During starvation, does the human body do anything to prioritize which organs receive nutrients? When food is scarce, the body slows its metabolic rate to conserve energy. Are there any other systems or processes that prioritize which organs receive nutrients?

The glycogen in the liver begins providing blood glucose. Muscle glycogen is used as fuel by the muscles, fat cells (adipose tissue) release fatty acids to manufacture ketone bodies in the liver and to be used by the brain as fuel, and body proteins are converted to glucose.

In short, the body's metabolism shifts to catabolic reactions.

If this continues for too long, you begin to see effects of starvation:

Inadequate tear production
Enlarged/tender liver
Muscle atrophy
Rashes, sores, or peeling skin

In short, deficiencies of energy, protein, iron, and zinc can really mess you up in the long term.


Evolutionarily speaking, why do humans have 46 chromosomes In humans, each cell normally contains 23 pairs of chromosomes, for a total of 46. Monkeys, chimpanzees, and Apes have 24 pairs (twenty-four pairs), for a total of 48.

What caused humans to have 46?

EDIT:
@TomD is right, I was asking why we have one less chromosome pair than chimpanzees (for example) [23 pairs instead of 24].

I think the OP is asking why we have one less chromosome pair than chimpanzees (for example) [23 pairs instead of 24].

The is an abundance of evidence, as alluded to above by shigeta, that human chromosome 2 is the result of a telomere-to-telomere fusion of two ancestral chromosomes (IJdo et al., 1991).  This event did not occur in our closest ancestors, hence we have one less chromosome pair.  In fact the sequence of human chromosome 2 contains the relic of an ancestral telomere-telomere fusion (IJdo et al., 1991).

The pdf of this key reference is freely available to all from PNAS

Reference

IJdo, J.W, Baldini, A, Ward, D.C, Reeders, S.T, Wells, R.A. (1991) Origin of human chromosome 2: an ancestral telomere-telomere fusion  Proc Natl Acad Sci U S A., 88 9051-9055.[pdf]

Actually it has now been shown that Neanderthals and Denisovans also exhibit the same chromosomal fusion as humans - http://m.motherjones.com/politics/2014/02/evolution-creationism-bonobos-neanderthals-denisovans-chromosome-two


What is the field of view for the human eyes? I'd like to know how much a person can see regarding the angles.

If it is a rectangle, I'd like to know it's height and width.

But if is another shape, I'd like to know which kind of shape and the angles.

I suppose that we can see something like this and if this is true I am curious about 4 dimensions:

"vertical" angle for both eyes
"horizontal" angle for both eyes
"vertical" angle for an eye
"horizontal" angle for an eye

It would be also nice if there will be some "areas" with percentages. I mean, something related to "central" vs "peripheral" view, because we see better something that is in front of us than something that is near us.

The general shape of the field of view has been answered in the related question "If human eyes watch an area, what's the shape of its capturing shape? Rectangular? Half spherical?"

Regarding the central view: yes, foveal view has a higher acuity than peripheral view.

Regarding the numerical dimensions of the monocular and binocular field of view: Monocular field of view  (measured from central fixation) is 160 deg (width w) x 175 deg (height h). The total binocular field of view is 200 deg (w) x 135 deg (h).

The region of binocular overlap is 120 deg (w) x 135 deg (h) (WebVision). The binocular foveal high-acuity part (central view) is about 6 degrees (5-15 degrees).


Does all of life on Earth use the same DNA compounds for all species? If an organism on Earth has got DNA, would it always have C,T,G,A?

Yes, there are no variations on this. There are 3 domains of life; Archaea, Bacteria and Eukaryota. All use these identical nucleotides. All use all four of them, and this is one of many lines of evidence for the single origin of life on Earth.


How difficult is it to make a shRNA/miRNA/siRNA to silence/knockdown NaV1.7 voltage gated sodium channels in humans? There have been various research projects that experimented with shRNA/miRNA/siRNA to specifically silence/knockdown NaV1.7 voltage gated sodium channels in small animals like rats & guinea pigs. (Example; my previous question: Is HSV-vector-mediated miRNA expression in dorsal root ganglia stable?

But I can't find any that's been done for humans... So I think it means scientists have not gotten to that stage (if they are interested in doing so), and I was wondering,

technically, how difficult do you think it is to make a shRNA/miRNA/siRNA that can silence/knockdown NaV1.7 in humans, given that they already know how to make it for NaV1.7 in small animals?
financially, how much money is needed to invent such a thing (and how hard to get a grant for it?)
if technically not too difficult, and not very expensive to invent just a sample, is this something not necessarily a professional researcher, but a student could try making as their research project?

The major hurdle for novel treatments to make it into humans is the assessment of its merits and added value over existing, proven treatments. And more importantly, the safety for humans has to be validated to a sufficient extent. The notorious from bench to bedside (Goldblatt & Lee, 2010) bottle neck. To answer your questions:

Technically, going from animals to humans may be a small step. Just increase the dose according to body weight. However, ethically it is a giant step. In fundamental research, lab animals are typically investigated only for the positive effects (e.g., amelioration of symptoms). In preclinical research, the animals have to be tested on side effects. Systemic injections, and even localized administration of potentially harmful virus vectors carries considerable risk. What if it returns to an infectious state? What are the side effects? Further, while animals can be treated systemically via iv injections, humans don't like needles. The FDA will put every possible danger and every possible discomfort to the patient into the spotlight.
Getting grants is hard. Going from bench to bedside is even harder, as the FDA, institutional review boards and the scientific community at large will scrutinize the plans.
To undertake clinical trials with humans is a team effort involving medical professionals, review boards, patients or healthy volunteers, an independent monitoring committee and so forth. It's not something you'll be doing in a few months. It can take years or decades to bring novel treatments to patients. It doesn't take one grant - it takes many, and development costs easily run into the tens of millions.

Reference
- Goldblatt & Lee, Am J Transl Res (2010); 2(1): 1–18


Do epigenetics determine the proteins a cell produces and therefore it's function? I'm having trouble understanding what epigenetics is in a simple sense.

How I imagine it is that if we had 2 twins with identical DNA and we let them live we will see that they'll develop differently. Their DNA will stay the same (unless the DNA gains mutations, which could lead to cancer...) but their epigenetic tags will differ. These epigenetics tags determine the execution of parts of the DNA and the way the twins live their lives determine how the tags will be distributed. It's hard for me to find an example.

Another way I think of epigenetics is for example the cells in the muscles have a specific epigenetic tags to produce the specific proteins needed to create the muscle and the cells in the skin for example have different tags, produce different proteins which produce the skin.

Is my understanding of epigenetics anywhere close to the truth?

Short answer: Yes, epigenetics play a role in determining gene expression, therefore protein expression and function.

Lifestyle factors like diet, smoking, alcohol consumption, and stress can change one's epigenome. A historical example of this might be the Dutch Hunger Winter of 1944-45; there is evidence that after the parents' generation suffered during World War II, the children who were conceived during this time and exposed in utero to famine had different epigenetic marks than their siblings who were conceived not during the famine.

Epigenetic regulation is also essential for cell differentiation in vivo and in vitro. Embryonic stem cells undergo many changes to their epigenome in order to become mature cells. One interesting example for further reading is the transcription factor NeuroD1, which binds to targets in the DNA to cause widespread changes in gene expression that are specific to neurons, and commits cells to a neuronal fate. It doesn't bind to thousands of neuronal genes; instead, it causes a "ripple effect" thanks to epigenetic mechanisms.

Longer answer: Epigenetic marks are added to the genome for many reasons, including the two you just listed, and I think it is helpful to understand what happens at a molecular level in order to understand "why" we have them and to better visualize what the epigenetic marks ("tags") are. This might help you to think of better examples on your own.

DNA spends most of its time wrapped around proteins called histones. A complex of DNA and histones is called a nucleosome. DNA-in-nucleosomes is called chromatin. Chromatin can then either be "loose" (called euchromatin) or "compact" (called heterochromatin). There are more detailed ways to define how accessible chromatin is, but this is the basic idea. Intuitively, loose chromatin is more easily accessible and the genes there can be transcribed actively. Compact chromatin is less active.

The looseness of chromatin is determined by how closely the nucleosomes interact, which is controlled by the histones' molecular properties. Whether or not the histone proteins interact to make the chromatin compact, or repel each other to make the chromatin loose, depends on what modifications they possess. These modifications are added by histone-modifying enzymes.

Histone-modifying enzymes are regulated by transcription factors (i.e. during the process of differentiation) as well as signals generated by extrinsic factors (i.e. during the organism's lifetime). The balance of activating and silencing activity is what adds and removes these marks to give a cell its individual epigenome.

So, in simple terms, epigenetic marks determine how accessible different parts of the DNA are, and a whole lot of factors (like cell identity and lifestyle) can determine where those epigenetic marks are.


largest bootstrap support I was reading about bootstrap in phylogenetics and it got me wondering that amongst all of the methods (UPGMA, Maximum Likelihood, Parsimony, Neighbour joining method) which method generally provides the largest bootstrap support? Or does that vary from problem to problem?

For sequence data, UPGMA is not really accepted anymore. Maximum parsimony and Neighbour-joining are usually used because they are quite fast and they give you a relatively good idea about the phylogeny.

You should not decide based on which method gives you the highest bootstrap.

For publication, it is recommended to use either Bayesian consensus tree (MrBayes is popular program) or a maximum likelihood tree (RAxML or MEGA are popular for ML). For maximum likelihood bootstrap (BS) is used and the confidence is relatively high if at least reaches 80 (%). For Bayesian, instead of bootstrap Bayesian posterior probability (BPP) is used. For BPP it has to be at least 0.95 to be significant.


What is happening in each iteration of PSI-BLAST? I understand that the first BLAST yields almost the same results as blastp. The second time the iterated blast generates different results as it uses different matrix based on our first result.

But I don't understand how exactly the second matrix is generated.

PSI-BLAST is Position-Specific Iterated BLAST.

I'm probably out of my depth here, but my understanding is that the results of the first, essentially standard, BLAST search are used to create a multiple sequence alignment. This alignment is then converted to a Position Specific Scoring Matrix (PSSM). (The linked Wikipedia entry shows this for DNA sequences, but the principle is exactly the same for protein sequences.) This matrix can then be used as the probe for the next round of BLAST, and the results of that alignment can be used judiciously to improve the matrix, and so on until the results converge.

Here is a link to some slides by Stephen Altschul which go into lots of detail.


Is there a durable surface that ants can't pass? I'm looking for a surface, that will be impassable for ant's yet not poisonous or easily decaying.

One idea is water - they really can't cross that. But water easily dries and is quite uncomfortable.

Is there something their legs will find uncomfortable? Something spiky for example?

I've found that ants do not walk through petroleum jelly. It is also convenient, as it isn't too messy, and can be whatever shape you want. I use it to keep ants from climbing into my hummingbird feeders. Make sure the area you treat is wider than the ant is long.


Why is succinate dehydrogenase attached to the inner mitochondrial membrane? Succinate dehydrogenase is attached to the inner mitochondrial membrane. All the other enzymes of the Krebs cycle are located within the matrix of mitochondria, though.

In biological systems, there is often a relation between structural properties and function. For example, two enzymes that function sequentially in a metabolic pathway are sometimes held in close proximity to one another by a scaffold  (e.g., in fatty acid synthesis). Is there a similar biochemical reason why succinate dehydrogenase is attached to the inner mitochondrial membrane, as opposed to being dissolved in the mitochondrial space?

The reason behind this lies in the properties of FAD+. Unlike NAD+, FAD+ is not free to diffuse within the mitochondrion, it is an integral part of the inner mitochondrial membrane. Its reduced form FADH2 contributes electrons directly to ETC.


Is this necrotizing skin infection caused by Staphylococcus aureus? A 5-year-old boy returns from summer camp with several minor cuts and abrasions on legs. He has fever
and extensive cellulitis, subcutaneous tissue and muscles are involved. Necrotic tissues were surgically
reomoved and broad spectrum antibiotics were used. Which of the following microorganisms usually
causes necrotizing fasciitis?

a. bacillus cereus
b. clostridium tetani
c. A-group streptococci
d. Micrococcus sp.
e. Staphylococcus aureus

It is so severe that I started think that Staphylococcus aureus is possible.
My previous answer was A-group streptococci, but I disagree with it now.

What is causing the case?

No. It is caused by A-group streptococci. Source Murray and empirical evidence.


Confluency or confluence, which term is correct to describe the % area covered by cells? I noticed that both of them are used in many scientific papers. Are these two terms, or can they be used interchangeably?

Searching Google Scholar for cell confluence returns 239000 hits, while searching for cell confluency returns 75000 hits.

A look at the context in which they are used supports my gut feel, which is that

1:  "confluence" should be used in contexts of "% confluence"

2:  "confluency" should be used in contexts where you describe high or low levels of confluency.


What is this (water-loving) bug? For some time we've been finding these little fellows in our apartment:

They seem harmless enough, but finding them is a bit... annoying. I found the fellow above in the bathtub, and it's not uncommon to find more than one.

Unfortunately, some started to appear near the kitchen sink as well. Or outside of the bathroom on the floor (at least that's where we noticed them).

I think this thing prefers darkness over light, and seems to be drawn towards wet places or just water. These critters are also surprisingly fast.

What is it? Should we be concerned about a pest problem, or is this just a minor, unwelcome guest?

PS. We live in Poland.

It is a Lepisma saccharina or silverfish.

It is rather common and yes, it's harmless.


Is cell senescence in culture comparable to that in vivo? A cell is 'senescent' when is has permanently left the cell-cycle. This can be caused by stresses, or by reaching the 'Hayflick limit' (the cell has reached its replicative lifespan, as defined by its telomeres).

Cells cultured in vitro can be used as models to study senescence (or sometimes 'ageing', although the distinction there is not necessarily within scope of this question) by growing the same population of cells for a long time (many passages). A common method to identify a senescent cell population is to use beta-galactosidase staining.

I was wondering to what degree senescent cells in culture (identified by beta-gal staining) are actually comparable to those you might expect in vivo. I ask because it seems to me that a terminally senescent cell may not actually survive long in an organism, so what we refer to as senescent cells in vivo are actually pre-senescent cells? I haven't got any basis for this, just a feeling. (Very scientific I know).

Senescence does not equal cell death, but is simply an arrested state in which the cell still remains viable (1). It has been shown throughout the literature that this state corresponds with an altered cell cycle profile different from contact inhibition or damage-induced arrest (2). This corresponds with an enlarged cell size, altered gene expression (3, 4), and the pH-dependent expression of β-galactosidase (5). This has been shown both in cultured cells and in animal models (6, 7).

Goldstein, S. (1990) Science 249, 1129-1133.
Sherwood, S. W. et al. (1988) Proc. Natl. Acad. Sci. , USA 85, 9086-9090.
Cristofalo, V. J. et al. (1998) Crit. Rev. Eukaryot Gene Expr. 8, 43-80.
Linskens, M. H. et al. (1995) Nucleic Acid Res. 23, 3244-3251.
Dimri, G. et al. (1995) Proc. Natl. Acad. Sci., USA 92, 9363-9367.
Swarbrick, A. et al. (2008) Proc. Natl. Acad. Sci., USA 105, 5402-7.
Efeyan, A. et al. (2009) PLoS One 4, e5475.


Role of the Hypothalmus in the control of Blood Sugar In homeostatic regulation of blood glucose, the receptor and effector is the Pancreas, but how does the control centre — the Hypothalamus — connect and link into this process?

Your question doesn’t make it clear whether you think that the pancreas must be under the control of the hypothalmus, or whether you are asking whether it has an influence on the pancreas in relation to the secretion of insulin and glucagon, which control the concentration of blood glucose.

First, it has been long known that secretion of insulin can be influenced by the concentration of glucose in isolated pancreatic islets in vitro, so it can not be true that the effects must involve the hypothalmus. This is implicit in most book or general information articles you might find on the web, but for an original reference a review by W.J. Malaisse in Diabetologia 9, 167–173 (1973) seems highly cited.

I know almost nothing about physiology, but on searching the web for the role of the hypothalmus in glucose homeostasis, found a most readable prize-winning postgraduate essay on the topic by Syed Hussein of Imperial College London. I trust that it is in order to append an edited extract of this:

  How does your brain control sugar?
  …altered delivery of glucose to specific parts of the hypothalamus can change insulin, glucagon and glucose levels [2]. …alterations in hormones and nutrient sensing by the brain in rodents leads to marked changes in glucose control. Evidence suggests that distinct regions of the brain have roles in controlling blood glucose in response to changes in glucose, insulin and fatty acids [ref]. These discrete brain nuclei regulate glucose output from the liver, insulin resistance, counter-regulatory responses to hypoglycaemia, glucose-stimulated insulin and glucagon release from the pancreas.
  How does your brain tell the pancreas and liver what to do?
  …blood glucose levels and hormones, such as insulin and glucagon, are influenced by the autonomic nervous system [ref]. This system …consists of two parts: a sympathetic nervous system which deals with ‘fight or flight’ responses such as stress and a parasympathetic nervous system which deals with ‘rest and digest’ and ‘feed and breed’ responses. This system arises in the brainstem of the brain and is under the control of the hypothalamus. Nerves from the autonomic nervous system innervate almost every organ in the body including the cells and blood vessels of the pancreas and liver. The ‘wandering’ vagal nerve, a key component of the parasympathetic nervous system, is shown to play an important role in this. This nerve is necessary for the brain to influence blood glucose. The autonomic nervous system can influence insulin release, glucagon release, liver glucose output and even the size and number of insulin producing cells in the pancreas [ref]. …Exactly how these nerve fibres regulate hormone release is still being slowly unravelled [ref].

The essay cites references which you may wish to follow up for further information.


Why do humans require vitamin B12 supplementation while herbivores do not? This question came about from reading the comments of this (very unclear) question, which the author did not properly clarify.

Vegans are often recommended to take vitamin B12 supplements, as the vitamin is not present in sufficient quantities within vegan food. This implies that plants do not produce (or need) vitamin B12 in their metabolic processes.

However, herbivorous animals do not require any vitamin B12 supplementation, yet contain significant amounts of vitamin B12 in their food products.

What, then, is so different about the digestive tracts of humans and other herbivores that prevent humans from obtaining sufficient vitamin B12 from bacterial sources? Can humans be supplemented with gut bacteria from herbivores, allowing them to obtain sufficient vitamin B12 while on a vegan diet without requiring supplementation?

The bacteria in the foregut of cud chewing animals (e.g. cows) provide enough B12 and other B vitamins. Uptake of B12 happens mainly in the small intestine. There are lots of bacteria in the human intestine but most fermentation of plant matter happens in the hindgut.

Hindgut fermentation also produces B12 but since this happens past the small intestine it is not sufficient to provide enough B12. Therefore non foregut fermenting herbivores (e.g. rabbits) get their B12 when they consume their own feces, which they do anyway to obtain higher digestion efficiency of plant matter. I would not recommend this process to any vegan human though.

As mentioned by bonCodigo, these animals need to take up enough cobalt, and their requirements for this element are higher than our own.

Source:
Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients
C. EDWARD STEVENS , IAN D. HUME
Physiological Reviews Published 1 April 1998 Vol. 78 no. 2, 393-427


Inability of vultures to digest diclofenac The population of Indian vultures has been rapidly declining since 2003. This is attributed to the diclofenac present in the carcasses which the vultures eat. Vultures seem to digest all sorts of food items but why can't they digest diclofenac? What is the mechanism which causes this?

Via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1618889/

  Post-mortem examination revealed extensive visceral gout in all diclofenac-treated birds (see electronic supplementary material). Histological examination revealed significant lesions in the kidneys, liver and spleen with extensive uric acid crystal deposition.

Via: https://repository.up.ac.za/bitstream/handle/2263/26027/Complete.pdf?sequence=7

  From the mechanistic studies both diclofenac and meloxicam were directly toxic to chicken and vulture renal tubular epithelial cells following 48h of incubation. It was later shown that this toxicity was associated with an increased production of reactive oxygen species (ROS), which could be temporarily ameliorated by pre-incubation with uric acid due to its anti-oxidant activity. When cultures were incubated with either drug for only two hours, meloxicam showed no toxicity in contrast to the cellular toxicity present for diclofenac. In both cases no increase in ROS production was evident. In addition, diclofenac influenced the excretion of uric acid by interfering with p-amino-hippuric acid channels. The effect on uric acid excretion persisted after the removal of the diclofenac. It was therefore concluded that vulture susceptibility to diclofenac results from a combination of an increase in cellular ROS, a depletion of intracellular uric acid concentration and most importantly the drug’s long half-life in the vulture.

The second link posits three mechanisms for the cause of renal failure in vultures (ref., pg. 26):

Ischaemic nephropathy with secondary visceral gout
Organic Anion Transporter antagonism
Secondary renal toxicity with or without toxic activation


Why didn't the polar bear change its color from white to black during evolution to absorb heat? Polar bears are white in color and white color is not a good absorbant of heat. Why then didn't they evolve a black color to absorb more heat?

Polar bears do not have white fur - they don't have pigments in their fur hairs which makes them clear and translucent. The outer fur consists of hollow fibres, which shatter a part of the incoming light (the visible part) which makes them look white. This gives a very good camouflage in a white environment.

It was initially thought (see reference 1) that the hollow fibers work in the same way as fiber optic cables and direct the UV part of the light (the visible was thought to be shattered) towards the black skin of the bears where it generates heat, but this hypothesis has been disproved. The UV part of the light is simply absorbed by the bears outer fur and doesn't reach the skin (see reference 2 for details).

The hollow hair helps with the insulation of the skin and can change the color due to environmental influences. The tend to get yellow after feeding on seals due to the fatty substances from the animals. There have also been reports from zoos that algae lived inside the hollow part of the fur making the animals more grey and sometimes even green (see reference 3).

Reference:

Light collection and solar sensing through the polar bear pelt
Is polar bear hair fiber optic?
The greening of polar bears in zoos


Can magnetoreception occur in humans? Magnetoreception is a sense which allows an animal to detect the Earth’s magnetic field in order to perceive direction, altitude, or location. Magnetoreception is present in bacteria, arthropods, molluscs and members of all major taxonomic groups of vertebrates.

  There are several hypotheses that magnetoreception could occur in humans due to cryptochromes, which are a class of blue light-sensitive flavoproteins, because they have been observed to detect magnetic fields in a number of species.

Furthermore, I read somewhere that magnetic bones exist in the human nose, specifically in the ethmoid sinuses. $^1$

Is there more research on those "Magnetic bones", and to what extent is magnetoreception possible in human-beings?

$^1$nature.com/nature/journal/v301/n5895/abs/301078a0.html

When we talk about 'can something happen', then I don't think the answer would need a reference.

Of course, humans can attain the ability of magnetoreception, but the main question is What good will it do to us? Instead it'd prove to be disadvantageous as:

We already have smartphones, compass for identifying magnetic field, so why will the body prefer to waste energy on something which can be done without wasting energy?
We all know that the earth has its own magnetic field. So whenever you wake up or go for a walk (just do any movement), you'll feel an irritating magnetic sensation. Why would that be useful?

Even if we don't talk about disadvantage, then also magnetoreception wouldn't prove to be much useful in whole human population. Randomly, some guys might get a few genetic mutations which would allow them to feel magnetic field, but that wouldn't be of any use to them.

BUT, to your interest, humans do have magnetoreceptors, in retinas. See this article:

  But cryptochrome isn’t unique to birds – it’s an ancient protein with versions in all branches of life. In most cases, these proteins control daily rhythms. Humans, for example, have two cryptochromes – CRY1 and CRY2 – which help to control our body clocks. But Lauren Foley from the University of Massachusetts Medical School has found that CRY2 can double as a magnetic sensor.

or this Wikipedia article:

  Humans are not thought to have a magnetic sense, but there is a chemical (a cryptochrome) in the eye which could serve this function.(2)

Source                                                           Source

So, acquiring magnetoreception might be easier than you'd expect, but it doesn't happen even in this condition. Why?, who knows? Maybe because our body rejected magnetoreception as useless. Maybe at some point of time, humans had the ability to feel/see magnetic field, but this feature now seems vestigial.

EDIT: Regarding "magnetic bones", every article that I could read only points to this Nature article you referred to in your question. So it doesn't seem like there has been much research on it, or maybe this article itself is enough to conclude the topic.

References:

1.http://blogs.discovermagazine.com/notrocketscience/2011/06/21/humans-have-a-magnetic-sensor-in-our-eyes-but-can-we-see-magnetic-fields/

2.https://en.wikipedia.org/wiki/Magnetoreception

3.http://www.ks.uiuc.edu/Research/cryptochrome/

4.http://www.microsystem-components.com/html/magnetoreception.html

5.http://www.nature.com/nature/journal/v301/n5895/abs/301078a0.html


What is Modulation Power Spectrum? I'm reading this paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4562283/ , but I cannot make sense of what MPS nor how should I read the pictures that make use of this method.

The authors say

  The MPS, beyond classical representations such as the waveform and spectrogram (Figure 1A and B, upper and middle panels), displays the time-frequency power in modulation across both spectral and temporal dimensions (Figure 1A and B, lower panels). The MPS has become a particularly useful tool in auditory neuroscience because it provides a neurally and ecologically relevant parameterization of sounds

I'm clueless about what the meaning of time-frequency power in modulation across both spectral and temporal dimensions. Can someone provide a brief explanation about this and MPS?

A time-frequency graph also know as a TF distribution, is a spectrogram, a spectrograph, a sonogram, a waterfall display of sound. They are all different names for the same thing. They look like this:

https://www.google.fr/search?q=dolphin+spectrogram&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiD3vv-9cvdAhUCzhoKHf4jDM0Q_AUIDigB&biw=1429&bih=734

Just as white light contains many wavelengths of colors, sound energy contains bass, mids and high all in the same moment in time, a bit like a water wave has multiple wave sizes, sound energy is the same with sound pressure levels.

Modulation refers to the variation of a simple signal, like tarzan modulates his voice using a kind of tremolo effect, so does a car alarm, and a bird has very varied squeak effects with tremolo effects and also changes from squeaks into clicks into hisses, spectral changes in the timbral quality of the sound. Modulation is a scientific word for the variations of the amplitudes and frequencies of a communications signal.

They write about temporal modulation and spectral(pitch) modulation, it's just hte changes on the time-frequency graphs.

Modulation power spectrum is a relatively obscure field of bioacoustics, it attempts to generalize the fluctuations and patterns of loudness and squeak spectrums into another graph, which is a bit like a secondary time and freqency graph derived from the first sound time and frequency graph, else a 2D graph as in the illustrations, which show sound fluctuation prevalence as an average of the TF graph(a averaged sound fluctuation prevalence of the spectrograph). so, if tarzan's voice oscillates every 1 second, he has a major modulation at 1Hz spectrally, and a minimal amplitude modulation, and they will graph that as a peak as 1Hz on the MPS graph.

We can see on this image that The human speech spectrogram on the top left is mostly at 500HZ, with some S and CH sounds at 2000hz.

For the MPS of the human voice, they have correlated Spectral modulations against Temporal modulations. It is easy to see that the human voice mosly changes at arond 1HZ, same as tarzan's voice, because syllables and pauses take about .5 to 1 second (average words per minute of a human is about 50, average syllables per minute is about 120). So it is easy to see a temporal modulation peak at 1Hz.
The less clear thing is that it is plotted against spectral modulation, which is 2-3 octaves of change, an octave being a doubling of wave speed and frequency. So we can say that the main spectral modulations of the human voice occur over 2-3 octaves at a speed of about 1Hz.
There is a secondary peak, which suggest that there is a change of about 1 octave that occurs at about 200-300 HZ. That is the gruff buzz that you hear in your own man voice, it is about 150HZ and it has about .5-1octave, the base frequency of your voice being 150Hz and various 3rds adn 5ths of an octave, and another octave at 350Hz, seems to be visible from that graph.
tarzan voice: https://www.researchgate.net/profile/Alexandre_Hyafil/publication/283260815/figure/fig2/AS:293940512215079@1447092287682/A-Phase-Frequency-coupling-can-be-mistaken-for-Phase-Amplitude-Coupling-Top-curves-An.png

MPS seems to have been used to study neuron responses in psycho-acoustics.

Neurons interpret sounds using some kinds of complex time and freqency variation(modulation) recognition(resolution) and the researchers use MPS as they say it fits well with the neuron psychoacoustics study.

I would suggest that there are many other ways of measuring psycho acoustic nerve responses and bioacoustics than only MPS, it is an over simplification of sound analysis, and the Digital-Signal-Processing forum on this website will inform you that there are also 100ds of other maths and analysis algorythms that you can run on sound to study Time-Frequency Graphs, and to define sound in many different ways than MPS.

very pure sounds like sine waves make tight lines on a time frequency graph, noise makes very scattered signals at all frequencies, and sounds with many harmonic modes make nice ordered lines of smaller subharmonics that reflect the base frequency of a signal, which resemble echoes of the original sound in parralel with it, and that are on a different frequency.

Time frequency graphs are quite interesting to study and there are probably some studies of bird calls on YT: https://www.youtube.com/watch?v=_FatxGN3vAM


Why is Botulinum toxin the most potent poison known? Botulinum toxin (trade name Botox) inhibits acetylcholine release in neurons and causes botulism, an acute paralytic disease which leads to nerve degeneration and takes a long time to recover. I've read the statement that Botox is the most potent poison we know a few times now and was wondering why exactly it is. All sources I've found only claim that it is, without explanation.

The biochemical mechanism of BT is pretty well laid out at Wikipedia already. The toxin is likely very potent because (1) it is targeted to neurons; (2) neurons endocytose BT; and (3) the BT light chain's protease activity is able to cleave a wide range of SNARE-complex proteins which effectively disrupt the neurons ability to secrete monoamine neurotransmitters, and peptide hormones. Basically, the neurons are completely inhibited from transmitting nerve impulses.


What's the effect of oxygen deficit on plants? As I know all cells require oxygen. So my question is how efficiently can plants operate in no-oxygen atmosphere? Do all plants produce enough oxygen for themselves? Can they consume their own oxygen or the oxygen will be quickly lost to the air? Is there a plant that consumes more oxygen than they produce?

During the daylight, the plant is photosynthesising faster than it is respiring so there is no net uptake of oxygen (the oxygen of course being produced in the as part of the photosynthesis).

Of course, this only applies for tissues where photosynthesis is occurring.  In the roots of the plant, oxygen must always be present in the surrounding soil/growth medium for respiration.  Therefore if there is no oxygen in the roots then the root cells will be unable to produce ATP from respiration and consequently die.  This will eventually lead to the death of the entire plant as it is unable to take up nutrients due to the lack of a functioning root network.

This is the cause of plant death when soil is waterlogged - the water fills spaces in the soil that would otherwise contain air (i.e. oxygen).

Certain plants (often crop plants), rice being given as an example in the comments below, are able to survive being waterlogged and the resulting low oxygen supply. However they can only do so in the short term.  Rice plants in particular have adaptations that allow the transport of oxygen from the aerial parts of the plant down to the roots.  This does of course mean that the rice can not survive being totally submerged for an extended period of time.  Plants such as rice may have better adapted anaerobic fermentation pathways that become the main producer of ATP when aerobic respiration has arrested thus allowing them to better cope when transiently submerged than other plants.

Molecular strategies for improving waterlogging tolerance in plants


What's the difference between an embryo and a fetus? The most I've been able to come up with is that fetuses are embryos slightly farther along in their development. Is that correct?

Yes, you are correct. You can read the wikipedia article about an embryo:

  An embryo is a multicellular diploid eukaryote in its earliest stage of development, from the >time of first cell division until birth, hatching, or germination. In humans, it is called an >embryo until about eight weeks after fertilization (i.e. ten weeks after the last menstrual >period or LMP), and from then it is instead called a fetus.


If a venomous snake somehow gets it's own venom in its body, will it be affected by it? Here is a hypothetical situation I had been thinking about that sparked my curiosity:

Let's a snake is just slithering around, not being attentive for some odd reason. It happens to pass a mouse, in which it didn't see (this is all just hypothetical), and the mouse freaks out and starts to run. When it does, it trips over the snake's tail, and, not knowing what is happening, the snake snaps back bites the mouse and gives it a good dose of venom. (Now, to my question).If the snake ate the mouse, would it's own venom, now in the mouse, hurt the snake?

(Since they are native to where I live, let's say the snake is a Water Moccasin)

An excellent question.  This fun mental floss article addresses that question, but from the perspective of one snake biting another snake:
Snake on snake violence

“The conventional wisdom is that they have circulating antibodies in their blood,” says Stephen Mackessy, Ph.D., a Professor of Biological Sciences at the University of Northern Colorado and an expert in venomous snakes. “This would protect them from their own venom, as well of venom from another snake in their own species.”
Hypothetically, if a speckled rattlesnake bit another speckled rattlesnake, the immunity they’ve built from being exposed to low levels of their own venom—kept in glands behind their eyes and secreted when they bite—would protect them from a fatal wound. (Even though the glands are closed, they still contain blood vessels that allow the venom to circulate in their system, causing mild exposure, Mackessy says.) But a speckled rattlesnake that meets up with a cobra might have a different day entirely.

The same principle should apply to venom ingested in dead prey. Antibodies against the venom would protect the snake. For what it's worth, I think your way of phrasing the question is more interesting and relevant than the way it was phrased in the mental floss article.


Cross section of actin network in neurites for a simulation I am developing I would like to know how the actin network in neurites is distributed.

Is actin confined to the periphery or is the whole neurite shaft containing actin with a rather constant density?

If you have any papers backing up the one or the other view don't hesitate to pass the link.

Thanks for answering.

Actin is required for the neurite architecture and is present throughout the shaft (along the direction of the neurite process)

See these images.

                                        [Source]

                                             [Source]

These are not from research papers but the sources are trustworthy.


What is this beetle? During a pit stop on the road from North Carolina to New York (somewhere in Delaware) I found the following (dead) insect in the car park:

As you can see from the quarter next to it (25 mm diameter) it is rather large - maybe six centimeters, including the "horns".

What was it?

Looks like it must be a male Dynastes tityus (Linnaeus, 1763).

There are photos for comparison, and a full description with maps and some interesting notes on habitat and behavior, on the University of Nebraska State Museum Generic Guide to New World Scarab Beetles


What is the direction of the processing of light by the (human) retina and how does it happen? Quoting Textbook of Medical Physiology by Guyton and Hall, 2016, page 647,

  ...the functional components of the retina, which are arranged in layers from the outside to the inside as follows:

  (1) pigmented layer, (2) layer of rods and cones projecting to the pigment, (3) outer nuclear layer containing the cell bodies of
   the rods and cones, (4) outer plexiform layer, (5) inner nuclear layer, (6) inner plexiform layer, (7) ganglionic layer, (8) layer of optic nerve fibers, and (9) inner limiting membrane.

  After light passes through the lens system of the eye and then through the vitreous humor, it enters the retina from the inside of the eye (see Figure 51-1); that is, it passes first through the ganglion cells and then through the plexiform and nuclear layers before it finally reaches the layer of rods and cones located all the way on the outer edge of the retina. This distance is a thickness of several hundred micrometers; visual acuity is decreased by this passage through such nonhomogeneous tissue. However, in the central foveal region of the retina, as discussed subsequently, the inside layers are pulled aside to decrease this loss of acuity.

I have attached Figure 51-1 for people who would like to see it.

My questions are: How does light travel to the inner parts of the retina first even when there are so many impeding layers preceding it? Why does it not stimulate the photoreceptors first? What is the pathway of the light after it travels to the the innermost retinal layer? Are the photoreceptors the first to be stimulated by the light?

As can be understood, I am quite confused, so if the framing of any question is reflective of erroneous understanding, kindly let me know. All help appreciated.

Short answer

Photoreceptors are the only cells in the retina that directly detect light; they can detect light through the other layers because those layers are so thin and effectively transparent: light passes right through to the photoreceptors.

Longer answer

The retina is fairly thin, and the bipolar/RGC layers don't contain much pigment. Have you ever looked at a thin slice of tissue under a microscope? You can do this and focus to different layers because single layers of cells are fairly translucent (remember they contain a lot of water): most light passes right through them. Some cells, such as red blood cells or photosynthetic plant cells, are harder to see through, but that's only because they are full of pigments.

The reason the photoreceptors respond to light in a way that can be detected biologically is that they contain special photosensitive pigments. In rods, this pigment is called rhodopsin and it is composed of a protein and a molecule of retinal. Most other cells in the retina don't have any such photoreceptors (there is a special class of retinal ganglion cells that is an exception, see for example here - these cells have a pigment melanopsin and contribute to light detection for circadian rhythms rather than vision).

Other cells in the retina respond to light only because they are sensitive to neurotransmitters released by photoreceptor cells and other retinal cells.

As far as why this is the arrangement, with photoreceptors in the back, it's really just a fluke of evolution and evidence that evolution and not design is the best explanation for diversity in biology. Eyes have evolved more than once in animals, however, and cephalopods like squid do not have their retinas arranged this way; in squid the photoreceptors are the most superficial layer.

Because the retina is so thin, this arrangement doesn't provide a large enough disadvantage to be selected against given the complexity in changing the organization. One exception to the thinness, however, is in the blind spot. The blind spot exists because all of the axons from the retinal ganglion cells have to exit the retina someplace. They exit in a big bundle, and there can't be any photoreceptors where that bundle is, so there is a spot where you cannot see. However, the position of the spot is not in the center of your vision, and that part of the visual field is usually covered by the other eye


Why does regular bread yeast fail to thrive in pond water? I thought I'd try adding regular yeast to water taken from my 75 gallon pond, with the idea that the yeast would be a good "bottom of the food chain" kick start to feed the little beasties, along with warmth and light, to allow the creatures to multiply faster than they would in the pond, to be added back the pond as feed. But to my surprise, the yeast won't grow in the pond water, at least, not like when you make bread with it. I've tried adding sugar, molasses, and "proofing" the yeast, but each time, the yeast does not thrive. Is something eating it as soon as it starts to grow, or is something using a nutrient it needs, or what?
The pond is established, with lots of plants, only a few fish, and ammonia levels are 0 ppm. It is an (apparently) thriving ecosystem. My question is, why won't yeast grow and froth up in that water?

A few random thoughts.

I think that one problem here is that by using dried yeast you aren't really measuring growth or survival. Over a short time period much of the fermentation that you see probably has very little to do with viable cells. Dead cells in dried yeast act as permeable packages of enzymes and can promote fermentation.

Following on from that, it may be that components of the pond water can poison the fermentation carried out by the dead cells.

Thirdly, if you are using frothing as a measure of CO₂ production it is possible that there are components of the pond water that collapse that foam by removing stabilisers (probably protein).

Next, Saccharomyces isn't an obvious choice for use as an aquatic micro-organism since it is adapted/selected for growth in high sugar concentrations.

If I was trying to do this I think I would try to culture from the dried yeast under conditions where you do see activity, add lots more sugar (as if you were brewing), and look for actual production of yeast cells. Yeast settles out of suspension very easily so you might be able to pour off most of the liquid and add the cells to your pond. But I have no idea how well such cells will do in a pond.


Does any organism use both photosynthesis and respiration? Chlorophyll and hemoglobin are very similar molecules, as far as I understand. The important difference being one using an iron atom and the other a magnesium atom. Do any organisms use both to get energy from both oxygen and solar rays? If not, is there any good explanation of why?

And do organisms that use chemosynthesis also use macro molecules similar to chlorophyll and hemoglobin?

tl;dr: Yes, all plants breathe.—

I'm not sure whether I understand the question correctly; because all plants use respiration! Some of the organic high-energy substances produced by photosynthesis are later "burnt" to produce energy in the same "respiration" process used by animals, producing CO2.

The difference to animals is that green plants synthesize their carbs (including the ones they burn for energy), fat and proteins from thin air, so to speak, while animals must eat them.

These antithetic processes, photosynthesis and respiration, are often tied to the day-night cycle. When light is available, the plants-only photosynthesis dominates so that the plant consumes CO2 and emits oxygen; at night, when photosynthesis becomes impossible, the usual common-place respiration causes the plant to consume oxygen and emit CO2, just like animals.

Only as long as the plant is growing, this cycle is tilted towards photosynthesis so that more oxygen is emitted than absorbed: the excess carbon and hydrogen is sequestered in the plant's growing biomass. But when the plant dies, all this high-energy biomass is burnt by animals and micro-organisms, making the overall balance carbon- and oxygen-neutral.2

So how do plants breathe — or rather, exchange gases with the atmosphere in general — if they don't have lungs or gills? The key is the large surface area of typical plants with leaves. Seen in this light, a tree looks well-designed for filtering stuff out of the atmosphere. Consider these two images. The first one is a lobe of a human lung3. The second one is a tree... or is it?

I found John W. Kimball's page about gas exchange in plants accessible and full of interesting information. Central to our discussion are three facts:

A plant's living cells, including the ones in the stem, are never far from the surface.
The rate (or "speed") of respiration, i.e. oxidizing carbohydrates, is lower than in animals. (Plants do not perform physical labor with muscles and do not have a brain, which are the two main energy consumers in the human body.)
Photosynthesis happens mostly in the thin leaves.

Because of these factors — smaller amounts of gases per time over shorter distances — plants do not need high-volume, long-distance gas transport in the fashion most large animals do, with blood circulation. The gas travels between and through the cells as needed, guided and regulated by mechanisms detailed in Kimball's text. The fluid traveling through the stem provides (lots of) water to the leaves in the upward direction and nutrients to the living cells downward, but apparently does not carry (much) gas.

The Arbor Day Foundation has a nice page detailing a tree trunk's structure with information about each layer's function. (I didn't know that the cells in the heartwood — the inner part of the trunk — are dead and do not participate in the transport of nutrients or water.1)

Your question seems to be triggered by a perceived similarity between the molecule giving blood its red color, hemoglobin, and the molecule which gives plants their green color, chlorophyll.

True, both are organic molecules with metal atoms embedded, but they are quite different, even apart from their color. Hemoglobin is a protein with a fairly complex spatial structure; look at the image on the Wikipedia page. It weighs as much as 64,000 hydrogen atoms, i.e. it has a molar mass of about 64,000 g/mole. Chlorophyll is also an organic molecule, i.e. it has carbon chains and rings, but it is not a protein. (In living cells Chlorophyll molecules are embedded in a protein complex, arranging them to work together; that is a different thing.) It does not fold in space, partly because it is not as big. Its molar mass is only close to 900 g/mole, almost 80 times lighter than hemoglobin. A model of one variety can be found on its Wikipedia page, too.

The jobs the two molecules do also are fairly different, even though both have to do with oxygen.

Hemoglobin has a transport job. It binds oxygen efficiently. The spongy, blood-heavy lung tissue absorbs oxygen, which dissolves in the blood and is bound to the hemoglobin swimming around in it. There is a lot of hemoglobin in our blood, increasing the blood's capacity for oxygen transport by a factor of 70 compared to just dissolving oxygen in water (and it dissolves actually quite well in water!). Thus, hemoglobin does not synthesize anything but simply transports gases, mainly oxygen, through the body to where they are needed. Some athletes dope by collecting their own hemoglobin and re-injecting it before a competition, thus increasing oxygen supply for their muscles.
Chlorophyll does not transport molecules but instead does some heavy chemical lifting. It absorbs light to harvest its energy through the mechanism called photosynthesis. The details are fairly complicated, but the big picture is not: It is a reversal of respiration, or chemically a reversal of oxidation, called reduction: Oxygen is separated from the hydrogen in H2O and carbon in CO2 and given off to the air. Doing this consumes the same amount of energy which is released during oxidation (be it by fire or by metabolization in the plant). The emerging oxygen-poor(er) compounds can be oxidized later elsewhere to release that energy, or can be used as building blocks for new cells.

1 My girlfriend thinks I'm stupid not to know that ;-).

2 Unless it is buried and taken out of the biosphere, fossilizing to peat and eventually coal, tar and mineral oil. Then the net CO2 balance of a plant's life is indeed negative, i.e. the plant has removed CO2 from the atmosphere; until somebody excavates the fossil fuels, re-injects them into the biosphere and and restores former CO2 levels and all the tropical climate which made the old jungles grow so well.

3 From wikipedia, https://upload.wikimedia.org/wikipedia/commons/a/a1/Lungs_diagram_detailed.svg. By Patrick J. Lynch, medical illustrator, via Wikimedia Commons. The "tree" is actually the same lobe, rotated and colored.


Neuroscience book recommendations I'm looking for a textbook in neuroscience for a rigorous introduction to the topic as an autodidact. I have no prior exposure to the field.

In particular, I'm interested in the chemical mechanisms of enzyme modulation, ideally something similar to Lehninger's Principles of Biochemistry where specific Protein Databank ID's are given, so I can load an enzyme in PyMOL and view where the inhibitors/activators bind, in conjunction with an explanation of the actual pathways involved from a molecular level.

I've read Wade: Organic Chemistry, and a good part of Clayden's Organic Chemistry, before self-studying biochemistry for 6 months, to give a little background of my knowledge.

I'm leaning towards Kandel's Principles of Neuroscience after reading some other suggestions here, but this seems like a gigantic text, and I'm unsure how detailed the biochemistry side of things is (which is my main interest)? Could anyone share some thoughts regarding that, or recommend an alternative smaller text with a specific focus on biochemistry?

I'm also concerned that a large amount of data and publications in the field of neuroscience fail replication (something as high as 60% I believe), so the book would need to contain only factual, widely accepted information and not cutting-edge speculative studies that haven't been replicated and widely accepted. Also, as little pharmaceutical-industry influenced as possible.

Ultimately, my interest lies in understanding how different medications and drugs cause different mental states, their exact pathways and mechanisms, and how they form tolerance. I'd like to one day conduct research in how to minimize said tolerance, eg: reverse receptor desensitization. Which book should I begin with to head towards this goal?

Thanks!

I don't have enough rep yet to comment on your question, but I have read the whole of Kandel's Principles of Neural Science in 2nd year of med school (last year) and I thoroughly enjoyed all of it!

I would recommend Part II: Cell and Molecular Biology of the Neuron to you, as this is where most detailed discussion about the molecolular structure of membrane proteins etc. is happening. And that's only about 110 pages. It probably doesn't go as far as what you are looking for, but I found it a very good introduction to the field of ion channels and how they work. The rest of the book is very interesting if you are keen to get a thorough overview of the whole field of neural science, but you won't find too much detail on the biochemical level there. Part III: Synaptic Transmission with about 150 pages is also a very good read.

For a specific focus on biochemistry you'll have to look for another book, but quite likely you'll find good candidates in the Selected Readings at the end of each chapter, here is one example of those lists from chapter 7:


Stained chestnut tree leaves The leaves of the chestnut tree in our back yard have, for a while, developed these stains on them:

..which don't appear to be a normal feature of this tree's leaves, at least according to the pictures on Wikipedia (I'm no botanist).

Also, the grass at the bottom of & around the tree does not (no longer?) grows around its root:

Its fruit, on the other hand, appear to me to be healthy:

We've only moved here for a few months, so am not sure whether it has always been like this or whether the tree only got infested in the last period.

Does the leaves' degradation + non-fertile ground around its root, signal that the tree is sick? If so, is there some "medicine" I can get for it myself, or would I have to speak to the administrators of the garden? Thanks in advance for any thoughts!

This looks like Horse Chestnut Leaf Miner (https://www.rhs.org.uk/advice/profile?pid=533).  It is very common, and infects most of the horse chestnut trees around here.  Some years are worse than others. It has been spreading for the past few years.  It doesn't seem to seriously harm the tree, but there is no cure I have heard of.  The link I posted from the RHS offers some ideas about collecting the leaves and composting them in sealed bags, until the moth larvae have died. Occasionally, trees have been found that are genetically resistant to the disease.

Don't worry about the grass, the tree needs the light and water from that bit of soil, but you could try some bark mulch around the trunk to cover the soil, and keep the moisture in.


Do apes and humans share 99% of DNA or 99% of genes? What is the difference? I made an answer on the Scifi.SE that can be read here. It is about how the characters in the story Jurassic Park might have gotten DNA for all the species shown.

In my answer, I said this:

  Apes and Humans, for example, share over 99% of their genes. That means the difference between our species is less than 1% of our genes. In fact, all life on Earth shares about 50% of it's genes.

but in the original posting (before someone edited it) I chose to use the word DNA instead of genes.

He left this comment in the section to explain the edit:

  Sorry, I'm a biologist, I can't help it. Humans and apes share 99% similarity in the coding sequences of their DNA, the ~5% that codes for genes, not on all the DNA. I simplified this to genes for the answer.

I have a basic high school understanding of DNA and genes, so I'm afraid I fail to see the difference between using "DNA" or using "genes" in my statement. I understand that genes are specific sequences of DNA that are used by the cell in some way. I understand that DNA is more generic, including all of the strands, whether they are used or not, whether they seem to code for something or not.

So is it wrong then to say that apes and humans share 99% of their DNA or is it equally correct to say "genes"?

So, a quick molecular biology lesson.

Proteins are the things that make up a good percentage of our cells (which make up a good percentage of us), and are the things that do the work of the cells - many are catalysts and are known as "enzymes".
Proteins are encoded by genes - while the statement that one gene
codes for one protein is not quite correct (one gene can code for
different variations of the same basic protein), it's a good way to
think about things in this context.
Genes are made up of DNA, a polymeric molecule that constitutes our chromosomes, the informational portion of which resides four “letters” (chemical bases).
However, now we get to the key part — although all genes are made of DNA,
not all the DNA of chromosomes makes up genes. In fact, as @terdon    mentioned in a comment, only about 5% (or less) of the 4 billion letters in the total DNA — the genome — constitute genes - those sequences that
directly code for protein.
The function of the rest of the genome is not entirely clear. Some is regulatory, some may be structural, and may be “junk DNA”. However it’s stuck      around for millions of years, so it we assume it must have some purpose. This non-coding DNA differs between species to a greater extent than the genes themselves do, so perhaps it somehow contributes to the differences between organisms.

From AndroidPenguin

Here are the links to a paper about the function of "junk" DNA from 2013.

Summary in NY Times
Abstract in Nature
ENCODE threads on nature.com


Is it possible to artificially select for flight in pigs? After reading this rant by Fodor, as a layperson, I was idly wondering whether it would be possible to artifically select for flight in  pigs. Of course by that time the porcine lineage will probably comprise an entirely new species, but what would be the first step in our breeding experiment? And how would it develop thence, hypothetically speaking?

Intro course to evolutionary biology
I doubt you can get much from the below answer. At the end of the day, the only thing that would really allow you to increase your knowledge is probably an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.
Question

Is it possible to artificially select for flight in pigs?

If by 'artificially select' you refer to selection on available genetic variance, then No, it is not! You'll need plenty of new mutations and it would take a very long time.
Selection
You cannot select for something that does not exist. Selection requires pre-existing phenotypic and genetic variation for the trait of interest. No pigs are flying today, so you cannot increase the frequency of individuals flying by selection.
You will need to wait for mutations that confer such flying ability. Of course, there won't be a single mutation that turns a pig into a flying pig. Simply because flight is really not a simple adaptation for a pig! There are few species you could have chosen for which flight would be harder to think of! You are going to go on a long step-by-step procedure, fixing mutations one at a time by selecting every one of them and that will probably take hundreds of thousands of years or maybe millions of years.
Step-by-step procedure
I suspect you would consider using their front limb for flying. Here is a potential and extremely simplified step-by-step procedure. Of course, if you were thinking of pigs flying using their ears, the procedure wold be drastically different!
You should probably start by attempting to modify their limbs then. You can maybe try to start by selecting for individuals that are better able to manipulate objects with the front limb. Also start selecting for lighter bodies. Also, remove any selection for the ability of fast displacement or moving in the mud as that would select for their current front limbs. Start with some very very simplistic manipulation and increase up to eventually ending up with individuals that have pretty flexible front limb. Make sure to select for front limb that can move perpendicular to the body axis.
Then I don't know if you should aim to make wings out of skin or out of hair-feather like structure. If you're aiming with feather-like structure, you can try play it out with sexual selection just like it evolved in birds. Let's say you're choosing skin wings. Then, maybe selecting for those having broad and thing front limbs might be a good way to go. In the meantime, you've reached anything like that, you probably managed to reduce the body size of your pigs to the size of a mouse with a very elongated body.
Select for jumping abilities and then slowly for flying abilities. You've got flying organisms who's ancestors were pigs! Be aware nobody is going to fund such a useless and incredibly long experiment.


How did the first sexual animal come to exist? I am more or less familiar with the evolution theory based on mutations.

Now, starting with a nonsexual being, how did the first organism that reproduces sexually come to exist.

This is a very broad field, with many complementing, overlapping, and contrasting theories. I suggest that you read this part of the Wikipedia article on this topic:

http://en.wikipedia.org/wiki/Evolution_of_sexual_reproduction#Origin_of_sexual_reproduction

Here is what I got from the Wikipedia article (this is just one hypothesis, read the article for all the others):

There are many advantages to sexual reproduction, two main ones are greater genetic variation and recombinational DNA repair (occurs during meiosis).

There are certain species that can reproduce both sexually and asexually. They choose to reproduce sexually during times when the environment is uncertain (changing). This provides evidence that greater variation is one reason for sexual reproduction.

Asexual organisms only have one copy of each gene, therefore if this copy is mutated in a bad way, they are out of luck. Organisms that sexually reproduce have two copies of each gene, when one goes bad, they can use the other copy to repair the original copy, during meiosis.

As you may know, stress has many harmful effects, one being that it leads to DNA damage. There are certain species of bacteria who, in response to stress, uptake/integrate nearby bacteria cell's DNA into their own. They can then use this new copy to repair their own copy in case they experience DNA damage.

This "trait" of up taking/integrating other's DNA may have been evolutionary selected for (because these organisms repaired their DNA, they survived and passed on their genes), therefore eventually leading to organisms that sexually reproduce.


Does darker skin color make it easier to live under sun? I have always thought darker colors absorb more heat from the sun, so if you are wearing a white T-shirt you will be cooler under sun than wearing a darker T-shirt, or a black piece of steel will be hotter under the sun than a shiny silvery one.

If this is true, then why is the same not applicable to skin color? It seems to me like the more sun in an area the darker the people's skin has become, isn't that the case?

It isn't about heat but ultraviolet light. Melanin is the pigment that makes our skin colour whatever it is and in darker skin there's more melanin. Melanin dissipates UV, which otherwise would cause skin cancer as it introduces mutations into DNA. Melanin production is stimulated by UV so that's why tanning beds work, our body senses the danger and responds by making our skin darker. Yes this makes us hotter but that's a small price to pay, melanin needs to be dark to do its job well.


Why do the most structurally well-characterized bacterial RNA polymerases belong to thermophiles? From Lewin's Genes (11th edition, page 515):

  The only bacterial RNA polymerases for which high-resolution crystal structures have been solved, however, are from two thermophilic bacterial species, Thermus aquaticus and Thermus thermophilus.

Is this just a matter of economy? I mean, as X-ray crystallography is exceedingly expensive and complex, did scientists consider enough to resolve the RNA polymerase structure of one species and deduce those belonging to the rest by homology-based folding prediction?

Or is it because thermophilic proteins are inherently more stable and thus easier to crystalize?

I think both of your suggestions have some merit: (1) it appears that Thermus RNAPs are more stable and easier to crystallize (2) RNAP is highly conserved and so it is not critical to crystallize it from every bacterial species.


Meaning of term ‘rapidly labeled RNA’ I encountered the term, “rapidly labeled RNA”, in the article: Rapidly labeled HeLa cell nuclear RNA. I. Identification by zone sedimentation of a heterogeneous fraction separate from ribosomal precursor RNA. (1966).
I would appreciate it if someone could explain to me what it means or implies.

Explanatory answer

Rapidly-labelled RNA was the RNA labelled by radioactive precursor during a short period (the pulse), terminated by swamping the system with an excess of non-radioactive precursor (the chase). This is known as a pulse–chase, and is described in the methods section of the paper cited in the question and reiterated by @SeRe as an answer. Such a pulse–chase preferentially labels RNA species that have short turnover times (i.e. half-lives of the same order of the pulse), and was thus regarded as a way of studying messenger RNA.

This strategy and its interpretation was an extrapolation from what was known about mRNA in the regulation of bacterial gene expression, but the descriptive term ‘rapidly-labelled RNA’ was used rather than ‘mRNA’ because there was no direct evidence to support such an assignment in nucleated mammalian cells. Indeed, there were major problems because the rapidly-labelled RNA in the nucleus was of a different size to the RNA that subsequently appeared in the cytoplasm, and, indeed, there was no simple precursor–product relationship between the two. In retrospect this is not surprising given what we now know about the splicing of eukaryotic mRNAs and the fact that most of them have much longer half-lives than bacterial mRNAs. However, at the time there was a school of thought that interpreted these results as evidence against the idea of mRNA in eukaryotes, and one of the purposes of the paper cited was to demonstrate that some of the rapidly-labelled RNA that appeared in the cytoplasm had properties consistent with mRNA.

The historic context

It may be necessary to explain to younger scientists that this work was done before DNA cloning, before RNA sequencing (never mind DNA sequencing), before the discovery of polyadenylation of eukaryotic mRNAs (the ‘handle’ for purifying them), in short, at a time when no specific mRNA had yet been identified or isolated (see, e.g., the Wikipedia article on The History of RNA Biology). As documented in Mathew Cobb’s excellent article ‘Who discovered mRNA?’, mRNA wasn’t really discovered but was an idea to account for the rapid response of the lac system (observed in genetic experiments) in terms of a previous unexplained labelled RNA with a DNA-like base composition observed associated with more abundant stable RNA (ribosomes) when bacteriophage infected E. coli. Subsequent work, presented in papers by Brenner et al. and Gros et al. in the same issue of Nature in 1961, in effect documented this RNA more precisely in phage-infected cells and showed that it differed from ribosomal RNA. The importance of the work of Mathhaei and Nirenberg in establishing cell-free systems for translating polyU and subsequently other artificial polynucleotides cannot be underestimated. However, it is important to recognize that the genetic code was not deciphered using genuine mRNA.

It was natural to assume the mRNA model extended to eukaryotic cells, but at that time there was no convenient system with an abundant mRNA like that of bacteriophage and so the presumed differentiating characteristic of short half-life was used, as seen in a plethora of papers on ‘rapidly-labelled RNA’. Many of these were opportunistic, claiming to document anticipated hormonal or other effects on eukaryotic gene expression. Consequently the demonstration that much of the rapidly-labelled RNA in the nucleus never reached the cytoplasmic ribosomal location had the effect of discrediting not only these papers, but the very idea that mRNA existed in eukaryotes. This may seem rather absurd today, but the foremost ‘eukaryotic mRNA denier’ (as he might be termed in contemporary parlance) was the eminent Oxford Professor of Pathology, Henry Harris FRS, who developed man–mouse heterokaryons and set out his ideas in a published monograph entitled ‘Nucleus and Cytoplasm’ (a copy of which I once possessed). So it is relevant that Warner et al. (1966) refer specifically to Harris in the discussion section of their paper, which describes work that addresses the issues Harris had raised.

If there is a moral to this story (and it is always easier to draw morals after the event) it is perhaps that Harris was happy to confusticate lack of proof with disproof in an area that was peripheral to his main concerns, and that the groups in New York — and Jonathan Warner, especially, having previously described polysomes in Alexander Rich’s lab — were prepared to accept the fact that the situation was more complicated than originally thought, but were not prepared to throw out the baby with the bath water.


"producer cell line" vs. "host cell line" in biopharmacology I'm translating a text that describes the creation and testing of a cell line that produces a drug (a protein) and also procedures for creation and maintenance of cell banks.

Example sentence:

  Assessment of the morphology, viability, and cell concentration of the producer cell line

I wonder if I can use host cell line instead of producer cell line, or "host cell line" would mean "a line that has not yet been subjected to transformation using viral vectors" (a line that cannot yet produce the needed drug; a "pure" line). Just making sure.

I would lean towards staying with "producer cell line". In my mind, a host cell line is hosting something, like a virus, while a producer produces something. The non-transformed cell line would be the parent cell line.

On the other hand, "host cell line" also implies hosting the recombinant protein product that is later purified, so there's an argument to be made for either phrase. I still prefer producer, though, as I think it's more directly descriptive of what the cells are actually doing - producing the protein of interest.


Are neurons clustered? How do neurons make thousands of connections? According to this source, a neuron can connect to up to 10,000 other neurons. Does this imply that neurons are clustered, that is, not evenly spaced? Argument:

Say axons are length $L$, and dendrites are length $D$. Say a neuron $N$ has 10,000 outgoing connections. Then there must be 10,000 neurons within distance $D$ of $N$'s axon terminal. Then each of those 10,000 neurons are within distance $2D$ of each other by the triangle inequality. Assuming $2D<L$, then all of those 10,000 neurons are less than an axon's distance from each other. But for this to be true, the 10,000 neurons must be closer to each other than they are to $N$. Since this argument holds for any neuron, we get the result that neurons must form clusters of around $10,000$ neurons, or their dendrites must be longer than half their axon length.

Similar to this question.

In addition to the comments pointing out other inaccuracies, I think the biggest, most obvious misconception that completely invalidates the whole premise is that axons most certainly do NOT have a single terminal; axons branch and make thousands of individual synapses along their length and at the ends of any branches. For excitatory projection neurons in the cortex, for example, the axons can stretch for many millimeters (or centimeters in larger brains), but also typically branch near their origin to contact the dendrites of neighboring cells.

The number of synapses and number of neurons contacted varies greatly across brain areas, species, cell types, etc.

You might be interested in "small world" organization, such as at link, which I suppose could be considered a form of clustering, but it has absolutely nothing to do with the mathematical distance explanation you are proposing.

The only correct equation you can write here is that the spacing S between neuron A connected to neuron B, must be S<=D+L, where L is the length of A's longest axon, and D is the length of B's longest dendrite; for many pairs, S << D+L. These equations will not lead you directly to any valid conclusions of clustering.


Can a person survive on blood in place of water? This question: Can you get enough water by eating only fish? asks if a person could survive on fish alone. Can a person survive on fish and/ or blood alone of any species if stuck at sea or animal blood as a last resort where there is no water or fire?

Obviously if it was a fresh water fish there is water, but there are fresh water mud skippers that can breathe air and the water to tainted to drink in that case a fresh water fish blood maybe safer than the water. https://chemistry.stackexchange.com/questions/115901/what-can-i-eat-that-will-help-metabolize-blood

Desalination would be the best way to process the blood but this is in emergency situation scenario.

From @PTwr Comment's Link: If you drink blood regularly, over a long period of time the buildup of iron in your system can cause iron overload. This syndrome, which sometimes affects people who have repeated blood transfusions, is one of the few conditions for which the correct treatment is bloodletting. https://what-if.xkcd.com/98/

Blood is not a good source of water.
1 liter of blood contains about 800 mL of water, 170 grams of protein and 2 grams of sodium (calculated from the composition of lamb blood).
When metabolized, 170 grams of protein yields the amount of urea that requires 1,360 mL of water to be excreted in urine (calculated from here); 2 grams of sodium requires about 140 mL of water to be excreted (from here).
This means that drinking 1 liter of blood, which contains 800 mL of water, will result in 1,500 mL of water loss through the kidneys, which will leave you with 700 mL of negative water balance.
Fish blood can contain less protein, for example, trout (check Table 1) contains about 120 g of protein (plasma protein + hemoglobin) per liter of blood. Using the same calculation as above (1 g protein results in the excretion of 8 mL of urine), drinking of 1 liter of trout blood, which contains about 880 mL of water, will result in 960 mL of urine, so in 80 mL of negative water balance.
Turtle blood can contain about 80 g of protein (plasma protein + hemoglobin) and 3.4 g of sodium per liter. Drinking 1 liter of turtle blood, which contains about 920 mL of water, will result in 80 x 8 mL = 640 mL loss of urine due to protein, and ~240 mL due to sodium, which is 880 mL of urine in total. This leaves you with 40 mL of positive water balance (to get 2 liters of water per day you would need to drink 50 liters of turtle blood, which isn't realistic.
In various stories (The Atlantic, The Diplomat, The Telegraph), according to which people have survived by drinking turtle blood, they have also drunk rainwater, so we can't conclude it was turtle blood that helped them. I'm not aware of any story that would provide a convincing evidence that the blood of turtle or any other animal is hydrating.


Why do plants store energy as carbohydrates and not as fats? In my introductory biology class, we are learning about biomolecules. The textbook says fats are a more efficient energy store than carbohydrates.

So my question is - why would plants store their energy as carbohydrates and not as fats, if fats are a more efficient energy store?

The question was:

  Why would plants store their energy as carbohydrates and not as fats, if fats are a more efficient energy store?

But before trying to answer it you have to be quite clear what is meant by efficient. Without qualification this term is meaningless. A little reflection will tell you that whatever positive properties are implied by ‘efficiency’ may have different importance in relation to the very different modes of existence of animals and plants. One will also want to test any explanation on the exceptions — the instances where animals store carbohydrates (generally polysaccharides) and plants store fats. With this in mind I argue as follows:

1. Carbohydrate is the straightforward solution

Plants synthesize glucose from carbon dioxide, animals take in carbohydrates in their diet and break them down to monosaccherides. Hence, storing excess as polysaccheride (glycogen in animals, starch in plants) involves developing and using a relatively simple polymerization/depolymerization system. One would therefore assume it to be the default. The question is then, “in what circumstances is it advantageous to store surplus as fat?”.

2. Fat is a more concentrated energy store, so is used to minimize weight

Dull eh? But that’s the answer. The following extract from Berg et al. explains this clearly (triacylglycerol is the chemical name for triglyceride or fat):

  Triacylglycerols are highly concentrated stores of metabolic energy because they are reduced and anhydrous. The yield from the complete oxidation of fatty acids is about 9 kcal g–1 (38 kJ g–1), in contrast with about 4 kcal g–1 (17 kJ g–1) for carbohydrates and proteins. The basis of this large difference in caloric yield is that fatty acids are much more reduced. Furthermore, triacylglycerols are nonpolar, and so they are stored in a nearly anhydrous form, whereas much more polar proteins and carbohydrates are more highly hydrated. In fact, 1 g of dry glycogen binds about 2 g of water. Consequently, a gram of nearly anhydrous fat stores more than six times as much energy as a gram of hydrated glycogen, which is likely the reason that triacylglycerols rather than glycogen were selected in evolution as the major energy reservoir. Consider a typical 70-kg man, who has fuel reserves of 100,000 kcal (420,000 kJ) in triacylglycerols, 25,000 kcal (100,000 kJ) in protein (mostly in muscle), 600 kcal (2500 kJ) in glycogen, and 40 kcal (170 kJ) in glucose. Triacylglycerols constitute about 11 kg of his total body weight. If this amount of energy were stored in glycogen, his total body weight would be 55 kg greater.

The animal exception — glycogen

A limited amount of fuel is stored as glycogen in animals. The increased weight load is offset by the advantage of rapid mobilization and the fact that glucose is obtained (animals cannot convert fatty acids to glucose).

The plant exception — oils in seeds

Plants do not walk around, so weight is not generally a consideration that would induce them to store their reserves as fat. They can develop large tubers under the ground, for example. However there is an advantage to minimizing weight in the energy reserves required for the development of seeds — it allows for easier spreading in the wind or through animal consumption. Thus one can rationalize why the energy reserves in seeds are oils (lower melting point triglycerides on account of their greater unsaturation).


Do babies resemble their father? An often heard theory is that newborns and babies resemble the father more than the mother, a theory apparently ignited by a Nature paper by Christenfeld and Hill (1995). Figure 1 shows one of the tests images. His subjects had to guess which picture was the real dad and which was the real mom. It turned out that tested subjects were indeed significantly better at guessing dads than moms.

Test stimulus of Christenfeld and Hill (1995). Which one is dad: a, b, or c?

It is suggested that paternal matching of a baby promotes identification of the father with his offspring. In turn, self-identification in his kin would prevent the father from doing harm and stimulate protective paternal behavior. This then is hypothesized to increase survival rates of his offspring and et voila, a trait is born (pardon the pun) that makes baby paternal look-alikes fitter than those that don't. This hypothesis seems to have become part of parenting folklore.

However, a Scientific American paper by Matson (2011) contests this view and puts forward several primary research studies showing no preferred resemblance between mother or father, or even predominantly maternal features in babies.

Is the resemblance between father and baby fact or fiction?

References
- Christenfeld & Hill. Nature (1995); 378: 669
- Matson, Sci Am (2011) online article

Credits for this question go to @KoustavPal for his comment in Y-chromosome and phenotype

Resemblance between parent and offspring is certainly true. Some traits are more obvious than others, for example skin colour would be very obvious. As babies mature they will gradually begin to look more and more like their parents, the features of babies often change rapidly, for example pretty much every baby has a little nose, but by the time they are a fully grown adult it probably resembles that of one the parents fairly well.

More obvious example would be height - imagine being presented with a baby and two males who are identical in every way, except one is two metres tall, and the other is 1.5 metres tall. As a baby it would be very difficult to assign paternity on the criteria of height/size, but as the child develops it would likely become easier and easier.

The resemblance between parent and offspring relates to the heritability of a trait but, because there can be temporal variation within an individual, heritability can only be properly determined by measuring the traits in parent and offspring at the same time point (e.g. father's height at 18 years old and son's height at 18 years old), otherwise it will introduce noise in to the estimation, likely reducing the estimate of heritability (and specific to your question, making it harder to assign paternity based on phenotypic characters).

In the context of your question: Ability to assign paternity would depend on a) the resolution with which the traits available can be distinguished among all individuals in the test and b) the variance among all individuals in the test. E.g. If the only trait available was number of fingers per hand, and all potential fathers and the child had five then the lack of variance would make it impossible to use this as a criterion, while if both one of the potential fathers, and the focal baby, had six fingers on one hand then there would be pretty good clue.

Whether babies more resemble their fathers more than mothers (which I think is the true question you are asking here) there is evidence from Drosophila that within-sex heritability is much higher than cross-sex for lifespan and aging, i.e. the lifespan of males (females) far more resembles the lifespan of the father (mother) than the mother (father). This would suggest that there is a sex specific element. Meanwhile there is evidence of high cross-sex genetic correlations in humans preventing males and females from becoming more different (thus maintaining resemblance to opposite sex parents). I would think that resemblance to the father could offer some benefit in assigning paternity by care giving males (stopping males devoting resources to other males offspring) but some of the resemblance could be generated by genetic correlations to sex-specific genetic variance, for example, males (females) will look more like their father (mother) in many ways purely because they are of the same sex, so it will heavily depend on the traits you look at to judge resemblance.

For a related answer about heritability on biology SE see:

Is it possible for a child to grow taller than their tallest parent?


What sort of seed pod is this? My son found this floating in a stream in Massachusetts, in the northeastern US. It was intact when he found it, but he cracked it open to see what was inside. I did some Google image searching, but couldn't find anything. Any idea what it is, and where it came from?

It's actually not a seed pod, but rather a gall (see here or here for more info about galls). Specifically, it most likely is a gall belonging to the Oak Apple Gall Wasp (Amphibolips confluenta). You can read about this species and its gall here.


Why ketoacidosis is less common in patients of Noninsulin Dependent Diabetes Mellitus? The other day my teacher said ketone bodies are mostly formed when insulin is less and NIDDM type diabetes mellitus has less chances to grow ketosis. https://medlineplus.gov/ency/article/000320.htm
P. S. I had read the difference between the type 1 and type 2 diabetes.

This is a good and important question. The answer is not obvious, or necessarily well understood. Hyperglycemic crises occur in both Type 1 and Type 2 diabetes. In type 1 diabetes, the crisis is more likely to be diabetic ketoacidosis (DKA). In type 2 diabetes, it's more likely to be something called hyperosmolar hyperglycemic state (HHS), though type 2 diabetics can develop DKA, especially later in the course of the disease. Both can be brought on by similar precipitating events (for example, infection) in an individual who has had diabetes for a very long time (and this is where we often see these patients now -- pneumonia or the flu in an older diabetic). With type 1 diabetes, though, it can be how diabetes is discovered in a young, otherwise healthy individual.
The key difference between type 1 and type 2 diabetes is that type 1 is an absolute loss of insulin production, typically due to autoimmune destruction of the cells of the pancreas that produce insulin. Type 2, on the other hand, starts as insulin resistance. In fact, insulin levels may be high early in the course, but the tissues do not respond appropriately.
Insulin actions in glucose and fatty acid metabolism
Broadly, a key role of insulin is to respond to increases in blood glucose by shifting energy metabolism from fatty acids to glucose.
In a healthy individual, insulin is secreted as blood glucose rises, and causes peripheral tissues, especially fat and muscle, to take up and use glucose. It also causes the liver to release less glucose into the bloodstream from glycogen stores and gluconeogensis, and instead to store it (in glycogen).
At the same time, since there is plenty of glucose available, insulin diverts fatty acids to fat cells, promoting their storage in and inhibiting their release. Insulin indirectly prevents fatty acid catabolism in the liver by promoting its storage in fat cells, but also directly inhibits liver ketogenesis, a process by which byproducts of fatty acid and protein catabolism are converted to ketone bodies that can be used by, among other tissues, the brain.
Impaired insulin signaling
In both DKA and HHS, despite high levels of blood glucose, the muscles, fat cells, and liver act as if the organism is starving. In response to this state, counter-regulatory hormones (catecholamines, cortisol, glucagon, and growth hormone) are released. The liver releases glucose from glycogen stores and generates even more glucose from other metabolites through gluconeogenesis.
The difference between DKA and HHS is how lipid metabolism is regulated. It is unclear why, exactly, in HHS insulin fails to regulate glucose metabolism but seems to succeed in suppressing lipolysis and ketosis, but that is the current hypothesis. In DKA, fatty acids are released from adipose tissue and delivered to the liver, where massive unregulated lipid catabolism and ketogenesis occurs. In HHS, the existing insulin seems to be effective at suppressing lipolysis and ketogenesis.
You can read more about the pathophysiology of both these diabetic hyperglycemic crises in this excellent review.


How has the use and subsequent ban of DDT affected insect populations? Living in Australia there were less ticks for example during the use of DDT, now there are more ticks prevalent here. I am wondering if any insect species have declined permanently as the result of the DDT use, and if some have repopulated disproportionately (compared to populations prior to the use of DDT- if there is such data) since it's cessation of use.

How has the use and subsequent ban of DDT (dichlorodiphenyltrichloroethane) affected insect populations?

Are there any studies on this?

The most thorough study on the matter appears to be entitled "Anthropogenic impacts on mosquito populations in North America over the past century". Their broad conclusion is that various mosquito populations decreased in abundance and variety during heavy DDT usage years. However they have revived in the past few decades. The only species that seemed to have a permanent decline is Ae. Stimulans.  While this study was only on mosquitos, it may be representative of wider insects - most revived but a small fraction faced permanent damage.

There is a large amount of more associative evidence that observes a large decline in insect biomass and can only predict pesticides, such as DDT, as the culprit. The NYTimes had a good article on this.


How likely is a lack of DNA match with a distant relative? How likely is a lack of DNA match with a distant relative?
I have recently gotten interested in ancestry research and have had a DNA analysis performed by a prominent commercial provider.
I've been working on my family tree for a few months now and have gotten into contact with a lot of distant relatives of mine, which has generally been quite delightful. In one particular case, we discovered that we actually have a double-relationship about 5-7 generations back in time, depending on how you count (common links go back to about ~1790).
We found this quite interesting, and this distant relative had a DNA analysis performed on their own genome as well.
Much to our surprise, however, we didn't find any commonalities in our DNA, which seems odd given the double-relation, and the fact that we have what we believe to be original and authentic documents of all the relatives forming the link.
Of course, we began speculating about the possible reasons for this. Maybe a misattributed child somewhere in the family tree? However, this seems unlikely, given the double nature of the link - most likely, we would need two misattributed children to explain the lack of any commonalities.
The other explanation would of course be that the DNA analysis provided by these companies is less reliable than we think, and that just by random mutations and "unlucky" inheritance, any common DNA might have been lost or scrambled beyond recognition.
I would like to calculate the probabilities of this happening in order to judge whether it makes sense to dig further into the original documents to try and clear up this mystery, or whether a mismatch by chance alone is sufficiently likely to explain this oddity. Of course, I don't need super precise numbers, but a back-of-the-envelope estimation would be nice - are we talking a few percent, or one in a billion? Also, I would be curious anyway on how to calculate probabilities like this, given the publicly available data on these tests.
What are the relevant quantities for this calculation (number of SNPs, I suppose), and how would one define and calculate a probability like this?
About myself
I'm a physicist with a strong background in data analysis with some basic understanding of biology and genetics. Don't be afraid to hit me with those numbers and probabilities, but please explain any genetics jargon you're going to use!

First, if you haven't read it already, I highly recommend Carl Zimmer's "She has her mother's laugh." for anyone interested in ancestry/genealogy.
In it, he presents the following figure showing the probability of sharing any autosomal DNA with a given ancestor as a function of the number of generations separating you from that ancestor. (notably, this analysis excludes the very real possibility of intermarriage within a family tree).

So, for example, if you were to look at one single ancestor from 10 generations before you, there's a little less than a 50% chance that you share any of that ancestor's DNA (remember that at 10 generations you have roughly 1,024 ancestors).
So, at 5-7 generations there's still a high probability that you both have at least some genetic material from the same common ancestor(s). But, it's much less likely that you both share the same pieces of that genetic material (probably in the 10-14 range on this graph).
Plus, very few (probably none) of the commercial DNA ancestry sites do full genome sequencing for ancestry comparisons. They look at a limited number of specific regions that can help identify familial relations. So, even if you do share common ancestral DNA, it's less likely that it would be detected without whole genome comparison.
Image Credit: https://gcbias.org/2013/11/11/how-does-your-number-of-genetic-ancestors-grow-back-over-time/
Edit
I just wanted to edit and reference that the above analysis was calculated by Graham Coop and colleagues. I did a little more digging and he's got a blog post (How many genomic blocks do you share with a cousin?) with a more relevant analysis for you're specific question, showing the probability of two "cousins" having zero shared DNA blocks as a function of how many generations back the two shared common ancestors.

Reference: https://gcbias.org/2013/12/02/how-many-genomic-blocks-do-you-share-with-a-cousin/


Why can't diamine oxidase be supplemented? I've read from an academic article that diamine oxidase cannot be supplemented  but it had no explanation as for why. I am curious as to why this?

  Food rich in histamine or red wine may cause allergy‐like symptoms
  such as sneezing, flush, skin itching, diarrhoea and even shortness of
  breath. The suspected reason is a diminished histamine degradation
  based on a deficiency of diamine oxidase. As diamine oxidase cannot be
  supplemented, a histamine‐free diet was implemented to reduce
  histamine intake.

The article nowhere mentions diamine oxidase(DAO) cannot be suplemented.
DAO supplementation
The link clearly supports DAO can be used. Though Triptans like sumatriptans are used because of cost.
Note: Research is of 2018, so not your fault.