How does the partial pressure of oxygen affect mental focus? On this Wikipedia page it says that lower oxygen levels can cause light-headedness. Is there evidence that higher partial pressure of oxygen can improve mental focus?

Long term exposure to hyperoxia actually does more harm than good. Though short term hyperoxia is recommended after brain injuries (http://www.medscape.com/viewarticle/741751_3) as a valid clinical strategy.

For lower concentrations of oxygen, there seems to be evidence that cognitive function is improved:

You can read more about that here: Chung, Soon-Cheol, et al. "Effect of 30% oxygen administration on verbal cognitive performance, blood oxygen saturation and heart rate." Applied psychophysiology and biofeedback 31.4 (2006): 281-293.

And also this:

  This study aimed to investigate whether inhalation
  of the air with 30% oxygen compared with normal air
  enhances cognitive functioning through increased activation in
  the brain. The verbal and visuospatial tasks were performed
  while brain images were scanned. The results showed that
  there were improvements in performance and also increased
  activation in several brain areas under the condition of 30%
  oxygen. These results suggest that a higher concentration of
  the inhaled oxygen increases the saturation of the blood
  oxygen in the brain, and facilitates cognitive performance.

Taken from: Sohn, Jin-Hun, Soon-Cheol Chung, and Eun-Hye Jang. "30% oxygen inhalation enhances cognitive performance through robust activation in the brain." Journal of physiological anthropology and applied human science 24.1 (2005): 51-53.

Though you have to be a bit careful about oxygen poisoning.

  While oxygen is an essential component for living organisms, the
  formation of reactive O2 intermediates is commonplace in aerobically
  metabolizing cells. The stability of a variety of reactive O2
  intermediates varies, but in some instances their interaction with the
  intracellular environment sets the basis for the pathophysiology of
  several disease states.

Adapted from: Cadenas, Enrique. "Biochemistry of oxygen toxicity." Annual review of biochemistry 58.1 (1989): 79-110.

  Pathophysiological processes are associated with increased levels of
  hyperoxia-induced reactive O2 species (ROS) which may readily react
  with surrounding biological tissues, damaging lipids, proteins, and
  nucleic acids. Protective antioxidant defenses can become overwhelmed
  with ROS leading to oxidative stress.

  The continuous exposure of newborn rats to 70–80 per cent oxygen at atmospheric pressure throughout the first 9 days of life significantly inhibited the growth of the brain which normally occurs during this period of life. The accumulations of DNA, RNA, total protein, and proteolipid protein which accompany brain growth during this period were all approximately proportionately depressed by the oxygen-enriched atmosphere. RNA/DNA and protein/DNA ratios were unaffected. The increase in brain mass in the first week of life reflects mainly cell proliferation, and since the decreased DNA accumulation occurred with no changes in RNA/DNA and protein/DNA ratios, we conclude that the effect of oxygen was to inhibit cellular division. We estimate that the oxygen exposure caused an approximately 7 per cent deficit in the cell population of the brain. These results indicate that the use of elevated concentrations of oxygen may have serious deleterious effects on the growth and development of the brain.

Taken from:* Grave, G. D., C. Kennedy, and L. Sokoloff. "Impairment of growth and development of the rat brain by hyperoxia at atmospheric pressure." Journal of neurochemistry 19.1 (1972): 187-194.*

Also hydrogen peroxide is  produced:

  Thus the H2O2 concentration in brains of rats exposed to room air is calculated to be about 7.7 pM, rises 60% when O2 tension is increased to 100% O2, and increases 300% at 3 ATA 100% O2, where symptoms of central nervous system toxicity first become apparent. These studies support the concept that H2O2 is an important mediator of O2-induced injury to the central nervous system.

Taken from: Yusa, T. O. S. H. I. K. O., et al. "Hyperoxia increases H2O2 production by brain in vivo." Journal of Applied Physiology 63.1 (1987): 353-358.

You can also always read the wiki page for oxygen poisoning: http://en.wikipedia.org/wiki/Oxygen_toxicity and also hyperoxia itself: http://en.wikipedia.org/wiki/Hyperoxia


When there is incomplete dominance of one allele, is one allele still considered recessive? When you have incomplete dominance between two alleles of a gene (say, on two different tail lengths blending into an intermediate tail length or two rose colours blending together), can you still call an allele recessive or dominant? If so, how would you tell which to call "dominant" and which to call "recessive"? Do you compare protein expression or measure the difference between the phenotypes of the two homozygous variants or something?
This is purely a terminology question -- I'm aware that the distinction might be a bit meaningless in practice. The closest I could find to an answer is this question, though I'm unsure whether they're measuring tail length to determine the difference between codominance and partial dominance or what.

No - if we have a phenotype, in your case the tail, which we can measure and treat as a numeric variable, and if a heterozygote's phenotype is exactly half-way between that of the two homozygotes, the phenotype is considered not to exhibit. Dominance exists only when the heterozygote's phenotypic value lies closer to one homozygote than the other.


Do any plants grow leaves beneath the ground? We have a pretty common California weed in our yard. When we dig in the ground, we often find small ones there, with green leaves!  It's as if they form green leaves before they come to the surface. While that seems counterintuitive, there's no purpose in having green beneath the soil, it doesn't seem impossible.

We had our yard redone 6 months ago. It's possible that some mature plants were buried- but would they stay green for six months?  Or perhaps they expect to be close to the surface, so after creating a couple inches of roots, they form green leaves, even though they're buried deep enough that they're not at the surface yet.

Is this a known phenomenon?  How common is it for plants to be able to make green leaves before coming to the surface?

Thanks much...

It is a known phenomenon. A good example of the same can be observed in Philcoxia minensis.

This plant is predominantly found in sandy areas of Brazil and its underground leaves photosynthesize using sunlight energy through the relatively opaque sand particles.

These leaves also play the function of trapping and digesting nematodes underground supplementing nitrogen in the leached soils. This article [with pdf] explains this mechanism in detail.


What is the effect of reduced gravity on human height? There has been talk recently of building a base on either the Moon or Mars. What I'm wondering is, if you are born and grow to adulthood on the Moon, where the gravity is a tenth of the Earth's, would you be taller than if you had been born and grown up on Earth?

As far as I am aware, no one has ever been born in space, so your answer cannot be answered directly. However, it is known that the absence of gravity results in an increase in body height by a few centimeters. This is due to stretching of the vertebral column, which is no longer being pressed together by the downward pull of gravity1. For example, the astronaut Richard Hieb, who spent 2 weeks in space, found that his height had increased by 1 inch (~2.5 centimeters)2. Loss of gravity also causes the blood and other fluids to migrate from the legs to the upper part of the body, resulting in swelling of the face and protrusion of the veins of the neck1. I assume that these effects reported at zero gravity at least partially apply to 10% gravity.

Sources
- Airbus Defence & Space
- NASA


Why do people with type O blood have anti-A and anti-B antibodies? People with type O blood have anti-A and anti-B antibodies, even without receiving a transfusion. Why?

To understand what's happening here, let's have a look at the actual ABH (or ABO) antigens:

As you can see, they are not very big molecules: quite the opposite, they are relatively small globosides.
That being said, how it's possible a type O individual producing anti-A and anti-B antibodies without having any contact with the antigens? And that is the same as asking "how it's possible a type A individual producing anti-B antibodies without having any contact with the antigen?"
The answer is: there was contact with the antigens, even without a blood transfusion.
According to Laura Dean (Blood Groups and Red Cell Antigens, chapter 5):

ABO antibodies in the serum are formed naturally. Their production is stimulated when the immune system encounters the "missing" ABO blood group antigens in foods or in micro-organisms. This happens at an early age because sugars that are identical to, or very similar to, the ABO blood group antigens are found throughout nature.

Thus, from an early age, we have contact with the antigens, coming from food or bacteria in our digestive system. As we get in contacts with antigens A and B, this is what happens:

People with type A blood: they will produce anti-B antibodies.
People with type B blood: they will produce anti-A antibodies.
People with type O blood: they will produce anti-B and anti-B antibodies.
People with type AB blood: they won't produce antibodies (regarding A and B antigens).

Source: Dean, L. (2005). Blood groups and red cell antigens. 1st ed. Bethesda, Md.: NCBI.


Iron metabolism in the brain I did an expression profiling from publicly available RNAseq data for mouse tissues. While for liver and testes I am getting expected proteins in the top highly expressed mRNAs, for brain I am getting ferritin (Ferritin heavy chain 1: Fth1) as the top expressed mRNA!

There are a few studies which report elevated ferritin and iron in neurodegenerative diseases while some others have implicated its role in ageing.

I haven't come across any study on iron metabolism in the normal brain. Does iron metabolism play an important role in the function of the brain?

PS :

The data that I am talking about, has the SRA accession number- SRR652247 (I tried all three runs submitted in SRA)
The mice used in the experiment were 11 weeks old
I used bowtie -> eXpress for quantification of RNAseq reads.

Many articles focus on the pro-oxidant function of iron (and globins in particular). It makes sense that levels may be higher in the CNS due to their role in respiration, which is increased secondary to the “absolute requirement” for glucose facilitated by constitutive GLUT3 expression. So perhaps ferritin is increased to maintain supply for neuroglobin synthesis?

Another thing to consider, Ferroportin1 (FPN1) (iron export protein) is expressed at relatively low levels in the brain when compared to i.a. bone marrow (HPA 2018). You could hypothesise that increased storage is required as a result of decreased transport. But I would look at expression of import proteins; TFR, DMT1, and ZIP 8/14, as that could very quickly throw this theory off.

References:

The Human Protein Atlas (HPA) 2018, SLC40A1, The Human Protein Atlas, 11 September 2018, www.proteinatlas.org


Why Goldman Equation cannot be used to calculate dynamic changes of membrane potential I'm reading about Goldman Equation and I've seen in some resources that it calculates the resting potential (not membrane potential in general) and that this equation cannot be used when membrane potential is changing. One example is in Kandel textbook:

  This equation applies only when Vm is not changing. Principles of Neural Science. Eric Kandel, Fifth edition. p. 135.

I don't really understand why this equation cannot apply when Vm is changing. Precisely, I understand that this equation defines how membrane potential changes taking into account permeability and concentration of ions. If you "give" to it the concentration-permeability changes for each moment, it'll show the Vm for each of these moments.

Could someone explain that to me?
Thank you very much!

What's the purpose of the Goldman equation?

I think that statement you posted from Kandel is a bit misleading, though not incorrect - I think he's just warning against a pitfall he's seen students make.

The Goldman Equation is an equation for steady-state voltage or in other words the reversal potential, not for Vm. It will only give you Vm in a (mostly) steady-state condition, like in the context of a resting membrane potential. However, that doesn't mean it isn't useful to calculate the Goldman equation voltage when Vm is changing or that it doesn't apply, but rather that it is not sufficient to use. It will still accurately tell you what the reversal potential is at any moment in time, but it can't tell you what Vm is at that moment.

How the Goldman equation can be helpful in understanding dynamic voltage changes:

Importantly, the rate of change of the voltage of the cell is going to be proportional to the difference between the reversal potential (from the Goldman equation) and the current voltage Vm, and after a long time the voltage will eventually asymptote to the Goldman voltage.

Therefore, if you know the current Vm, and you calculate the reversal potential with the Goldman equation, you can make some inference about what will happen to the voltage at the next moment in time: it will change in the direction of the reversal potential by a magnitude proportional to

Vm - Ereversal

Why the Goldman equation is not sufficient while Vm is changing:

I suspect what Kandel and others are warning about is that this isn't quite enough information to know what happens in the next moment of time:

It takes time to reach a steady voltage, and you need to know the membrane capacitance, which isn't represented in the Goldman equation, to know what the actual change in voltage is after $\delta$t, or how long it will take to reach a particular voltage.

Also, because of voltage-dependent conductances in a neuron, the permeabilities to different ions are also changing as a function of Vm, so the reversal potential is also changing constantly.

Furthermore, simulations of Vm sometimes need to consider the changing concentrations of individual ions, because the reversal potential will change as ion concentrations change. Therefore, it typically makes more sense to think about the driving force of individual ions given by the Nernst equation rather than the Goldman equation which gives you the net reversal potential across all ions.

Summary

In summary, authors that warn against using the Goldman equation when Vm is changing are reminding you that voltage changes take time and depend on membrane capacitance as well as changes in conductance from voltage-gated channels. However, the Goldman equation is still a correct way to calculate the instantaneous reversal potential at any moment in time (but not Vm), even if Vm is dynamic.

You could edit Kandel to say:

  The Goldman equation only outputs the present Vm when Vm is not changing; also, when Vm is changing, the output of the Goldman equation is also changing due to changing conductances and ion concentrations.

..but you can see this is a bit verbose.


Can muscles work as brakes? When I walk downhill I lose potential energy.  If I descend 100m in, say, 10 minutes I lose potential energy at a rate of about 114J/s (114W).  Where does the energy go?  Not into kinetic energy provided I don't run or fall, not into heat, for there is little friction to create such heat.  My leg muscles appear to be acting as very efficient brakes, absorbing the potential energy but turning it into what? Chemical energy?

Yes, muscles do work as brakes; it's a process called eccentric contraction.

The energy balance of an eccentric contraction is a pretty difficult question. Some fairly recent research (Linari et al., 2003) found that a low velocities more energy is consumed (i.e. released as heat) even during eccentric contraction, while at high velocities, the muscle does store some energy from the eccentric motion. In frog muscles, at least.

So muscles do work a regenerative brake... in some conditions.

It's an active research topic where exactly this (non-heat) energy gets stored. Current models (in the previously cited paper) cannot account for all of what's measured experimentally; only 34% of it could be explained.


Male behaviour during breeding season The mountain blue bird build nests to attract females and exhibit aggression towards other males during breeding season. Which of the following is likely to give the birds maximal evolutionary fitness?

a) stronger aggressive behaviour only during egg laying

b) stronger aggressive behaviour during nest building rather than during hatching of eggs

c) stronger aggression when egg is first laid than during nest building

d) greater aggression during hatching eggs than during nest building

a) stronger aggressive behaviour only during egg laying
c) stronger aggression when egg is first laid than during nest building
d) greater aggression during hatching eggs than during nest building

These all occur after the stage which determines fitness. Egg laying (a and c) and Egg hatching (d) occur after the male has won the right to mate.

b) stronger aggressive behaviour during nest building rather than
during hatching of eggs

Assuming the behavior increases mating success and fitness, the answer is B because this is the only strategy that attracts more females and gets rid of rival males before it is too late (i.e. before the female mates). This is also assuming that the female can/will only mate once.
In chronological order the answers run "B,C/A,D" (C & A are really one and the same in my eyes). Mating occurs between B and C.


How migration creates Linkage Disquilibrium I want to know how admixture and migration creates linkage disequilibrium? I am reading about it but I really don't quite get it.

Imagine one population is fixed for A1 at locus A and for B1 at locus B. Here is a representation

--- A1 --- B1 ---

Another population is fixed for A2 at locus A and for B2 at locus B. Here is a representation

--- A2 --- B2 ---

Further imagine that the recombination rate between loci A and B is 0 $(r=0)$. Any migration rate will cause some individuals --- A1 --- B1 --- to be present in a --- A2 --- B2 --- population (and/or vice-versa). So linkage disequilibrium is complete.

If the recombination rate is in between 0 and 0.5, then there will be some level of linkage disequilibrium at equilibrium that can be calculated for a specific demography (incl. migration rate).


What type of lizard is this? The photo was taken in southern Florida.

It may be green anoles (Anolis carolinensis). They are harmless I think...


Retina Transplant Difficulties Why is retina transplant not as easy as the normal eye donation and transplant (I think the latter involves the cornea ) ?
This says that a new method has come up but why isnt the process similar and simple as the normal transplant ?
What are the difficulties in retina transplant ?

This is a diagram of a cross-section of the cornea:

It is an amazing but relatively simple structure, the shape of which is responsible for about 60% of our focusing power, and the clarity of which allows light to enter. It is avascular (no blood vessels), and the non-mylenated nerve endings are very tiny and present in the epithelium.
Transplanting this relatively simple tissue is easy (well, not do-it-at-home easy, but easy.) The only problem with cutting all those nerve endings is that the new cornea will feel nothing if there's dust in the eye, etc. This is a problem, but nothing compared to blindness.
This is a diagram of a cross section of the retina:

As you can see, it is not nearly as simple as the cornea. The nerves (to the left: yellow, light blue, medium blue and darker blue), which collect information from the rods and cones (pink and purple) are very numerous, and absolutely vital to the ability of the brain to interpreting information from these photoreceptors. Therefore, a cut piece of retina immediately loses the ability to send any information to the brain. To transplant it into an eye with a damaged retina would do nothing to improve vision. Also, it is not easy surgery. It's very difficult.
What has been called "retinal transplants" in the recent past have been tiny pieces of embryonic retina, about...

4 millimetre square of retinal tissue, complete with retinal progenitor cells and the retinal pigment epithelium that nourishes them. The tissues were placed in the sub-retinal space beneath the fovea, the area of the retina responsible for sharp central vision.

Note, they didn't try to connect nerves or blood vessels. And, it came from an embyro (so the supply is a problem.) The improvement in vision - which was significant in 7 out of 8 recipients (one patient going from 20/800 to 20/160) - is not long lasting, and believed to have been not from the transplanted retina connecting to the existing retina, but from the release of growth factors from the embryonic tissue improving the health of the degenerating retina.
The newest in "retinal transplants" (which might be better called stem-cell-supplied growth factors implanted in the retina) actually derives from the patient's own stem cells:

A Japanese woman in her 70s is the first person to receive tissue derived from induced pluripotent stem cells, a technology that has created great expectations since it could offer the same regenerative potential as embryo-derived cells but without some of the ethical and safety concerns. [No news yet on whether it worked.]
In a two-hour procedure... a team of three eye specialists lead by Yasuo Kurimoto of the Kobe City Medical Center General Hospital implanted a 1.3 by 3.0 millimetre sheet of retinal pigment epithelium cells into an eye of the Hyogo prefecture resident, who suffers from age-related macular degeneration, a common eye condition that can lead to blindness.

TL;DR: It's not as easy as taking cadaver retina and replacing a patients retina (that would result in immediate and permanent blindness). Whereas corneal transplantation is very easy.
Corneal Innervation and Cellular Changes after Corneal Transplantation: An In Vivo Confocal Microscopy Study
Retinal transplants see fleeting success
Japanese woman is first recipient of next-generation stem cells


Can bacteria, viruses, and cancer cells be destroyed by resonance? Radiotherapy has been used to treat cancer.

Can the resonances by coordinated electromagnetic waves (and/or other forms of waves), of various frequencies, amplitudes and pulse rates, directed from various directions, be used to destroy harmful viruses, bacteria or cancer cells in a human body, without damaging the other parts of the human body?

(* NOTE * This question was posted here in Physics Stack Exchange too, but is possibly going to be closed in that forum as some claimed it is not so much about Physics.)

Your question included "other forms of waves" so I'm going to assume that the use of ultrasound to destroy cancer cells qualifies.

A paper published in the British Journal of Cancer in 2009: "[High-intensity-focused-ultrasound in the treatment of primary prostate cancer: the first UK series]"1 describes the use of a "Sonablate 500" device used to treat 172 men with prostate cancers at two hospitals in the UK, and its use is described as resulting in "acceptable short-term levels of cancer control."

However, the paper does lament the deficiencies of research in this area, the number of other treatments available, and the lack of longer-term follow-up to this research.

The answer to your question appears to be yes, with the qualification that this is an example using sound waves, rather than electromagnetic waves - isn't radiotherapy, mentioned in the first sentence of the question, electromagnetic waves?


Where does the proton come in the reduction of NAD? In our curriculum biology textbook the reduction of NAD+ is depicted as follows:

NAD+ + 2 H+ → NADH + H+

If this proton in the products was not present in the reactants, then where does it come from? Alternatively, if it does not take part in the reaction, then why is it depicted?

In a very simple way the equation describes the reaction. NAD is reduced using 2 hydrogen atoms. The two hydrogen atoms can come from one reactant (lactic acid fermentation) or from two (in a reaction of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate; as shown in the figure below).

First of all, I will pick a particular example from glycolysis, catalyzed by glyceraldehyde-3-phosphate dehydrogenase.

Phosphate by its own has one hydrogen at cytosolic pH (because of the pKA). Thus in this reaction, there are two hydrogen atoms. One hydrogen atom is in the form of a hydride (a proton and two electrons) from the aldehyde group. This hydrogen atom is used to reduce NAD+ to NADH. A second hydrogen atom (in the form of a proton) comes from the phosphate. In the bisphosphoglycerate form, the proton dissociates from the phosphate group and is in solution.

The eventual fate of the electrons that were used to reduce NAD+ to NADH is the electron transport chain (in the mitochondria). In some cases, though, for example muscle cells in an anaerobic environment, or other species that don't have an electron transport chain, the electrons are used in fermentation of pyruvate to alcohol or lactic acid. When NADH donates its electrons in either case, it is then oxidized back to NAD+.

References:

Glycolysis
NAD
Lactic acid
fermentation
HPO4


Why do polyneuropathies affect the extremities first? Polyneuropathy is an anatomic pattern of nerve damage most commonly seen in Diabetes mellitus.

To quote Robbin's Pathology,

  In most polyneuropathies, axons are affected in a length dependent fashions leading to deficits that start in the feet and ascend with disease progression. The hands often start to show involvement by the time deficits extend to the level of the knee, resulting in a characteristic 'stocking and glove' distribution of sensory deficits

What is the reason behind longer neurons being preferentially affected?

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

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

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

References:

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


What are good resources for self-learning modern molecular biology concepts? My learning of molecular biology ended in the early 90's (and with early 90's era information). While I don't aspire to be a molecular biologist, I do aspire to better understand modern approaches better.

Short of going back to school and taking classes, what are good resources for learning on my own? I'd like to get to the point of being able to understand Nature, Science, Cell, etc. Is this even a feasible goal?

Sure it's feasible! Of course, there are lots of papers that I can't read even with a recent education, but you should be able to make a good dent by:

Getting a good modern textbook like Molecular Biology of the Cell by Alberts et al. This is becoming a standard text and gives pretty good coverage of the field. I find that it doesn't always get as detailed as I would like, but such is the nature of textbooks I think. Another textbook that some people like is Molecular Cell Biology by Lodish et al, although I don't have experience with it myself.
Watch online lectures. MIT OpenCourseWare has a pretty good molecular biology course. It may get basic for you at times, but the lecturers are well-respected molecular biologists and geneticists.
Read reviews in things like Nature Reviews to get a 30,000-foot view. Review authors often touch on concepts that primary literature assume you know. Armed with a good text, you should be able to get a good idea of what people are talking about. On a similar note, the "News and Views" commentary articles that accompany "high-impact" papers are great for giving people unfamiliar with the field a taste of why a certain paper deserves attention.
Come back here and ask!


What kind of larva is this? (Southern CA, USA) I need help identifying this larva:

(Click images for full size versions).

There's about a dozen of them in my parents' bathtub and I'm not sure what they are or where they are coming from.

They are about a centimeter long, maybe a little less. They look flat and are hardly noticeable. When they are upside down they look more like a maggot.

My parents didn't even notice until I pointed them out. They move around very little and stay at the bottom of the tub. I haven't seen them anywhere else.

That looks a lot like a Common Southern California Termite. I would check any wood that you have around your home just to prevent any damage. If you want more information just look it up online, but that's most likely what it is.

Note the eyes, the short, segmented antennae, the mandibles (better seen in your second photo.)


carbohydrates and lipids as a source of energy? why? Why carbohydrates and lipids basically used as a sources of energy? Why only proteins are used as building blocks of all the creations? Yes there are some parts of cells like cell walls in which carbohydrates are used but 98% portion of cell is made up of proteins? Why it so?

First, it is a matter of the energy that food can provide. Here fat wins clearly (from the Wikipedia article on Food Energy):

Fat: 37 kJ/g
Ethanol (drinking alcohol): 29 kJ/g
Proteins: 17 kJ/g
Carbohydrates: 17 kJ/g
Organic acids: 13 kJ/g
Polyols (sugar alcohols, sweeteners): 10 kJ/g
Fiber: 8 kJ/g

Proteins and Carbohydrates have approximately the same energy content. But the advantage of carbohydrates (and especially glucose) is that is can be taken up by the body and the cells pretty fast, while proteins need to be digested and broken up, before they can metabolized further. Also plants make primarily sugars (or derivated polymers like starch), so carbohydrates are readily available in the food.
Fat and sugars are chosen for nutritional reasons, since they have a higher energy content and are available for it.

Structural components are build by proteins, since the 20 amino acids allow a much greater diversity in the protein chains than it would be possible for fats or carbohydrates. The building blocks are relatively small and simple but they all have the same basic structure (carbogroup, aminogroup and the sidechain) which allows linking via the functional group and the sidechain influencing their behavior (hydrophobic, hydrophilic, charged, etc.).


Is it harmful for someone to consume things full of bacteria if they don't get physically sick from the bacteria at all? Or as another example - what if you touch a surface that's contaminated with potentially pathogenic bacteria (like the ones at http://arstechnica.com/hardware/news/2008/05/study-keyboards-make-excellent-homes-for-nasty-bacteria.ars) and introduce those bacteria into your body and don't get sick. Then could there be some other damage that the bacteria could do your body? Like, at the very least, maybe promote a not-particularly-noticeable increase in inflammation in the regions where the immune system decides to fight the bacteria? Inflammation only starts to get noticeable when some really high threshold gets crossed.

By "sick", I mean, that the symptoms of the infection become noticeable enough to cross the threshold of being unpleasant to the person carrying the infection. I'm sure that there may be some sub-threshold effects that come in first.

And why is this important? We have to establish some sort of balance between using too much soap/other cleaning agents and not using enough of it. If we use too much, the bacteria could develop antibiotic resistance. And if we use too little, there could be an increase in the types of bacteria that cause chronic infections that don't get noticed, even though some of us might not even get physically sick more.

It really depends on what you consume, how much of it you consume, and the state of your immune system. Let me give you some examples. Yogourt is full of bacteria, and yet we can eat it without issue. The bacteria likely don't survive digestion, but if they do, they will quite happily live in our intestines contributing to the already existing population of good bacteria.

Streptococcus is a genus of bacteria that contains some species that live all over us. They are on our skin, in our upper respiratory tract and intestine. If the species, S. pneumoniae makes it into our lungs, this can cause a bacterial pneumonia. There are likely few bacteria making it into our lungs on a regular basis, and normally our immune system can fight this off without concern. If we some how become immune depressed or compromised (for a number of medical reasons) then that's when we become symptomatic and ill.

On a more extreme side, if we have a bacteremia it is called a bacteremia. There are benign cases of this every time your brush your teeth and bacteria are able to enter tiny cuts in your gums from the brushing action. A healthy person fights this off. If a bacteremia is left unchecked, because of a lack of immune response or trauma, this can develop into a sepetcemia, a toxic infection of the blood. This can be very life threatening and is quite serious.

In general, we always have bacteria all over our hands which we likely transmit to our food or otherwise ingest. This is normally not a problem, but there is an appreciable risk of getting some kinds of viral or bacterial infection (eg, strep throat or a cold). Washing with soap (and to a lesser degree, using hand sanitizers) minimizes this risk.


Are we deaf to water's taste/smell? If we hold a rose in front of our nose for an hour, we can barely notice the smell after that duration, since the smell receivers ( Or the brain, I'm not an expert ) get used to it, and become sort of deaf.

Now my question is, are we deaf to the smell or taste of water simply because our body is consisted mostly of water and we are deaf to it, or is it because we do not have any receiver for this liquid?

If so, is this shared between all the living organisms?

UPDATE

By water, I mean pure water. Now what we practically have is never 100% pure, but a good place to start is distilled water.

I've come across multiple articles about this, but they lack of evidence and scientific proofs.

These are 3 of them:

Ask Anything: What Does Water Taste Like?
Does ordinary water really have no taste [...]
Water taste in man

It appears that little is known regarding how water is detected in mammalian mouth and throat. However, a recent study published in Nature Neuroscience(1) showed that acid-sensing taste receptor cells (TRC) participate in taste responses to water.

First, the team screened knock-out mice in order to identify which TRC were involved:

  They used genetic knockout mice to look for the cells, silencing different types of TRCs, then flushing the rodents’ mouths with water to see which cells responded. “The most surprising part of the project” was that the well-known, acid-sensing, sour TRCs fired vigorously when exposed to water, Oka says. When given the option of drinking either water or a clear, tasteless, synthetic silicone oil, rodents lacking sour TRCs took longer to choose water, suggesting the cells help to distinguish water from other fluids.(2)

Then, the acid-sensing TRCs thus identified were artificially activated using optogenetics techniques:

  They bred mice to express light-sensitive proteins in their acid-sensing TRCs, which make the cells fire in response to light from a laser. After training the mice to drink water from a spout, the team replaced the water with an optic fiber that shone blue light on their tongues. When the mice “drank” the blue light, they acted as though they were tasting water, Oka says.(2)

Source:

(1) Zocchi, D., Wennemuth, G., Oka, Y., The cellular mechanism for water detection in the mammalian taste system, Nature Neuroscience 20, 927–933 (2017) doi:10.1038/nn.4575

(2) Scientists discover a sixth sense on the tongue—for water, Science


Does the bending of a tree's trunk in the wind stimulate and strengthen root growth? Recently Southern California experienced extreme wind velocities and afterwards the news reported over 300 trees had fallen in San Diego County. I had either heard or read somewhere that the action of the wind and bending of a tree assists to strengthen the roots ( I suppose as long as the wind is not strong enough to pull the tree out of the ground). And so that brings me to the point of my question.

Does some kind of mechanism exist within the tree that connects mechanical bending of the trunk with increased rate of root growth? I can imagine that bending might stimulate fluid movement through the phloem & xylem, and perhaps this might be the mechanism. Or does the bending cause a release of some type of growth hormone? Or perhaps the mechanism is epigenetic?

I suppose that if such a mechanism were to exist it would provide one means of evolutionary weeding; removing the weaker part of the gene pool. Perhaps that's what happened in San Diego this last week.

In tree growth there is principle called The axiom of universal stress whereby the growth is in such a way as to equalise the stress across the whole of its structure. The roots, the stem and the branches are one continuous system and can not be thought of as separate.

On a simplistic level for a branch to grow, there must be a corresponding equal and opposite growth in the stem and roots. Of course it is not quite like this as the growth happens across the whole structure at the same time.

The trees on the edge of an even-age stand of trees will have grown to be more stable against wind. They are referred to as being a wind-firm edge to the stand. The trees that have grown up within a stand, with the shelter of their neighbours will not have the same stability in the face of wind, so that if the stand is opened up too quickly it can lead to wind-blow. In uneven-age woodlands, the same principle is true but the dynamics make it less pronounced.

The reason for mentioning this is just to illustrate that, absolutely the wind, and other external factors, gravity being the obvious one, will have an effect on the growth of the roots, as well as the rest of the tree. As the wind exerts a force on a tree that  force will travel through the structure and into the roots and into the ground.

To come back to the specific question then.

  Does some kind of mechanism exist within the tree that connects mechanical bending of the trunk with increased rate of root growth?

Yes, and no. Because the increased rate of growth will be across the whole structure, but not equally. It will put on growth at the points where the stresses are, in order to self-optimise the loading including within the root system.

The next time you cut either the stem of a leaning tree, or a branch of a tree, take a look at the orientation, and thickness of the rings. You will see that in broadleaf trees (or more correctly angiosperms) the rings on the side under tension will be thicker. In conifers (or gymnosperms) it is the opposite. The thicker growth is found on the compression side.

Here is a great photo of compression wood in a conifer from http://www.copperman.co.uk/didgeridoo/how_to_make_a_wooden_didgeridoo/what_is_wood_2.php

The same principle will be happening in the roots also.

As to the actual physiological mechanism that causes this response I have not yet come across a definitive answer. The consenus, at least as far as I know, is that it is not fully understood.

The closest I have come across so far is from this phd in 1994. http://etheses.whiterose.ac.uk/2438/1/DX184141.pdf

I dare say there has been more work done on this in the last couple of decades.


What species is the smallest bird? What species is the smallest living bird in the world? What circumstances limit the bird size from the bottom?

The smallest bird in the world is the bee hummingbird.

I think the minimum size is only limited by the size of organs. I mean that certain organs need to have a minimum size to maintain their function in the organism.


Is this a bedbug or a book lice or what? So basically i found this thing in my home. It's super small so I had to zoom it for you. Whiteish/yellowish colour. We had bedbug problem back in our dorms and I'm worried I somehow managed to transfer them home but I don't know if it's a bedbug nymph or a book lice or what kind of insect, so I'd really appreciate someone's opinion on this.

Edit: It's really small, like. really small. my mother wouldn't even see it and thought me crazy. Just zoom made it look bigger. I'd say 1.5mm maximum at the very best. Moves kinda quickly and I thought it jumped two times when i was trying to capturing but maybe it was just me doing it to it. Living in Europe, Slovakia specifically.

This is not a bed bug, but some sort of book louse (order Psocoptera). Bed bugs have a more compact body shape, even in the early stages:
 (from http://www.bedbuginspectiongroup.com/facts/)
Compare this with a book louse, and I think it is much closer to your specimen:

(from https://commons.wikimedia.org/wiki/File%3ABook_louse_01.JPG)
Also, here is a page comparing them: http://bedbugger.com/2008/03/04/book-lice/
Hope you stay bed bug free!


Numbering amino acid residues While reading about primary structures of protein, I came across the following image.
What do the numberings $n-1, n, n+1$ in the below image refer to?
I thought about it : The amino acid residues are numbered from 1 to n starting from the N-terminus to the C-terminus .
But the image below shows only a part of the protein.. so why is the last residue numbered $n+1$ instead of $n$ also, why is this shown as termination?

I looked out few papers.. but they seem to be very technical and beyond the scope of my understanding.

This question is a bit hard to answer for me without more context.
However, it is clear that the n refers to the tyrosine which is highlighted in the figure as well (especially the interaction of its phenol). The other positions (n+1, n-1) are shown relative to the tyrosine.
I'm unsure about the role of tyrosine in the primary structure of proteins, but maybe this is more clearly explained where you found the figure. I'm also unsure if the glutamic acid is terminal.


How does anger relate to blood pressure? Anger is an emotion generated by neural processes in the brain and is associated with elevated blood pressure. How can an emotion, which is totally related to brain, result in blood pressure changes?

Anger is a common emotion in most animals and it is highly related to stress. At time of anger body usually releases stress hormones and  the body's way to respond to stress is by sympathetic nervous system activation which results in the fight-or-flight response.

Anger is an emotional response related to one's psychological interpretation of having been threatened. Often it indicates when one's basic boundaries are violated. Sheila Videbeck describes anger as a normal emotion that involves a strong uncomfortable and emotional response to a perceived provocation.
Anger may have physical correlates such as increased heart rate, blood pressure, and levels of adrenaline and noradrenaline. Some view anger as an emotion which triggers part of the fight or flight brain response.
http://en.wikipedia.org/wiki/Anger

Stress and anger trigger the release of stress hormone Cortisol in the body. Mild releases of Cortisol can give the body a sudden burst of energy,it also may increase the heart rate to 180 times a minute and  blood pressure from 120 over 80 to 220 over 130.
Anger is processed in hypothalamus and amygdala,the roles of two peptide hormones, corticotropin-releasing hormone (CRH) is responsible for the production of Cortisol (Primary stress hormone) and  arginine-vassopressin (AVP) produces Vasopressin, which triggers blood pressure by increases reabsorption of water by the kidneys, this results in contraction of blood vessels which raises blood pressure.

The human stress response involves a complex signaling pathway among neurons and somatic cells. While our understanding of the chemical interactions underlying the stress response has increased vastly in recent years, much remains poorly understood. The roles of two peptide hormones, corticotropin-releasing hormone (CRH) and arginine-vassopressin (AVP), have been widely studied. Stimulated by an environmental stressor, neurons in the hypothalamus secrete CRH and AVP.
CRH, a short polypeptide, is transported to the anterior pituitary, where it stimulates the secretion of corticotropin (4). Consequently, corticotropin stimulates increased production of corticosteroids including cortisol, the primary actor directly impacting the stress response (5). Vasopressin, a small hormone molecule, increases reabsorption of water by the kidneys and induces vasoconstriction, the contraction of blood vessels, thereby raising blood pressure.
http://dujs.dartmouth.edu/fall-2010/the-physiology-of-stress-cortisol-and-the-hypothalamic-pituitary-adrenal-axis#.VH7k8cnQoX0


New speciations among Darwin's finches In this video it is claimed that Darwin's finches arrived at Galápagos Islands just a few hundred years ago. Have there been new speciations over the past 200 years?

According to oneZoom.org (see the node of interest here), the large ground finch and the large cactus finch share a common ancestor about 170k years ago. Looking among Darwin finches on oneZoom.org, I could not find a more recent speciation event. I could not find their references for their estimates though.

However, part of the difficulty here lies in the exact definition of species one is willing to use (see this post). While it is not reported in oneZoom.org, grant and grant (2009) reported an evidence of reproductive isolation within the G. fortis species.

  Speciation, the process by which two species form from one,
  involves the development of reproductive isolation of two divergent
  lineages. Here, we report the establishment and persistence
  of a reproductively isolated population of Darwin’s finches on the
  small Gala´pagos Island of Daphne Major in the secondary contact
  phase of speciation. In 1981, an immigrant medium ground finch
  (Geospiza fortis) arrived on the island. It was unusually large,
  especially in beak width, sang an unusual song, and carried some
  Geospiza scandens alleles. We followed the fate of this individual
  and its descendants for seven generations over a period of 28
  years. In the fourth generation, after a severe drought, the lineage
  was reduced to a single brother and sister, who bred with each
  other. From then on this lineage, inheriting unusual song, morphology,
  and a uniquely homozygous marker allele, was reproductively
  isolated, because their own descendants bred with each
  other and with no other member of the resident G. fortis population.
  These observations agree with some expectations of an
  ecological theory of speciation in that a barrier to interbreeding
  arises as a correlated effect of adaptive divergence in morphology.
  However, the important, culturally transmitted, song component
  of the barrier appears to have arisen by chance through an initial
  imperfect copying of local song by the immigrant. The study
  reveals additional stochastic elements of speciation, in which
  divergence is initiated in allopatry; immigration to a new area of
  a single male hybrid and initial breeding with a rare hybrid female.


What did (domestic) cats evolve from? I have received this question during a recent discussion about pet birds and cats. We know that birds evolved from the dinosaurs before the mass extinction that happened about 66 million years ago.
However, I could not find such clear information about the most prolific creature on the Internet.
This article suggests Felis attica (reclassified to Pristifelis attica) as an ancestor which seems to have lived about 12 million years ago.
I am interested in filling the gap between the mass extinction and Felis attica to have an answer for my question, but I cannot find an article diving even further in cats history.
Question: What did (domestic) cats evolve from?

The carnivora can be seen in this phylogeny tree which comprises most of today's mammals. They suggest that rodents, elephants, monkeys, dogs and sea mammals all diverged from about 30 million years before the asteroid, until 5 million years after. The placentals and marsupials had a common ancestor previous to 100 million years ago.
Image from genomic study:

Previous to the Felix clade we have Feliforma, which includes mongooses and hyenas.
Image from wiki Feliformia:

There's a tree here
The last common ancestor of cats and dogs was about 40-55 million years ago. Feliforma family tree.
If you want to see previous to that, there are some basal carnivora, where the Feliforma are at the end of the tree.


What are 'acid stable' amino acids? I tend to see terms amino acid, acid stable amino acid, and free amino acids used often in the field of nutrition, but they are sometimes used interchangeably which confuses me.

I know that:

amino acid is a general term to describe organic compounds that encompass both essential and non-essential amino acids.
free amino acids is a general term for amino acids that are not broken down from a protein source; instead it exists in its original form 'freely'.
acid stable amino acid ... no idea

Is that right (correct me if I'm wrong)? What is the larger relationship amongst all three terms? Would consuming a free amino acid be better than one from a protein, or from an acid stable amino acid? Why would one choose to consume a particular class of amino acids over another?

The amino acids asparagine and glutamine have hydrolysable amide groups on their R groups, as shown here:

Note the leftmost amide group on both amino acids. When exposed to acid, these groups would hydrolyse, releasing ammonia.

This was of interest when people used to determine amino acid compositions by acid hydrolysing purified proteins (example paper which does this) and then running them through HPLC or mass spectroscopes. This method, however, fails to distinguish asparagine/aspartate and glutamine/glutamate due to their acid-unstable nature.

So to answer your question, an acid-stable amino acid is any amino acid that does not degrade under acid treatment.

Additional amino acids that degrade under such treatment can be found here, and includes serine, threonine, tyrosine, tryptophan and cysteine in addition to the two above amino acids. These amino acids degrade by alternative pathways distinct from the one by which the above amino acids degrade.

Finally, assuming you are talking about amino acids in dietary supplements, the reason acid-stable amino acids are reported is because acid hydrolysis is usually the method used to hydrolyse the proteins into amino acids, and therefore the manufacturer would not be able to produce acid-unstable amino acids by this method, leading to that label on your supplements.


Why is untreated trypanosomiasis invariably fatal in humans? If left untreated, African trypanosomiasis will invariably kill the patient. The human immune system is unable to clear the infection.

I am aware of a few other infectious diseases with this property and I have a rudimentary understanding of the reason why. For example, I'm told that rabies has evolved to be uniquely good at attacking the brain because that's the only way it can spread to other hosts, and the neuroimmune system, being quite different from the peripheral immune system, is not capable of dealing with a virus that has this property.

I do not understand why the human immune system is ineffective against trypanosomiasis. One explanation I was offered is that the human immune system is just not very good at fighting parasitic infections (compared to viral and bacterial infections). However, this can't be the full answer, because there are other parasitic infections that may go away on their own without treatment.

African trypanosomiasis, or sleeping sickness, is caused by the protozoan Trypanosoma brucei, a single-celled eukaryote.  Being eukaryotic, it has a cell nucleus and a larger genome than most bacteria; it also has a flagellum with which it can propel itself.  Infection with T. brucei occurs via the bite of a blood-sucking fly, one of several species of tsetse fly.

The mammalian immune system has a difficult time with T. brucei because of an effective set of adaptations.  The protozoan's surface maintains a dense coat of a particular glycoprotein on its surface which generally hide other necessary surface features such as chemical receptors and ion channels. Since it is this glycoprotein that the adaptive immune system will encounter, that molecule is the one which it will develop antibodies to recognize.

Within a few days the protozoans would be recognized and soon eliminated by the immune system except that T. brucei at random times changes the glycoprotein used as its surface coat.  The mechanism that does this is called a variant surface glycoprotein (VSG) expression system.  The organism has a repertoire of about 1500 different proteins to  select from to use for a new glycoprotein coat.  The overall effect is that by the time the immune system is able to flood the body with the antibody type it has developed, most of the T. brucei population is not recognizable by those antibodies. T. brucei devotes a significant portion of its genome and its protein production to this immune evasion system.


Shell in garden snail I was wondering that how does shell of garden snail "grows " with growth of snail.
Small snail possess shell as its size but as it grows shell grows. How do they enlarge cavity inside shell?

The snails enlarge the shell by adding material at the lip.  The addition of material is sometimes noncontinuous and shows up as rings, sort of like tree rings.  You can see the growth rings in this photo.

I found the photo here http://ediblesouthflorida.ediblecommunities.com/things-do/snails-slugs-millipedes-oh-my

As the shell spirals outward the diameter of the added rings gets larger and larger.  It has to get larger if it is to spiral - addition of the same sized rings would make a donut-like torus.


Caterpillar identification It has since cocooned I think but it was a weird circumstance. I kept adding leaves for it to eat, and it decided it was done, and cocooned under a wilted leaf.  I'm wondering if anyone can ID the species, and the following: I think it is a real cocoon, as there is no dead or rot smell.

But the cocoon was under the wilted leaf, and is now quite firmly attached. In the pics below, I've turned the leaf and cocoon over. Does the cocoon know "up"? And does it know it before or after making the cocoon? If it was stuck on its "up and out" direction, can turing it over be harmful? I.e. I turned it over so now it's trying to emerge towards the ground, can it figure out how to find 'up'?

Locale: Southwestern United States
Found in: found it in a moist garden bed (tomatoes, radishes, peppermint, basil) eating radish leaves
Description: About 2 inches long, 1/2 inch long hairy, black/grey hairs, body is black/grey with yellow striped markings

Cocooning position: wilted leaf / \, stick |, cocoon (), ...

 /|\
/()|\

Summary: It made the cocoon with the leaf on top of it, and it would never make it out in that case, so I turned it over. Is that okay? Can we still see the winged form come out? Like I said, it doesn't smell dead... in fact smells better than when the caterpillar was pooping everywhere.

Aside, this is the only tag I could find that might fit. Please feel free to edit tags to get this answered. TY

Caterpillar

Cocoon after being turned over, you can see it's kind of wrapped in the leaf

Although a definitive ID will likely never be possible with such low quality photos, you probably have a Western Tent Caterpillar (Malacosoma californicum).

According to the USDA Forest Service, mature larvae are about 2 inches (4.5-5.1 cm) long and are highly variable in color and markings.

This insect is the most variable of the North American species of Malacosoma, in which six subspecies and several unclassified forms have been recognized.

Although this species eats primarilly trees and shrubs (e.g., see here and here), the Minnesota DNR suggests that garden plants can also be targeted.

Cocoons are of white silk dusted with a white to yellow powder. Your image appears to show that.

The Western Caterpillar is found throughout western North America:

 [Source: USDA Forest Service]


What are the ways to test for protein in the canine urine? I know that one way is to use the reagent sticks and the refractometer, but this is inaccurate. Is protein distinguishable when using a microscope? Is it time sensitive(i.e. have to test it right away)?

After some research, I could primarily find two tests for testing the protein content in dog urine.

1) The Urinalysis dipstick test (reference) which has a chance of giving false positive results (reference). Here is the link to a lab test done using the dipstick method and the results that the researchers got.

A sample Dipstick (reference)

2) The second test would be the benzethonium chloride test (reference).

  This test precipitates the protein and increases the turbidity of the
  sample. The turbidity is proportional to the protein concentration.
  This technique is very sensitive and can yield accurate results in
  samples with very low protein concentrations (< 20 mg/dL).

A lab study done using this procedure to precipitate protein (reference).

  The urine sample is best read within 30 minutes of collection
  otherwise certain factors (like crystals, bacteria and cells) may
  alter their composition (dissolve or multiply) over time. If you
  collect a urine sample at home, please drop it off at your veterinary
  clinic as soon as possible (reference).

Reasons for excess protein if present in the urine of your pet is listed in this article.


How does "inheritance of methylation" of DNA and/or histones work? What are the current models/ideas describing the mechanisms explaining inheritance of methylation on DNA resp. histone level?

Is there evidance of this "setup" information being really duplicated/inherited during a cell division process?

Pointers? Articles? What is the current state of knowledge regarding this?

Jon Wilkins has a nice introduction to imprinting.  He does a nice job of introducing the idea methylation and how these patterns are maintained during development and cell division.  Further, he links to some interesting papers on the subject.


How is single nucleotide polymorphism denoted? Currently I'm studying an article on TERT promoter mutations in human melanoma and find myself unfamiliar with included denotations,I would appreciate it if someone could explain to me what C228T in the sentence below means.

  Two tumors with a C228T transition also contained an adjacent C>T transition (at position chr5,
  1,295,229), which is indicative of a dinucleotide CC>TT transition

C228T is a mutation from Citosin to Thymin at the 228th basepair.

Maybe this website helps? Nomenclature for the description of mutations and other sequence variations
I see they write the mutation different (following their format it would be 228C>T), but the general idea is the same.


Source for Specific Models of Birds' Habitat Suitability This source gives a very detailed analysis of what habitats are best suited for many different species. However, this is a government funded project and, to the best of my knowledge, not published in a peer-reviewed paper. In addition, this project has officially been depreciated for 18 years.
There are 2 features of this project that are very attractive to my own project. First, each habitat is ranked as a value between 0 and 1. Second, it ranks 31 habitats, each with very precise differences (e.g. a conifer palustrine forest habitat is ranked separately from a deciduous palustrine forest). Compare this to other sources, such as the IUCN Red List which only says 'Yes' or 'No' to whether a species has been observed in a habitat and only tracks 18 habitats that are very broad groups (e.g. all forests are ranked together).
Can anyone direct me to a more modern and/or peer-reviewed source that has one or both of these benefits?

A quick google reveals several databases of bird habitats, which appear to be at least somewhat more recent.
I believe that the one closest to what you describe is here (there may not be a single publication but they do have a lot of associated publications on their site). But this climate change geospatial database (with a newer version here) and this more local database may also be helpful.


Does crude oil or kerogen contain ancient DNA? According to wikipedia by the formation of oil there are a lot of organic materials present including DNA. Is it possible that this DNA is conserved somehow for millions of years?

According to Live Science, the temperatures are in the 120 to 300 degree-Fahrenheit range (48-148 degree-Celcius) when crude oil is forming. DNA in "dry" conditions completely degrades at temperatures above 190 degree-Celcius. Which means that there could be DNA in the oil itself if there are some surviving cells, however, outside the cells there are DNases which will chew up DNA.

So the DNA they are talking about is like the DNA studied by Gong et. al, where they're looking at the live bacteria in the crude oil, which would be descendants of the bacteria that was around when the oil first began its degradation from organic material.

On both NCBI and PLOS ONE there appear to be a number of papers studying the bacterial growth in crude oil. Which would be why you may have seen articles about DNA in the oil.


Do all chromosomes in one human body contains same genome? As I understand it, each nucleus of a cell contains multiple chromosomes. Each chromosome has multiple DNAs. Each DNA contains some specific gene sequences. That sequence is called Genome.

My question, do all chromosomes in cells in a human body contain same types of genomes (i.e. gene sequences)?

Yes, all cells contains the same genome. This is because, for a given individual, all of its cells comes from the zygote, a singular cell formed after fecondation of the maternal ovum and paternal spermatozoa, through repeated cell division (mitosis). This is a process which replicates quite exactly the genome that will be passed to the newly formed cells.

There are some exceptions however, such as :

Red blood cells, and platelets : these cells lack a nucleus, and don't contain DNA at all.
Cells bearing mutation(s) : even though the replication machinery try to make an exact copy of the DNA, error(s) may happens.
Gametes : ovum and spermatozoa are produced through meiosis, a specific replication mechanism that keeps only half the genome, and may produce new sequences through recombination.
Lymphocytes undergo V(D)J recombination and somatic hypermutation which alters their DNA, a process that is necessary to the working of our immune system.


How much energy does a neuron use for information processing as opposed to just surviving? That is, as part of a neural network in a brain.

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

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

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


Do mammals and birds have a common warm-blooded ancestor? Is it homogeneous or did they converge?  Did we both evolve from warm-blooded reptiles that are extinct maybe?

Welcome to Biology.SE.

Did you say warm-blooded?

The term warm-blood is very unclear. The correct terms are endo-, exo-, poikilo- and homeo- therm. In short…

Source of heat

endo = inside
exo = outside

Variation in inside temperature

Poikilo = varies
homeo = does not vary

Any combination of these two axes exist. For example: If the temperature in the environment never varies you can be homeotherm without needing to be endotherm. A fun example also are the large dinosaurs that are thought to be homeotherms because their metabolism produce some heat and they are so large that they remain warm thanks to this heat source. However, they were probably not able to regulate actively their temperature. Therefore, I would tend to qualify dinosaurs as homeo-exo-therm but I wouldn't be surprised if someone prefers to call large dinosaur homeo-endo-therm individuals. Hope that makes sense to you.

By warm-blooded I will assume you meant endotherm.

MRCA of mammals and birds (and other things)

The Most Recent Common Ancestor (MRCA) lived 301.7 millions years ago (see on tolweb and on OneZoom). This MRCA was exotherm. In consequence, birds and mammals endothermy are an example of convergent evolution (even if they are not using exactly the same mechanisms).

References to go further into the evolution of endothermy in birds and mammals

Grigg et al. 2004
Hillenius and Ruben 2004
Ruben 1995


Is there a negative correlation between the mRNA produced by the cell and the time of extraction? I am doing some data analysis about gene expression time series. When I plot mRNA produced by P. Furiosus cells irradiated by gamma radiation against the time of extraction, it seems that there is a negative correlation between them. Is it a good result from a biological point of view ?

$\gamma$-irradiation produces single- and double-strand DNA breaks, depending on the dosage, and activates DNA damage repair pathways like p53. During this time, the cell cycle arrests and most if not all mRNA production ceases. For sub-lethal doses of $\gamma$ rays, I would expect to see newly-produced mRNA levels drop off fairly quickly with time following the initial dose, then possibly begin to ramp up again later as the damage is repaired and the cell cycle arrest checkpoints released.


Can someone help me identify this spider? Can someone help me identify this spider? Saw it in Malawi; aprox. 5 to 6 cm. Seems like a Solifugae but I cannot go any further... I thank you in advance!

According to museum.wa.gov.au, there are four solifugid species in Malawi. Ceroma johnstonii, Ceroma zomba, Zeria niassa and Zeria paludicola.

Ceroma johnstonii has a grayish-brown tint, not the dark brown, almost black coloration (and red) of your solifugid. Ceroma zomba is only 8 mm in length, much too small even if your estimate of 50-60 mm was referring to the legspan.

Zeria niassa is only 24-28 mm in body length, significantly smaller than what you saw unless you meant legspan. Zeria paludicola is also smaller than your 50-60 mm estimate, so it must have been the legspan, not the length. The only photo I could find of any Zeria species is from eol.org and is of an unspecified species. In the photo, it has a dark brown coloration and a very faint tinge of red on the side of the abdomen.

So your image is either of Zeria niassa or Zeria paludicola.


Contact Inhibition of Cell Division: Signaling Pathway The following article refers to contact inhibition of cell division in epithelial cells, specifically MDCK cells: Collective and single cell behavior in epithelial contact inhibition.

In their review of the literature, there are a number of possible signalling pathways implicated in contact inhibition of cell division. These pathways are outlined in the following quotes:

  It is widely accepted that contact inhibition requires establishment of E-cadherin-mediated cell-cell contacts and subsequent maturation of the adherens junctions (AJs) that link E-cadherin and F-actin in a synapse-like complex involving numerous other proteins

  One possible pathway involves β-catenin, a mediator of Wnt signalling, that, in addition to its function as a transcriptional cofactor, is associated with the AJs at the cell surface

  A contact inhibition role has been reported for NF2/Merlin, a tumor suppressor gene that encodes a membrane-cytoskeletal scaffolding protein, which most likely acts via the Hippo kinase pathway, controlling nuclear localization of the transcriptional activator YAP—itself a known regulator of cell proliferation.

  Contact inhibition is known to involve the MAPK pathway, which, in turn, promotes cell cycle entry by regulating the expression of cyclinD1. Also implicated are Nectins—a family of cell adhesion molecules that are involved, together with integrins and other proteins, in the regulation of cell motility and proliferation. Yet, this accumulated knowledge falls far short of a comprehensive picture of contact inhibition.

In the article, the findings were as follows:

  Our findings show that contact between cells is not sufficient for inhibition of mitosis in MDCK cells. Instead, inhibition of cell proliferation is a consequence of mechanical constraint that causes successive cell divisions to reduce cell area.

Where, in the discussion, they note the following:

  Our measurements also suggest that inhibition of cell division is a distinct single cell state rather than a global state induced by cell-cell signalling across the layer, as illustrated in Fig. 4E. In fact, confluent MDCK cell cultures with an average cell density corresponding to the morphological transition are often sufficiently heterogeneous in local cell density that highly motile cells and completely arrested cells coexist in the same colony. Thus contact inhibition is a local phenomenon...

Published later, the article Spatial constraints control cell proliferation in tissues showed that reducing the amount of space in a tissue prevented entry into S-phase. Actually stretching the tissue quickly reactivated the cell cycle, and compression leads quickly to arrest. More so, they found that cells had no memory of past constraint, and were able to suggest a model of growth in relation to the spatial constraint.

I'm editing my question because the way I posted it initially, to me, was unanswerable. Being said, I suspect that at this point cell volume and extracellular contacts are synergistic. This is probably going to need two separate questions, but:

1) How does the mitotic entry machinery roughly respond to cell volume? I'm currently reading into Cdc25/Wee1 regulation in addition to some stuff about internal fluidics that are influenced by water, ion channels, etc. but I still don't fully understand.

2) What's a relatively straightforward downstream pathway (core elements), starting at the adherens junctions, that illustrates how cell-cell signalling gets the STOP signal to the mitotic entry machinery (based on what we know)? This might require some much more in-depth knowledge about the field, however, but articles with some good figures are appreciated, too.

How does the mitotic entry machinery roughly respond to cell volume?

This is a broad question but luckily there is one article that addresses this precise question in detail. However, it is very likely that more discoveries are made on this topic in future.

Neurohr et al. (2019) have extensively studied the effect of cell volume on mitotic re-entry and cell cycle progression. They used Saccharamyces cerevesiae with temperature sensitive alleles of CDC28 to arrest the cells in G1 phase. At this stage high glucose concentration (2%) led to increase in cell volume compared to that of starved (0.1% glucose) or protein synthesis inhibited (2% glucose + cycloheximide) cells. Using this model they find that cytoplasmic dilution causes impairment of transcriptional regulation during cell cycle progression. This is because the transcription factors do not scale with cell size.

Read the paper for more details.

  What's a relatively straightforward downstream pathway (core
  elements), starting at the adherens junctions, that illustrates how
  cell-cell signalling gets the STOP signal to the mitotic entry
  machinery?

This is again a broad question if you expect all details. However, google scholar search on "contact inhibition pathway" suggests that the main downstream pathway is the Hippo signalling pathway.

Top hits on this topic:

Zeng, Qi, and Wanjin Hong. "The emerging role of the hippo pathway in cell contact inhibition, organ size control, and cancer development in mammals." Cancer cell 13.3 (2008): 188-192.
Kim, Nam-Gyun, et al. "E-cadherin mediates contact inhibition of proliferation through Hippo signaling-pathway components." PNAS 108.29 (2011): 11930-11935.
Gumbiner, Barry M., and Nam-Gyun Kim. "The Hippo-YAP signaling pathway and contact inhibition of growth." J Cell Sci 127.4 (2014): 709-717.


What is the population limit that makes consanguinity an issue? A recent incident brought in the news one of the last uncontacted people - the Sentinelese:

  the Sentinelese appear to have consistently refused any interaction
  with the outside world.

  There is significant uncertainty as to the group's size, with
  estimates ranging between 40 and 500 individual

If I understood correctly, the Sentinelese have a rather small population for dozens if not hundreds of generations and I am wondering if consanguinity is not issue (e.g. serious childhood effects) for them.

Question: What is the population limit (lower bound) that makes consanguinity an issue?

I don't have a great knowledge in population genetics but I think your question can be answered by the relationship between loss of heterozygosity and the effective population size.

For an ideal asexually reproducing genetically diploid population, the heterozygosity is lost with increasing generations according to this equation:

$$H_t=\left(1-\frac{1}{2N}\right)^t H_0$$

where $H_t$ is the heterozygosity at the generation $t$, $H_0$ is the heterozygosity of initial population and $N$ is the population size.

If you analyse this equation then you'll note that heterozygosity exponentially reduces at rate inversely proportional to the population size.

For real populations you have to replace the population size with effective population size. Effective population size for a sexually reproducing population would be:

$$\frac{1}{N_e} = \frac{1}{4N_m} + \frac{1}{4N_f}$$

Where $N_e$ is effective population size, $N_m$ is number of males and $N_f$ is number of females.

You can find the derivation of these formulas in Principles of Population Genetics by Hartl and Clark.

Other than that, the probability of extinction is also higher, the smaller the population is.

When would consanguinity be an issue depends on other factors too such as initial heterozygosity, presence of deleterious alleles in the gene pool and other environmental factors. I don't think there is some kind of mathematical/practical lower bound. The minimum viable population is approximated using simulations.


Why do cells not store glucose? I understand that glucose is soluble and hence it is not stored by cells. However, my teacher said that I also have to say that "it would have an osmotic effect on the cell." I don't understand what that means.

The issue here can be explained by colligative properties:

In short, colligative properties are properties that depend upon the concentration of the molecules, but not upon the type of those molecules. And osmotic pressure is a colligative property.

That being said, have in mind that 10 molecules of a huge polysaccharide in a given volume or 10 molecules of a small monosaccharide in the same given volume will have the same osmotic pressure.

So, let's imagine that the cell needs a given amount of glucose. Let's say 1000 molecules, just for an oversimplified example. The osmotic pressure can be calculated by (assuming Van't Hoff factor is 1):

  π = MRT

Where M is the molar concentration, R is the ideal gas constant and T is the absolute temperature.

Thus, the osmotic pressure created by those 1000 molecules can be calculated taking into account their molar concentration.

However, If we simply polymerize those 1000 glucose molecules into a huge polysaccharide (be it starch, glycogen or cellulose, it doesn't matter)...

  1000 molecules of glucose → 1 molecule of starch

... the molar concentration will be 1000 times smaller, and the osmotic pressure will drop 1000 times.

As the actual numbers are way higher than this simplified example, we can clearly understand that cells avoid storing glucose to prevent a deadly osmotic pressure, in which the cell bursts due to the amount of water that moves in (specially animal cells, which have no walls that could prevent the membrane from rupturing).


What does 5' and 3' mean in DNA and RNA strands? What are 5' and 3' in DNA and RNA strands? Please clarify with some images and please use simple English.

The 5' and 3' mean "five prime" and "three prime", which indicate the carbon numbers in the DNA's sugar backbone. The 5' carbon has a phosphate group attached to it and the 3' carbon a hydroxyl (-OH) group. This asymmetry gives a DNA strand a "direction". For example, DNA polymerase works in a 5' -> 3' direction, that is, it adds nucleotides to the 3' end of the molecule (the -OH group is not shown in diagram), thus advancing to that direction (downwards).


What kind of bug or insect is this? One of my friends has seen this insect-like species in water in the mountainous area in Iran (near Qom).

Looks like some species of tadpole shrimp. I couldn't tell you what species. There's really no other basis for identification other than these are extremely unique. As you can imagine, they're endemic to a variety of wetland environments. The take home point, however, is it's a crustacean rather than an insect.


Protein construct design I am trying to create some constructs of a certain protein deleting well defined domains (at either terminus) to determine interaction regions with other proteins etc., 3 constructs with varying start/end sites have ended up being aggregated in E coli (while the full length protein expresses reasonably well). My question is what considerations one should use to determine start/end sites to maximize chances of getting soluble, purifiable protein. The criterion I used were:

Preferably loop region in known x-ray structure
Use hydrophobicity plots to minimize hydrophobic residues at both termini
3-4 residue linker between protein and affinity tag (GST/6xHis)

From personal experience with an earlier construct, this can turn out to be an idiosyncratic exercise but I was wondering if I was missing any crucial parameters.

EDIT: I also played around with the PDB file of the non-truncated protein to check whether huge hydrophobic patches were exposed on deletion of the domain(s), and I didn't find any such patches that could potentially be exposed and lead to aggregation

Did you identify structural domains in the protein using Pfam or some other domain detecting peptide search?

It's pretty useful to cut your constructs at the boundaries of structurally independent domins in the protein if you know where they are.  Hydrophobicity plots might lead you to cut right in the middle of a protein fold, only exascerbating inclusion body formation/protein precipitation.


lifespan of Nautilus compared to other cephalopods Most cephalopods live uncharacteristically short lifes compared to other creatures of their size and intelligence. The octopuses with the longest lifespan for example, the giant pacific octopus, only live for up to 5 years.
This is quite long for cephalopods already, as some of them only live for as little as half a year.

The reason for this short lifespan is not aging itself (meaning loss of information in the epigenome and similar effects), but their reproduction. The maturation of their reproductive organs results in the deactivation of their degestive glands, so they basically starve themselves to death.
When the reproductive glands of an octopus are removed, their lifespan increases greatly.

Nautilus are an exception to this low lifespan of cephalopods. They live to be over 20 years old.
Why do nautilus live so long and is it possible to grow other cephalopods with similar lifespans by introducing nautilus genes?

On a basic level, the difference in lifespan is due to the fact that the nautilus has a vastly different reproduction strategy from other living cephalopods.  While most other cephalopods exhibit a rather extreme form of r-Strategy reproduction, the nautilus is, relatively speaking, a K-Strategist.  To explain, r-Strategy is when a species produces many offspring, but puts relatively little investment into each one under the expectation that most will die.  K-Strategy, on the other hand, produces relatively few offspring, but put much greater investment into each one.

As you stated, in most cephalopods, sexual maturity triggers a shutdown of the digestive tract, as they put all their energy into reproduction, during which one spawning episode will result in hundreds or thousands of eggs.  After fertilizing the eggs for males, and for females after laying those eggs (allowing for a delay of a relatively short incubation period in some species, including most or all varieties of octopus), the adults die, having produced enough young to guarantee the next generation.  This lifestyle of a single massive reproduction event before dying is called semelparity.

However, with nautiluses, each mating results in only about a dozen eggs.  These eggs are much larger than the eggs of any other cephalopod, have a considerably longer incubation perios, and by extension, the hatchlings start out larger and better-developed.  However, technically, nautiluses aren't true K-Strategists, like humans or whales, which have only one offspring at a time and put a massive amount of investment into that offspring.  Instead, they are more like cats or dogs, Median Strategists, who fall somewhere between the extremes.  While for r-Strategists like other cephalopods, semelparity can produce enough young to ensure the survival of the species, this is not the case for Median or K-Strategists.  Instead, they must reproduce multiple times over the course of their life, a strategy called iteroparity.

While in all cephalopods, the gonads are destroyed by the process of reproduction, in nautilus females, the gonads regenerate after spawning, allowing them to mate again the next year.

It should also be noted that despite this, the nautilus spends a relatively small portion of its life sexually mature.  It takes roughly fifteen years for a nautilus to reach breeding age.

While my knowledge of genetic engineering is pretty much limited to what appears in the news, based on this information, it seems like to lengthen the lifespan of other cephalopods to be on par with that of a nautilus, you'd have to completely change the way they reproduce and the rate at which they mature, which I tend to suspect is beyond our current abilities.


How much light can pass through the human eyelid? My sister tells me that at night when the lights in the room are off that she can see the ambient outdoor light from neighboring buildigns and streetlights through her eyelids (i.e., when her eyes are closed). I, on the other hand, can't see anything. I can easily fall asleep even when the lights in the room are on; my sister can too, but when I tell her to sleep with the lights on because I have work to do, she just stares at the light and says that she can't sleep.
So, quantitatively, how much light would be able to pass through a normal human being's eyelids. And would ambient outside light be enough to pass through?

Short answer
About 0.79% of the light gets through on average, but there is variability across wavelengths and individuals. (variability between individuals seems to be correlated with density of macromolecules in the eyelid).
Long answer:
This is called "eyelid spectral transmittance".
Lucky for you, Bierman et al (2011) sought to determine the answer to this question.
Using a custom LED wand that actually emitted light under the eyelid for a sensor on the outside to read, they found quite a bit of variability both across wavelengths as well as across 27 test subjects.
They report their findings in terms of optical density, which is explained as follows:

A measure of the transmittance through an optical medium. Optical density equals the log to the base 10 of the reciprocal of the transmittance.... In spectroscopy, optical density is the measure of absorbance, and is defined as the ratio of the intensity of light falling upon a material and the intensity transmitted. Abbreviation OD.

We can use the equation  A = -log10(1/T) to convert their findings of OD to transmittance and then multiply by 100 to get a percentage of light that can pass through.

Their result of an OD of 2.1 ± 0.3 SD = a transmittance of 0.79%

They do note that  eyelid thickness, and/or the density of macromolecules in the eyelid account for most of the variation in transmittance between subjects.

 Bierman, A., Figueiro, M.G. and Rea, M.S., 2011. Measuring and predicting eyelid spectral transmittance. Journal of biomedical optics, 16(6), p.067011.


Is a flower having 12 petals trimerous or tetramerous? Suppose if a flower has 12 petals. Then 12 is a multiple of both 3 and 4. So which category of flower is it? Is it trimerous or tetramerous?

Suppose if a flower has 12 petals. Then 12 is a multiple of both 3 and 4. So which category of flower is it? Is it trimerous or tetramerous?

Merosity, in the context of your question, is the number of petals in the corolla.
Refer to "Gray's Botanical Textbook: Structural botany", on page 176, section 322:

"322. To designate the particular plan, such familiar terms of Latin derivation as binary, ternary, quaternary, quinary, unary, &c., are sometimes employed, denoting that the parts of the flower are in twos, threes, fours, fives, or sixes. More technical and precise terms, equivalent to these, are composed of the Greek numerals prefixed to the word meaning parts or members, as Alonomerous, for the case of a flower of one member of each ; Dimerous, of two, or on the plan of two members of each ; Trimerous, of three, or on the plan of three members ; Tetramerous, of four, or on the quaternary plan ; Pentamerous, of five, or on the quinary plan ; Ilexamerous,$^{[1]}$ of six, or on the plan of six members to each circle. But, in Monocotyledons, so-called hexamerous blossoms are really trimerous, the sixes being double sets of three.
[1] These may be shortly written 1-merous, 2-merous, 3-merous, and so on up to 10-merous (decamerous), 12-merous (dodecamerous), &c.".

Because counting is done using Greek cardinals a corolla with 12 petals is dodecamerous. One with 4 sets of 3 is trimerous, and one with 3 sets of 4 is tetramerous.


Why does hair turn grey or white, and why does it happen later for some? The question is pretty simple: what is happening molecularly when hair turns grey or white? I would imagine that it is due to the lack of a particular compound. I'm also interested in why some people's onset of grey hair happens much later than others.

Each individuals hair colour is determined by the particular pigment they produce (called melanin - the same stuff in your skin that makes you tan).

As the body ages this pigment (produced by the melanonocytes - cells that reside in the hair follicle) is produced less and less, until the hair is no longer coloured, and appears grey.

This is unique to each individual because it is a genetic (and therefore highly heritable) trait. Because it is in no way linked to mortality there is no selection pressure against greying hair.

The reason that the pigment is not longer produced is the gradual depletion of the stem-cell pool with age. This is common to many tissues, hair follicles being just one. As the 'pool' of stem cells is depleted, the melanocytes are no longer replaced as frequently, and thus less pigment is produced as we age.


Is complete linkage found in all four chromosomes or only Y-chromosome of Drosophila? Male Drosophila shows complete linkage. Is it observed for all four chromosomes or only the Y chromosome?

All chromosomes. There is no crossing over in males in Drosophila. Check out the related question Why doesn't recombination occur in male Drosophila? for sources and context.


Knockout Rat Phenotype Database? Is there a database where I might list the phenotype of a certain rat knockout and/or search for other similar phenotypes?

There is a International Mouse Phenotyping Consortium, which has the goal of characterizing the phenotypical changes of homozygous knockouts for each of the 20,000 genes in the isogenic mouse line C57BL/6.  The International Knockout Mouse Consortium is responsible for creating the knockouts and the two consortiums work together closely.

There is also a Knockout Rat Consortium, but I haven't found a Phenotype Change database for rats.

Opinion:

the Jackson laboratory

http://jaxmice.jax.org/

Is the industry leader in transgenic mouse production. Their list of mouse strains is almost a db in itself but currently no db exists that I'm aware of. I take it your looking for something similar to what's available for c elegans:

http://www.celeganskoconsortium.omrf.org/


Is it possible to use PCR to test for Machado-Joseph disease? Machado–Joseph disease (MJD) is a rare inherited neuromuscular disease that is caused by a mutation in the gene ATXN3. The protein encoded by this gene contains "CAG" repeats in the coding region, and the expansion of these repeats from the normal 12-44 to 52-86 is the most common cause of the disease.
It is well known that amplification of repetitive DNA by PCR is prone to errors, mainly caused by misalignment/slippage of the polymerase during the elongation phase.
Does anyone know if there exists a specialized PCR protocol or polymerase that could accurately amplify the repetitive region of ATXN3 such that one could then use gel electrophoresis or Sanger sequencing to approximate the number of CAG repeats?

This paper describes an allele-specific PCR protocol to detect CAG repeat expansion in MJD patients:
Maciel P, Costa MDC, Ferro A, et al. Improvement in the Molecular Diagnosis of Machado-Joseph Disease. Arch Neurol. 2001;58(11):1821–1827.


Why aren't animals diverse in phenotype? I am not comparing a cat with leopard.

I am just saying that we humans are all one type of creature and we are diverse (I am not saying we are class of mammals and phylum of etc and kingdom etc, because my religion doesn't believe in it).

So consider the class of cats they are one type of species so why aren't they diverse in phenotype like us?

Why do other animals, plants, unicellular organisms not have diversity in their phenotype and how they can recognize each other, like a bird always brings food to his offspring and it can't make mistake by giving it to other offspring of its own species?

So can I say they aren't diverse because of in their meiosis division their chromosomes don't cross over and random assort (alignment)?

In your question, your assumption that animal species are less diverse phenotypically than humans is wrong. I am sure you will appreciate @terdon's answer to this post and @rg255 answer to this post.

Don't forget that we are good at detecting differences among humans (because we evolved for this purpose). We are doing much worse at telling apart animals from other species just because we have not evolved for this purpose. This is the reason why we tend to see human faces when looking at clouds but we rarely see sheep faces! Several studies (here and here) showed that sheep are able to recognize each other (and we even know the number of neurones needed to remember one face). They are probably better at telling two sheep apart than telling two human apart.

Another interesting fact is the so-called cross-race effect. We, humans, are better at recognizing faces of people from our own ethnic group than faces of people from other ethnic groups. For example, a Japanese is very good at Japanese faces recognition but not good at recognizing European faces. Same is true the other way around.

As @user568459 said in the comments: some people are not able to recognize faces. This is due to a cognitive disease called Prosopagnosia (also called face blindness). Those suffering from this disease are not better at recognizing sheep faces than human faces.

  So consider the class of cats they are one type of species so why aren't they diverse in phenotype like us?

There is no good definition I think of what is phenotypic diversity (no accurate and objective index to measure it) but at first sight I would tend to think that cats are more diverse than humans. One of the main features one would probably raise when talking about human diversity is skin color. And in terms of color, cats are much more diverse than humans. You may think of an extraordinary diversity when thinking of Norwegian that are taller than Indonesian (I may not have chosen the two extremes) by several centimeters on average but think about cats! The average cat weight 4 to 5 kg but some cats weight less than 2 kg and some other (like the coon cat) weight more than 10 kg (World Record: 21.3 kg). Imagine a human ethnic group that would on average weight 5 times more than another ethnic group! And think also about cats' hair length or tail shape! Humans vary in terms of facial feature (lips size, nose shape, etc.) so do cats. Some look like their face was smashed against a wall while others have a long muffle. Again I welcome you to have a look to this post.

  how they can know each like a bird always brings food to his offspring and it can't make mistake by giving it to other offspring of it's own species?

As I said above humans evolved to recognize their own. Many species also evolved in order to recognize their own. In some species individuals use smell rather than visual features in order to recognize each other (odor is also a kind of phenotypic variation). But still some species are poor to recognize each other. For a bird, it seems rather easy to not feed the wrong individual as all their offspring are usually together in the same nest. However you might be interested the lifestyle of the cuckoo who parasites nests of other bird species. Cuckoos' babies and particularly the inner beak resemble to the babies of the species they parasite and often the parents (often the mother only is involved in feeding the young) get fooled and feed the cuckoo.

  So can i say they aren't diverse because of in their meiosis division their chromosomes don't cross over and random assort (alignment)?

No, you can't say that! Because they are diverse and because for many of the species you may think about, cross-over does occur. Their genetic diversity as well as their phenotypic diversity is as high than in humans. There is nothing extraordinary about humans (except their brain and the related fact that we predigest our food by cooking it) compare to other lineages. And there is nothing extraordinary to have one extraordinary feature (such as a big brain) that you can't find in other lineages! Many lineages are extraordinary in some sense.


What kind of grasshopper-like insect is this? We found this thing in our basement. Not quite an average grasshopper. Any ideas?

That is a "cave cricket", in the family Rhaphidophoridae. These are common in basements, and harmless.


Does sour food cause sweating? While eating sour food or candy, I start to sweat if it's sour enough. My body feels much hotter although my actual temperature is the same, my forehead starts sweating a lot and I feel like it just got twice as hot wherever I am.

Is this a biological phenomena or is my DNA just stupid? Is it somehow related to the digestive system, that sour food is harder to digest?

In general, sweating is caused by too much heat, even if you're not aware of the heat. This can happen if the bowel moves and so raises the core temperature. Such movement is often accompanied with sweating, and since you only feel the normal temperature on the skin, it is cold sweat. But at the same time your core is hot so you think it's cold, but it will later mix to normal.

Anyway, it points to unusual bowel movement. This can be due to food allergy or, in a milder form, in food intolerances which are quite common. When it comes to sour ingredients, they are often in fruits, so I'll make a shot in the blue and say that you have a food intolerance against some fruits. You can check this hypothesis by trying chemically pure acetic acid to sour your food. If that doesn't result in sweat/hotness then it's probably the fruits.

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

The Wikipedia points even directly to salicylate in fruits but I think you cannot exclude allergies against essential oils like limonene and such. Plants are really chemistry factories and not all is well that you can get with them.


Bed bug or booklouse? I found this creature climbing on the lower part of a wall inside apartment. Can you distinguish if it's a bed bug nymph or a booklouse? Sorry the photo quality isn't great, because it's so small (2 mm). Thanks in advance!

After looking it up, I can, with some confidence, confirm that this is a book louse in the larval stage, as seen in this picture:
https://bpca.org.uk/write/MediaUploads/Pages/A-Z/Booklice/booklice-1.jpg
I hope this answers your question!