the reasons that allergies that cause sneezing, such as hay fever, continue as long as the factor causing the allergy is present.


I don't have it with me, but the book Adventures among Ants by Mark Moffett, which I highly recommend if you're even vaguely interested in ants, describes the creation of paths such as this. Some ants apparently build underground "highways" of a sort, and such a sunken path is indeed an intermediate step in the construction of such. I can't remember the specific reasons given in the book but I expect protection (if not from the elements, then from other insects and rival ants in particular) and efficiency (it minimizes ants wandering around for that bit of their journey) would be involved. Given how short the path in the photo is it might also be an underground path that the ceiling caved in on for a section.

I am not saying that this is what your photo shows, or even that the ants you were looking at typically make such paths, and I realize that I am technically not even answering your question, but I hope that a confirmation that this is a phenomenon that happens and the recommendation of a book that will answer your question is a decent start.

EDIT - Found the book !

The ant species described in this section is the Marauder ant, a species from India so probably not the one you saw. But the motives described in the book could be transferrable. A few quotes from the chapters "Roads" and "Defense":

  Marauder colonies maintain a fast, steady, well-protected flow of food and labor on their trails. Whereas small ant colonies, like people in small societies, are able to access and distribute the supplies they need without roads, larger groups depend on an infrastructure so complex that in the marauder ant it rivals human highway systems.(...)

  Marauder colonies avoid both gridlock and species confrontations, like that with the Diacamma worker [an encounter described at the beginning of the chapter where killing that errant worker of another species involved major disruption in the flow of traffic], when trails are in good shape. Highway construction efforts are part of the society's logistics, providing supply lines for fresh combatants on the front lines as well as streamlined routes for bringing home the plunder[2]. Trunk trails are well looked after - that's how they can be distinguished from the fleeting paths created by raids

The note after "plunder" points to the following:

  The lower cost to ants of sticking to clear paths rather than going over rough ground is addressed in JH Fewell 1988, Energetic and time costs of foraging in harverster ants, Pogonomyrmex occidentalis, Behav. Ecol. Sociobiol. 22:401-408.

A description of the building of the trails, which matches some of how the picture looks like:

  Each worker size class participates in the creation of the roadways. All the castes eliminate surface irregularities along a trunk: while the medias[medium-sized caste] and majors[big ones] chisel out embedded roots and pebbles, minor workers[little ones] extract grains of soil, establishing the road's slightly concave shape in cross-section. The dross is discarded along the edges of the trail, where it accumulates in embankments(...). When the ground is moist, the minor and media workers build up the ramparts into a complete soil cover, or thin-roofed arcade, fabricated from soil extracted from the trail surface or from mining shafts - blind-ended tunnels near the trail used specifically as quarries.

Giving some reasons for their existence:

  To what use is all this effort? Not, it seems, as protection from the elements. The earthworks fall apart in rain, and disintegrate when the earth is dry. Arcades are thin enough to puncture with a tap of a finger, which means a route is weatherproof only when it travels through an underground tunnel, perhaps dug and then abandoned by other animals. Alternatively, near the nest the ants may make a subterranean route of their own: over time, construction crews can scratch away so much soil from the trail surface that the highway sinks from view, at which point the ants seem to be able to construct a thicker, rainproof cover that becomes flush with the surrounding land.

  The main function of this relentless building is defense. Because trunk trails extend for dozen of meters, they travel through territory controlled by other ant species. Marauder ants must therefore be organized to protect the trunk trails from aggressive neighbors or even from hapless passerby such as the Diacamma.(...)

  ...after an arcade has been completed[,] the Diacamma workers could now walk over the trunk trail, blissfully ignorant of the industry below them. if a trail should sink underground, it is as protected as a passage in an army bunker, safe even from human footfalls.

  Bulwarks constructed over trails and provisions prevent battles among competing marauder ant colonies as well. Where they are absent, combat can last a day and engage thousands of minor workers, which pour along the line of contact between the armies.


What is optical density in Lowry's protein estimation method?

The OD measurement is the output of what the photometer measures. It is actually the amount of light which is scattered or absorbed by your sample - scientifically called extinction.
A blank is used to be able to substract the influence of reagents, light that is scattered on the surfaces of the cuvette (which is probably also not completely clean) and so on. Every of this influences reduces the amount of light which should reach the detector on the other side of the probe and give you false extinction readings. If you are using a colored detection sample (which colors deeper or looses color during the reaction) this is more obvious. The solution already has an extinction on its own which is not of interest. So you make a blank (which basically substracts all these influences from you sample reading) to correct for this. How this is done depends on the photometer. Some make a correction reading at the beginning, while others use a second cuvette (a blank cuvette) which is permanently measured.
It means that the protein gives you this extinction. Without a calibration curve (made from serial dilutions with known protein concentrations) it is impossible to make any further comment on this number.


This would be a suggestion rather than a precise answer.

Your sample being pond water a highly probable candidate of the first two photographs would be Euglena sp., though the red eyespot is not visible.

They are freshwater Excavates   and according to Washington State Lake Protection Association a common pollution-tolerant genus in Washington water bodies.

Another picture reference: A website


Are there any substance that are more dangerous at low dose than at higher dose?

Yes. Taking antibiotics (and by extension antivirals and antineoplastics) at low doses is dangerous, as this creates an evolutionary pressure to evolve antibiotic resistance (or rather, incorporate through horizontal gene transfer). This is dangerous because an infection resulting from these bacteria will then be harder to treat.

In the paper "Experimental evolution of resistance to an antimicrobial peptide", Perron et al. gave E. coli the chance to evolve resistance against a novel antibiotic. When given a high dose initially, most bacteria died. When exposed to low doses, the bacteria evolved resistance in 600 to 700 generations.

For the same reason it is strongly advised to finish a course of antibiotics even after symptoms fade.


Why doesn't submersion in water kill fungi?

There is a lot of anecdotal evidence that frequent visits to the pool help with fungal infections. Surely, someone from the scientific community must have noticed too, right? So why don't we frequently hear people suggesting to go swimming to treat these infections?
Because scientific results suggest the opposite!
Incidence of occult athlete's foot in swimmers

In our results, 22 swimmers had positive cultures (15%), 8 of these cases had no lesions (36%). They included 7 infections with Trichophyton mentagrophytes (87.5%) and one with T. rubrum (12.5%). We observed one case with a dual infection. Only one sample from the inanimate environment was positive. This study showed a significant incidence of occult athlete's foot in swimmers. To control this endemic problem, adequate preventive measures must be taken.

Foot Infections in Swimming Baths

A 10% random sample of all bathers at a public swimming bath were examined for tinea pedis and verruca.
The overall incidence of tinea pedis was 8·5% and of verruca 4·8%. The incidence of tinea pedis in 205 male adults was 21·5%, in 288 boys 6·3%, in 60 adult females 3·3%, and in 220 girls 0·9%. The incidence of verruca in juveniles ranged from 4·2% in boys to 10·5% in girls.
It was clear that both infections spread within the baths, and since a relatively small proportion of users admitted to taking precautions to avoid contracting or developing infections it seems advisable that more publicity about recommendations on foot care should be provided.

Onychomycosis in Icelandic Swimmers

The prevalence of
culture-positive onychomycosis was 15% in women and 26% in
men. Our results suggest that onychomycosis of the toenails is
at least 3 times more prevalent in swimmers than in the rest of
the population.

Does this mean that not only is going to the swimming pool not a cure of fungal infections, but it is actually the cause? Well, maybe not. While the articles show that there is a larger incidence of fungal infections among swimmers, they only show correlation, not causality. People who partake in sports activities have a bigger chance of having these infections than the general public. These are also the people who are more likely to go swimming.
To settle the matter for good, we need an article named "Prevalence of fungal infections among occasionally swimming couch potatoes" :-)


The connection between eyes and food pipe had to do nothing with the motion sickness because the visual inputs and outputs to these sensory information are processed in the brain itself, So there is not need for eyes and food pipe to be connected together in order to cause nausea.

  Vasovagal response or vasovagal response or vasovagal attack (also called neurocardiogenic syncope) is a malaise mediated by the vagus nerve. When it leads to syncope or "fainting", it is called a vasovagal syncope, which is the most common type of fainting.

(from http://en.wikipedia.org/wiki/Vasovagal_response)

This case is most commonly seen in adults and adolescents. There are several syndromes which comes under the vasovagal syncope which consists of symptoms like loss of consiusness,lightheadness,nausea,sweating,tinnitus,confusion,altered heart rate,fuzzy thoughts,cloud like spots in vision etc.

  Vasovagal syncope occurs in response to a trigger, with a corresponding malfunction in the parts of the nervous system that regulate heart rate and blood pressure. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting and confusion.

(from http://en.wikipedia.org/wiki/Vasovagal_response)

Several pshychiatric disorders can cause vasovagal response like,

Agoraphobia
Obsessive–compulsive disorder
Social anxiety disorder
Blood-injury phobia
Hemophobia
Traumatophobia
Trypanophobia

http://www.nwocc.com/Pt%20Education/neuro_syncope.pdf http://en.wikipedia.org/wiki/Vasovagal_response

  When it comes to seeing red, the faint feelings could be tied to a phenomenon called blood-injury phobia. According to WebMD, this condition evolved as a way for humans to cope with threats:

  "The idea is that back in time, when someone was coming at someone else with a sharp stick or rock, a kind of genetic variation allowed certain people to faint in response," explains Tyler C. Ralston, PsyD, a clinical psychologist in Honolulu, who treats people with blood-injury phobias. Warriors who fainted looked dead and were passed over during battle. The blood pressure drop also might have helped those who were wounded avoid bleeding to death. Survivors then passed on the "fainting" gene.

(from: http://www.popsugar.com/fitness/Why-Sight-Blood-Makes-You-Feel-Faint-3061135)

"Overcoming Obstacles in CBT" written by Yvonne Tone and Michael McDonough states a condition about a patient having similar psychological problem described in the question. Here the patient's panic is associated with "gory images" of injury or illness, and his responses included intense nausea, pale skin, sweat and sometime fainting. He also reports avoiding gory scenes on TV/filim and medical programmes. The problem is identified as co-morbid panic/agoraphobia and blood injury phobia.

http://books.google.co.in/books?id=1uIYqkKgKRYC&pg=PA44&dq=nausea+and+gory+images&hl=en&sa=X&ei=qLZ2VJPMJ420uAS8qoHIBA&ved=0CB0Q6AEwAA#v=onepage&q=nausea%20and%20gory%20images&f=false


What are the uses of Helical Wheel Projections in Structural Biology?

Helical wheel projections can be useful anytime you have a protein or peptide with one or more α-helical regions. They allow you to see whether any "property" is present along one side of a peptide. This can be useful in recognizing potential protein-protein interacting motifs such as leucine zippers.

The wikipedia article on "Helical wheels" also looks like a good place to start learning more about this.


Regulation of Glycolysis and other pathways at ‘irreversible’ reaction steps

As far as glycolyis is concerned, the answer is straightforward. In certain cells and tissues there is a pathway working in the opposite direction — gluconeogenesis — in which the ‘irreversible’ steps of glycolysis are, in fact (and of necessity), reversed by a different enzymic reaction in which the position of the equilibrium is in the opposite direction.

Obviously if it is metabolically appropriate for glycolysis to occur it is inappropriate for gluconeogenesis to occur. The only way of turning e.g. glycolysis off while at the same time turning gluconeogenesis on is by regulating the activity of the different enzymes at these three steps.

Glycolysis is, therefore a special case in sharing many reactions with another pathway working in the reverse direction. What about pathways in which the interconversions only proceed in one direction. Classic examples are biosynthetic pathways that are regulated by what is known as ‘feedback’ or ‘end-product’ inhibition. An example (for which I happen to have my own diagram) is the synthesis of isoleucine from threonine in bacteria:

When the concentration of isoleucine increases to a certain amount (sufficient for the cell’s needs) this inhibits the enzyme threonine deaminase, preventing the wasteful conversion of threonine to isoleucine.

The main point is not the position of equilibrium of the threonine deaminase reaction (I haven’t checked it yet) but that it is the first unique step in the synthesis pathway. Hence regulating this step prevents the unnecessary removal of threonine in a way that does not allow the wasteful accumulation of intermediates.

Moral

There is an old party game in which you pass a pair of scissor to your neighbour saying “I pass you these scissors crossed” or “I pass you these scissors uncrossed”. The initiates then tell you whether you have performed the operation correctly. The uninitiated player assumes that what is important is whether the scissors are crossed. In fact, it is whether or not your legs are crossed. Beware of false associations.


While not specifically answering why ambidextrous persons are rare, one potential explanation is that mixed-handedness and/or ambidexterity seems to be related to adverse effects. For instance, some studies have shown that mixed-handedness (which might not be exactly the same as ambidextrous, depending on how you define the terms) is related to ADHD symptoms (e.g. Rodriguez et al. 2010) and patients with schizophrenia have an overrepresentation of mixed-handedness (Green et al, 1989; Orr et al, 1999) and ambidexterity (Crow et al, 1996).

A potential reason for the adverse effects seems to be that mixed-handedness and ambidexterity is related to delayed or weakened dominance of one cerebral hemisphere, which is important for language development (see e.g. Crow et al, 1996). See also this quote from Intelligence and the ‘Intelligence Quotient’ (Crow, 2001 from Encyclopedia of Genetics):

  Handedness, reflecting cerebral dominance, is a trait that is associated with quantitative variation. Whether this variation is a correlate of human cognitive ability, as would seem plausible if it underlies the specific characteristic of language, has been much debated, but it now appears that lesser degrees of lateralization (‘hemispheric indecision’) are associated with delay in the development of verbal, and also nonverbal, ability (Crow et al., 1998). Thus it appears that lateralization is associated with significant variation in the rate at which words acquire meaning, and that this variation reflects a dimension that is specific to Homo sapiens.

This is not my area of expertice thought, and others more knowledgeable about the field can maybe expand on this or explain more in detail.


If some exons are missing in one of the samples then the introns will, by definition, be different. What this allows is for the bounds of the outermost exons to vary a bit. This is particularly useful for exon 1, which often has lower coverage.


Do bald people not grow hair, or does their hair simply fall out immediately?

I'm no expert on the whole matter, but I know that at least when it comes to male pattern baldness, it is caused by a hormone called dihydrotestosterone. As those men with the right (or wrong genes, however you choose to look at it) age, this hormone causes the hairs to progressively lighten and thin up until the hair stops growing altogether. The hair follicle dies out basically.


I believe it's a Dieffenbachia, see also this question & answer from Gardening.SE:

https://gardening.stackexchange.com/questions/9765/what-is-this-thick-stemmed-houseplant-with-variegated-leaves

though I am not sure of the species, it could be Dieffenbachia seguine which shows a similar coloration and is one of the taller species (I believe some of the others stay bushy).

On the linked answer, @TeresaMcgH warns:

  By the way, one of the common names for this plant is "dumb cane" because the sap can cause numbness and swelling in the mouth and throat if ingested. So watch pets and small kids around it if you have such at home.


Wikipedia has a quite didactic article on this: https://en.wikipedia.org/wiki/Anatomical_terms_of_location#Axes

These terms are complementary with a mathematical coordinate system: if you are describing a system of axis for a cylinder, you will need to specify that (e.g.) $z$ is along its symmetry axis, here you will say that $z$ is along the rostro-caudal (or antero-posterior) axis. Also, in biology, axes do not have to be straight lines, see the neuraxis:


Is there a biological basis for race (re: Nicholas Wade's article)

I think it's best if you check out Wikipedia article on Race. Race is not a taxonomic term. In a nutshell, you can't define it in a useful way that has anything to do with the usual associations of the word, or gives it a practical value in science.

The problem with arguing about the existence of races in humans is that this is an argument about a word without an agreed definition, so there's never a true or false. This author is merely making some controversial extrapolations from quite obvious biology: Of course human genomes change over time, and it is also possible to an (impressive) extent to trace genetic lineages geographically. Of course there are subgroups that share a small set of characteristics not found in the rest of the human population. Some of these subgroupings are for example medically relevant.

Essentially, "race" ends up a loosely defined term that has something to do with subgrouping a species based on whatever criteria chosen. The reason why it's not a useful word to argue about in humans is because whatever subgrouping you might make, and for whatever purpose you are subgrouping, there are better, more meaningful (and quite importantly, less controversial) terms to describe those subgroups.


Does the Miller-Urey experiment explain the origin of life?

This is a common question. I think the experiment and its conclusions are often misunderstood.
Originally, the null hypothesis was that the ingredients for life could not have come about spontaneously, from inert, inorganic molecules. There was no evidence of strictly physical, non-biological processes being able to produce compounds that were necessary for the proteinaceous life as we know it. In other words, abiogenesis was therefore not supported by any line of positive evidence... until the Miller-Urey experiment. The experiment showed that the ingredients could arise through plausible, natural conditions prior to the existence of life! It bridges the gap between inert, inorganic, non-biological, and the rich soup of complex molecules that would - arguably - be necessary for anything like abiogenesis to even be a consideration based on empirical observation.
Of course the presence of amino acids is not evidence for the abiogenic origin of life. Life is not protein nor amino acid alone. But demonstrating that complex biological ingredient chemistry occurs spontaneously in large abundance - that sounds like a great take-off point for an abiogenic origin of life! That's really all the experiment achieved. In its historical context, it is a very impressive discovery, but it is certainly not a complete explanation, merely something that makes myriad biochemical explanations possible (and perhaps even plausible!). Perhaps you can now better appreciate why it excited and continues to excite biochemists working on trying to understand the chemical origins of life. The Miller-Urey experiment is foundational.
As for the transition from RNA to an RNA-protein origin of life, I quote briefly from another answer elsewhere here:

Regarding the transition from RNA-only to RNA-protein world, peptides
function as cofactors for some ribozymes. Amino acids and peptides are
known to have existed in the prebiotic environment and have been found
in space (glycine has been found in comets, along with other 70 amino
acids).


What is the primary cause of death for small animals in urban and suburban areas?

Cats, windows, and cars appear to be the leading causes of avian (bird) deaths:

 Major sources of anthropogenic bird mortality in the USA [from Fig 2b, Loss et al. (2015)]
Cats and vehicles are likely leading causes of death for many small non-avian animals as well.

Loss et al. (2013) estimated that 6.3–22.3 billion mammals are killed by free-ranging domestic cats in the USA each year.

The Wikipedia article for roadkill provides the following discussion of vehicular deaths:

In 1993, 25 schools throughout New England, United States participated in a roadkill study involving 1,923 animal deaths. By category, the fatalities were: 81% mammals, 15% bird, 3% reptiles and amphibians, 1% indiscernible. Extrapolating these data nationwide, Merritt Clifton (editor of Animal People Newspaper) estimated that the following animals are being killed by motor vehicles in the United States annually: 41 million squirrels, 26 million cats, 22 million rats, 19 million opossums, 15 million raccoons, 6 million dogs, and 350,000 deer.

I welcome others to corroborate these claims with a more reputable source in the comments. (I will try to do so myself and will update as I find them.)

DISCALIMER: I was previously only aware of Loss et al.'s work, so the emphasis of my post is on their papers. I did not otherwise search exhaustively for data. Noticeably absent from my post is mention of deaths caused by pest control (trapping and poisoning). I may update this post with more info as I come across it.

 Citations
Loss, S.R., Will, T. and Marra, P.P., 2013. The impact of free-ranging domestic cats on wildlife of the United States. Nature communications, 4(1), pp.1-8.
 Loss, S.R., Will, T. and Marra, P.P., 2015. Direct mortality of birds from anthropogenic causes. Annual Review of Ecology, Evolution, and Systematics, 46, pp.99-120.


What determines the shape of the center-surround receptive fields of retinal ganglion cells?

The center-surround structure is created by the horizontal connectivity of the horizontal cells (Periman et al., 2012)  that receive input from multiple photoreceptors (Fig. 1).

Fig. 1. Retinal patch showing the connectivity between a horizontal cell and photoreceptors. Source: Harvey Mudd College

The horizontal cell passes on the congregate output to the bipolar cell, which in turn drives the retinal ganglion cells (RGCs) that send their axons to the optic nerve and send the signal on its way to the brain.

The photoreceptors are connected in two concentric circles to the horizontal cell. When light stimulation of the inner patch (center) evokes an excitatory response in the RGC, and the outer circle (surround) inhibits this response, the receptive field is said to have an ON-center configuration. In the reverse scenario, it is OFF-center (Fig. 1). This center-surround configuration is one of the first visual processing steps in the visual system and enhances contrast in the perceived image.

Fig. 2. ON and OFF center-surround receptive fields. Source: Brain Connection

Reference
- Periman et al., Webvision. The Organization of the Retina and Visual System. Utah


Do identical twins have the same fingerprint?

Identical twins have, despite the name, neither identic fingerprints nor identic genetic fingerprints.

Fingerprints: According to the papers listed below the fingerprints show higher similarities (the "structure" is the same), but they can be distinguished and are not the same.

On the similarity of identical twin fingerprints
Can identical twins be discriminated based on their fingerprints?

Genetic Fingerprint: Although identic (or monozygotic) twins share the same DNA, they are not the same and can still be distinguished with a DNA fingerprint, if enough regions are analyzed. The difference comes from small mutations (so called "single nucleotide polymorphisms", one base mutations) which occur in each of us individually. The other difference comes from epigenetic modifications of our genome (basically adding methyl groups to our DNA) which are also not the same between identic twins (there is an interesting video on this on Youtube). However, when using standard forensic kits it is usually not possible to discriminate between identical twins. Differences are detected with whole genome sequencing.

Have a look at these publications:

Identical Twins' Genes Are Not Identical
Finding the needle in the haystack: Differentiating “identical” twins
in paternity testing and forensics by ultra-deep next generation
sequencing
Epigenetic contributors to the discordance of monozygotic twins.


Will the N- or the C- terminal soluble domain be on the extracellular side?

Luminal/cytoplasmic orientation of single-pass transmembrane proteins is mostly dictated by positively charged residues residing on the cytoplasmic side (positive-inside rule) and negatively charged residues being suppressed on the cytoplasmic side/preferred on the luminal side (negative inside depletion/outside enrichment rule).

Since your molecule has a positively charged Lys residue on its N-terminus and a negative negatively charged Glu residue on its C-terminal side your protein would most likely acquire a type II integral membrane protein topology, i.e. the C-terminal part would be directed towards the extracellular space while the N-terminal part is in the cytosol.

Further references can be found here:

Baker JA et al., Charged residues next to transmembrane regions revisited: “Positive-inside rule” is complemented by the “negative inside depletion/outside enrichment rule” BMC Biol. 2017 pubmed

Ott CM and Lingappa VR, Integral membrane protein biosynthesis: why topology is hard to predict. J. Cell. Sci. 2002 pubmed


Just because you have removed the Nitrogen and CO₂ won't help you keep a higher vapour pressure of H₂O in the air. You Could REMOVE all the other gasses and just have O₂ at its normal partial pressure at 1/5 bar total pressure and breath fine, but there would be a fire risk in this environment due to no non O₂ molecules to quench excited O₂.

The only way to have a high enough vapour pressure of H₂O for something like diving would be to heat it, but I don't think a lungful of very hot water vapour would be terribly good for you.

You can't just pressurise water vapour to any pressure you feel like; it will condense fairly easily.

To avoid Nitrogen's toxic effects, divers often use Helium to replace it as pure Oxygen is deadly at high pressures.