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

I can't think of any reason why it would be good for a kidney to have lobules. It would be good if the kidney needed to have a large surface area, but I don't see a reason why it would have to, since there is no diffusion or another proces that needs larger area.

Is there any reason why it would be beneficial for a kidney to have
lobules?
Is there a known reason why the kidney of a cow has lobules,
while the kidney of a human hasn't any?

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

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

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

However this is not related to its function.

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

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

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

One observation that they do make is that

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


How quickly are plants able to sense changes in light intensity? Evidently due to the process of photosynthesis, plants are able to "sense" light (as demonstrated by the phototropic response). My question is, how quickly are plants able to perceive changes in light intensity?
I.e. if there is a strong light shining on a plant, and at t=0 the light is switched off, is there some delay τd before the plant exhibits a response to the change in light intensity?

The delay for UVR8 photoactivation seems to be in the range of picoseconds depending on the wavelength:

Global analysis in terms of a model of parallel decaying
components indicated four lifetimes of 14.7 ps, 370 ps, 1.9 ns,
and 5.9 ns.

The photodynamics of the Trp ensemble in UVR8 can be summarized as
illustrated in Figure 5B. We observe excited state decay in the
few-hundred- picoseconds to nanoseconds time domain to the triplet
intermediate U460.

<img src="https://i.stack.imgur.com/Sz4zK.png" alt="Tentative photocycle of UVR8
photoactivation as observed in vitro." />
For a better understanding of photoactivation mechanism times, you can read the following article:
Proton-Coupled Electron Transfer Constitutes the Photoactivation Mechanism of the Plant Photoreceptor UVR8
Journal of the American Chemical Society 137(25) · May 2015


Problem in understanding Operon Is there a good book that explains operons: lac operon and trp operon in details.

I was reading  the functioning of the trp repressor protein from 'Principles of genetics-by Snustard and Simmons',they have mentioned that the binding of the repressor-corepressor complex to O$_t$$_r$$_p$ prevents the transcription of the structural genes. But they don't explain how.

Khan academy says that the repressor-corepressor complex physically comes in the way of the RNA polymerase. They have used this diagram below which shows that the large RNA polymerase cannot bind to the promoter site due to steric hindrance.

I'm looking for a more authentic source to study exactly how this RNA polymerase is being prevented from transcribing the DNA in both the operons.

Chapter 31 in the Voet and Voet biochemistry book (I have the 4th edition) link has a rather extensive explanation on this subject. It is rather pricey but you can find a copy of this one in nearly every university library. It generally is a good resource if you want to know more about the DNA or Protein structure of a basic process


How does the human body extract energy from ethanol? I was talking about alcohol and obesity with a colleague. I always thought the only cause of that is the sugar that is found in most alcoholic beverages. But my colleague pointed out that ethanol itself provides calories to human body.

I checked that and it seems to be the case. What I don’t understand is how is it possible. On wikipedia I found following statement:

  If catabolism of alcohol goes all the way to completion, then, we have a very exothermic event yielding some 1325 kJ/mol of energy. If the reaction stops part way through the metabolic pathways, which happens because acetic acid is excreted in the urine after drinking, then not nearly as much energy can be derived from alcohol, indeed, only 215.1 kJ/mol.

The statement relates to these reactions:

$$C_2H_6O (ethanol) → C_2H_4O (acetaldehyde) → C_2H_4O_2(acetic acid) → acetyl-CoA → 3H_2O + 2CO_2$$

Now note that the wikipedia calls the pathway "exothermic". However, I don’t think that human body can derive energy from heat. Or can it?

Since most articles claim that ethanol alone has positive caloric value, how exactly is this energy extracted and used or stored as fat?

Preamble

The question suggests unfamiliarity with the nature of biochemical oxidations and their relation to energy transfer in biology. The naïve reader is recommended to consult a text for a coverage of this subject: all I feel is appropriate here is a general summary followed by a brief indication of the key reactions.

General principles of energetic value of and biological oxidation of foodstuffs

The energy available from the oxidation of foodstuffs such as starch, fat and alcohol may be represented as the thermodynamic Gibbs Free Energy change (ΔG) in their complete oxidation.
This value can be determined chemically by bomb calorimetry in which the oxidation is done directly by oxygen and the energy produced is in the form of heat.
In biological oxidations the immediate oxidant is a molecule (an enzyme cofactor) such as NAD+ (or NADP+ or FAD), and *part of the Gibbs Free Energy change is translated into chemical energy in formation of the reduced compound — NADH etc. Only some is lost as heat*; but enough to give an overall negative ΔG, that causes the reaction to proceed.
The reduced coenzymes can be used to produce ATP by oxidative phosphorylation (involving oxidation by oxygen) or in reductive processes such as the synthesis of fatty acids, depending on the organism’s energy requirements.
Likewise, the molecular intermediates produced in the course of the biological oxidation (e.g. acetate) can be oxidized completely by oxygen (the terminal electron acceptor of the electron transport chain) to carbon dioxide and water (with production of more NADH in the tricarboxylic acid cycle, and hence more ATP), or can be converted to other metabolic intermediates or used as the precursors of other molecules, including storage molecules.
If the organism has a sufficient supply of energy (ATP) already, surplus intake of foodstuffs will lead to the deposition of energy reserves.

The case of ethanol

The question rightly states that ethanol is converted to acetaldehyde and then to acetic acid, but fails to include the oxidant, NAD+, which is an essential participant in the biological reactions:

[ADH: alcohol dehydrogenase; ALDH: aldehyde dehydrogenase ]

Thus, two molecules of NADH are produced, providing either ATP or reducing power.

The question assumes that after conversion of the acetate to acetyl-CoA it will be oxidized in the tricarboxylic acid cycle*. However in a fed subject with sufficient energy the cycle is suppressed and the acetyl-CoA will be converted to malonyl-CoA, the precursor of fatty acid synthesis. These processes require both reducing power (NADPH, which can be obtained from NADH) and ATP (ditto):

*The quotation states that “acetic acid is excreted in the urine…”. I have no knowledge of what proportion of ethanol is disposed of in this way, but I would imagine it is small — certainly not enough to prevent beer belly. However this is not the main reason why “catabolism of alcohol” does not “go(es) all the way to completion”.

Postscript

The biochemistry above is covered in Section 30.5 of Berg et al., entitled “Ethanol alters energy metabolism in the liver” (freely available to read online). This explains in more detail why the acetate is not metabolized in the tricarboxylic acid cycle. It does not discuss fatty acid synthesis, as the emphasis is on the more immediate pathological consequences of excess intake of alcohol.


Do only large birds float? So, I've noticed a pattern in water fowl (here meaning birds who can take off and land on water, who float in the intervening time) tend to be larger birds.

The smallest I know of are gulls.

Are there any smaller water fowl? Anything the size of a partridge? Or a wren?

If it is only large birds, why is this?

There are many seabirds smaller than partridges. The smallest seabird (according to the National Trust of Scotland) is the European Storm Petrel, which weighs in at an average of 28g. That's not quite as small as the European Wren (6 - 10 g), but it definitely counts as 'small', nonetheless.

Being seabirds which spend their life at sea except during breeding, storm petrels float well.

Below is a European Storm Petrel weighing in at less than 35 grams in Fig. 1.


Can motor neurons in the brain stem start movements? Supposedly (consciouss) movement is started in the cerebral cortex. But some time ago I've read a research which stated it might be possible some movements (not specified which ones, probably mean automated ones) start in the brain stem. That research was in one of those research file websites, it wasnt an article and it didnt have any mainstream visibility. Then I didnt hear anything more in this line, but you hear many times about these babies "born without a brain" who lacks most of its brain, 80% of its brain or who lacks cerebral cortex yet they move. Where are those movements started? Can motor neurons in the brain stem start movements?

Yes, movements (including fairly complex ones) can start in or be driven by the brainstem (and spinal cord).

Central pattern generators are key to producing coordinated rhythmic movements, including those for locomotion, chewing, and breathing: these are also located in the brainstem and spinal cord.

There have been many experiments done to study brainstem control of locomotion (see Shik and Orlovsky, 1976), particularly in decerebrate cats. You can induce a walking motion independent of cerebral control in these animals just by moving the floor (e.g., using a treadmill).

More generally, voluntary motor commands from cortex are mostly just a "suggested plan" - the specific patterns of muscle activation are determined in the brainstem and spinal cord, with input from proprioception and modulation by the cerebellum and brainstem nuclei such as the red nucleus.

In humans, spontaneous movements are also common in ~50% of brain-dead patients (Saposnik et al. 2005), although definitions of brain death typically include the brainstem, so these should be thought of as spinal rather than brainstem movements.

Saposnik, G., Maurino, J., Saizar, R., & Bueri, J. A. (2005). Spontaneous and reflex movements in 107 patients with brain death. The American journal of medicine, 118(3), 311-314.

Shik, M. L., & Orlovsky, G. N. (1976). Neurophysiology of locomotor automatism. Physiological reviews, 56(3), 465-501.


What happens when our muscle tense? Is the tensing of muscles equivalent to stretching them? I am trying to understand what tensing of the muscles means.

Muscles are designed to contract i.e., when they tense they get shorter. Their stretch is a passive process, typically facilitated by antagonist muscles in case of skeletal (striated) muscles. Consider the biceps and triceps antagonists in the upper arm in Fig. 1:

Fig. 1. Left: The biceps actively contracts to bend the arm and is called the agonist. The triceps is inactive and is passively stretched by the biceps, called the antagonist. Right: To stretch the arm, the reverse happens, i.e. the triceps contracts and is now called the agonist. The biceps is now inactive and is called the antagonist and it is passively stretched by the triceps. Source: Pilates Studio

At the molecular level, the tensing of muscles can be readily seen as contraction, as opposed to stretching (Fig. 2):

Fig. 2. Muscle fibers contract actively and stretch passively. The passive stretched state is depicted in the upper panel. Under the influence of ATP (active part) the muscle fibers condense and the muscles contracts. source: Emaze Presentations.

Further Reading
- Do both ends of a muscle contract?


Why do trees prefer their sunlight a bit diffused? I don't know what "a bit diffused" here means.

Do other plants also "prefer their sunlight a bit diffused"?

     Mount Pinatubo was the most powerful volcanic eruption in nearly one hundred years. Within two hours of
the main blast, sulfuric ash had reached twenty-two miles into the sky. By the time it was done, Pinatubo
had discharged more than 20 million tons of sulfur dioxide into the stratosphere. What effect did that have
on the environment?
      As it turned out, the stratospheric haze of sulfur dioxide acted like a layer of sunscreen, reducing the
amount of solar radiation reaching the earth. For the next two years, as the haze was settling out, the earth
cooled off by an average of nearly 1 degree Fahrenheit, or .5 degrees Celsius. A single volcanic eruption
practically reversed, albeit temporarily, the cumulative global warming of the previous hundred years.
     Pinatubo created some other positive externalities too. Forests around the world grew more vigorously
because trees prefer their sunlight a bit diffused. And all that sulfur dioxide in the stratosphere created
some of the prettiest sunsets that people had ever seen.

Dubner, Levitt. SuperFreakonomics: Global Cooling, Patriotic Prostitutes, and Why Suicide Bombers Should Buy Life Insurance (2009). p 176.

The studies are very complex and varied. There is evidence that strong omnidirectional light can get through to the understory of dense foliage more effectively.
Here is a Dutch study for crops in dutch greenhouses using light-diffusing rooves which maintain the quantity of light while making it omnidirectional. They report higher growth from diffuse light. https://www.researchgate.net/publication/40803021_The_Effect_of_Diffuse_Light_on_Crops
Studies of tree rings after volcanic eruptions have also found an overall higher growth for the periods following 5 major eruptions.
quotes: Under the presence of clouds, some studies have reported increases in both photosynthetic carbon gain (due to light levels closer to optimal) and water use efficiency, with less impact of photoinhibition due to excessive sunlight (Germino and Smith 2000; Gu et al. 2002)
This research suggests higher growth from direct sunlight in open forests and higher growth in dense, shaded forest under cloudy condition (research)


Difference between Fulminant and Acute Meningococcemias Fulminant seems to mead rapid.
There is however some articles with both phrases: "fulminant meningococcecemia" (about 5000 Google matches) and "acute meningococcecemia" (about 3000 Google matches).

I am thinking Neisseria meningitidis and its pathogenesis

  Portal entry nasopharynx (pili)-> attach epithelium cells -> bloodstream (bacteremia); upper respiratory tract infection -symptoms; may be asymptomatic in transient flora; fulminant meningocococcemia (regardless of meningitis)

What is the difference between the two diseases?

When we say "Fulminant meningococcemia" we mean failure of adrenal glands due to haemorrhage of infectious origin, or Waterhouse–Friderichsen syndrome

and acute is related to time of signs appearance, opposed to chronic disease.


Why are newly grown leaves red? After a period of heavy rain, several trees in my garden will put out an impressive burst of new leaves, with an incredible vibrant red colour, almost the colour of port wine. The new leaves will then slowly turn green.

I understand that the leaves turn green once they start producing chloroplasts and chlorophyll, but what is responsible for this initial red colour that is so very vibrant? And what biological role does it play?

It is anthocyanins that are produced to protect the developing photosystems (chlorophylls) from being damaged by sunlight.

As you have noted, it dissipates as the photosystems become adapted to the ambient light levels. Were you able to shade your trees for several weeks, you would likely also see their leaves turn red right after you removed the shade (easily done with trees in pots). Again, it is anthocyanin positioned in the leaf in a layer above the chloroplasts, but it will not be as vibrantly red because of the green chloroplasts below.


Why does sex last so long? I wonder why (especially human) sex lasts longer than just a few seconds?

My thought is that the shorter it takes a man to ejaculate, the lesser is the risk that he gets interrupted by a rival or a predator. Therefore, men who ejaculate quickly get an evolutionary advantage in the long-term.

But, as human sex lasts several minutes, I'm obvioulsy wrong with my argument. Anybody knows why?

There are plenty of animals with brief procreative periods, as you suggest. In chimps, sex takes 10 to 15 seconds - much less time than humans. So the question is really why have humans evolved to be different?

I don't think any of the answers based on fitness are particularly compelling. It's not like sex feels like running a marathon or less physically fit people can't manage to ejaculate in their partners so it seems unlikely that the lengthy sex act serves to distinguish fitter individuals.

Instead, I think the difference probably lies in the pair-bonding role of sexual activity. Humans form unusually long-lasting, typically monogamous or largely monogamous, bonds that function to provide the support needed during the lengthy childhood that humans undergo. The prolonged, and highly pleasurable, sex act likely functions to help maintain these bonds in order to keep the couple together and provide the stable support needed to maximise the chances of successfully raising a child to adulthood.

Unfortunately, to the best of my knowledge, there is no high quality empirical evidence that would convincingly answer the question so any answer must be somewhat speculative.


Do human women smell different before they enter labour? Surfing youtube I found a video where a cat shows a protective behaviour towards a pregnant woman soon to enter labour.

In the miriad of average (dumb) comments I found another person stating that her cat felt precisely (via olfactory means I guess) that her (the woman's - not the cat's) day had come to give birth and started acting weirdly.

Do mammals leave a clear olfactory footprint before labour? And is this footprint noticeable by cats and dogs?
Is this definetely myth? Is this something yet to study? or is this something well known?

If the latter is the case: is it based on the sense of smell? is there anything to read to study the topic?

It is not a definite myth but is a subject of much debate. However, it may well be that it is from smell (olfaction). We certainly know that cats have a significantly larger number of scent receptors, being approximately 200 million, compared to the 5 million receptors humans have. Cats also have an organ called the Jacobson's organ found in many animals that helps to pick up scents even more, especially chemicals - hormones.

As an example, the primary hormone released to progress labour is oxytocin, which causes the body to perform homeostatic positive feedback (initial stimulus is increased until an end result). This begins when the baby's head puts pressure on the cervix, which triggers contractions. This in turn starts oxytocin release which speeds up both the frequency and intensity of the contractions.

This increased concentration of oxytocin could well be what the cat is smelling as animals are well known to detect human hormones such as adrenaline in situations of fear. Although oxytocin is usually present in the body even apart from childbirth, in the moments leading up to labour and just afterwards, the oxytocin concentration is at its highest concentration. The cat probably sensed the 'abnormally' strong smell and began to behave accordingly as it recognised it from instinct (cats release oxytocin in labour too).

It's still all very hypothetical though so I don't know of any authoritative investigations for you to have a look at – it’s one of those anecdotal subjects which has yet to have any concrete evidence.


How does fluoride prevent tooth decay? Fluoride is a common active ingredient in tooth paste to prevent dental caries. It is also added or removed from the water supply in some communities for the same reason, but in children only.

My understanding is that the fluoride in tooth paste reacts with minerals in saliva then bonds to the tooth enamel. The fluoride in water is ingested and is somehow added to the developing bones and teeth of growing children, to the benefit of making decay resistant teeth.

What is the biochemical pathway of each process? A perfect answer will also discuss fluorosis and when that occurs and why.

Your understanding is correct to some extent. Tooth enamel mostly consists of a mineral called hydroxyapatite ($\ce{Ca_{10}(PO4)6(OH)2}$) (Staines et al, 1981).  Though this makes enamel the strongest material in the body, it is susceptible to degradation. In acidic environment, hyrdoxyapatite gets dissolved and leads to cavities (Brown, p. 688). The reaction is:
$\ce{Ca_{10}(PO4)6(OH)2_{(s)}~+~8~H+_{(aq)} -> 10~Ca^{2+}_{(aq)}~+~6~HPO4^{2-}_{(aq)}~+~2~H2O_{(l)}}$
To overcome this, fluoride is added in toothpastes. Fluoride ($\ce{F-}$) reacts with hydroxyapatite of enamel to form fluoroapatite via demineralization and remineralization cycle. The 3 main mechanisms through which it happens are (Rošin-Grget et al, 2013):

Iso-ionic exchange of $\ce{F-}$ for $\ce{OH-}$ in apatite:
$\ce{Ca_{10}(PO4)6(OH)2~+~2~F- -> Ca_{10}(PO4)6F2~+~2~OH-}$

Crystal growth of fluorapatite from a supersaturated solution:
$\ce{10~Ca^{2+ }~+~6~PO4^{3-}~+~2~F- -> Ca_{10}(PO4)6F2}$

Apatite dissolution with $\ce{CaF2}$ formation:
$\ce{Ca_{10}(PO4)6(OH)2~+~20~F- -> 10~CaF2~+~6~PO4^{3-}~+~2~OH-}$

Instead of preventing cavities, fluoride just controls the rate of formation of cavities (i.e. it repairs, not prevents, tooth decay), due to which its repeated exposure on enamel throughout the day is important (Cate et al, 2013). However, the effects of fluoride are minimal once it gets swallowed (Ismail et al, 2008).
Talking about fluorosis, the cause behind it is dissolution of hydroxyapatite due to higher concentration of fluoride (see the 3rd point in mechanisms, it requires higher level of fluoride to occur). Apart from this, formation of fluorohydroxyapatite is also a cause of fluorosis, the reaction being:
$\ce{Ca_{10}(PO4)6(OH)2~+~F- ~+~H+ -> Ca_{10}(PO4)6(OH)F + H2O}$
Dissolution of fluoroapatite causes depletion of enamel layer, causing fluorosis.
References:

M. Staines, W. H. Robinson and J. A. A. Hood (1981). "Spherical indentation of tooth enamel". Journal of Materials Science. 16 (9): 2551–2556. doi:10.1007/bf01113595.

Wikipedia contributors. "Tooth enamel." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 25 Apr. 2017. Web. 1 May. 2017.

Rošin-Grget, K; Peroš, K; Sutej, I; Bašić, K (Nov 2013). "The cariostatic mechanisms of fluoride". Acta medica academica. 42 (2): 179–88. doi:10.5644/ama2006-124.85. PMID 24308397. Retrieved 31 March 2014.

ten Cate FM. Contemporary perspective on the use of fluoride products in caries prevention British Dental Journal 214, 161 - 167 (2013) PMID 23429124

Ismail AI, Hasson H; Hasson (2008). "Fluoride supplements, dental caries and fluorosis: a systematic review". J Am Dent Assoc. 139 (11): 1457–68. doi:10.14219/jada.archive.2008.0071.


When did death due to aging first appear? As I understand it, single-celled organisms that reproduce via mitosis essentially live forever. When a cell divides, one cannot say that either one of the new cells "is" the parent and the other the child, neither is older than the other, and we might say that the original cell is still alive as long as either of the cells resulting from the division is. With humans the pictures is very different, of course: we have no trouble telling parents and children apart and no one lives longer than about 120-something years.

When in evolutionary history did organisms stop living forever? Was it with the advent of multicellular life with differentiated cells? Sexual reproduction?

(Not an evolutionary biologist, but I couldn't resist :)

I don't think your premise is correct. In (symmetric) cell division, we should consider that the old cell "disappears" and two new cells appear; neither of the two daughter cells is the parent cell, they are both descendants of it (hence the term "daughter cells"). The parent cell is gone. Therefore, at least for symmetric cell division, the lifetime of a cell equals the length of a cell cycle. So cells are not immortal --- only the cell lineage is.

Asymmetric cell division (as in stem cell division, not budding) is more tricky. Here it might seem as if there really is an immortal cell (the "stem cell") generating "mortal" offspring. But I think the situation is really the same as in symmetric cell division: most of the cell cycle mechanisms are identical, and again two new daughter cells are generated, and the parent cells disappears. The asymmetric part is that only one of the two daughter cells are "permitted" to continue the line. Again, the cell line is immortal, the cell is not.

But this is still true in higher organisms: the germline is an immortal line, while the somatic cells are not. So the key difference between higher organisms that have a clear life span and unicellular organisms is the appearance of cells that do not generate offspring, but instead support the cells that do.

I'm not sure there is a sharp transition from single cells to the germline/somatic cell situation. Intermediate cases are found in all sorts of single-celled organisms where certain cells "decide" that it's better to support their (genetically identical) neighbor in some way to rather than divide themselves; these are a form of "somatic" cells. All sorts of community behavior in bacteria and other microorganisms could be viewed in this way. During evolution this behavior has gradually got encoded into the DNA itself, with more and more sophisticated "support systems". Higher animals are really just the latest version of this, where the entire body is really just a support system to ensure survival of the germline.

I would suggest reading Richard Dawkin's books on this subject, especially The selfish gene. They are well written and quite accessible.


Can PCR detect phosphorylated protein? I'm trying to detect the level transcriptional protein inside cells. However, the cells contained both of this protein that is phosphorylated and not phosphorylated. Can RT-PCR detected the level of both of them? If yes can it detect them separately?

No. PCR (and quantitative PCR, or qPCR) rely on primers. They will amplify DNA flanked by primer regions, and this 'multiplied' DNA will be detected (and quantified).

PCR can be used to detect DNA. Reverse transcription followed by PCR (RT-PCR) can be used to indirectly detect RNA. Neither method is used to detect protein abundance, or post-translational protein modifications such as phosphorylation. This is because the modifications are not inherently encoded* in the nucleic acid sequence. They occur only on the protein level. Also, the abundance of a transcript tells you very little about how much protein will actually be produced from it, and how long this protein will remain in your biological system. A single mRNA can result in two very differently-modified proteins, and PCR would not be able to distinguish between an mRNA producing one kind or another. Also, phosphorylation is often a temporary modification, it's good to remember that.

*unless you have transcript variants (that produce protein isoforms) which omit or gain sequences that are modifiable, in the environment of a specific biological system.


Are microsatellites viable markers for GWAS? I'm just reading some papers on genome-wide association studies and find that most of them use SNPs as a marker. I understand that they're the most polymorphic and thus the best for accurate correlations, but would microsatellites provide another viable method to check for genetic correlation?
They're highly polymorphic and small enough to showcase differences, while maybe allowing for more statistical significance.

Microsatellites could be used for GWAS. Actually they were the basis for linkage studies and were also used in the first association studies. The main reason why they have been replaced by SNPs is that in the human (or other organims') genome, there are by far more SNPs than microsatellites.
GWAS rely on linkage disequilibrium between the marker and the real causal variant. LD decreases quite fast with distance, thus, the more markers you use, the more likely you are to genotype a marker in LD with the causal variant. In the end, I would strongly recommend to use SNPs to perform GWAS.


Do archaea undergo the same horizontal gene transfer processes as bacteria? Do archaea also undergo processes like conjugation, trasformation, etc.? If not, do they have their own horizontal gene transfer methods? Can bacteria conjugate with archaea?

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

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

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

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

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

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


Questions about a fossil I have a plant fossil that my dad once found for me at a beach in Denmark, Europe about 15 years ago.

Is it possible to identify what kind of plant it is? There is a fossil water bubble suggesting that this plant lived under water.
What kind of process did the plant undergo in order to become a fossil?
Is it possible to find out how old it is?

Unfortunately, this is not a fossil, but a pseudofossil: a pretty deposit of iron or manganese called a dendrite.


Is "reaction center" the same as "photosystem"? I have a diagram which labelled a part of PSI (Photosystem I) as "reaction center". But I have read on several websites that the reaction centers are PSI (the whole complex, not just a part of it) and PSII.

So, which one is correct? And if the reaction center is only a part of these PSI and II complexes, what does it contain? And what does it do?

Reaction centers are specific sites within the photosystems where the adsorbed photon energy is transferred to electrons.


Spermatogenesis in humans - timing of phases and chromatin modifications I'm interested in the timing of events during human spermatogenesis, ideally with some references I can build off of. Specifically, I am trying to pin down the number of days for:

Spermatogenesis, beginning to end (I have come across 65, 75, and 100).
Leptotene stage
Zygotene stage
Pachytene stage
Spermatozoa maturation and histone-protamine transition
Time in epididymis (I have come across 12 days)

Again, I want to know the timing of these events in humans, not mice or rats. Specifically, I am trying to pin down the major epigenetic reprogramming stages, with a focus on those occurring in mature males.

Spermatogenesis (Beginning to end):

64 +- 8 days (range 42 to 76)

There is considerable individual variation. This includes time in epididymis.

Amann 2008 argue for 74 days based on early study by Clermont 1972.
Also argue that biopsies are still needed on top of radiolabelling.

Substages:

Calculated from Amann 2008, Figure 1 using percent time in 16 day cycles.

Leptotene:

26.5 days (~70 days total - 26.5 days = ~ 43.5 days pre-ejaculation/conception)

Zygotene:

31.2 days (~70 days total - 31.2 days = ~ 38.8 days pre-ejaculation/conception)

Pachytene:

32 days (~70 days total - 32.0 days = ~ 38 days pre-ejaculation/conception)

Histone-Protamine transfer:

68.8 days (~70 days total - 68.8 = ~2 days pre-ejaculation).

The resolution of the data doesn’t really let us get at Epididymis vs. histone-protamine transfer, though.

Time in the Epidymis:

10-14 days.

References:

  Misell LM, Holochwost D, Boban D, Santi N, Shefi S, Hellerstein MK,
  Turek PJ. 2006. A Stable Isotope-Mass Spectrometric Method for
  Measuring Human Spermatogenesis Kinetics In Vivo. The Journal of
  Urology 175:242–246.

  Amann RP. 2008. The Cycle of the Seminiferous Epithelium in Humans: A
  Need to Revisit? Journal of Andrology 29:469–487.

  Durairajanayagam D, Rengan AK, Sharma RK, Agarwal A. 2015. Sperm
  Biology from Production to Ejaculation. In: Schattman GL, Esteves SC,
  Agarwal A, editors. Unexplained Infertility. New York, NY: Springer
  New York. p. 29–42. Available from:
  http://link.springer.com/10.1007/978-1-4939-2140-9_5


Triangulation number of the SARS CoV-19 virus Is the triangulation number of the SARS CoV-19 virus capsid, in the sense of the Caspar-Klug theory, known?   In case the Caspar-Klug theory does not apply to it, is it known what is its tiling, in the sense of the viral tiling theory of Twarock (and coauthors)?
I am a mathematician, trying to learn the geometric and group-theoretic aspects of virus structures.

Coronaviruses, like many viruses with a lipid membrane, are pleomorphic. The individual particles don't have a consistent shape. Here is a cryo-electron micrograph of SARS-CoV-1:

It might not be obvious, but each particle seen here is unique, they are not different rotations of identical copies. Since there is no consistent symmetry, there can be no triangulation number.

The image is from the following reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1563832/


What is this 2-3cm insect found in South-Eastern Brazil? Noted in South-Eastern Brazil rainforest at low level - about 2-3 cm from head to tail.

Maybe a Cassadine Beetle?

Maybe a cassadine beetle ?

You are correct! This insect does belong to the subfamily Cassidinae (common referred to as "tortoise beetles"), and is of the species Stolas aenea.


How much penicillinase is needed to deactivate 125mg of amoxicillin? How much penicillinase is needed to deactivate 125mg of amoxicillin?

Penicillinase in penase concentrate from CPC.
20,000 Levy Units/ml/min

I need IU of 125 mg of amoxicillin.

Please note that the problem is with finding the right parameters for amoxicillin, not penicillin G.

My goal is to test an amoxicillin product (i.e. it contains more than just amoxicillin) so the overall problem is more complex, I wanted to keep the question focused.

I would like to know the minimal amount of penase needed to deactivate 125mg of amoxicillin (that's the amount of amoxicillin in the product) in a reasonable amount of time, say 5 minutes. I want the minimal amount of penase because I am not sure what is its influence on bacterial growth, I am going to test that separately. Maybe I am going wrong about the whole problem?

I think that this paper could be helpful in general: Microbiological Applications of the Inactivation of Antibiotics and Other Antimicrobial Agents but it's behind a paywall and I can't access it at the moment. So far, I failed to find any other useful resources.

As March Ho has pointed out, we could do with a bit more information on this one.

I am going to attempt the calculation for penicillin G, and the necessary information seems to be available.

From here, A Levy Unit (LU) is the amount of penicillinase that inactivates 593 IU (International Units) of Sodium Penicillin G  per minute at 25°C and pH 7.0
From here and here, the specific activity of penicillin G is about 1667 Units/mg
I am assuming your concentrate is 20,000 Levy Units/ml (not 20,000 Levy Units/ml/min, which does not make sense to me)
Therefore 1 Levy Unit will inactivate (593/1667)mg, or 0.356 mg, of penicillin G per minute, pH 7.0 and 25oC
2.81 Levy Units will inactivate 1 mg penicillin G under identical conditions
351 Units will theoretically inactivate 125 mg penicillin G in 1 min under the conditions stated.
Your concentrate is 20000 Units/ml, or 20 Units per microliter.  So you will need (351/20) microlitres, or about 17.5 ul.
This assumes that the enzyme continues at a constant rate given by the specific activity right until the end.  This might not necessarily be the case, as one would expect the rate to slow down as the substrate concentration falls below Km.  Personally, I would use at least a 10-fold excess. 176ul - Seems a lot?

Please feel free to provide further information, or to edit the answer in any way you feel is necessary


Are mosquitoes attracted to blue lights in particular? I've been confronting the fact since childhood that mosquitoes are attracted to lights, especially blue lights. Now I know that all insects including mosquitoes are attracted to bright light but I never got it verified that if they are specially attracted to blue light or not. Is it true or just another urban myth?

It is not an urban myth. UV and blue lamps are good insect attractants. They have been used for many decades in insect traps, and these too work for mosquitoes. These lamps are routinely used in ecology at insect sampling sites. In some cases, such as with diurnal moths, yellow lamps can also be good attractants. The reason why UV is applicable is because insects are equipped with three photoreceptors, namely the UV-, blue-, and green-sensitive photoreceptors. Below you can see the spectral sensitivity curves of the genus Apis, which is typical for many insects.

As to why they are good attractants is probably variable across species, because it would depend on the neurological encoding of this information. For instance, some species may use this information to determine night and day, or may be superstimuli for nectar as used by plants to advertise themselves for pollination. Or it may simply be for some other reason.


Understanding these SNP annotations I am looking at the PharmaPGKB database for SNPs and trying to understand what the following annotation means:

rs1801131 at 1:11854475 in CLCN6, MTHFR (VIP)

Ok, the SNP identified by rs1801131 occurs in the first chromosome, at position 11854475.

Then, the two genes' identifiers come. The position 11854475 is inside the gene MTHFR. Why do they also annotate the SNP to the gene CLCN6 (which is a "neighbour" of MTHFR) ?

It is because the two genes overlap:

CLCN6 is on the plus strand and MTHFR is on the minus strand. The SNP is annotated to both because it falls in a region of the genome claimed by both genes.


How do scientists transfer the specific DNA in Optogenetics? I'm a bit new to genetic modification and I was wondering in Optogenetics (a field in neuroscience) how the scientists transfered the desired DNA strand from the light-sensitive ion channel opening cell (I forgot the name) to the specific neuron that will grow these cells sensitive to green light and trigger an action potential in the neuron? (open the neuron ion channels)

I don't understand how scientists know exactly which strand of DNA to cut from the source and where to put it in the target. I mean, if scientists can do this, why not cut the legs growing part of my DNA and insert in a butterfly and boom, you have a butterfly with legs, no?

Well for one, just having a gene doesn't mean you can make it work as intended, and indiscriminately tweaking the genetic material can produce unwanted effects. For example, if I overexpress p53, a common tumor suppressor gene, the cell undergoes apoptosis (1). If I break/delete the same gene, the cell might undergo apoptosis or it might become cancerous. Human development is of course regulated by hundreds of genes at a time, however, so legs on a butterfly is far more complex than just a single gene.

A common approach for inserting genes into a host genome is the lentiviral transfection. Generating a lentiviral vector is detailed here. A similar strategy for transfection using HEK293 for viral production is described in the following paper. I have no knowledge of optogenetics but I tried my best to find a paper in the field that employs the method in practice. In case you have no access to the article,

Viral Production

  HEK293T cells (ATCC, UK) were cultured in Iscove’s modified Dulbecco’s medium (Sigma-Aldrich, Germany) supplemented with 10% (v/v) FCS (Sigma-Aldrich) and penicillin–streptomycin–glutamine (Sigma-Aldrich) in 5 × 150 mm dishes. After 80% confluency was reached, cell were transfected in serum-free medium with the helper plasmids pRV1, pH21 and pDFΔ6 and pAAV1/2-hSyn-BLINK-IRES-eGFP or pAAV1/2-hSyn-IRES-eGFP at a molar ratio of 1:1 with CaCl2. On the next day, the medium was replaced with serum-containing medium, and 48 h after transfection cells were harvested, pelleted and resuspended in lysis solution (150 mM NaCl, 20 mM Tris, pH 8).....

Culture & Transfection

  Hippocampal neuronal primary cultures were prepared from embryonic day 18–19 (E18– E19) rat hippocampi as previously described43. All the experiments were approved by the Institutional Animal Care and Use Committee of University of Milan and by the Italian Ministry of Health (#326/2015). Neurons were transfected at 7 days in vitro (DIV7) via the calcium-phosphate precipitation method with 4 μg of plasmid DNA for GFP for the experiments assessing the axonal and dendritic distribution of BLINK2 reported in Fig. 2c. Neurons were infected with AAV1/2-hSyn-BLINK2-IRES-eGFP at DIV10 and fixed at DIV12 for the immunocytochemistry assays.

There's more to the method, but in short they transfect the 293 cells with these plasmids that create a functioning virus enclosing their plasmid of interest, and then they harvest the virus and use that to further transfect their neural cells with the gene(s) of interest.


Reason behind using inducible promoter for heterologous expression Protocols often seem to use regulatable promoters when expressing a heterologous gene in a host like yeast where they add something like IPTG to induce expression from (say) the lac promoter.

Is there a reason to do this as opposed to using a constitutive promoter? i.e. Is there reason to think that regulatable (inducible) promoters have higher expression levels than constitutive promoters?

In other words, what utility is there in having an external "switch", i.e. the IPTG to turn on expression on-demand rather than just boost the default expression level using a promoter not requiring induction?

The goal here is small biomolecule synthesis by industrial fermentation of a transgenic yeast.

Example Protocol:

L21 Star™ (DE3) E. coli cells (Invitrogen) were co-transformed with the plasmids pACYCDuet-4506 and Ct94-pETDuet and transformed cells were selected on carbenicillin (50 μg/ml) chloramphenicol (34 μg/ml) LB-agarose plates. Single colonies were used to inoculate 5 mL LB medium with 50 μg/ml carbenicilin and 34 μg/ml chloramphenicol. The culture was incubated overnight at 37° C. The next day 2 mL of TB medium supplemented with the same antibiotics were inoculated with 0.2 mL of the overnight culture. After 6 hours incubation at 37° C., the culture was cooled down to 28° C. and 1 mM IPTG, 2 mg/mL mevalonate (prepared by dissolving mevalonolactone (Sigma) in 0.5N NaOH at a concentration of 1 g/mL and incubating the solution for 30 minutes at 37° C.) and 0.2 mL decane were added to each tube. The cultures were incubated for 48 hours at 28° C. The cultures were then extracted twice with 2 volumes of ethyl acetate, the organic phase was concentrated to 500 μL and analyzed by GC-MS as described above in Example 3. In these conditions sesquiterpene production above 200 mg/L was routinely achieved. Beta-santalene was produced.

Heterologous promoters often express genes that are toxic to the organism when expressed in too high quantities. When the genes are expressed constitutively, the organism will either grow slowly or die before they reach a high density suitable for production of the protein.

As such, it is not about expressing the genes all the time, but expressing the maximum amount of gene product over the shortest period of time. It doesn't make sense for the cells to express the gene product all the time, if they can't reach sufficient densities first. More product will be made if the cells are allowed to grow to a relatively high density, then inducing expression on all of them. This would allow relatively large production levels in a short period of time.


Death because of no radio waves I read somewhere that a man dies if he is isolated from natural electromagnetic fields and waves. (I imply fields of radio frequencies and below.)

Is it true?

I've never heard of such a thing, and a quick Scholar search didn't yield anything significant. In fact, artificial radio waves are used in things that usually save lives, like MRIs.

If we were truly agnostic about this, we could say that it might or might not have an effect on human survival due to the general lack of evidence or even indication of a claim, but like the orbiting teacup, it's safe to assume that given our current extensive set of knowledge of biology, radiowaves do not affect human at all, and that as it has not been observed, the claim doesn't have a scientific basis.


Genetically speaking, are dogs exactly similar to humans and chimps both? Richard Dawkins mentions in his book The Greatest Show on Earth that dogs are exactly similar to both humans and chimps. Supposing that a cell contains the genetic similarity between 2 species, he says

  The human/dog cell should have an identical resemblance score to the chimpanzee/dog cell because humans and chimpanzees have exactly the same degree of relation to dogs. It should be identical, too, to the monkey/dog cell and the lemur/dog cell. This is because humans, chimpanzees, monkeys and lemurs are all connected to the dog via their common ancestor, an early primate (which probably looked a bit like a lemur)

He later says that this will be found within "statistical margins of error".

Because the common ancestor of both chimps and humans was more similar to chimps than to humans, it stands to reason that chimps will be more genetically similar to the common ancestor than humans. Therefore (not a direct therefore), dogs and humans can't be exactly similar as dogs and chimpanzees are, even theoretically. Humans and apes are even more dissimilar. Therefore ape/dog cell will not be exactly same value as the human/dog cell.

Please explain where I am wrong.

Dawkins is overgeneralizing.  Genetic distance is a fairly new field, and a heated topic, since your answer depends upon which genes you are comparing.  If you picked ONLY strongly-conserved genes for your genetic distance comparison, then you'd find that humans, bonobos, dogs, mice, mosquitos, shrimp, and bakers' yeast are all equally distant (and that the distance is small).  But if you pick ONLY very weakly-conserved genes for your genetic distance comparison, you can get crazy results -- humans are more closely related to yeast than to horses, for example.  (Creationists have had a heyday making fun of some early genetic distance studies that, in retrospect, had poorly-chosen genes.)  So biologists doing genetic distance comparisons try to pick genes that are common to many species, and that have some drift to them, but not so much that the answers are obviously goofy.  Another problem that has arisen is that sometimes an entire gene in several species appears to have been obtained from a very dissimilar species, in a different phylum or kingdom even.  (Current theory is that this is the work of viruses.)  The "tree of life" paradigm might need to be changed to the "web of life."  Needless to say, there's still a lot of argument about which (and how many) genes to pick for genetic distance studies.


Changing genetic code of E. coli to accept synthetic amino acids? I read in my Biology textbook that an experiment has been done in which one of   E. coli's stop codon has been altered to accept a synthetic amino acid. I do not get how it can be done. Taking the fact into account that every permutation of the 4 natural nitrogenous bases codes for a particular amino acid means that if the stop codon, let's say UGA, is altered to UUA it will code for Leucine. How does this leave a possibility for the production of a codon which codes for a synthetic amino acid? I will appreciate your kind explanation. Thank you a lot.

This has been done by engineering a synthetic tRNA that can recognize the stop codon. The synthetic tRNA possesses a non-natural amino acid that is processed normally by the Ribosome and incorporated into the growing polypeptide chain.


Which filament slides past which? Somehow I haven't found anyone on the internet can answer this: during muscle contraction, does the thin myofilament slide past the stationary thick myofilament, or does the thick myofilament slide past the stationary thin myofilament?

thick filaments slide over thin as cross bridges are formed by thin filament which slides thick filament and sandwich like structure is formed and Z-line disappears


How does gene editing in one cell affect other cells? I have read about gene editing and I have some questions concerning this technology:

With gene editing, are we correcting the genes in all the cells or a single cell?
If the gene editing is done for only one cell, then how (or can) it affect other genes in other cells?

Gene editing is not done on a single cell but a bunch of cells. However, it still does not affect all the cells. Gene editing/therapy for the entire organism works in these cases:

Stem cells are edited, which give rise to many other somatic cells. Usually done in case of gene therapy in which the stem cells are obtained from the patient, edited and re-implanted.
Some embryonic cells are edited and reimplanted in the developing embryo which gives rise to what is known as a chimeric organism (some cells in the body carry the edit while others don't). Now some of the edited cells will give rise to germ cells which in turn give rise to gametes. In the next round of breeding the chimeric parents would give rise to a fully transgenic (with edited gene) organism.
For unicellular organisms, it is pretty obvious: you just use a selection marker or extensive screening to select for the cells carrying the edited gene.


Where do the bacteria within the vagina originate from? I understand that it's feasible the bacteria within the gastrointestinal tract originate from the food we eat and air we breath, but where does this population of microbes originate from?

Most of the initial colonisation is said to be coincidental ('happenstance' as the textbook puts it!) exposure.

It's then fairly predictable depending on:

type of delivery (as Larry commented);
feeding; and
receipt of antibiotics.

In terms of feeding, there are differences in flora between babies fed human milk and those that are given cow's milk.

There's a section called 'Establishment and Composition of Normal Flora' in chapter 187 of Principles and Practice of Pediatric Infectious Diseases (3rd ed) by Long which discusses the above.

It's also said that hormones may influence indigenous flora. For example, premenarcheal and postmenopausal vaginal flora are very different to those present during the childbearing period.[1].

Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 7th ed. 2009. Churchill Livingstone.


To characterise diameter of capillaries in organs I know that there exist Continuous capillaries (skeletal muscle, adipose tissue, connective tissue, pulmonary circulation), Fenestrated capillaries (small intestine, renal glomerulus, exocrine glands), and Discontinuous capillaries (sinusoids; liver, spleen, bone marrow and hypophysis).

However, I am not sure how to characterise these.
The diameter of capillaries is different for each.
I have not managed to find any figure which present the relationship of diameter of these capillaries.
I have reviewed books Guyton, Pocock and Lange.

What are the diameters of capillaries in different organs?

This question is dependent on the specific patient at hand.
I think in the normal situation the diameter of the capillaries is about the same in each organ.
Better question would be: how does the diameter changes in relation to the venous and arterial ends of the capillaries?
Then, think about how big portion of the capillaries are in the venous end in the organ.

I cannot say that 50% of capillaries are on the venous end of the organ and 50% on the arterial side.
This is again an open research question.


Anyone can identify this moth? Found on the ceiling of my flat.
Place: London, UK
Date: 9th of August
Size I would say slightly more than inch and inch and half (3-4cm) wingspan
Suspect on the photo:

That looks very much like a brown color morph of the Box tree moth (Cydalima perspectalis), which has been seen in the UK since 2008. The size is about right (around 4.0-4.5 cm wingspan).
This species is an invasive pest outside of its native range (Asia).

By Nagy Sándor (NagySandor.EU) CC BY 3.0, Link
According to the Royal Horticultural Society this species has been invading the UK from the southeast with London a likely place to find them.


Could humans choose to establish fibre digesting colonies in our guts? Humans don't digest fibre, and nor do any animals, but some creatures have micro-organisms (bacteria, I'm guessing) in their gut which digest fibre for them.  My question is, could humans take some sort of pill and establish our own fibre-digesting colonies in our intestines?  Has this been tried?  Supposing it could be done, would you suppose it would have any negative effects on our health?  (i.e.. would those whose gut digested fibre for them be stuck on a low-fibre diet?).

Purpose of question: just wondering.  It would be cool to be able to eat bark.

Probably not without some substantial evolution to change our physiology, depending on what you are wanting.  If you just want to digest fibre, that might be done, but if you wanted to see nutritional value out of it, its not clear that's going to be worth it..

Soluable fibre is currently used by the human body, so you are probably be asking about insoluble fibre.

It might be possible to do a little of this experimentation - I'm not recommending this - but there would be several likely issues depending on your goals in such a project, which could vary.

the human gut microenvironment probably will not accommodate the bacteria you need and they might not grow in significant quantity.
the human gut is not physiologically arranged for digesting such fibre - ungulates generally have four stomach chambers that they can use to store some of the hard for the longer time it takes to break the fibre down.
the nutritional value of plant fibre is low XKCD has some numbers on this and a cow can eat 10kg of plant matter a day and in doing so they don't tend to move that much.  Humans have to eat a greater volume of vegetables to get the calories they need.  Is getting that last 2-5% or so of the energy from digesting fibre worth the trouble? Eat one more apple or a handful of grain.

Lastly, there would likely be some impact on human health - if you succeed then you would be modifying fibre's role in human diet as it stands - which is to help keep the intestines cleaned out.


Why are there six reading frames if only one strand of DNA is referred to as the ‘coding strand’? We need to consider six reading frames when considering the potential of DNA to encode protein (three frames for each strand). But only one strand is transcribed into RNA — the so-called coding strand. It would therefore seem to me that there are actually only three reading frames to consider. Why, then, do people refer to six?

Another point concerning reading frames is the definition of Open Reading Frame — ORF. One text defines ORF as:

  “An ORF is a continuous stretch of codons beginning with a start codon
  (usually AUG) and ending with a stop codon”

whereas another text defines it as

  “An ORF is a continuous stretch of codons that do not contain a stop
  codon (usually UAA, UAG or UGA)”

It seems to me that the first definition is correct. Which is the generally accepted definition for ORF?

The coding strand refers to the DNA strand with the same base order as the RNA transcript for a particular gene. As one gene is always entirely present on a single DNA strand there are indeed 3 reading frames possible in this strand, with only 1 actually containing the correct codon sequence for this gene.

However when we view an entire genome it is entirely possible for one gene to be present on one strand with another gene present on the other,  meaning that the coding strand for one gene is the non-coding strand for the other. This is why there are 6 possible reading frames for the genome as a whole as both strands can (and do) contain genes.

As to the ORF, both definitions seem to be in use. In the context of trying to discover genes by looking for long ORFs the first definition is probably more helpful as following the second definition could lead to a lot of falsely predicted genes (for an extreme example a long stop codon free sequence that has no start codons either would be considered a possible gene even though that should be impossible).


Why is the origin (patient zero) required to cure a virus? I'm not sure if it's just a movies thing but I always notice that the original strain of a virus is required to cure a virus, why is this? is this even true?

Nope. This is a total movie fallacy/exaggeration.

How worthwhile it would be to isolate the original strain is debatable, but certainly not necessary for vaccinology purposes.

On one hand, the inital strain might be interesting to study if its an aetiological agent which has never caused human disease before. It would be the first 'snapshot' of the genomics/transcriptomics of an organism/agent which has been able to jump a species barrier perhaps, or has evolved to survive at our body temperature, evade our immunity and so on.

However, as the infection progresses through a population, in order for it to stay infectious, it must by definition have maintained the molecular patterns that permitted it in the first place, so isolation of the 'zero-th', 10th or even 10,000th infection shouldn't make any real difference from a therapeutic standpoint. It may even be the case that as subsequent infection has in effect, passaged, the organism, that the later strains may even be more dangerous than the initial one.


How do marine mammals control buoyancy? Presumably, as a whale or seal dives, its lungs get compressed by the increasing water pressure, and it gets less buoyant.

Under this model, for a given amount of air taken in at the surface, the animal has a very specific depth D at which it is neutrally buoyant. Any deeper, and the lungs shrink, making it negatively buoyant. Any shallower, and the lungs expand, making it positively buoyant.

In other words, until it reaches depth D, the animal is positively buoyant. To get to depth D, the animal would have to do a lot of work swimming down, fighting against its own floatiness.

The amount of air that keeps you neutrally buoyant at 10 meters will inflate to twice the volume once you surface, keeping you pinned there. Speaking as a scuba diver, I can say that it would take a lot of work to dive back down to 10 meters. (We deflate our air vests at the surface and re-inflate at depth from our incompressible tanks, something animals don't have.)

For very deep divers like sperm whales, swimming down against positive buoyancy seems like a huge energy waste, the kind that one might expect wouldn't be tolerated long by evolution.

So do marine mammals do anything to compensate for the effect of fluctuating lung size on their buoyancy? One guess is that they actually exhale fully before diving, thus making lung buoyancy a small player in the overall body buoyancy. Another guess is that they compress the air with their chest muscles at the surface in order to sink. These are just guesses; I'd love to hear the real story.

From what I can tell, marine mammals can't dynamically control buoyancy during a dive. They ease the beginning of the dive by starting with a small lung volume to reduce buoyancy.

Pinnipeds like seals do this by exhaling half their breath before diving.

Deep-diving whales actually breathe in before diving, but their lungs are small relative to body size to begin with. This makes their surface buoyancy weak enough to swim against without great difficulty (unlike humans).

As they dive their lungs compress rapidly with depth:

V = Vs / (1 + D/10)

V is lung volume, Vs is lung volume at surface, and D is depth in meters.

At 90m, the lungs are already at 10% original volume. Pretty soon they've shrunk enough that their effect on buoyancy is negligible compared to the density of the incompressible tissues. Presumably, these are close to neutrally buoyant (though the fact that dead whales sink suggests that they're slightly negatively buoyant).

Thanks to @souvik-bhattacharya for the ucsc.edu link.


Identify this insect Please help identify this insect - genus, species and anything interesting about it. Also - please outline your general methodology for identifying such insects

Note, this is posted separately due to comments in this other thread.

Okay, to identify to Order level you can use the key here (although it's actually not as user-friendly as I'd expect; I might suggest they revise it). The key characteristic is that the forewings are uniformly hardened. So, starting at question 1:

"Insect has wings" - yes; go to 2.
"Two pairs of wings" - yes (wing cases/elytra are the first pair); go
to 7.
"Fore wings hard or leathery" - yes; go to 8.
"Fore wings of uniform texture throughout" - yes; go to 9.
"Fore wings (elytra) hard and veinless, meeting in centre line" -
yes; go to 10.
"Abdomen without forceps: elytra commonly cover whole abdomen =
Coleoptera [beetles]".

So we know it's a beetle.

There's a key to beetle families here. Starting at question 1:

antennae are "clubbed or thickened" so go to 5.
"Elytra covering all of abdomen" yes, go to 7.
"Head not stretched forward into a beak" - go to 9.
"the last few segments [of the antennae] clearly wider than the rest" - no, so go to 24.
the elytra (wing cases aren't "soft (easily bent, folded or even
rolled up)" so go to 28.
this is a tricky one, but basically you can (just) see that all the tarsi (feet) have the same number of segments, so we go to 29.
29: "      Beetle usually elongate and parallel-sided; antennae very long often longer than head and body; most antennal segments very elongate (at lease twice as long as wide)" - sounds like our beetle, so that makes it a longhorn beetle. (Some of the other criteria - eye nothces etc - only apply to some species, but this key is a UK-specific one).

So we have a longhorn beetle (Coleoptera: Cerambycidae). In theory you shouldn't need to geographical location to get this to species level as it could be an introduced species etc; in practice most keys are specific to certain geographical regions so you might need to provide the collection location to get it to species level. You could start by Googling "longhorn beetle identification key" and give it a go though.


Conversion rate of topical Retinol to Retinoic Acid (Tretinoin)? I'm wondering if someone out there has more information than me. Retinoids have well known metabolic pathways in vivo, and it's usually something like: Retinyl Palmitate --> Retinol --> Retinaldehyde (Retinal) --> Retinoic Acid (Tretinoin) which is the biologically active form of the Retinoids.

Retinoids are used in cosmetics all the time, and while Retinol is available OTC, Retinoic Acid (Tretinoin - a.k.a. "Retin-A" by brand) is available by prescription only since it is a 'stronger' version of Retinol. It's not difficult to find 1% Retinol creams or higher, but Retinoic Acid treatments top out at 0.1%.

However, I can't help but wonder 'why'? One study I was able to dig up was here: Retinoic Acid Biosynthesis and Metabolism PDF. The table on page 5 shows Physiological Concentrations - starting at 50 microM for Retinol and ending at "<50nM?" suggesting an ultimate conversion rate of a little less than 10% which would make the 1% Retinol treatments roughly equivalent to a 0.1% Retinoic Acid treatment (and a 2% Retinol treatment to a 0.2% Retinoic Acid treatment - double what's available by prescription).

Do other studies/other evidence support the rate of conversion of Retinol to Retinoic Acid to be roughly 10% or suggest than a 1% Retinol topical treatment is equivalent to a 0.1% Retinoic Acid topical treatment? Or are there some other interfering factors that reduce the utilization of Retinol to Retinoic Acid that I'm missing?

My guess is that the effect you describe is due to compartmentalisation: both retinol and retinoate are practically lipophils and so will localize in membranes and other lipid "pools", while both human retinal dehydrogenase enzymes are cytosolic. Probably the only occasion they have to get at their substrate is when it's bound to RBP. This however introduces another factor complicating the simple model.


Bayes theorem for mutations MEN 2A is a dominant inherited disease caused by a mutation in the RET proto-oncogene.
The probability of being sick when you have the mutation of the RET proto-oncogene varies with age and is assumed to be 40% at 40 years of age.

With autosomal dominant inherited diseases, this formula can be used, where p indicated penetration and D is the sick allele:

P(II inherits D given that II is healthy) = $\frac{1-p}{2-p}$

The uncle of the son III1 in the tree has the disease so he assumes it comes from I1 or I2. The father of the son II2 is 40 years old with no symptoms.

What are the odds of the father having the mutation?

What are the odds of the son having the mutation knowing the % in the first question?

I just used the formula above as so for the first question: $$\frac{1-0.4}{2-0.4} = 37.5\%$$

I'm having problems with the second though and I assume to use Bayes formula.

I've tried as so:

$$P(\text{son mut given dad mut}) = \frac{P(\text{Dad mut given son mut}) \cdot P(\text{son mut)}}{P(\text{Dad mut})}$$

I know the probability of the dad having the mutation is 37,5% and the probability of the dad having the mutation given that his son has the mutation is 100%. However I can't seem to know what to put in the probability of the son having the mutation? Any help appreciated, thanks! Sorry for a long question.

I don't understand your calculations and I don't understand why you're trying to use Bayes formula. I don't know the $\frac{1-p}{2-p}$ formula and I don't understand what it is supposed to calculate. It seems to me that you're overthinking a simple problem.

We don't have all the information and need to make a bunch of assumptions but if I understand the question correctly then..

Probability that the father carries the mutant allele

I neglect the probability that a new mutation occurred and that the son is the first carrier of the mutant in the lineage. I assume that we have a probability of 0 of being sick if we don't carry the disease. Because MEN is a pretty bad disease, the autosomal dominant alelle causing the disease is probably kept at pretty low frequency. From wiki, I read that MEN 2A has a frequency of 1/40000. This means that the probability of being homozygous mutant is $\left(\frac{1}{40000}\right)^2 ≈ 10^{-9}$. I think we can safely assume that the sick kid is heterozygous. Given that the kid is heterozygous, the mutant allele comes either from the mother or from the father with equal probability. So the probability it comes from the father is $0.5$ and the odds are $\frac{p}{1-p}=\frac{0.5}{1-0.5}=\frac{0.5}{0.5}=1$

Knowing that the father is heterozygous, what is the probability that a given kids receives this mutant

By the law of segregation, the probability is 0.5 and the odds are 1.


BWA-MEM single strand or doublestrand alignment In whole genome secondary analysis does BWA-MEM use a double stranded fasta reference or are reads aligned to only one, single stranded fasta reference?

BWA-mem (like most aligners), takes a normal single-stranded fasta file (I've never seen one with both strands listed) and aligns to both strand.


Question about flux and changes in net flux of molecules across a membrane I've been reading a book called Principles of Human Physiology by Stanfield 5th edition, and was reading a chapter on membrane transport when I came across a figure question which will be posted below.

It says "As time passes, does the one-way flux from side 2 to side 1 increase, decrease, or stay the same?"

I have unfortunately been unable to comprehend why and how the answer is "Increase". I would suppose it stays the same, correct? There is no possible way that a flux would occur, unless by individual molecules (regularly) passing through each side on a equal basis.

It was a topic on Simple diffusion.

P.S. This book, as i've noticed hasnt been quite explaining some things in a clear-cut way to understand as a beginner, and also it has had some mistake within it.

Diffusion is just the random movement of particles. Over time, the solute will randomly distribute throughout the entire available volume. Under initial conditions, there is no solute in side 2 and so it cannot move to side 1 (thus flux from side 2 to side 1 is 0). At equilibrium, the net flux is 0 but there is still flux from side 1 to 2 and from side 2 to 1 (which is equal and opposite) due to the random motion of the solute. So, flux from side 2 to 1 goes from 0 at initial conditions to some non-zero value at equilibrium (ie it increases).


Electronic cigarettes (e-cigs), any health risks? Background:

An electronic cigarette (e-cig or e-cigarette) is a battery-powered device which simulates tobacco smoking patented in 1963 by Herbert A. Gilbert.

It generally uses a heating element known as an atomizer, that vaporizes a liquid solution. Some solutions contain a mixture of nicotine and flavorings, while others release a flavored vapor without nicotine.

Question:

Are there any health risks uniquely associated with e-cigs as compared with normal cigarettes?

Since the question is about risk specific to e-cigarette as opposed to classic cigarettes, what's left is the potential harm from the chemicals in refill-fluids (apart from nicotine): polyethylene glycol, glycerol, alcohol, linalol, flavours. You can find cytotoxicity experiments (e.g. http://www.sciencedirect.com/science/article/pii/S0890623812002833), that show that the most harmful components may be the flavouring compounds. Some other articles (I can't find a reference right now) point out that the moderate heating of the fluid might create harmful byproducts, differently from those in regular cigarette: acroleine, formaldehyde. The use of e-cigarette is probably too recent to have long-term studies that answer your question.


Which is a good methodology to find out a domestication process? I just started with my course in genomics and I'm working with domesticated animals (cows, chickens, pigs, etc) and I would like to know which methodology is better to trace the process of domestication since the origin of these species. I'm thinking of using SNPs of a particular gene to identify punctual traits that were selected, but also I was suggested to do a complete screen analysis and identify all the polymorphisms present in each variant and compare them with the species that gave them origin.

Yes, everyone use SNPs today for such analysis. Some RADseq is probably the way to go.

Detecting selection is not an easy task as many technics exist which differ by their assumptions and by the applicability. You should probably try to find papers having done the same type of analysis with the same types of data and eventually talk with authors. Your lab might already be experienced in such analysis.

What test to detect genomic signatures of selection? might help but the suggested algorithms are mainly for the analysis of within species variation. Procedure like mcdonald-kreitman test and other more advanced methodology to detect selection over a phylogeny (such as OUWIE if you have phenotypic traits) might be of interest. You could also simply use some rank tests when having many independent domestication events. The exact methodology you end up using very much depend on your data (how many independent domestication events do you have for example, do you have phenotypic traits, ...).

  compare them with the species that gave them origin

Do you really have sample of the ancestor? Most of the time people simply consider a non-domesticated descendant of the non-domesticated common ancestor. Don't make the mistake of considering an extant lineage as if it was a descendant. This extant lineage evolved too!


Single stranded DNA in gel electrophoresis From http://www.nfstc.org/pdi/Subject05/pdi_s05_m01_01.htm :

  ... The separation medium contains a denaturant in order that the
  electrophoresis is conducted on single-stranded DNA fragments.
  Single-stranded DNA fragments are more similar to each other than
  double-stranded DNA fragments are to each other. Double-stranded DNA
  produces more electrophoretic diversity due to its three-dimensional
  structure.

Questions :

What is the denaturant they are talking about?
It's mentioned that double-stranded DNA
produces more electrophoretic diversity due to its three-dimensional
structure. Why should dsDNA have more 3-D structures than ssDNA? ssDNA can form hairpins and other structures. Which structures can dsDNA form?

As already mentioned formamide can be used. However formamide has to be incubated with the nucleic acid sample and heated. Urea can be included in the gel (8%). DNA can also be denatured using NaOH. NaOH, however, cannot be used for RNA because it will cause alkaline hydrolysis.
I don't much agree on this point. Though dsDNA can produce diverse structures, as buzrw mentioned, so can ssDNA (in fact more diverse). Moreover, linearization solves the issue of supercoiling. We never compare circular plasmids with each other on the gel. Long linear dsDNAs can form structures but then in such cases gel electrophoresis is not a very suitable method for comparison. PFGE might be a better option in such cases.


What happens to deep sea creatures if they reach the surface? Since deep sea creatures are adapted to incredibly high pressures, I would assume they would not be able to survive in the low pressure environment of the surface.  What exactly happens physiologically to a deep sea fish if it reaches the surface?  Would cell walls rupture?

It varies depending which creature is considered. The faster they are made to lower the pressure and raise the temperature, the worse the effects are. Some animals have a liver, which can help to counteract toxic effects at lower pressures, and some fish at 2000m have an air bladder, so they explode if they are hauled up.

Deep sea fish sometimes arrive at the surface with their inner organs popped out of their mouth.

They have different lipid types than us, because lipids are packed together differently at high pressures, and lowering the pressure on their lipids can make them malfunction.

Chemicals can act differently at high and low pressures, so a chemical that can be inert at a low pressure, can produce a different reaction at high pressure, producing gas, precipitating into component chemistries. Urea can be toxic at high pressures and fine at low pressures.

Proteins fold and change shape under pressure, so deep sea animals can use different proteins that may chainge their shape and function at lower pressure.

Dolphins can get the bends if they are scared back to the surface by deep sea exploration industries, too fast for their bodies to adapt.

here are some info sources:
http://www.deepseanews.com/2016/03/under-pressure/
https://www.quora.com/Do-deep-sea-animals-experience-decompression-sickness-if-brought-to-the-surface


What about this bat? This happened in LaGrange GA. We heard some crawling around behind one of the faux-wood shutters on our front porch. So I eased it back and saw this:

If you can't make out the scale, the furry part was about 3 inches long. I didn't want him hanging out right there so I took the shutter off and tried to carry it to the woods but he jumped off. I videoed this:

https://photos.app.goo.gl/NsAFrcry8nJmykzQ7

He definitely had trouble flying but he didn't seem to be sick. He didn't look like a baby to me but I'm not familiar. Any idea what his problem was? He's currently either in the holly bush right next to the house or made his way to the woods in the back yard. I've heard horror storied about rabies so I avoided direct contact the best I could considering how cool this was to see one this close.

Short answer
Appears to be an evening bat (Nycticeius humeralis) or little brown bat (Myotis lucifugus).
 Long answer.
You can see a list of common bat species in Georgia through the Georgia Department of Natural Resources. (A high-res image of a visual poster can be seen here).
According to Greenhall and Frantz (1994)1, three of the species found in Georgia are among the species most found in and around buildings: big brown bat (Eptesicus fuscus), evening bat (Nycticeius humeralis), and little brown bat (Myotis lucifugus)
Your image is relatively good, but it does not provide enough detail of key structures to definitively say which species it is. (see Morgan et al. (2019)2 for a key).
If we go simply based on size, the evening bat seems to be closest to your specimen:

E. fuscus is typically 4.1-5.1 inches in length (source), which is larger than your specimen
Your specimen is larger than a typical M lucifugus (1.8-2.3 inches, source).
N. humeralis is more similarly sized (average is 3.4 inches, source).

It appears that your bat has a broad nose, which would hint toward big brown bat (Eptesicus fuscus) or an evening bat (Nycticeius humeralis).
According to GeorgiaBiodiversity.com:

The evening bat is commonly confused with the big brown bat due to its fur color and broad muzzle. However, the evening bat is much smaller and does not have a keeled calcar. The evening bat's rounded tragus distinguishes it from all other small bats except the eastern pipistrelle, which has tri-colored rather than bicolored dorsal fur. The evening bat also has just two upper incisors instead of the four typical of all myotis.

Wait, keeled calcar? Huh?

A calcar is the spur of cartilage coming off the lateral side of the ankle of bats. The image below roughly dmeonstrates the difference between keeled and not keeled.

 Left is keeled; Right is not keeled. Source: Fig 12, Morgan et al. (2019)2
Your specimen does not appear to have a keeled calcar, which would suggest further that this is more likely an evening bat versus a big brown bat.
However, the little brown bat also lacks a keeled calcar....
Though many sources do not directly compare the little brown and evening bat, Morgan et al.'s (2019) key splits these species at the same step, suggesting they have much in common. Morgan et al.'s  differentiating characteristics for these species include:

Hair on hind foot extends beyond tips of claws; tragus long and blunt; underwing lightly furred to elbow: Myotis lucifugus (Little Brown Bat).
No long hair on foot; tragus is short, blunt and curved; underwing, muzzle, and uropatagium are hairless: Nycticeius humeralis (Evening Bat)

According to Greenhall and Frantz (1994)1,

[the evening bat] bears some resemblance to the somewhat smaller little brown bat (M. lucifugus) but can be identified by its characteristic blunt tragus.

To reiterate, the "sharply-pointed" tragus (source) of M. lucifigus and the presence of long toe hairs extending beyond the length of the toe claws (source) would both definitively point toward the little brown bat vs the evening bat. However, neither characteristics is really distinguishable in your photograph.
As such, I don't feel fully confident to rule one out over the other.
It's 3 am though, so perhaps I should stare at your image more in the morning after some rest...I'll update further if I notice anything definitive.

 1. Greenhall, A.M. and Frantz, S.C., 1994. Bats (Myotis lucifugus). The Handbook: Prevention and Control of Wildlife Damage, p.46.
 2. Morgan, C.N., Ammerman, L.K., Demere, K.D., Doty, J.B., Nakazawa, Y.J. and Mauldin, M.R., 2019. Field identification key and guide for bats of the United States of America. Occasional papers (Texas Tech University. Museum), 360.


DNA complementarity against reverse complementarity I am sorry to bother with this question (i study genetics for about few hours, because I need to understand my data) and I am really confused about these two terms, because I dont know if the books uses word "reverse" interchengeably or what is going on here.
The main problem I am totally confused about are words reverse complementarity and complementarity of two DNA strands. Since I know that strands runs in antiparallel directions and two DNA strands are complementary to each other:
i.e. sequence ACTCTG is complementary to TGAGAC and vice versa.
But my question is: are two DNA strands reverse complementary to each other? Because at least in two books I have read that two strands of DNA are. But if I would apply it to my previous example and use reversion, then no way I can get to my other strand. Is the word reverse in this context use as antiparalel (5' - 3' and 3' - 5') or am I missing something and it's true that if I take the whole DNA strand, I can use complement and reverse it and it will be my other strand?
Again I am sorry to ask this really basic question, but I am so confused about this terms.
Nice day to all and thanks if someone will have time to answer my question.

I agree that the definitions can be somewhat confusing when first encountered.
Each nucleotide has a complement A-T, C-G. But the DNA strand are reverse-complementary because when aligned from 5'->3' they are not (necessarily) complementary.
For example:
DNA strand 5'-ATCCGG-3'
complement 3'-TAGGCC-5'
reverse    5'-CCGGAT-3'
Since we want to write all sequences in the same direction we must call the strand reverse-complementary


What is this (seed/berry)-like object and where is it coming from? I've been finding these little green (seed/berry) like objects in my garden for three years now.

This picture shows either a large variant or simply  a later lifecycle stage of development.

At their smallest, they look artificial - kind of like nerds candy - almost too green to be natural.  In the picture above, it is obvious that the item is a berry, but at the smallest sizes, my first thought was that it was fertilizer.  And indeed, I would've continued to think that if not for two things:

We re-mulched our garden two years ago, and didn't fertilize (nor have we ever, but this house is only 3 years old).
When you squeeze even the smallest sized objects, they squirt juice or water.

When the larger berries are crushed, many little seeds come out along with liquid; and it looks almost like a miniature pickled tomato.

There is nothing in my garden that produces any kind of visible berries; and I've never seen one of these attached to a plant.  That is part of what makes them so odd (and part of what made me think they were fertilizer); I always find them mixed (sometimes deeply) in soil or mulch.

If no one knows after a couple days, I'll go take a picture of one of the baby ones to help.  Any thoughts?

Location: Brighton, MI (USA).

Update:. Here are some other shots.  These are both flash shots because it is overcast today.  These are also of the younger variant because I couldn't find any  of the mature berries today.  Hope this helps.

Barring further details or photos, your fruits remind me of the drupe  from a hackberry (Celtis spp.)  tree.

Hackberry drupes are relatively small, often being only about 6-10mm in diameter.

Examples:
1,
2.

Do you have any warty looking trees nearby?
(like this).

Do you ever see the fruits in a different color? (purple, black, red, orange)?


What part of food gives the blood red color? Roughly, what I know is, when we eat food it goes into our: Stomach > Small Intestine > Large Intestine > Rectum. So, it just moves through a digestive pipe.

What I don't understand is, what part of the food is responsible for blood's color and how does the food that we eat mixes with blood?

The red colour of blood isn't actually to do with food at all.  The primary purpose of the blood is to carry oxygen to all the cells that require it to release energy.  Red Blood Cells are filled with an iron containing pigment called haemoglobin.  When it has oxygen bonded to it, haemoglobin  has a bright red colour - it is this that gives blood its red colour.

In terms of how food enters the bloodstream, it is first broken down into extremely small constituents.  This is done by mechanical action (i.e. chewing and the squeezing movement of your digestive system) and by chemical action through the use of enzymes.  Enzymes are proteins that are secreted by various glands in the mouth (and are therefore contained in saliva), stomach and both intestines.  These chemically break large food molecules down into small products such as glucose (sugar) and amino acids (protein-building blocks) amongst other things.  These then move across the wall of the intestines and into the bloodstream, which are separated by only one cell:

Unfortunately that's the best image I could find.  The intestine is everything outside of the pink layer (which is the wall of the intestine).  The small molecules are able to pass through the pink layer and straight into the blood stream.  The picture shows a fold in the wall of the gut, which increases its surface area so allows more molecules to diffuse across.


How do I know whether or not a nuclear gene is single copy? As a part of a phylogenetic study, I need to find a nuclear gene that meets the following requirements:

Single copy gene;
Highly variable gene;
Gene longer than 400 bps;
Gene that gives information at the species/genus level in Gastropoda.

My candidate genes are the following: 5.8S, 18S, 28S, ACT, APN54, EF-1alpha, endo-1,4-beta-glucanase, GSTM, GSTO, GSTP, H3, ITS1, ITS2, MCP, MYO.

However, I do not know where to find whether or not they are single copy.

The simple way to do this is to use blast to search the genomes your interested in for sequences similar to your gene. If there's another copy it'll turn up in the blast results (so will orthologous genes - but they'll have lower scores than an actual copy). That relies on the annotation and genome being correct, of course.