Non-Lifestyle related diseases Given the obvious importance for global health, I've found it easy to track down lists from Google of the top lifestyle related causes of death (like heart disease, lung cancer etc), but as a consequence it proven difficult to find a source of the opposite, the leading causes of death which have no (or very little) relation to lifestyle choices (like smoking, obesity etc).

What I'm interested in is those chronic and generally quite fatal disease which just happen for either genetic or spontaneous reasons, or perhaps due to environmental causes which are so ubiquitous as to be unavoidable.

I'm not looking for an exhaustive, or even very large list, the top five to ten would do, and I understand that there's no clear distinction between lifestyle and genetic factors, but obviously health organisations make some estimate of what is mainly the cause otherwise lists like these would not be possible. I just want the opposite list.

To clarify in the light of some answers, I'm looking for diseases which one might contract in adulthood (this could include pathogens) which could in a normal healthy person living within reach of modern medicine still present a more than 50% chance of being fatal. Basically I'm after a risk figure (my field of research) which would act as a baseline presuming a safe, healthy life.

So the CDC has a list of total leading causes of death

https://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm

  Number of deaths for leading causes of death
  • Heart disease: 614,348
  • Cancer: 591,699
  • Chronic lower respiratory diseases: 147,101
  • Accidents (unintentional injuries): 136,053
  • Stroke (cerebrovascular diseases): 133,103
  • Alzheimer's disease: 93,541
  • Diabetes: 76,488
  • Influenza and pneumonia: 55,227
  • Nephritis, nephrotic syndrome, and nephrosis: 48,146
  • Intentional self-harm (suicide): 42,773

Cancers can be further subdivided into types which may or may not be related to lifestyle. There are lung cancers and skin cancers that are not linked to smoking or skin damage respectively. Cancer is very complicated.

Most of the causes on this list have lifestyle or environmental components to them. Influenza and pneumonia have less to do with lifestyle and more to do with the immune system either being too robust or not robust enough but the immune system is influenced by lifestyle as well.

To get a list of diseases that are the leading causes of death and not influenced by lifestyle or environmental, you'd probably be looking at genetic diseases like cystic fibrosis for example.

The WHO has a list of these monogenetic diseases. These are diseases that are caused by a single gene (either one or two copies of the gene depending on the disease) and are independent of lifestyle and environment.

  Thalassaemia
  Sickle cell anemia
  Haemophilia
  Cystic Fibrosis
  Tay sachs disease
  Fragile X syndrome
  Huntington's disease

You can read more about these diseases here: http://www.who.int/genomics/public/geneticdiseases/en/index2.html


What are the hairs/spikes on the edges of these leaves for? Windows 7 has a wallpaper/background which shows an attractive, leafy plant with fine hairs or spikes on the edges. What might these be for, and what sort of plant is it?

My initial (uneducated) guess is some species of Sempervivum, with the hairs serving some purpose like water-collection?

Windows 7 leaf background http://p1.pichost.me/i/32/1555532.jpg

I believe the hairs are known as trichomes. They can be uni- or multicellular. Depending on the plant and type of hair, they can serve one or more of several purposes. They may interfere with feeding by small and/or large herbivores, depending on how annoying to the palate they are. Some plants use hairs to keep frost away from the surface of the leaf. They can serve as nucleation points for water droplets in areas where the plant's primary source of water is fog. On the other hand, they can also help reduce transpiration in windy areas by breaking up the flow of air across the leaf. Finally, in hot/dry areas, they can reflect some sunlight to protect the leaf's tissues.

So, the function really depends on the type of plant and its habitat. I'm not a botanist, so I can't confirm whether or not your guess of Sempervivum is correct, but if it is, then the hairs would likely help reduce transpiration in hot, dry, windy areas, and possibly block some sunlight.


Identification of insect I am trying to identify this insect on a hibiscus plant. Google googles is unable to identify it.

It's a Japanese Beetle Popillia japonica - they are invasive in most of North America and some of Europe now.

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

They are spreading rapidly west in the United States and many areas are reporting the largest numbers ever observed, for example:
http://www.wisconsinrapidstribune.com/story/life/2017/07/19/japanese-beetles-invade-central-wisconsin/490140001/

http://www.omaha.com/living/japanese-beetle-swarms-are-worse-than-ever-this-year-and/article_77257d36-6c28-11e7-839a-877ff3c8538b.html

For control around your plants, it is recommended to manually remove them; brushing or placing them in water with some dish soap works well. They tend to congregate with other individuals of the species, so if you take them off your plants that will tend to limit the numbers that join them. However, they likely do the most damage to gardens etc as larvae, and there doesn't seem to be a good, specific way to control them at that stage.


Finding a easy and cheap method for dyeing dNTP I want to measure OD to know the concentration of dNTP. Any idea for dyeing dNTP at cheapest price and easiest way ?

There may be such a dye, but I'm not aware of it.  The standard way to measure dNTPs, and nucleic acids in general is by absorbance at 260 nm. This article has a table of molar extinction coefficients for dNTPs (Table 10.2). They are

        wavelength      molar extinction coefficient
dATP    259 nm          15,200
dCTP    280 nm          13,100
dGTP    253 nm          13,700
dTTP    267 nm           9,600

In practice for routine work with DNA you can use 260 nm and assume that an absorbance of 1 corresponds to [DNA] = 50 µg ml-1. Using an average of the values in the Table, and disregarding the fact that these are actually at different wavelengths, and using an approximate average dNTP MW of 500, I calculate an absorbance for a 50 µg ml-1 solution of all 4 dNTPs as 1.3, so that's a reasonable agreement given all of the assumptions I've made.

There are fluorescent dyes that can be used to measure DNA, but these rely upon the presence of stacked bases, so are not useful for free dNTPs.

So, bad news if you don't have a UV spectrophotometer. There are plans available for construction of simple spectrophotometers using Lego and a few optoelectronic components. These tend to use LEDs as a light source, but I don't know if UV LEDs are available.


What's the technical difference between fainting (and being unconscious) and falling asleep (and sleeping)? This is actually a popular question along google results but the answers usually sound like:

sleep is voluntary (oh is it?) and healthy
fainting is result of accident and is not normal

I read those answers and I'm like: "You don't say?". So yeah, I know that falling a sleep is a result of some preparation to planned unconscious state, whereas fainting is some defensive reaction trying to protect you from moving (or maybe thinking) when you shouldn't.

But I fainted once and when I woke up it was pretty much like waking up from sleep - including the fact I don't remember the moment I fainted. This gave me an idea that maybe, if you faint in your bed, you'll just fall asleep and wake up in the morning, which would be actually pretty sweet.

Therefore my question is, what's specifically going on when you faint and when you fall asleep. Is there any part when these two situations merge and the final state is the same - you're asleep?

And to my original idea: If you hold your breath to the point where you faint in your bed, what will the result be?

For this answer I assume that we are talking about sleep in healthy individuals as well as fainting as an isolated event without underlying disease or injury.

The most common form of what we call "fainting" is vasovagal syncope. It is caused by a drop in blood flow to the brain (cerebral hypoperfusion) e.g. by (false) activation of the parasympathetic nervous system and inhibition of the sympathetic system, resulting in low blood pressure or drop in heart rate (reviews 1,2,3). This can be triggered by the Bezold-Janisch reflex. Syncope can also be a symptom of underlying diseases or a side effect of drugs.

The reduced blood flow results in a transient loss of consciousness, a 'shut down' of the brain, which we don't really understand. It is sometimes accompanied by a flattening of an EEG signal, even though the data doesn't seem to be very consistent. Consciousness is defined by two factors, arousal and awareness. The fainted person cannot be 'woken up' and is not aware of the situation (as you said, you don't remember the moment of fainting). But this state normally only lasts for a few seconds or 1-2 minutes.

Sleep, on the other hand, is a mechanism highly regulated by the brain, circadian rhythms and hormones. The brain is thought to switch between the states of sleep and wakefulness by an interplay of different sleep-promoting and wake-promoting areas, including the hypothalamus.

You can argue that sleep is not a state of unconsciousness, since dreaming or even lucid dreaming are connected to a conscious experience. While sleeping lasts longer than the unconsciousness during syncope, it can be reversed by an external stimulus. The sleeping person can be woken up, even though the arousal threshold is increased (loud noises from the alarm are needed). The brain, in fact, is highly active during sleeping (as can be seen in characteristic EEG signals), with energy use close to the state of wakefulness in REM sleep and about 85% during non-REM sleep.

Since these are two different mechanisms, you should not be able to switch between them. After fainting you should regain consciousness very fast. Activation of sleep mechanisms is unlikely in a healthy individual, where sleep regulation is normal and syncope is a rare event.


Why are all human beings not black in color? Archaeologists and historians strongly claim human beings originated from the African continent, where the default color is black for humans.
Why are all human beings not black in color?

First let's look at the difference between light skin and dark skin: darker skinned people have higher concentrations of melanin than those with lighter skin. Africa is located around the equator, a place where the sunlight is very intense. Melanin protects the skin against harsh, damaging rays, which is very beneficial in Africa. But a high concentration of melanin also decreases the skin's ability to produce vitamin D3 (1). Vitamin D3 is a vital nutrient to many physiological processes. Deficiencies in vitamin D3 has been known to cause things like rickets and osteomalacia (2).
So in Africa, having a high concentration of melanin in your skin conferred a great fitness benefit: you could go outside without getting cancer. But when humans relocated to places farther from the equator with reduced sunlight, having a high concentration of melanin in the skin actually became harmful because it would make darker skinned people more likely to have vitamin D3 deficiencies. Given this change in the fitness conferred by the trait of dark skin, individuals with lower concentrations of melanin in their skin were more likely to survive and reproduce in these new conditions. After many generations, the allele(s) that cause lighter skin became more common than those that cause darker skin.
Hope that was helpful!

T.L. Clemens, S.L. Henderson, J.S. Adams, M.F. Holick, INCREASED SKIN PIGMENT REDUCES THE CAPACITY OF SKIN TO SYNTHESISE VITAMIN D3, The Lancet, Volume 319, Issue 8263, 9 January 1982, Pages 74-76, ISSN 0140-6736, http://dx.doi.org/10.1016/S0140-6736(82)90214-8
http://www.everydayhealth.com/drugs/vitamin-d3


Do any plants exhibit hormonal changes similar to puberty? Just what the title states.

Are there any plants/trees that exhibit a growth spurt at a definite interval after the shoot appears?

In flowering plants (the angiosperms) there are several developmental transitions in the life of the plant. I won't list the plants, because the list includes pretty much all of them (although the magnitude in the change of developmental pace differs widely between taxa and environments).

First there is seed germination, which is controlled hormonally. Absence of germination is usually imposed by abscisic acid, whilst germination is caused at the appropriate time by gibberellic acid and ethylene (among other things; Holdsworth, Bentsink & Soppe, 2008).

Next, in many herbaceous species there is a transition between a spreading growth stage (e.g. rosette growth) and the flowering stage. The 'growth spurt' here is the differentiation and elongation of the flowering stem, and then subsequently the sudden flowering of buds. The transition is also controlled hormonally, by a variety of hormones including auxin (Zhao, 2010), gibberellic acid, ethylene (Schaller, 2012), and the long anticipated, recently confirmed florigen (Choi, 2012). Ethylene and abscisic acid then play important roles in the next developmental transition when seeds and fruits are produced and dehisced.

Small RNAs are also now being revealed to play a large role in controlling the timing of developmental, but they are upstream of the hormonal changes. In particular some key miRNAs are involved in auxin-based regulation of branching, and in embryogenesis (Nodine & Bartel, 2010), and RNA silencing is involved in the switch from rosette growth to flowering growth (reviewed in Poethig, 2009 and Baurle & Dean 2006).

 Bäurle I, Dean C. 2006. The Timing of Developmental Transitions in Plants. Cell 125: 655–664.
 Choi CQ. 2012. A Blossoming Field of Research: How Florigen Is Transported to Create Flowers. PLoS Biol 10: e1001311.
 Holdsworth MJ, Bentsink L, Soppe WJJ. 2008. Molecular networks regulating Arabidopsis seed maturation, after-ripening, dormancy and germination. New Phytologist 179: 33–54.
 Nodine MD, Bartel DP. 2010. MicroRNAs Prevent Precocious Gene Expression and Enable Pattern Formation During Plant Embryogenesis. Genes Dev 24: 2678–2692.
 Poethig RS. 2009. Small RNAs and developmental timing in plants. Curr Opin Genet Dev 19: 374–378.
 Schaller GE. 2012. Ethylene and the regulation of plant development. BMC Biology 10: 9.
 Zhao Y. 2010. Auxin Biosynthesis and Its Role in Plant Development.


How long do zebra fishes remain transparent? As larva, zebra fishes are transparent, at least up to 5-6 days. I wonder what would be the upper limit of the transparent period. This is of relevance considering purposes for imaging.

The question primarily relates to normal zebra fish, and not especially to transgenic breeds.

The upper limit of transparency time of zebrafishes is anywhere from two to three weeks for normal zebrafish for optimal high-resolution imaging. However, there is a modified species of Zebrafish called 'Casper' which is now the preferred zebrafish strain for studies in cancer and other research, because the length of transparency lasts into adulthood.

Sources:

http://medicalphysicsweb.org/cws/article/research/51394
https://biology.mit.edu/people/lisa_steiner#research_summary
http://www.the-scientist.com/?articles.view/articleNo/34834/title/Models-of-Transparency/


In which reactions of glycolysis is magnesium involved? I am currently studying the metabolic pathways for biochemistry and I am not quite clear in which reactions of glycolysis magnesium is involved.
So I have now found out that magnesium is present in the three ATP-dependent reactions (1st, 3rd and 10th reactions), but also in the 2nd, 7th, 8th and 9th steps.
According to this diagram:

In our university we have been tought, that Magnesium is present in all ATP reactions, but also in Step 2... this is what causes confusion for me:

In the 1st step where glucose is converted to glucose-6- phosphate by the enzyme hexokinase, in the 3rd step where fructose-6-phosphate is converted to fructose-1,6-bisphosphate by the enzyme fructose-1,6-bisphosphatase and in the last reaction where 2 phosphoenolpyruvate is converted to pyruvate by the enzyme pyruvate kinase.. In this 3 reaction Magnesium is needed as they are ATP dependent reaction and Magnesium stabilises the ATP in this reaction and help the reactions to proceed faster.


Altruism in viscous (asexual) populations The viscosity of a population is the tendency of offspring to remain
near their place of birth. Taylor 1992 ("Altruism in viscous populations") provides a model to study how viscosity affects the evolution of altruism in a patch-structured population. In Taylor's model, the marginal inclusive fitness is given by
\begin{equation}
  W = bR -c - s^{2}(b-c)R
\end{equation}
where $R$ is the relatedness of a mother to random offspring born on her breeding patch and $s$ is the probability the offspring will remain on the natal patch. The altruistic act creates $b$ offspring with average relatedness $R$ and $-c$ offspring with relatedness 1.

My question is about the term $s^{2}(b-c)R$. Taylor explains this term as follows:

  these b - c extra offspring remain on the natal patch with probability
  s and will therefore displace s(b - c) random individuals competing
  for the next generation breeding spots on that patch, and these will
  be native to that patch with probability s and in this case will have
  average relatedness R to the actor. Thus these displaced individuals
  will have average relatedness sR (p. 353)

My question is: Why is the average relatedness $sR$ (as opposed to $R$)? In other words, why is the term that accounts for competition among relatives $s^2(b-c)R$---as opposed to $s(b-c)R$?

The $sR$ that your looking at is the average relatedness of the next generation.  This assumes that the new immigrants into the the population are completely unrelated. So if the population is completely viscous ($s=1$) the average relatedness of the next generation equals that of the current generation.  On the other hand, if the population is not viscous ($s=0$) the next generation would be entirely unrelated because it would only be made up of unrelated immigrants.

The $s(b-c)$ is the number if individuals that are displaced by new offspring.  Again if all of the new generation sticks around ($s=1$) then the number of displaced individuals equals the number of new individuals.  And if all new progeny leave ($s=0$), there are no displaced individuals.


Did I just watch a spider die? So I'm sitting in my office and all of a sudden a small spider is gliding down on a web string from the ceiling, right in front of my eyes, and down onto my desk. It proceeds to make a few awkward movements which looked like it was having problems correctly coordinating its legs. Then it flipped on the back and had its legs curled up (like it was dying).

A few seconds later it suddenly started moving with the awkward movements (like it was trying to walk) for a few seconds before collapsing again. It's been doing this on and off about 3 to 4 times. As far as I can tell, the unconscious periods are becoming longer and the waking periods shorter.

What's happening here? Is it dying (of stress / bitten by a female spider / old age) ?

Edit: The whole process has now been going on for over 30 minutes. During the times it moves, it looks like it cannot use the foremost pair of legs. Here are two pictures of the (really tiny) spider with a shopping cart token coin for scale:

Spiders do curl up their legs when they die. Since they do not have muscles for extending the legs at their joints, they control the haemolymph pressure in the legs by using the blood pressure spike from their heartbeat to extend their legs out or walk. And with no heartbeat (when the spiders cease to exist), they curl up upon death.

Source: http://www.informationsociety.co.uk/why-do-spiders-curl-up-when-they-die/


Does RNA serve as the genetic material of some plants and animals along with viruses? My teacher mentioned that some plants and animals have RNA as genetic material but did not substantiate his statement  with examples. I'm wondering if it is so?
I have searched the internet but have found no such information.

There are no animals or plants with RNA genomes. There was a mistaken belief in the 1920s that plant genetic material was RNA whereas animals had DNA, but this was finally disproved by JN Davidson in the 1940s.


Regulation of the TCA cycle and glycolysis by adenine nucleotides Why is the tricarboxylic acid cycle regulated by the ADP/ATP ratio as stated in the following quote :

  Isocitrate dehydrogenase is allosterically stimulated by ADP, which enhances the enzyme's affinity for substrates.1

while glycolysis is regulated by AMP/ATP ratio as in the following quote from the same book :

  Why is AMP and not ADP the positive regulator of phosphofructokinase? When ATP is being utilized rapidly, the enzyme adenylate kinase (Section 9.4) can form ATP from ADP by the following reaction: 2

I want to check my hypothesis that it is because the TCA cycle needs acetyl-CoA ( which can come from glycolysis and other sources such as beta-oxidation of fatty acids) in order to operate, so it gets acetyl-CoA from many sources and isn't dependent on glycolysis alone, and that's why it is affected by ADP (which increases upon initial exercise) while AMP stimulates glycolysis (increases after more exercise) to give more acetyl-CoA and that's rate of the TCA cycle is faster than glycolysis?

References

1,2 J.M. Berg et al. (2002). Biochemistry, 5th ed. New York: A H Freeman.

Summary

Glycolysis and the tricarboxylic acid cycle (TCA cycle) are distinct processes which are not necessarily linked sequentially. It is therefore not surprising that their modes of regulation are not identical and, in fact, involve far more complex regulation than mentioned in the question. The use of AMP rather than ADP as sensor of energy deficit depends on the action of adenylate kinase, which may differ between cytoplasm and mitochondria.

Relationship Between glycolysis and the TCA cycle

The expectation evident in the question that glycolysis and the TCA cycle should be controlled in exactly the same way assumes that either the two processes are inextricably linked or at least that the functioning of the TCA cycle is dependent on that of glycolysis. This is not the case, although the student can be excused this misimpression from the (perhaps unavoidable) way the topics are generally treated sequentially in text books of biochemistry.

The primary function of glycolysis is to produce ATP directly from ADP. The end-product of the pathway, pyruvate, is in some circumstances converted to acetyl CoA for the TCA cycle, and the NADH generated used for production of ATP generation via the electron transport chain (etc) and oxidative phosphorylation. However pyruvate has a variety of other possible fates depending on the type of organism or — in higher organisms — the tissue, and their overall metabolic requirements. For example in anaerobic metabolism — including exercising muscle tissue mentioned by the poster — the pyruvate may be reduced by reactions that regenerate NAD+ from NADH, e.g. conversion to lactate. It can serve as a precursor of the amino acids, alanine, valine and leucine. It can also be converted in the reaction catalysed by pyruvic carboxylase to oxaloacetate, the key intermediate that allows acetyl CoA to enter the TCA cycle. The importance of direct synthesis of oxaloacetate in this way is that it allows continuation of the cycle when intermediates are used for synthetic purposes (discussed below), in which circumstances oxaloacetate becomes depleted.

As regards the TCA cycle, there are sources of acetyl CoA other than pyruvate produced by glycolysis, and it has functions other than energy generation. Acetyl CoA can arise from the breakdown of fatty acids and of certain amino acids. In multicellular organisms, pyruvate can also be produced from lactate taken up from the blood, although in liver cells it is likely to be used for gluconeogenesis. And certain bacteria — acetic acid bacteria such as Acetobacter — can utilize the ethanol produced by fermentation in the TCA cycle. In addition to its function in energy generation some of its intermediates (α-ketoglutarate, succinyl CoA and oxaloacetate) are precursors of biosynthetic pathways, and the production of citrate from acetyl CoA is a means of transferring the latter out of the mitochondrion, where it is reconverted to acetyl CoA by the citrate cleavage enzyme (ATP citrate lyase).

It is therefore not surprising that there will be differences in the regulation of glycolysis and the TCA cycle, and, indeed, that there will be differences between different organisms — something generally not mentioned in elementary texts.

Regulation of Glycolysis

The prime function of glycolysis is the direct generation of ATP (“at the substrate level”), and flux of glucose through it is controlled by the regulatory effects of both ATP (–ve) and AMP (+ve) on phosphofructokinase, which was established and rationalized by D. E. Atkinson (Biochemistry 1968, 7, 11, 4030-4034) in terms of a response to the overall energy charge of the system.

This arises from the ability of adenylate kinase to reconvert ADP to ATP:

               2ADP → ATP + AMP

[from Atkinson and Walton (1967) J. Biol. Chem. 242 3239–3241]

It can be seen that AMP is a much better indicator of low energy charge than ADP in the circumstances represented by the graph above.

Citrate is also a negative effector of the enzyme, providing co-ordination between glycolysis and the TCA cycle. (Hormonal regulation via protein phosphorylation occurs in the tissues of higher eukaryotes.)

Regulation of the conversion of pyruvate to acetyl CoA

In order to enter the TCA cycle, pyruvate needs to be converted to acetyl CoA by the pyruvate dehydrogenase complex. The regulation of this enzyme determines the extent to which this occurs, and, hence, the extent to which pyruvate is metabolized by other processes. Negative regulators here are high concentrations of the reaction products, acetyl CoA and NADH, although in higher eukaryotes hormonally induced protein phosphorylation is important.

Regulation of the TCA cycle

Then first regulatory enzyme of the TCA cycle, isocitrate dehydrogenase, responds to the concentration of the key molecules involved oxidative phosphorylation: it is stimulated by ADP and +, and inhibited by ATP and NADH. It is worth reflecting on the consequences of inhibition. If a build-up of citrate occurs, this can feed back and inhibit phosphofructokinase in glycolysis. However the citrate can move to the cytoplasm of eukaryotes and be converted to acetyl CoA (for fatty acid synthesis) by the citrate cleavage enzyme, which is stimulated by ATP and inhibited by ADP.

A later regulatory stage is α-ketoglutarate dehydrogenase, which is inhibited by ATP, NADH and its product, succinyl CoA. Inhibition of this enzyme would allow a build-up of α-ketoglutarate, which is a precursor of several amino acids.

This the existence of several regulatory steps in pyruvate oxidation and the TCA cycle allows the use of the cycle for both energy generation and as a source of synthetic precursors. Hence it should be evident why its control is similar to that of glycolysis in some respects, but exhibits key differences.

[Berg et al. Biochemistry 5th ed, Figure 17.18]

But why isn’t AMP a regulatory molecule in the TCA cycle?

Glycolysis and the TCA cycle do not need to march in step, although when they are both responding to the need for ATP their key enzymes are regulated by adenine nucleotides, among other molecules. The original question (or a modification of it) remains as to why is AMP a positive effector of phosphofructokinase, but not of isocitrate dehydrogenase, which responds to ADP. It is interesting that in the section of Berg et al. discussing the concept of energy charge, a rather lame rider is added without further explanation to the effect that the ATP/ADP ratio can also act as an index of energy status.

I don’t know for certain, but suspect that the conditions under which Atkinson’s equation for energy charge is valid do not hold in the mitochondrion. This is supported by Sobol et al. (1978) Eur J. Biochem. 87 377–390 who found concentrations of AMP in rat liver mitochondria to be much lower than would be expected from equilibration with ATP and ADP through the adenylate kinase reaction. They suggested additional reaction of AMP with GTP in the mitochondrion might be responsible and also cited reports that adenylate kinase was absent from the matrix of rat liver mitochondria.
At least in rat liver, this would explain AMP would not be a useful regulatory molecule, whereas the ATP/ADP ratio would be indicative of the requirement for oxidative phosphorylation.


How can space-time affect ageing? I recently watched the movie -"interstellar" and I came through the question that how can ageing be affected by space-time? Wherever I look, I get it as a fact that it's kind of ageing slows down in space, but I don't understand why.

How can space-time affect internal cellular metabolism? And if it is related to our biological clock, then can it be a sufficient explanation for this kind of drastic ageing changes?

According to Einstein's Special Theory of Relativity, moving objects measure shorter in their direction of motion as their velocity increases until, at the speed of light, they disappear. It also tells us that moving clocks run more slowly as their velocity increases until, at the speed of light, they stop running altogether.

Hence,  astronauts traveling at great speeds for long periods of time return to earth younger than had they stayed on earth.

Technology, however, limits the velocities of astronauts, the differences are hence minuscule: after 6 months on the International Space Station (ISS), the astronaut crew had indeed aged less than those on Earth, but only by about 0.005 seconds. Hence, your notion that there are drastic changes do not find solid ground in the light of current technology. The effects would be greater if the astronauts were traveling nearer to the speed of light (299,792,458 m/s).

It is the mere physics behind it. Everything slows down relative to a slower moving observer. Not just metabolism, but time itself.


Have we succeeded in building a living organism from inanimate material? Following the Miller-Urey experiment where we were able to produce organic compounds with basic primitive atmospheric gases, high potential and water in a closed system. Have we been able to create a living organism fully functional with only inanimate material (dead material, or atoms, or anything that is not coming from a living organism such as a clone, or already existing DNA)?

I mean building a living organism from scratch. Are we able to do this?

It depends on your definitions.

we have built organisms with an entirely synthetic genome. basically the genome was "printed" from a computer file and inserted in a cell which had its DNA removed, it continued to function and replicate just fine.

We have not built a modern cell from scratch, mostly because even the simplest living cells today need to compete with other more complex cells so they are still extremely complex in their own right. The simplest possible cells would never survive in the current world due to competition and "predations" so we don't know exactly how it has to be arranged to function.

You may want to look at the much more modern experiments like the Urey-miller one, Jack Szostak has been trying to work up to what you are looking for, his lab has created RNA from abiotic (non-life) sources.
This is probably the closest since we know a slightly longer sequences of RNA can be self-replicating. And Harvard scientists have put manufactured self replicating RNA in an artificial lipid capsule and gotten it to function.
 Getting the right sequence of RNA to form by itself is possible but would probably need several billion repetitions of the first experiment.


Database of Geographic Range of Species Is there a database of organisms which would contain their queriable geographic location?

I would need to perform a rather simple query, such as Animals of <Location>, where Location is some well defined geographic area such as Czech Republic or Europe.

So far I have found multiple lists on Wikipedia and other webpages, however they seem to be quite incomplete as their intersect is quite small. Moreover, I have found EOL (Encyclopedia of Life) collections but they appear to struggle the same way.

This is to a large extent a question of how reliable the data in the database needs to be. Reliability (and spatial scale) will differ between datasets and between species groups within datasets, and it is difficult to give a general recommendation. I doubt that you will find a single database with good coverage over all taxonomic groups, even if it is in the form of country checklists. For the most reliable information, curated country checklists for specific taxonomic groups will probably be best, but these have to be searched for individually for each taxonomic group of interest.

As a starting point, you might want to look at the occurence data that can be found in gbif.org (The Global Biodiversity Facility). The data found there is certainly not complete, and it will be misleading for many species. However, for the current distribution of relatively well-known groups of species it will give you a good idea of their distribution. This has to be evaluated on a case-by-case basis though. You can access the data in gbif using external tools, for instance using R through rgbif (there is also tools for python or other languages). At the blog recology.info you can find a tutorial on how to get a species list for a particular country using rgbif (more specifically the function density_spplist).


How to prevent blobs under the microscope? My task is to take photographs of fungus spores under a microscope at x100 using oil immersion.

My problem is that I get all these little blobs. How do I prevent the blobs?

So, I have been instructed to first put the spores on the glass slide, then add a teensy drop of water to it (I use a syringe so I have exact control over the droplet) and then put the coverslip on top of that.  Then I tap the coverslip down with the eraser-end of a pencil to force the excess water out from under the coverslip.  The immersion oil goes on top of that and then I can view the spores and take the photos.

This is what I mean:

All those little blobs aren't supposed to be there.  I can't tell what are spores and what aren't, or if these spores have ornaments or not.  However, I happen know this spore does have ornaments (rhodotus palmatus).

At least some of the blobs that you have appear to be air. Seating the coverslip carefully will help to prevent air-bubbles from forming under the coverslip. Lay one edge against the fluid and slowly ease it down.

You mention using an oil immersion lens. It is possible that water has come into contact with your lens. Oil finding its way beneath the coverslip could also introduce refractory blobs as well.


What is our skin made up of? Again, it is a basic question. What is our skin made up of? is it made up of many cells arranged in a systematic way or is it just like any layer say of a book?? what is the difference? where is the living and dead thing coming into picture? is it the fact that skin can self-heal makes it living and in turn made up of cells??

The human skin is indeed made off a number of different layers, the three most important are epidermis, dermis and hypodermis (also called subcutaneous fat), see the figure (from here) for details:

All three layers can be subcategorized further, I'll only give a few details here. More can be found for example in the Wikipedia article on skin.

Epidermis: Top layer of our skin, is covered with the stratum corneum, which consists of several layers of dead cells, which protect the layers below. New cells of the epidermis are made at the border between dermis and epidermis and travel upwards (actually the top layers are worn off). The epidermis is the place where the pigmentation takes place due to melanocytes embedded in the keratinocytes of the epidermis.

Dermis: The next layer is the dermis where a lot of important functions on the skin happen. Sweat and oil are produced in the dermis. The feeling of the skin is also mediated in the dermis where the ends of the nerves are embedded. The hair roots of the hairs of the skin are also located here as well as the blood capillaries which supply the skin.

Hypodermis or Subcutaneous fat: The last layer is the hypodermis. It attaches the dermis to the underlaying muscles and bones and houses bigger blood vessels and nerves which go up into the dermis. The fat layer is also important for controlling the body temperature and storing fat reserves.


Why does UVA penetrate deeper than UVB, though it's weaker? Even though UVA radiation ranges in longer wavelengths (315–400 nm) than UVB (280–315 nm) and thus is less energetic, UVA is able to penetrate deeper into the skin and even reach the dermis. Why is there such a discrepancy?

Our skin contains quite a lot of water and I think this is answers the question: The absorption of UV light by this water goes drastically up when you shift to shorter wavelengts with a minimum absorption in the UV-A spectrum.
See this figure (from here):

So water has a very low absorption around 340-350nm (UV-A) and a very high absorption at shorter wavelength (UV-B and UV-C). This also explains why we get a lot more UV-A through the atmosphere than for harder UV-Radiation.


Do trees really get a large share of their mass from the carbon in the air? I remember hearing that trees and other plants actually obtain a large amount of their mass from the carbon floating in the air, not the ground beneath them. Does the makeup of air actually contain enough carbon to support this theory, and is a tree's surface area actually large enough to obtain the amount of carbon it needs directly from the air?

The vast majority of a tree's carbon comes from the air, which averages 0.03-0.04% by volume (300-400 ppmv) CO2.  This is fixed through photosynthesis and eventually stored as glucose which the plant can then use for its metabolism.

Doing some quick math, this means that in order to produce 1 kilogram of carbohydrates (e.g. cellulose) a plant needs to process on the order of 2000-3000 cubic meters of air (and ≈550 g or mL of H2O), which would fill a cube measuring 13-14 meters on a side.  Note this is an ideal figure; a plant's fixing efficiency will likely fall as it depletes the air of CO2.

Plants do take a great deal from the ground, namely water, fixed nitrogen (for proteins),  phosphorous (for nucleic acids), and several ions (sodium, potassium, calcium, among others)


Rod and cone photoreceptors are neurons? i mean the photoreceptors have axon and dendrite and body cell or it is not neuron
any more   . can we say outer segment of photoreceptor cell is dendrite ? of course these have body cells but i am not sure they are neuron or not

Photoreceptors are considered neural based on embryonic origin: they derive from neuroepithelial cells like neurons do.

Neuroepithelial cells also produce non-neuronal cells like some glial cells.

It doesn't make much sense to worry too much about whether a rod/cone photoreceptor is a neuron or not. They don't have long axons or dendrites, but they need not have either to be called a neuron. They make synapses, but these synapses are highly specialized and different from other types of neurons; that isn't sufficient to not call them a neuron. They don't fire action potentials, but they need not fire action potentials to be called a neuron. They do release neurotransmitter, but there are other cells that also release neurotransmitters that are not considered neurons. Ultimately, deciding whether a cell is a neuron or not is a matter of semantics, not biology.

Most texts I am familiar with consider them neurons because of their neural origin, which differentiates them from other sensory cells that derive from other tissue.


Are these birds in video real? What are they called? I recently came acroos this video   :  https://m.facebook.com/story.php?story_fbid=1053324651468913&id=492140647587319

I want to know whether these birds are real or edited? If they're real,  what are their names?

Yes, they are real, that's not a CGI. That footage belongs to The Cornell Lab of Ornithology, and those are birds-of-paradise.

The first one is a Wilson's Bird of Paradise (Diphyllodes respublica). Here is an image of it:

The second one, showing a courtship display, is a Superb Bird of Paradise (Lophorina superba). Here is an image of it:

And the courtship display:

The third one is a King Bird of Paradise (Cicinnurus regius). Here is an image of it:

The next one is the Wahnes's parotia (Parotia wahnesi). Here is a picture of it:

The last one is a King of Saxony Bird of Paradise (Pteridophora alberti). Here is its picture:

Finally, here is the only correct way (just kidding) to watch any video with birds of paradise: narrated by David Attenborough! Have a look:

https://www.youtube.com/watch?v=nWfyw51DQfU


What are Codominant vs Dominant Genetic Markers? When talking about types of genetic markers, the adjective "dominant" and "codominant" are often used. I don't fully understand their definitions and found contradicting definitions.

Foll and Gagiotti (2008)

Typically reading from  Foll and Gagiotti (2008), they list give two examples of markers of each type

Codominant markers

SNP
microsatellite

Dominant markers

RFLP
AFLP

reddit

This reddit post indicates that RFLP are codominant markers (unlike stated in  Foll and Gagiotti (2008)).

wageningenur

On wageningenur.nl (random website I never heard of before), they define dominant and codominant markers based on gene expression suggesting that the terms dominant and codominant used for markers have the same definition than those used for allelic effects on the phenotype (dominance, recessivity, overdominance, etc..).

Questions

What are the definitions of dominant and co-dominant genetic markers?
Can you please offer examples for each type and explain why they fit in one or another category?
Do the terms dominant and codominant have the same definition when used to describe a marker and when used to describe allelic effects on the phenotype (dominance, recessivity, overdominance, etc..)?

From wikipedia

  If the genetic pattern of homozygotes can be distinguished from that
  of heterozygotes, then a marker is said to be co-dominant.

This definition seems to be different from the one used to explain allelic effects. For example, as you would know a SNP is basically a feature of the DNA sequence. It is more of a genotype rather than a phenotype. Markers are supposed to be phenotypes (can be a molecular phenotype too for example a marker for stem cells etc). SNPs do create allelic variants but they may or may not contribute to different phenotypes. Consequently, the allelic variants may exhibit dominance or co-dominance with respect to each other. So, going by the definition used in classical genetics, you cannot call SNP as a "dominant"/"co-dominant" marker.

That is a weird usage of the terminology but people have done it so the deed cannot be undone. I would avoid future usage of such misleading terms. Having said that SNP would fit the definition of a "co-dominant marker" if it is observed by DNA sequencing .

Personally, I would consider RFLP a technique and not a marker per se. RFLP can be used to differentiate SNPs but sometimes it may not even resolve different strongly visible phenotypes (its efficacy basically depends on the polymorphism at restriction sites). Heterozygotes however, would have a different band pattern compared to homozygotes. So it should be a "co-dominant" marker.

AFLP, as far as I know is simply PCR amplification of restriction fragments. It would be "co-dominant" for the same reasons. However, just a PCR based screen would not differentiate between homozygotes and heterozygotes and would thus be a "dominant" marker. Now again, these are techniques and not, in a true sense, "markers" whereas SNPs and microsatellites are actual DNA features. So these cannot be even compared. A technique, depending on its resolution, can be "dominant" or "co-dominant" as per these definitions.

For general interest

I would want to reiterate that these definitions, for some reasons mentioned above, are quite flawed and are therefore misleading (they may have been okay at certain point of time but are obsolete now). Please avoid their usage in your papers and reports and if possible point these flaws out, so that they do not propagate.


Membrane potential after exposure to glutamate Neurons were kept in a physiological solution. During the resting
  phase, the membrane potential in the axoplasm of neurons was negative
  compared to the extracellular space and a potential difference of -70
  mV was observed in this phase. Neurons were then treated in two
  different experiments with either gamma-amino butyric acid (GABA; an
  inhibitory neurotransmitter) or glutamate (an excitatory
  neurotransmitter) and the membrane potentials were recorded. Choose
  the correct statement/s:

  (A) The resting membrane potential of -70 mV would not change with
  either GABA or glutamate treatments.

  (B) The membrane potential would be even more negative than resting
  phase with GABA treatment.

  (C) The membrane potential would be positive when the neuron was
  exposed to glutamate.

  (D) The membrane potential would be more negative than resting
  potential after glutamate treatment.

I feel, since, glutamate is excitatory, so resting potential should decrease when exposed to glutamate and increase when exposed to GABA. So (A)&(D) automatically gets eliminated and (B) is correct answer. I am confused at (C)

I believe C is also correct. The excitatory neurotransmitters open $\ce{Na}$ channels which makes the cell membrane more permeable to sodium as compared to potasium and therefore the equilibrium membrane potential would be much closer to the nernst potential for sodium. Now, since the concentration of sodium outside is much greater than inside, the nernst potential for sodium is positive with respect to the inside of the membrane. This makes the overall potential also positive.

If you want further clarifications regarding the calculation of the equilibrium and the nernst potential across the membrane, feel free to ask.

ADDENDUM

The approximate concentrations of sodium and potassium inside and outside a cell are :-
$$\ce {Na+_{in}}=10 \text{mmoll}^{-1}$$
$$\ce {K+_{in}}=105 \text{mmoll}^{-1}$$
$$\ce {Na+_{out}}=140 \text{mmoll}^{-1}$$
$$\ce {K+_{out}}=5 \text{mmoll}^{-1}$$

The Nernst potential is given by $E=-\frac{RT}{nF}\ln\frac{\text{in}}{\text{out}}$

Which for the given concentrations comes out to be $+67.7mV$ for sodium and $-78.1mV$ for potassium. During a sufficiently strong action potential, the relative permeability of sodium with respect to potassium becomes $10$. Using the GHK equation(ignoring the contribution of chlorine) gives us a net potential of $+47.5mV$.

The graph of the action potential clearly indicates that at the peak of the AP, the membrane potential is positive. Source : Graph of action potential


Is taking a shower unnecessary if good bacteria surround our skin? David Whitlock, a scientist, has not taken a shower for 12 years. Instead, he sprays a bacterial mist containing live bacteria to remove odor and maintain the number of good bacteria.

It is because using soap can remove good bacteria on our skin. So he chose not to take a shower but to spray the mist.

This kind of behavior sounds strange to me. But can it be very effective to maintain good bacteria and prevent disease?

I cannot do like him but I am just curious.
Thanks.

the Phrase "good bacteria" doesn't mean it's not gonna be harmful to you . actually they called : normal flora . they are refer not just to bacteria they include all types of microorganisms .
http://www.ncbi.nlm.nih.gov/books/NBK7617/
I give you an example : there is some bacteria in our bowel they help our digestive system to work better . but these bacteria in case of some infectious disease or in the people with Immunodeficiency disease like AIDS turn to be pathogens .
the vision of David Whitlock is not irrelevant in fact in the field of industrial biotechnology we use micro organism to clean and digest environmental pollution like oil spills & ... just like him use bacteria too clean out his body but in fact the thing is he put non pathogens bacteria on his skin so there is no place for other bacteria .
but as a professional view  there amount of normal flora on our skin is 10 times more than our cells so you can not think our skin is a surface and you can just wipe every thing on it just by showering and ... I'm telling you these thing are odd and there is no scientific evidence that support this odd things . maybe in 100 years when we ran out of drinking water we force to make cleaning sprays base on this view . but you know such a crazy but possible thing in theory .


In men, why do over 80% of sperm have abnormal form? Here is the percentage of normal forms among fertile mens according to the centile (Source: Cooper et al. 2010):

2.5: 3%
5 (below this is Teratozoospermia): 4%
10: 5.5%
25: 9%
50 (median): 15%
75: 24.5%
90: 36%
95: 44%
97.5: 48%

Men who have less than 4% of their sperm that have normal morphology are diagnosticated with Teratozoospermia (also called Teratospermia) and are likely to be infertile, though technically 5% of fertile men have Teratozoospermia.

I read on the internet that abnormally-shaped sperms are bad and useless because their abnormal shape prevents transport through the cervix and/or prevents them from adhering to the ovum.

But I think that if they were really that bad, Mother Nature would not have engineered the average men with 85% of their sperm abnormally-shaped.

And I also heard that even animals have a big fraction of their sperm that are abnormally-shaped.

So, in men, why do over 80% of sperm have abnormal form?

So I've dug a bit into how a 'normal morphological' form is defined and characterised, since assessing morphology into 'normal' and 'not normal' is always a very tricky thing.

Looking into the method section of the source you cited, we get:

  All laboratories generating the data analysed here used standardized
  methods for semen analysis [...] The various editions of the manual provided similar
  methods for assessing sperm concentration, motility and morphology but
  provided different criteria for categorising morphology.

So the  problem begins already with the fact that there is not one, but multiple different recommended practices.
(For anyone interested the different staining methods used were: Bryan–Leishman [B], DiffQuik [D], Haematoxylin and Eosin [H], Papanicolaou [P], Quickdip [Q] and Shorr [S]. Of thses H, S and P were used for generation of the 'normal morphology' reference set).

Clearly this problem was also obvious to the authors, so they tried to restrict the data they used:

  Although all centres reported using WHO procedures, the recommended
  methodologies have changed over time, and many centres have
  experienced difficulties with the subjective assessments of
  morphology. Data on normal sperm morphology were only included if
  results were reported as determined according to the so-called
  ‘strict’ (Tygerberg) method (WHO, 1992, 1999).

Fortunately these WHO guidelines are available on Google Books and they require the following points to met (most of which were defined by 95% confidence intervals of control samples):

head length 4.0-5.0µm
head width 2.5-3.5µm
head length-to-width ratio 1.5-1.75
well defined microsomal region compromising 40-70% of the head area
mid piece should be slender, <1µm
[mid piece should be] 1.5x size of the head
[mid piece should be] axially attached to the head
Cytoplasmic droplets should be less than half size of the head
Tail should be [...] approximately 45µm long

Plus one very important sentence:

  This classification scheme requires that all 'borderline' forms be considered abnormal

This sentence is important, because it means that each criterion stated has to be fulfilled for a single sperm to classified as morphological normal.
If we take only the numeric requirements (which should cover ~95% of the normal value distribution for a healthy population) and assume that they are not correlated, this means that for any given single healthy sperm we have a $0.95^9 = 0.63 = 63\%$ chance that it is within the 95% interval of all defined parameters.
This means that applying this strict categorisation scheme should even for a 100% healthy population only result around 63% sperm cells categorised as morphologically normal (ignoring that the parameters are probably not interdependent which would make it a bit better).

If we now take into account that the analysed samples were probably not 100% healthy cells and remember that the (reported) difficulties of assessing morphology, I think that the reported values for 'morphological normal' are not as quite as unexpected as they might seem.

Note: all bold highlighting in the quote blocks was added by me.


Virus immunity from animal to humans There are number of virus which have animal as reservior and jump to human to cause disease. Why dont we use antibodies of animal to cure humans?
Like rabies in bats.

I think you're asking why don't we take antibodies from previously-infected host animals and treat humans with them. In principle, that could work, but it's impractical as you describe it. You give the example of "rabies in bats". Imagine trying to get enough blood from a 25-gram bat to treat a single person. Farming bats is hardly practical, and if you're bleeding wild bats, you're probably collecting both known and unknown viruses that you're then injecting into your patient. So this is completely impractical with wild animals, which are the donors of most of the diseases in question.

However, there's nothing magical about the antibodies from the original wild animal. (This seems to be widely misunderstood, probably from movies that make medically idiotic and impossible claims.) Any antibody can be potentially valuable for treatment, whether it comes from the original host or not, and whether it comes from the live pathogen or from a vaccine made from the pathogen.

So a more practical approach is to infect a large, easily-handled domestic animal with the pathogen in question; or better yet, with a vaccine made from killed pathogens, so there's no risk of the animal getting sick or or infecting your patient. This used to be done with rabies, in fact, using equine hyper-immune serum to treat rabies patients (Production of hyperimmune antirabies serum in horses).

However, there are major problems even with this approach. It's difficult, it means keeping large numbers of large and potentially uncooperative animals around for long period, etc. Here is a WHO document reviewing some of the problems with this approach.

A third approach is to make monoclonal antibodies. This is the most popular approach now; it lets you make sterile, safe antibodies with completely defined characteristics, with minimal risk of contamination, under controlled conditions.

There are many monoclonal antibodies out there that are used in modern medicine, including some that are used to treat pathogens. However, it's worth pointing out that antibodies are not magical panaceas; they're often much less effective than conventional antibiotic or antivirals and are often more expensive and less practical to use.


Energy produced from respiration Why is the amount of ATP Produced from anaerobic respiration is less than the amount produced from aerobic respiration?

Anaerobic respiration does not completely oxidize the glucose, and as a result, pyruvate is not completely broken down, yielding fewer ATP molecules, and there are leftover molecules: lactic acid in animals and ethanol in yeast. This is because anaerobic respiration does not utilize oxygen, which is required for the electron transport chain, where most of the ATP comes from in aerobic respiration. In aerobic respiration, the glucose molecule is completely oxidized, and so (through the Krebs cycle and the electron transport chain, which requires oxygen and which produces the majority of the ATP) is completely broken down into carbon dioxide and water.


Estimated cost for diy biohacking How much would it cost (more precise the better) if i wish to start a diy bio lab in my own house. Assuming that all I want is a functional set and to create maybe simple things like glowing bacteria/glowing fish/deadly virus（jk)

" ... you can get started for around $500 or less with a little improvisation and patience." -- How to Set Up Your Own DIY Bio Lab

The $500 is pretty minimal and you won't get much done with that -- they mention other equipment (like a PCR machine) -- and you'd need to be extremely handy to be able to build all the equipment by hand.  More likely you're looking at thousands or several thousands of dollars.

Several sites give guidance:

A How-To For DIYbio Lab Equipment
Genome at Home: Biohackers Build Their Own Labs

Getting reagents may not be easy; I don't know how readily companies sell to individuals.

Don't forget that some experiments may require approval by animal care committees etc, unless you want to be arrested for animal abuse.

You might look into biohacker collectives, which are shared spaces where multiple "hackers" can use common equipment.


Peach pits with two seeds: Are the seeds identical twins? I have Prunus persica peach pits that have two seeds.

My question is simple:

Do the seeds have the same DNA? (are they identical twins?)

Polyembryony occurs when a single fertilized egg produces more than 1 embryo. This is the process that produces genetically identical twins.

Although polyembryony is common in some plants, I found limited information about polyembryony in peaches. I decided to broaden my search into drupes more generally. Drupes or "stone fruits" are the fruits with a fleshy outside (exocarp and mesocarp) and a hard inner shell (endocarp) around typically a single seed. Peaches are part of this category, as are almonds (the almond itself is the inner seed), cherries, and coffee.

The best citations I found reach back into history a bit.

From Webber, J. M. (1940). Polyembryony. The Botanical Review, 6(11), 575-598.:

  Cases of the first class of false polyembryony
  commonly occur in such drupes as almonds, plums and peaches.
  Although these drupes normally have a single seed within the hard
  seed-like endocarp, sometimes two or even three are found. ' During
  formation, each of the plural seeds develops from a separate
  ovule, provided with a separate funiculus and micropyle. Similar
  cases of such false polyembryony have recently been reported in
  Coffea (63) and Sandoricum (47, 49).

This passage would suggest that most likely what you are observing is false polyembryony. Immediately prior to this passage, the "first class" refers to:

  those in which more than one ovule develops in a normally 1-ovulate seed-like structure or locule

as contrasted with the second type:

  occasionally two of the developing ovules unite to form what appears to be a single composite ovule.

Another source, Zdruikovskaya-Rikhter, A. I. (1970). The phenomenon of polyembryony in the peach. Tr. Nikitsk. botan. sad, 46, 173-177. is in Russian and only available to me in abstract form in English. The abstract reads:

  In a number of varieties, two and sometimes three megaspores were functional, giving rise to several embryo sacs. On fertilization, embryos develop in these, causing the phenomenon of pseudopolyembryony.

Therefore this source seems to agree with the first.

However, a more recent paper Martínez-Gómez, P., & Gradziel, T. M. (2003). Sexual polyembryony in almond. Sexual plant reproduction, 16(3), 135-139., focused on almonds, suggests that certain almond cultivars are prone to true polyembryony, though it seems like the additional seeds are often a bit stunted and have high mortality. They also reference a paper purporting to mention polyembryony in peach, Toyama, T. K. (1974). Haploidy in peach. HortScience, 9, 187-188., though I cannot find this article in anything but Japanese - the title, however, suggests that these may be haploid polyembryos, which also occur with the almonds - these are indeed from division of the same embryo, but because they are haploid they would not actually be genetically identical, since each is taking half of the diploid chromosomes.

With only these limited descriptions to go by, which seem to be mostly observational rather than backed by any systematic study, I would hesitantly conclude that most likely what you are seeing is a fruit in which two separate ovules developed together, and therefore could be as genetically different as any two different peaches from the same tree. True polyembryos seem to be possible in stone fruits, but as a mostly rare occurrence that is only common in particular strains - when it does occur, it may be via haploidy, which means the seeds will still be genetically distinct.


Analysing the results of real-time PCR I want to evaluate the level of gene expression by real-time PCR.  I have five controls that are "clinically" the same. I calculated the "fold change" of the target gene regarding each control.

What if the result of "fold change" for my target gene is different for each control? I mean it is up regulated according to three of them and down-regulated according to the rest two.

Is the intervention biased? Or should I consider the average?

Please provide more information: fold-change relative to what?

If you did what I think you did (single control gene that you calculated fold change to of your gene of interest) I'd say this is the wrong approach. What you need is a set of genes which have similar expression levels across all your samples (controls and cases) to be able to compare your gene of interest to some common baseline. Selection of such genes should be the first step in the project, and it might be a good idea to use one of the established approaches - I recommend Jo Vandensompele's GeNorm (link to the paper) method. It goes like this: from a panel of potential control genes you select two or three that are most stably expressed across your experimental conditions, and then use these two-three control genes along with your gene of interest in a qRT-PCR. You then normalize the signal from your gene to a mean of the control genes.

It has been repeatedly shown that using a single control gene, even a so-called 'housekeeping gene' is misleading, because those genes do change their expression levels in some conditions. Also, using several control genes protects you against potential problems due to unequal amplification efficiency in different samples/groups. However, if you have multiple gene of interest, they all must have comparable amplification efficiency.


Is inbreeding really efficient at producing homozygosity? Inbreeding results in homozygosity.

I've come across this concept many times  and there's a question that comes to my mind every time I read it.

Let us suppose the character we are trying to establish is dominant trait controlled by a biallelic gene and the two individuals (animals) we have selected to inbreed  both have the genotypes Aa.

Aa x Aa = AA/ Aa/ aa in the ratio 1:2:1

So the possibility of having a homozygous dominant is 25% while that of heterozygous is 50%.
As the breeder has no access to technologies and find out the genotype of the F1 individuals there's a possibility that he would choose two F1 individuals with Aa genotype once again (which has the highest possibility of occurrence). And the same is repeated , production of F2 offsprings with 50% possibility of heterozygous individuals.

Edit:

So getting a homozygous dominant individual is very less likely to happen.

My question, is inbreeding really efficient at producing homozygosity?

And the same is repeated , production of F2 offsprings with 50% possibility of heterozygous individuals.

That's not correct.

Let's start with a population with 100% of heterozygotes:

100% Aa

And, just to create a highly exaggerated model, let's suppose that these individuals perform the most drastic case of inbreeding: self-fertilization. Inbreed occurs when an individual perform sexual reproduction with a closely related organism, and no one is more closely related to someone than himself!

After the first "inbreeding" generation, we'll have:

25% AA
50% Aa
25% aa

So, 50% of heterozygotes.

If this population inbreeds again, we'll have at the second generation:

37.5% AA
25% Aa
37.5% aa

So, 75% of homozygotes versus 25% of heterozygotes.

In the third generation:

43.75% AA
12.5% Aa
43.5% aa

And in the fourth generation:

46.875% AA
6.25% Aa
46.875% aa

Thus, in only 4 generations, we have 93.75% of homozygotes versus 6.25% of heterozygotes. Mathematically, the heterozygotes never disappear. Biologically, however, if a population shows self-fertilization, heterozygotes disappear in few generations.

Now, let's get out of this overly exaggerated example with self-fertilization and back to your question, where the organisms perform cross-fertilization:

The problem with your reasoning is that (correct me if I'm wrong) you're starting with a couple (Aa) and supposing that all their descendants will mate randomly. Of course, the allele frequencies will remain the same. But that's not inbreeding. By definition, inbreed is a non-random mating system. For a real inbreed to occur, the mating individuals should be more closely related than
those drawn by chance from the population.

In conclusion, given enough time, inbreeding (and genetic drift as well) has the effect of eradicating heterozygotes from the population.


What is the chemical composition / empirical formula of Herpes Simplex 1? Viruses such as polio are so well documented that a search for "empirical formula polio" gives you something like

 C332,652
 H492,388
 N98,245
 O131,196
 P7,501
 S2,340

We know that the virus consists of 70% protein, 22% phospholipid, 6.5% DNA, 1.5% carbohydrate (from the book Herpes Simplex and Pseudorabies Viruses by Kaplan)

Is there any information on the actual chemical composition of HSV1 and varieties?

Thanks!

The Herpes viruses have a unique four-layered structure: a core containing the large, double-stranded DNA genome is enclosed by an icosapentahedral capsid which is composed of capsomers. The capsid is surrounded by an amorphous protein coat called the tegument. It is encased in a glycoprotein-bearing lipid bilayer envelope 1.

You can watch an animation of infection and steps of replication here, and below the video, they say that

  HSV is a nuclear replicating, icosahedral, enveloped DNA virus. The HSV envelope contains at least 8 glycoproteins. The matrix or tegument which contacts both the envelope and the capsid contains at least 15-20 proteins[2].

In this definition of the structure, they at least assigned some values to the makeup. Additionally, in wikipedia, the viral genome is listed which I would recommend you take a look at as well. It can be found here but here is the synopsis of the table

UL1 through UL56
US1 through US12
RS1, ICP0, LRP1, LRP2
RL1, LAT

Additional resources:

HSV Genome 2nd link
The use of microarrays to analyze gene expression
Structural properties of HSV promoters
Animation of the Construction of a HSV-1 DNA Microarray for Global Analysis of Transcript Abundance
Animation of the Time-dependant Changes in HSV-1 Transcript Abundance During Productive Infection
Some Genetic Functions Encoded by Herpes Simplex Virus type 1
Herpes Simplex Virus Oligonucleotide Probes used in the DNA-microarray


Why do we have such a wide range of responses to pathogens and carcinogens? I was reading an article recently debunking the idea of 'boosting' your immune system. It occurred to me that - presuming it's right - our immune systems are all pretty much the same (with the exception of the immunocompromised). Given this, I wondered why there is such a disparity in how people respond to pathogens or carcinogens.

Most people would be quite happy, for example, to say that poor food hygiene causes food poisoning or that smoking causes cancer, but in actual fact, most of the time they don't. People who have poor food hygiene standards have them every day, but they're not sick every day, they're sick once in a while. Only 25% of heavy smokers actually get lung cancer, even with something like Asbestos, only 1 in 10 former Asbestos workers actually get Mesothelioma.

What is it that protects most people from these diseases despite definitely encountering the pathogen/carcinogen concerned?

I realise the most obvious answer is the immune system, but that just shifts the question to why this doesn't protect everyone all the time. Presumably the immune system doesn't just have a day off every now and again

This answer will address only cancer.

There is no such thing as standardized exposure to carcinogens in humans; while it would go a long way to answering your question, it would be unethical.

Also, it is unlikely that two people who do consume identical amounts of a carcinogen have identical environments or identical genetics.

Cancer used to be thought of as a carcinogen-host interaction; expose a (rodent, in my studies) to adequate levels of a carcinogen and cancer will occur. We tried to figure out exactly why. Then it was thought of as a host + environment (This was decades ago.)  The immune system was found to play a role; another level of complexity was added.

Mapping the entire human genome has made us aware of how simplistic these (and most) models were. There are tumor-suppressor genes. There are genes that matabolize carcinogens differently from other genes. There are genes that direct repair of DNA better than other genes. The possibilities are just beginning to surface.

To answer your question more directly,

  Although many studies have focused on carcinogen metabolism and cancer risk, more recent studies are considering DNA repair.

I would not go so far as to label DNA repair as Immunology.

I don't know why my father, who had a 120 pack year history of smoking, had absolutely no ill effects (not a trace of COPD, and certainly not cancer, no heart disease, CVD or other) and why my mother had COPD at a 40 pack-year history, but I'm sure it was genetic.

  Sporadic cancers are caused by genen-environmentn interactions rather than a dominant effect by a specific gene, environmental exposure, or gene-environment interaction. New paradigms, where we categorize genes as caretaker or gatekeeper genes, will allow for new hypotheses to be tested and will require advanced methods of analysis.

And, in another study,

  Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes.

Cancer Risk and Low-Penetrance Susceptibility Genes in Gene-Environment Interactions
Integrative Epidemiology: From Risk Assessment to Outcome Prediction
Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009)


Blast a sequence against multiple databases I would like to BLASTP a list of protein sequences in fasta format against multiple protein databases. Since I'm only interested in the first hit of each database, it is possible that BLAST result would need to be parsed.

Do you know if this strategy is a good one, or you suggest me others?

Thanks for your help. Best regards, Bernardo

To scan multiple databases:-

Download all the databases that you intend to match against (all databases will have a download option)
Download standalone BLAST executables from NCBI
Pool all the sequences from the different databases and make a BLAST database using the program makeblastdb (it is better to check for redundant sequences and remove them for improved performance)
Run blastp with desired parameters against this database
The first hit wont mean much. Use cutoffs on E-value or Bit-Scores or precentage identity

Now, if you vaccine targets a protein it is good to study the protein sequence conservation. BLAST isn't a really good option for studying conservation by comparing different orthologs. Use tools for multiple sequence alignment like ClustalW or T-COFFEE. In my opinion it is also better to use BLOSUM for scoring the alignments compared to PAM.

It might also be important to look at the protein structures. You can try VAST if possible.


Why is sorbitol used in buffers? Many protocols in my lab use sorbitol in buffers.  For instance, in co-immunoprecipitation, we include it at a final concentration of 200 mM in our lysis buffer. I'm not entirely sure why though.  I believe it might be as a crowding agent. But even if this is the reason, I'm not entirely sure what this means.  Could someone explain?

Generally, sorbitol is one of those 'old tricks' in the book which is thrown into cultures or buffers for several reasons. Here are a few that I have heard of:

Bacterial cultures (e.g. E.coli BL21) that are optimised to express (produce) protein, because sorbitol is thought to increase the expression of soluble protein. I have even heard of people (who work with very difficult proteins) that add to a final of 0.6M sorbitol in their culture media (note that the cultures grow very slowly).
In buffers intended for proteins, as it is thought to increase the solubility (i.e. avoid aggregation), similar to other sugar such as glycerol or osmolytes such as betaine.
Sorbitol is considered (chemically)  to be relatively inert, and many will therefore prefer to add sorbitol over e.g. glycerol or sucrose as a stabalizating agens when they work with proteins.
When you work with glycoproteins, you are generally depending on the addition of some sugar to stabilise the protein of interest - both during isolation, purification and analysis/testing.

The last point here could answer you question, as immunoglobulins are glycoproteins, you are generally depending on a high concentration of some sugar - such as sorbitol - to work with these proteins (i.e. antigens and antibodies) in e.g. immunoprecipitation.
I don't believe that sorbitol is a crowding agent - as this would perhaps facilitate aggregation, the opposite of the intended purpose. Adding crowding agents it typically done in protein crystallography with the addition of various PEGs to 'get the' proteins to form crystals. Instead, I think that sorbitol may (somehow) interfere with the proteins solvation shell - in the same way that is speculated for osmolytes (e.g. betaine or various sugars); however, this is something that I dont know much about and should be investigated.


Is there a publically available database of microbes that details what their wastes and food sources are Is there a publically available database of microbes that contains what their wastes and chemical food sources are in addition to other traits.

So that I could do like a sorted search for microbes that eat Ammonia or excrete sulfuric acid?

Cant seem to Google this one.

You could try to look into the kegg database. It's main purpose is to describe biochemical pathways, but it also has information on which species actually have these pathways (not sure how well this annotation is for bacteria though).

You should be able to pinpoint a few key pathways that start on free ammonia or have sulphuric acid as a sink/endpoint and then check for all annotated species. I wouldnt expect such lists to be comprehensive, but it should give you at least a starting point.

As an example the Nitrification and Anammox sub-pathways of the Nitrogen-metabolism page show direct usage/incorporation of free ammonia. If you click on some of the enzymes/genes (the boxes with numbers) and follow through to the 'taxonomy' box under genes, you'll get a list of some bacteria species each.


Variations in Genome Sizes Why is there wide variation in genome size amongst groups of protists, insects, amphibians and plants, but less variation within groups of mammals and reptiles?

You're asking about the C-value enigma, in particular this kind of diagram:1

The quick answer is that there is no "why" in evolution; things happen and if they're beneficial they tend to stick around more than the deleterious things.  The longer, (slightly) more satisfying answer is non-coding DNA.  Thanks to non-coding DNA the size of a genome doesn't even correlate to the number of genes.  The human genome, for example, has over 20,000 genes but is less than two percent protein-coding; the flower Utricularia gibba, however, has over 28,000 genes with about two orders of magnitude smaller of a genome, due to the fact that its genome is 97% protein-coding.  In short, there is no real meaning to be found in genome size variation due to non-coding portions, which while they are sometimes important regulators can often be just transposons (40% of our genome).  I will also point out that all of those groups you mention have species with significant polyploidy.

The are a number of other interesting ideas.  In the process of researching this, I stumbled upon the Animal Genome Size Database, which is an absolute gem of a treasure trove.  It's an unbelievable mine where I've spent a good half-hour just reading.  In particular, the statistics pages list interesting correlations for certain groups.  Mammalian genome size, for example, correlates:

Positively with red blood cell size, despite lack of nuclei
Negatively with metabolic rate
Not at all with developmental rate or longevity

For amphibians, however, there is:

Positive correlation with red blood cell and nucleus sizes in both frogs and salamanders
Negative correlation with developmental rate in many groups
Negative correlation with brain complexity in both frogs and salamanders
No strong relationship with metabolic rate in either frogs or salamanders
Some association with intensity and frequency of metamorphosis

If you have time, I highly recommend reading through T. Ryan Gregory's PhD thesis entitled The C-Value Enigma.  It's around 350 pages, but each chapter is in separate pdfs and is the most in-depth treatment I've seen, despite being about a decade old.  It's been moderately life-changing for me to read, some of the interpretations he presents challenged my thinking on the subject of genome evolution entirely.  Should genomes be treated as individuals, and what would that mean?  I digress.  Chapters 3, 4, 6, and 7 are what you'll want, in particular the last twenty or so pages of chapter 7.

Dr. Gregory now has a faculty position and his lab's research page is a little easier to read.  I love this image:

  As genome size increases in eukaryotes, the percentage of the genome composed of genes (white circles) becomes smaller. Conversely, the percentage of the genome made up of transposable elements (black circles) increases with genome size.

It seems like the best way to look at genome size and find some meaning is within a specific group.  There are correlations, for example, that are present in frogs and salamanders, but not in either group alone.  Some of the groups are very unbalanced; in insects, only Orthoptera tend to have very large genomes.  Interestingly, a number of those groups also undergo some form of metamorphosis, but the correlations aren't what you might have expected:  insects that develop quickly and metamorphose have smaller genomes, but "[i]n a more general sense, small genome size seems linked to rapid diversification... Conversely, insects without metamorphosis may possess very large genomes..."


Cold adaptation in proteins, at sequence & structural level When looking for cold adaptation in unicellular eukaryotes there is not much work found. Most of the time general sequence comparative sequence analysis between marine mesophile & psychrophile also does not give clear results. If I am planning to study at structural level (homology modeling) will I get answers? What type of parameters can I look to study? Which proteins are expected to provide cold adaptation apart from ice binding or antifreeze proteins because IBP & AFP cant be found by sequence comparison. Is it possible to give some ideas regarding this?

Thanks

There are research groups working on this exact question; understanding cold adaptation in enzymes. You can read about this in several articles such as 'Computation of enzyme cold adaptation', or 'Molecular Structural Basis for the Cold Adaptedness of the Psychrophilic β-Glucosidase BglU in Micrococcus antarcticus', or 'Specific amino acids responsible for the cold adaptedness of Micrococcus antarcticus β-glucosidase BglU'
On a general level there are several sructural characteristics that are typically found. They are usually far more flexible (i.e. less salt-bridges and other such stabilising bonds). The flexibility come from having fewer strong bond between and within the polypeptide chain, and even containing disordered regions. The flexibility also means that they are usually far less stable, and more difficult to work with. They are industrially interesting, as developing enzymes that can work at low temperatures can reduce the cost of running reactions. This is essentially a step towards a greener-industry. There are also speculations about various ratios and abundance of the amino acid types, and where they are located.  You would have to read articles on specific proteins to investigate this.
From a practical view-point, cold adapted enzymes are usually isolated from arctic microorganisms and characterised in the lab - in order to determine their temperature tolerance. The structure of such enzymes are then solved (after lots of work) and form the basis for understanding cold-adaptation.
To answer the question more specifically, no its not realistic to know if something is coldadapted directly by looking at the protein sequence (on its own), this has to be determined experimentally in the lab. However, if the protein is from a cold adapted organism (typically arctic bacteria) there is reasons to assume it is cold adapted before you test it in the lab. You can also apply som bioinformatics (e.g. blast search) to determine if its related to cold adapted proteins.  Also, If that specific type of protein that you are looking at, is well studies, you could also try to make homology models and see if its structurally similar to cold-adapted relatives or if it is more structurally similar to its mesophilic or even thermophilic counterparts. This is however very speculative, and i would not put too much weight on theoretically assumed adaptations - you should at minimum know that the protein of interest is from a cold adapted organisms, to even begin to look (computationally) on why and how it could be cold adapted.


If red blood cells have no mitochondria how are they able to metabolize glucose? I have read that red blood cells (RBCs) metabolize glucose. However they don't have any mitochondria because there is just so much hemoglobin that there is no room for mitochondria without expanding the cell.

So how is it possible for them to metabolize glucose if it is mainly O2, CO2, H2O, fatty acids (in cell membrane), and hemoglobin?

In humans (and all mammals), red blood cells lack mitochondria and therefore has no functional TCA cycle. They metabolize glucose mainly via glycolysis, forming lactate which is released from the cells; this yields 2 ATP for each glucose molecule, much less than complete oxidation (ca 30 ATP), but enough to support the red blood cells' energy needs.

There is some oxidation of glucose to CO2 in red blood cells though. This occurs mainly in the pentose phosphate pathway or "shunt", where 1 carbon of glucose is released as CO2, and the energy extracted is used to reduce NADP to NADPH, which functions as an antioxidant. The resulting 5-carbon sugars (pentoses) are then rearranged to a 3-carbon sugar (glyceraldehyde phosphate) which enter glycolysis again. Hence the term "shunt": 5/6 of the glucose carbon that enter actually comes back to glycolysis again.

By varying flux through the PPP, cells can balance the use of glucose for ATP (energy) or NADPH (antioxidant). Studies estimate that in human red blood cells, 10--30% of hexokinase flux is diverted through the PPP, and the remainder through upper glycolysis (see this and this article). This corresponds to 2--5% of glucose carbon released as CO2, and the remainder metabolized to lactate.

Note that the above apply to mammalian red blood cells. Red cells of other vertebrates, including birds and fish, retain both their nucleus and mitochondria, and their metabolism is different.


what is this mushroom and how to grow this mushroom? What is this mushroom?

And how to grow this?

This is an Ascomycota from the genus Morchella, called morel:

Morels are edible: despite the Wikipedia page I linked above saying that Morchella has hydrazine, according to Ammirati, Traquair and Horgen (1986):

  There is no evidence that Morchella species contain gyromitrin* or related compounds.

* A hydrazine compound.

Source: Ammirati, J., Traquair, J. and Horgen, P. (1986). Poisonous mushrooms of the northern United States and Canada. 1st ed. Minneapolis: University of Minnesota Press.

PS: Your second question ("how to grow this?"), however, seems to be off topic here at Bio SE.


Can someone help me identify this insect We found this insect in the basement of a friends house. It is about 1 inch in size. My friend lives in Canada

This guy looks very close to one of the variants of the very dangerous Triatoma.

I'm not sure what you should do in Canada about those guys, but in Brazil you should report them to your Disease Control Center. Triatoma has a very nasty bite and it can trasmit the Chagas Disease.

It is a bit weird to find this one in Canada - they are usually found in tropical places.


Identification of this insect These insects lived inside the wood of my bed in little round holes. They bite, lеаving very itchy red marks. And when crushed stink really bad. In the picture the lines are notebook lines for size comparison.
   I live in Eastern Europe, so I don't think they are fire ants, if they are ants at all.
Any suggestions would be appreciated!

This looks like an ant, but I cannot say which species. Their small size, colour, bite and being found indoors made me think of Pharaoh ants (Monomorium pharaonis), but I haven't heard that they smell bad. Ghost ants (Tapinoma melanocephalum) are rather similar and have a foul smell when crushed, and have been found indoors in Europe. They usually have a dark head/thorax and lighter abdomen though. They can also be separated from Pharaoh ants by having a one segmented petiole (the Pharaoh ant has two). A closely related species to the Ghost ant is Tapinoma sessile, which also smells but has a uniform colour (usually darker than your specimen though, see picture at bugguide.net). The petiole not being clearly seen in your specimen points towards the two latter species, or other species with a short/hidden petiole (see hidden petiole at antkey.org). However, these are only a couple of suggestions, and there are probably many other possible species.

Termites have larger mandibles (jaws) relative to their size, and no distinct narrow division between thorax and abdomen (your specimen does). Your animal also has eyes (termites don't) and I think you can spot a long first antenna segment, which ants have (hard to see in the picture though).


Nocioception (pain perception) in subcutaneous tissue There seem to be no nocioceptors (pain and temperature sensitive nerve endings) in subcutaneous fat. there are nocioceptors and other receptors in veins running through fat, but these can be avoided. Does this mean that subcutaneous fat can be cut, or otherwise traumatised, such as with diathermy (burning) without causing pain?

"no nociceptors in subcutaneous fat"

Well nerves innervate tissue, but only the layers of skin above the hypodermis (Subcuteaneous fat layer).
You are correct.
If one was to burn below this layer they would not feel pain in that area due to having no nociceptors.
There is a great Kharn Academy video on this topic here.


Was HindII the first restriction endonuclease to be extracted? Background:

Guided by wikipedia and pmc I found this paper by Hamilton O. Smith. and .Daniel Nathans.

  A
  restriction
  enzyme
  is
  a
  component
  of
  a
  restriction-modification
  system
  of
  a
  given
  specificity
  within
  an
  organism.
  The
  R-MT
  system
  consists
  of
  two
  enzymatic
  components,
  a
  restriction
  endonuclease,
  and
  a
  modification
  enzyme
  sharing
  similar
  (or
  identical)
  recognition
  specificity.
  We
  would
  like
  to
  propose
  that
  the
  genus-species
  designation
  be
  used
  as
  an
  R-M
  system
  name
  according
  to
  the
  following
  rules.

  (1)
  The
  genus
  and
  species
  name
  of
  the
  host
  organism
  is
  identified
  by
  the
  first
  letter
  of
  the
  genus
  and
  the
  first
  two
  letters
  of
  the
  species
  to
  form
  a
  three-letter
  abbre-
  viation
  in
  italics.
  For
  example:
  E.
  coli,
  Eco
  and
  H.
  influenzae,
  Hin.

  (2)
  Strain
  or
  type
  identification
  follows
  the
  genus-species
  abbreviation
  in
  non-
  italicized
  symbols,
  e.g.
  EcoB
  or
  EcoK.
  In
  cases
  where
  the
  R-M
  system
  is
  genetically
  specified
  by
  a
  virus
  or
  pla,smid
  the
  italicized
  genus-species
  abbreviation
  of
  the
  host
  is
  given
  and
  the
  symbol
  for
  the
  extrachromosomal
  element
  follows
  in
  non-italics,
  e.g.
  EcoPl,
  EwRI,
  etc.
  In
  occasional
  cases
  where
  it
  might
  be
  necessary
  to
  specify the
  host
  strain
  as
  well
  as
  the
  extrachromosomal
  element
  the
  strain
  identification
  symbol
  may
  be
  inserted
  parenthetically,
  e.g.
  Eco(B)Pl.

  (3)
  When
  a
  particular
  host
  strain
  has
  several
  different
  R-M
  systems,
  these
  are
  identified
  by
  Roman
  numerals,
  thus,
  the
  R-M
  systems
  from
  H.
  injluenzae
  strain
  d
  would
  be
  HindI,
  HindII,
  HindIII,
  etc.

Main question:

Now HindII was -

extracted from  Haemophilus influenzae
the strain was strain Rd, so d
and it was the 2nd enzyme to be isolated? Hence II.

So how is it the first Type II RE?

  H.O. Smith, K.W. Wilcox, and T.J. Kelley, working at Johns Hopkins University in 1968, isolated and characterized the first restriction nuclease whose functioning depended on a specific DNA nucleotide sequence. (wiki)

The explanation here is quite simple: HindI, despite having been isolated/discovered before HindII, is a type I Restriction Enzyme, not a type II:

  A type I restriction enzyme from Haemophilus influenzae, Hind I, which requires adenosine 5'-triphosphate and 5-adenosyl methionine, was studied for its activity on transfecting and transforming deoxyribonucleic acid (DNA) [...] Most of the restriction enzymes from Haemophilus belong to type II restriction enzymes according to the classification system proposed by Boyer. These enzymes require only Mg2+ for their action in contrast to type I enzymes that require Mg2+, adenosine 5'-triphosphate (ATP), and S-adenosyl methionine (SAM).

(Source: Biological Properties of a Haemophilus influenzae Restriction
Enzyme, Hind I)

Thus, in fact, HindII was the first type II Restriction Enzyme isolated/discovered, as it's well documented.

PS: As a bonus, here is a table with the main differences among RE types I, II, III and IV (Source: Thermo Fisher Scientific):

Type I:

Multi-subunit protein with both restriction and methylation activities
ATP requirement
Cleavage site a variable distance from recognition site

Type II:

Specific recognition sequence
Cleavage site within or close to recognition sequence
Generates 5′ phosphate and 3′ hydroxyl termini at cleavage site
Mg2+ requirement for most

Type III:

Two-part recognition sequence in inverse orientation
Cleavage site a specific distance away from one of the recognition sequences
ATP requirement

Type IV:

Cleavage of only methylated DNA
Cleavage site approximately 30 base pairs away from recognition site


Are omeprazole and other members estrogenic and/or antiandrenergic? As of 2020, omeprazole is a widely used OTC medicine for various types of acute heartburn and some other gastrointestinal disorders.

Almost every time I read about it I read that one of the possible side effects is gynecomastia, which Wikipedia defines as "noncancerous increase in the size of male breast tissue".

As a non chemist (let alone biochemist), it is unknown to me why should it at least theoretically cause gynecomastia.

Are omeprazole and other (chemical family) members estrogenic and/or antiandrenergic?

There is not a lot of evidence that the compound itself is estrogenic, but it may affect how estrogen is metabolized in the body, leading to feminizing outcomes.

Pubmed is a good source for information in the biomedical literature- here is a pubmed search that has more information on those terms.

Looking through some of the results of that search, I find that there seems to be a fair amount of evidence that omeprazole has something to do with gynecomastia, but the association is not strong:

A review of the literature has some conflicting information. One study of general practice in Britain suggested no detectable statistical relationship between taking omeprazole and gynecomastia. However, a smaller study suggested that in people who experienced gynecomastia who were also taking omeprazole, removing omeprazole helped in the majority of cases. I suggest reading the section of that review on omeprazole. The conclusion of the review is that omeprazole probably has a role in gynecomastia.
There is a literature of studies (mostly in Spain?) ascribing omeprazole a role in gynecomastia. One example.
There is evidence that omeprazole has a chemical effect on estrogen metabolism. However, it was much less strong than some other drugs examined.
There is evidence that omeprazole slows the metabolism of estradiol, an active estrogen compound (see Figure 2 in the review linked above).

Overall, people seem to say it (and related compounds) probably has something to do with gynecomastia, but it is not a principal contributor on average. Possibly it shows a synergy with some other drug or some lifestyle variable.


Evolutionary Cell Structuring I'm a total novice when it comes to biology, and I'm really just looking for an answer to a question that has been posed to me by people who deny evolution fervently.

Evolution dictates that we've gone from simple, single cell organisms to complex, multicellular organisms. If we consider the hand, for example, the hand is made up of various cells. Those cells are created according to DNA, which acts like a cell-level instruction manual.

Where are the "instructions" for where those cells go? I.e Where are the instructions that state that various cells have to line up in a thin, long, appendage structure to form a finger, or hand.

This isn't a particularly difficult question, I imagine. If it's been asked before, apologies. I don't know any of the technical terminology; this is just something that I would like to learn about.

The main governing principle is very simple and one of the most elegant mechanisms in biology. It is based on concentration gradients.

Briefly, certain cells secrete signaling molecules (called morphogens) that are detected by other cells. These molecules then activate the transcription of genes in the target cells. Since the molecules in question are produced by a subset of cells, their concentration varies according to the distance between the receiving cell and the producing cells. Different concentrations of the signalling molecules have different effects and this allows the formation of really quite complex patterns.

This can be illustrated very well using Wolpert's classic French Flag Model:

So, different concentration thresholds of the morphogen result in different patterns of gene expression. This simple system can give extremely complex results (such as yourself, for example). It gets more complex when there are multiple morphogens acting in tandem. Say morphogen1 is produced by cells on the left and morphogen2 by cells on the right, cells in the middle will have varying concentrations of both morphogens and will react accordingly:

Just about every pattern formation during development boils down to differential concentrations of diffusing morphogen molecules, it really is a wonderful example of how simple systems can give rise to extremely complex results.

On an unrelated note, this has absolutely nothing to do with evolution. At least no more so than any other biological process. If your friends do not accept evolution, I don't see how they can use this as an argument. Even if a god created humanity in his or her image as these people tend to believe, babies are still born and they still develop in the womb. As far as I know, even the most fundamentalist Christians do not believe in a mechanic god that puts babies together in the womb from some kind of IKEA kit. Even if humans sprung fully formed from the hands of this god, individual infants are still formed out of multiple cells. There is therefore a need for a mechanism that can coordinate this process, whether this mechanism evolved or was designed is irrelevant, it is still there and extremely easily observable (images taken from here):

The image above shows the locations and concentrations of various morphogens in a fruit fly embryo. You can see the concentration gradients clearly.