Why does a caloric reflex test induce sideways movement of the eyes? By my understanding the semi-circle canals in the inner ear are oriented in each of the 3 dimensional planes to sense rotation of the head. When the head moves, the fluid inside of the canals does not move with it causing relative motion (like the objects inside of a suddenly breaking car), moving hairs on the walls of the canal.
In the caloric test we inject cold water into the ear which causes a convection current in the canals hence moving the hairs and mimicking head movement. However, I can't understand why the horizontal canal is disrupted, since convection currents move in the direction of gravity. It seems logical that the canal oriented up/down would be most affected. The cold causing water to move downwards, mimicking rotation about the anterior/posterior axis.

The horizontal (= lateral) semicircular canal isn't truly horizontal.  Have a look at this lovely image from Wikipedia, which gives a nice explanation.  If you keep track of the helicotrema of the cochlea there, which is on the lateral aspect, you can see that the horizontal semicircular canal connects with the utricle higher laterally than medially.
This is somewhat confirmed in Maxwell, 2016 Figure 1 which illustrates that the "horizontal" semicircular canal is only horizontal when the eyes are lowered by 30 degrees from a standard anatomical position.  (Bearing in mind that the two lateral semicircular canals are not coplanar, but diverge by 15 degrees).  That paper also confirms that buoyancy is a key mechanism in the caloric test.
Because the lateral end of the horizontal canal is higher, treatment with cold water will draw the endolymph away from it to the medial end, and hence away from the ampulla ("ampullofugal lymphokinesis").  The patient would feel they were turning laterally relative to the the position of the fluid (taken to be fixed in space).  This leads to two types of eye motion - the vestibulo-ocular reflex to maintain fixation by moving the eyes medially, and saccades to follow the position of the "moving" stationary object that the patient is trying to focus on by moving the eyes rapidly laterally.


How is excretion of metabolic wastes from a cell related to its size? As with anything that is taking place within a cell, the metabolic waste too must be proportional to the size of the cell. In particular the surface area to volume ratio. But how is the waste excretion related to the concept of above ratio and how to determine it?

The critical element here is that building materials that need to be absorbed, or waste materials that need excretion have to cross the cell membrane. The larger the surface of the cell's membrane relative to its volume, the faster the exchange rate.

The book section you linked in the comments mentions the following on p.14:

  The volume [of a spherical cell] increases by a factor calculated by cubing the radius, [...] the surface area increases by a factor calculated by squaring the radius. [...] This means that a large cell has relatively less surface area to bring in needed materials and to rid the cell of waste [...]. Cells are limited as to the size they can attain [...]. Cells that are larger [...] have modifications that allow them to function efficiently. This is accomplished by shape changes such as from spherical to long and thin, [or] have infoldings or outfolding to increase their surface relative to their volume.


Cell growth conditions for preparing electrocompetent cells Usually the protocol for preparing electrocompetent E. coli cells calls for growing the cells at 37deg and 225rpms until they reach OD of 0.3. I was wondering, is there any reason they should grow at optimal conditions for growth, instead of at suboptimal, for example at 30 degrees? Also, what is the physiological/epigenetic difference between a culture of OD 0.2 vs 03. vs 0.3?

I'm new so I can't make this a comment, and I don't think the other commenter addressed your questions so here it goes: I don't think there will be much difference, if any, between 0.2 and 0.3 OD. Once you get higher and the cells start transitioning into a stationary phase is a different story. Did you mean to ask about 0.03 OD as well (you wrote 03.)? I'm not an expert in E. Coli, but they would probably be less likely to produce proteins that are contact inhibited. Sub-optimal temperatures may have a minor effect on growth, but I don't believe this will initiate much change or induce production of large amounts of cold shock proteins.


Can roots have cuticle, especially aerial roots? In my school biology book, it is written that cuticle covers the epidermal cells in aerial parts of plants and root epidermis doesn't have cuticle. My question is that whether aerial roots, in plants like kalanchoe, also not have cuticle?

Do all kinds of roots not have cuticle?

According to this article, Selaginella aerial roots have a thick root cap that possesses a cuticle. Roots that have breached the soil do not have cuticles.


Have creatures ever evolved to become less intelligent? Inspired by https://worldbuilding.stackexchange.com/questions/58533/is-intelligence-the-natural-product-of-evolution , I'm wondering if creatures have ever become less intelligent as a result of natural selection and evolution.

It seems plausible, because the brain can use a lot of energy, and I've heard of other aspects of an animal atrophying because they're not useful any more, such as vision in the Mexican blind cavefish.

One possible candidate I can think of is the koala: it's described as having a low brain to body mass ratio, doesn't have a great need for intelligence, and may have a need to minimise energy usage.

I'm mainly interested in cases of natural selection, as opposed to artificial breeding - I wouldn't be surprised if we selected animals to be less intelligent.

Unfortunately, measuring intelligence (assuming we would have a strict definition) is not a thing that can be done from fossil record or genetic data. The only thing one can do is to compare brain mass (or at least size of the cranial cavity) from fossil record. In this regard, no need to go very far for an example, humans are an example. From wikipedia

  The evolutionary history of the human brain shows primarily a gradually bigger brain relative to body size during the evolutionary path from early primates to hominids and finally to Homo sapiens. Human brain size has been trending upwards since 2 million years ago, with a 3 factor increase. Early australopithecine brains were little larger than chimpanzee brains. The increase has been seen as larger human brain volume as we progressed along the human timeline of evolution (see Homininae), starting from about 600 cm3 in Homo habilis up to 1500 cm3 in Homo sapiens neanderthalensis which is the hominid with the biggest brain size. The increase in brain size topped with neanderthals; since then the average brain size has been shrinking over the past 28,000 years. The male brain has decreased from 1,500 cm3 to 1,350 cm3 while the female brain has shrunk by the same relative proportion.

Note however, that wikipedia does not cite any reference and I failed to find one!

Note, also that one should not confound cranial cavity (the thing that is actually measured) with brain size and more importantly no confound brain size with intelligence. Wikipedia goes on saying

  However it is argued that another essential element of brain evolution in humans is rearrangement (Hoffman et al. 2004). Larger brains require more wiring, but more wiring can become inefficient (Hofman 2001). The brain has therefore become reorganized for efficiency. Furthermore, the average body size of nethanderthals was larger which led to bigger brain size (see Brain-to-body mass ratio).

I could not find the Hofman papers but I probably just did not look hard enough (and am a bit tired right now)! One might want to read Healy and Rowe 2007 for a criticism of the inference that can be done from measures of cranial cavity.


What's this insect (Oregon, USA)? Any ideas? This was taken in July on the beach of Bandon, OR, in the USA.

Your picture most likely shows Lichnanthe rathvoni of the family Glaphyridae.

The older answer is almost certainly not correct in any of its guesses; all of the possibilities listed are Palaearctic (see the sites https://fr.wikipedia.org/wiki/Epicometis_hirta, https://en.wikipedia.org/wiki/Tropinota_squalida, and http://www.coleo-net.de/coleo/texte/oxythyrea.htm for confirmation; the first and third will need translating for those not fluent in French and German, respectively).

Referring to Part V of M. H. Hatch, The Beetles of the Pacific Northwest (1971) (which covers the states of Idaho, Oregon, and Washington, and the province of British Columbia, in their entirety, and the western part of the state of Montana), and assuming the subfamily Cetoniinae is correct, I had thought this was Trichiotinus assimilis Kirby; there are inconsistencies between this photo and those provided by bugguide.net (see http://bugguide.net/node/view/22486); specifically, the elytra here are well-separated apically, and the coloration is quite different.  A review of Volume 2 of American Beetles showed me my error: the insect is a member of the family Glaphyridae (formerly a subfamily of Scarabaeidae), and the genus Lichnanthe; returning to Hatch, 1971 shows only L. rathvoni LeConte from the covered area; photos of that species in bugguide.net (see  http://bugguide.net/node/view/115846) show some variation in markings from the photo here (which is to be expected), but are structurally fairly close.

The genus Lichnanthe was most recently revised in the following paper:

Carlson, David C..  1980.  Taxonomic revision of Lichnanthe Burmeister (Coleoptera: Scarabaeidae).  Coleopterists Bulletin, 34(2):177-208.

which is available through JSTOR (a subscription, one-time payment, or access through a university will be needed).


NCBI E-utility to Find Shortest Citation Path Between Two Publications I'm trying to perform a thorough review of Hi-C and RNAi developments and have found myself looking at publication A (2011) and publication B (2015). B doesn't cite A explicitly but I'm sure there are papers linking the two and I'd like to find them. Are there existing utilities to help with this? I've used NCBI E-utilities in the past but would prefer not to rewrite an application that already exists.

I'm going to pursue Neo4j. Example usage, similar to what I'm looking for, is given here. (per a tip from the blog's author in response to my cross-posting on biostars)


Are there eukaryotes without introns? This question on the function of introns in eukaryotic genes made me think: I know that more basal organisms have smaller introns and fewer alternatively spliced exons compared to mammals. But are there eukaryotes whose genomes have no introns at all?

I don't believe so.  I have never come across a eukaryote that does not have introns although there are some genes that do not contain introns.  Some eukaryotes like ciliates actually contain other non-intronic intergenetic regions that seem to be nonfunctional.  These are called Internally Existed Sequences and are removed from the germ-line active micronucleus before going to form the transcriptionally active micronucleus.  Interestingly, introns are also present in these organisms and are present in both the micro and macronucleus.  These introns are spliced out in textbook fashion.  I believe one of the organisms where introns was discovered was in Tetrahymena thermophila with the intron in the rDNA sequence.


what does Pro→Glu substitution mean? Considering the paper:

A single amino acid in E-cadherin responsible for
host specificity towards the human pathogen
Listeria monocytogenes

in the abstract portion, what does Pro→Glu mean? Does it mean that, in place of Glu(glucose), pro-16 is placed?

You are looking at a protein here, which is mutated in the higher host specificity, so glucose is not involved here. What is written here are the amino acids in the three-letter-code, the notation Pro→Glu means that Proline (Pro) is replaced by Glutamic acid (Glu).

The notation Pro16 means the proline on amino acid position 16 in the protein. You often find this replacements noted as Pro16Glu or P16E (in the 1-letter-code)


Help reading chromatogram A genetic variation is found in this chromatogram:

It says that the "reference sequence" is the top line and that I can use the general genetic code to find the reading frame.

I can see that there are two N's instead of a G and a C. However I don't know what this means. I'm also not sure how I'd find the reading frame? I suppose I could look for a start and stop codon but I could read them both ways?

Last question: Is this change likely pathogenic? I'm not sure how to classify a variation as pathogenic or not.

The traces you have come from Sanger sequencing. N in genetics means nucleotide (surprising right?). N is used when the base at a given location is unknown (or could be any base pairs).

In your case you have Ns because the base-calling software is unable to determine the nucleotide. The first N is due to two peaks overlapping (G and A signals) and the second one should be a C rather than a N.

From what I can see, you have no apparent mutations so no those changes are unlikely to be pathogenic. A mutation can be called when you know a base in the reference is modified in your sample, which is not the case here (simply N -> G and a N -> C). The signals for your Ns look very similar between your reference and your sample therefore not suggesting a mutation.

For the reading frame, you have to look for a start (ATG) and a stop codon (TAG,TAA or TGA) to identify the open reading frame (ORF). Multiple software do that and here a link to an online NCBI tool called ORF Finder.

As you pointed out the ORF can also be in the reverse strand. You don't want to look at the reverse sequence but at the reverse complementary sequence. Usually tools to detect ORFs have the option to look at both strands.


What happens when lightning strikes us? How is it fatal? How does a person die due to lightning? Is the cause of death similar to that due to electric shock? Why do minor shocks don't show similar effects in small magnitude (like paralysis in that part)?

Minor shocks definitely can paralyze a part!  Get on youtube and watch videos of people who cant let go of electrical wires or who are hit by tasers.

Paralyzing a part does not kill you.  Lightning can kill in two ways.

Arrhythmia.  Having arrhythmia or asystole is what kills most people hit by lighting.  As regards lesser shocks - the handymen who are hanging on to a live wire and can't let go (because their hands clamp down) can stay that way for a while.  Eventually the current produces an arrhythmia in the heart and that is what causes death.  If someone goes down this way from lighting or a lesser shock, you might be able to get them back with CPR.

When you see a whole herd of animals killed by a single strike, that is why. The heart is sensitive.  I do not understand why people's hearts do not similarly stop when they are hit with tasers.  I think sometimes they do.

Resistive heating.  Lightning can burn you.  Mostly the electricity goes over your skin and concentrated at conductors, like your phone.  That hurts but won't kill you.  Lightning going thru you can burn you on the inside which can damage your organs.  That is rare.

https://www.cdc.gov/mmwr/preview/mmwrhtml/00052833.htm
https://en.wikipedia.org/wiki/Lightning_strike


What is a selectively neutral genotypic change? I am reading the paper "Neutral evolution of mutational robustness". Because I am new to neutral evolution, I have a few questions.

Firstly, from my understanding, genotypic neutrality means the genotype is not responsible for an increase in fitness. What else can we say about genotypic neutrality? Does it have something to do with the population being randomly selected?
Secondly, how to understand a neutral network exactly? Another article says "by linking every pair of genotypes that are mutually accessible through mutations, genotypes organize themselves into neutral networks", so what means "mutually accessible through mutations"?
Thirdly, the neutral network is like an assumed black box we know nothing about, is it right? That is why in the original article with title "neutral evolution of mutational robustness", the authors mentioned that "one can infer important structural information about neutral networks from data on evolving populations."

Mutations in DNA or RNA sequences do not necessarily result in significant changes in the functions of the proteins they encode (or in the case of RNA ribozymes, ribozyme function ). This is because, for a variety of reasons, the change in DNA/RNA sequence may not significantly alter the structure and function of the ribozyme/protein (the function that contributes to the fitness of the organism). If two alleles of a gene with different sequence have equivalent function (again with regard to the function of the gene that provides fitness) the differences between them are selectively neutral.

The neutral network consists of every variation in the sequence of the gene that can be reached from another sequence (of equivalent fitness) by a single base pair mutation (these aren't the only type of mutation, possible, but they are common and more likely to be neutral than more drastic changes). So for example (using an unrealistically short sequence), if I had a gene with the sequence  0 AACAATGCTGACTGA, and alleles 1 AACAATGCTGACTAA, 2 AACAATGCTGACAGA, 3 AACAATGCTGACTGG with equivalent function, 1, 2, and 3 would be directly linked to 0 in the neutral network as they all differ from 0 by a single base pair. The sequence 4 GACAATGCTGACTAA if of equivalent function would also be in the network as it differs by one base pair from sequence 1.

Each gene in the network being mutually accessible through mutations means that I could start out with any of the above sequences and reach any of the others through a series of single base pair mutations that traverse the network (i.e. I could mutate 0 into 4 by first mutating to 1, another network member, then to 4).

The genotypic space includes the sequences of all extant alleles of the gene. This paper suggests that there is a tendency for these sequences to form these networks and especially to evolve towards highly interconnected networks. This is the structural information the author refers to. It should be easy to imagine how this might confer robustness to deleterious mutation. Let's think about our sequences from above, imagine if every sequence was only linked to two other selectively neutral sequences forming a long chain. The sequence AACAATGCTGACTGA is 15 base pairs long with 45 possible single mutations, if only two of those are selectively neutral, the chance of mutating to a neutral network member is low, and even if you do hit on a neutral mutation, your chance of hitting another neutral mutation next time (reverting back or moving on down the chain) is still only 2/45. Now imagine that the neutral network is highly interconnected, with sequence 0 linked to sequences 1, 2, 3 and several other neutral 1 base pair changes, imagine those sequences are linked through each other by other neutral intermediates (being 2 base pair mutations away from 0). Not only is the chance of a single mutation being neutral higher, but subsequent mutations (remember that these include reversions from prior mutations) are more likely to stay within the network (you're more likely to come back around to 0.

Would you have more long-term success walking around a fitness plateau or walking across a fitness rope suspended over the abyss?


Why is the probability of fixation of an allele equal to its frequency? Introduction

In a panmictic population, the probability of fixation of an allele at a neutral locus is equal to its frequency at that time. I will refer to this probability of fixation as calculated at time $t$ as $P_{fix,t}$.

If $p_t$ is the frequency of the allele $A_1$ at time $t$, then the probability of the allele $A_1$ to reach fixation (rather than disappearing) is $P_{fix,t}=p_t$. Typically, the generation when the mutation occurred, the probability of the new allele to get fixed is $P_{fix,0}=p_0=\frac{1}{2N}$, where $N$ is the population size.

Question

This simple and classic result makes very good intuitive sense to me. However, I would fail to provide a mathematical proof.

Can you please demonstrate that $P_{fix,t}=p_t$?

Several proofs are given here (p. 9). My favorite comes from the genealogical argument:

Consider the situation where there are $2N$ alleles: $A_1$, $A_2$, $A_3$ ... $A_{2N}$.

By the genealogical argument, we may state that at $t = \infty$, all alleles at this locus will be direct descendants of one particular allele present at $t = 0$.

Allelic variants at this locus are selectively neutral, so $Pr(A_{1fix})$ $=$ $Pr(A_{2fix})$ $=$ $Pr(A_{3fix})$ $= ... =$ $Pr(A_{2Nfix})$. For any given allele present at $t = 0$, the probability of fixation is therefore $\frac{1}{2N}$.

Now define allelic variants $A$ and a as complementary, non-overlapping groups of the initial alleles, such that $n_A$ + $n_a$ $=$ $2N$. From the above, the probability of fixation of an allele within group $A$ is $n_A * \frac{1}{2N} = \frac{n_A}{2N} = p_0$.


Banana cultivar identification I found a cultivar of banana that I haven't seen before (and that was significantly different from the standard Cavendish cultivar) in a market in Hong Kong today, due to the language barrier (Mandarin Chinese vs Cantonese), I was unable to ask the store owner about the name of the banana.

This is a picture of the banana, pictured next to a pack of standard AA batteries, as well as the peeled banana and a transverse section of the banana.

Can anyone identify the specific cultivar of this banana?

I found the same cultivar of banana being sold in a market while on a recent trip to Sulawesi, Indonesia. I was told by the owner that this cultivar is locally known as the pisang kepok, or alternatively the Saba banana. This cultivar is thought to originate from the Philippines.


Is diabetes (type 2) a genetic disease? My friend's father has diabetes (who was diagnosed with diabetes long after my friend's  birth). The doctor told the friend that he has more chances of getting diabetes than a normal person and he must make lifestyle changes as he is more likely to get the disease. Does it mean that diabetes is genetic (hereditary)?

The trouble with questions like this--"is this disease genetic?"--is that diseases are complicated phenotypes that arise from interactions with both individuals' genetic makeup and also the changes in gene expression that happen as a result of the environment of that individual over their lifetime.

To put it another way: neither nature without nurture nor nurture without nature are particularly interesting, because the first amounts to a little vial of DNA in a microcentrifuge tube and the second amounts to, uh, a whole lot of nothing.

In the case of Type II diabetes, there is both a strong environmental component--persistent obesity in humans is so likely to lead to diabetes that one of the two original mouse obesity model strains was named 'db' for diabetes--and also a genetic component that affects the likelihood of developing Type II diabetes in a number of ways. Some genetic variants may be less likely to develop obesity even under the high-fat diets that typically are used to create obese phenotypes in mice. Some variants may be more or less likely to develop insulin resistance even in the presence of high levels of adipose tissue. Both of these variations would affect your likelihood of getting Type II diabetes... depending on your environment and the level of body fat you carry, and that last one is going to be dependent on not only your genetic makeup but also your environment and (almost certainly) epigenetic influences from your parents.

With respect to Type II diabetes and actual specific genetic variations that have been identified, there's the twin study cited in another answer here, which was done in Danish twins and really just looked at whether there was a genetic component done at all. GWAS studies have, predictably, resulted in several candidate loci, all with relatively small effects on risk--which makes sense, because metabolism is a complex thing and many players are probably involved in competing roles. (I'd link more, but I'm new here--hitting up a Google Scholar search for "type ii diabetes genetic variance" nets you a whole bunch more GWAS studies talking about specific types of variation noted.)


Does anyone know if there is a term to describe the following process? I'm actually currently studying physics but this came up in my textbook (taken from Giancoli 7th edition section 16-10):

The random (thermal) velocities of molecules in a cell affect cloning. When a bacterial cell divides, the two new bacteria have nearly identical DNA. Even if the DNA were perfectly identical, the two new bacteria would not end up behaving in exactly the same way. Long protein, DNA, and RNA molecules get bumped into different shapes, and even the expression of genes can thus be different. Loosely held parts of large molecules such as a methyl group can also be knocked off by a strong collision with another molecule. Hence, cloned organisms are not identical, even if their DNA were identical. Indeed, there can not really be genetic determinism.

I'm aware of different biological processes that can affect gene expression but this is random kinetic motion! Would you call this one of the epigenetic mechanisms that can affect gene expression? If so it would underlie ALL epigenetic mechanisms because all molecules have random kinetic motion.

The two terms of main interest to you
Cellular noise

Cellular noise is random variability in quantities arising in cellular biology. For example, cells which are genetically identical, even within the same tissue, are often observed to have different expression levels of proteins, different sizes and structures. These apparently random differences can have important biological and medical consequences
Cellular noise was originally, and is still often, examined in the context of gene expression levels – either the concentration or copy number of the products of genes within and between cells. As gene expression levels are responsible for many fundamental properties in cellular biology, including cells' physical appearance, behaviour in response to stimuli, and ability to process information and control internal processes, the presence of noise in gene expression has profound implications for many processes in cellular biology.

There is also the term developmental noise.

Developmental noise is a concept within developmental biology in which the phenotype varies between individuals even though both the genotypes and the environmental factors are the same for all of them. Contributing factors include stochastic gene expression and other sources of cellular noise.

Developmental noise is often sounds like a synonym of cellular noise, but it is supposed to include more processes that are causing phenotypic variation then cellular noise. For example, it is common to consider "micro-environmental variation" as being part of developmental noise and not of cellular noise.
The way your phrased your question
In your question you describe only sources of cellular noise. However, you end up saying Hence, cloned organisms are not identical, even if their DNA were identical. I just want to highlight that, there are other reasons than cellular noise for which two clones differ. These include micro-environmental variance, physiological noise, epigenetic variance and macro-environmental variance (often just called environmental variance). Note that I had never encountered the term "physiological noise" before, I just made it up but I wanted to highlight that noise also happen in among cells processes, not only within cells processes.
Intro to quantitative genetics
For a short introduction to quantitative genetics and the different sources of phenotypic variance (genetic variance, environmental variance, developmental noise, etc..) and how the concept of heritability fits into this discussion, please have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?


Where can I find resources of the biological processes occurring after death of a mammal at various temperatures? Using google I usually end with results in cell death. I found some layman articles, but that does not help.
My main interest is the brain part.

I believe William Bass has written on this, probably in the Journal of Forensic Sciences, but no specific articles come to mind. I'd start by looking for his articles, then probably with a variety of search terms using a filter for that journal. It's not open access, so you'll need to use a library or institution that has a subscription.


Identify this insect - genus, species Please help identify this insect - genus, species and anything interesting about it.

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

I'm

This one is most probably a longhorn beetle (Cerambycidae). The long elytrae (protective forewings) and the long curved antennae are quite typical.

Yours looks a bit like this one: https://en.wikipedia.org/wiki/Rosalia_longicorn
It is probably a different species, though.


Green feather-like formations in tap water - what is it? (with pictures) These things recently appeared in my tap water Copenhagen Denmark, this summer 2013. They are very small, and have a feather like structure. I've called the water supply, and they thought that it was some tracer put in there by humans to trace if the warm water supply leaks into the tap water. But I could not show them the pictures.

What are they? Are they dangerous?

For size comparison: the green stuff is located on the top right of a piece of A4 paper.

I have had a biologist out taking some samples of the water. She examined them in a microscope, and identified the algae as blue-green algae/cyanobacteria. She could not identify the species further.

She said the reason probably was that my pipes where exposed to sunlight, and also that the pibes with hot and cold water ran too close to each other, creating a nice lukewarm temperature for the algae to thrive in.

I'm of course going to change the pipes :)


Effect of Western chicken and GH I heard this clause from my teacher one week ago:

  Chicken are grown in half a year until eaten in Baltic countries - Estonia, Latvia and Lithuania, for instance, [probably in other parts of Europe, too]. How do you imagine this to happen so fast? - - Growth hormones are used to grow them fast. This affects your endocrine system and can replace its natural function. We cannot even know the withdrawal symptoms when you stop eating food of growth hormones. - - Eat pork instead. No growth hormones used in their life cycle because not needed and not so useful in practice.

I started to think what. Can this really be true that the effect of growth hormones is big economically on poultry but not on pork so it is not used.
The size of chicken is small compared to pork so they have different muscular structure.
So probably more musculature in chicken and bigger effect therefore.
Why does growth hormones have bigger growth effect on chicken?

Is it true that growth hormones are used more in the growth of chicken than pork in Western countries?

I do not understand the critique presented against poultry industry here, in favour of pork industry.
Probably, there is some truth too.

Poultry raised for meat in the US (called broilers) reach butchering size in 5 to 8 weeks (compared to 10 weeks for half the size 40 years ago. It's not a GH miracle; it's a result of generations of selective breeding (as cows have undergone for unhealthy udder size).

GH use is illegal in the US and many other countries. Honestly, it's an unnecessary additive/expense.

I raised poultry for more than a decade, mostly chickens and ducks (but almost everything else as well). Once I bought 25  1-day-old broiler chicks (early broilers were a Plymouth Rock X Cornish) alongside my usual mix.  Within 2 weeks the broilers were at least 3 or 4 times the size of the other chicks, and more than a couple of them died (under ideal conditions - all free-range outside, cooped only at night). By 10 weeks, they were enormous.

They were also dumber than a bag of hammers, unfortunately. I felt so sorry for them that I let them live out their natural lives, which wasn't terribly long, partly because of their docile stupidity.

Growth hormone is unnecessary in the poultry industry.

Murray McMurray Hatchery: Jumbo Cornish X Rocks
Modern Meat Chicken Industry


Do human populations differ in core body temperature? Human body temperature is a very complex and tightly regulated system. Hypothermia or fever of only 1-2K (i.e. changes of about 5%) already cause major symptoms and changes of 3-4K (i.e. about 10%) are life threatening. Many humans live under relatively cold outside temperature conditions and maintaining an inside 36-37 degree C in these conditions is very energy consuming (most probably a reason why the body temperature in the periphery is several degrees lower), indicating very strong evolutionary constraints on not changing the core temperature too much (I remember a professor in biology classes in university saying that most fungi have a growth minimum around 37 degree C). However, other mammals have higher or lower body temperatures than humans which suggests that the 36-37 degree C of humans are not a universal gold standard (in mammals).

Probably, for a long time in hominin evolution maintaining the core body temperature was not extremely energy consuming due to tropical conditions. This could have changed during the out-of-Africa migration some 100-60 thousand years ago. Of course this is somewhat difficult assess because early modern humans started to wear protective clothing. In fact, wearing clothes is a most probably adaptive trait to save energy while maintaining core body temperature. Still, it is unclear to me whether physiological adaptations took place as well. Furthermore, there is considerable variation between individuals and also within individuals, the latter in response to environmental conditions and/or behaviour (e.g. exercise), which in principle allows natural selection to change the trait and also shows that slight shifts in body temperature are not harmful individuals.

My question is: Are there significant differences in core body temperature between human populations? Please note that my questions is not why the (average?) human core body temperature has this particular value or why it is different from other mammals or birds.

There is a somewhat related question (also on Skeptics.SE) about lower core body temperature in Japanese people. As far as I know, this difference is rather a measurement thing than a real biological difference, so my question remains unanswered.

Yes there are different physiological temperatures in different ethnicities. To know which temperature range differences are inherited and which are learnt by living in different climates requires surveys of people who are from the same region.

This study states a 0.35 degrees difference between a japanese and a malaysian, 36.95 and 37.3, it's alot.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929238/

The following study states states a 0.15 degree difference measured with similar precision,
https://www.ncbi.nlm.nih.gov/pubmed/20824480

This graph shows that the human body temperature is 36.2 at rest, at night/morning and 37.5 in the middle of the day. :
http://millar.bio.ed.ac.uk/andrewM/WE%20book99/Part2-examples.html#tth_sEc8.3.4.2

That may account for the 1 degrees difference in Japanese studies, they measure first thing in the morning/ at rest/at night, and japanese body temperature of 0.15-0.35 lower that some other ethnic groups.

There are geographic differences if you test the homeostasis response of different populations, the inner body temperature responses, the temperature of the extremities, sweating responses, the physiological responses and the blood cell characteristics.

Mitochondria has also been shown to be selected by climate type. Populations living in colder environments have lower mitochondrial diversity and that the genetic differentiation between pairs of populations correlates with difference in temperature, and they have found certain genes mutations in the ND3 and ATP6 that seem to be independantly implicated in similar climate adaptations.

The temperature is measured in lots of zones of the body and of the extremeties and the capillary flow. That doesn't account for habituation and acclimatization to tropical or northern climates.

The tropical population was found to have different thirst and sweating efficiency, and to change temperature at different rates to compensate for the same ambient conditions and exercise.

Some schools in China enforce that children run around in shorts in the snow in the winter and at playtime so that they regualte their body in the cold. Some northern people are apparently able to override the unconcsious response of the physiology that can raise body tempereture very effectively, and be able to hold in cold tanks for surprisingly long times.

Cold and hot weather are a strong force on natural selection, as illustrated by mitochondrial adaptations, because an advantageous in temperature regulation brings about a global performance advantage. The physiology of temperature regulation has been subject to many theories and studies, and they have found physiological conditionings can be honed by genetic adaptations in different populations.

Even chimpanzees have similar temperatures:

The cycles of increasing and decreasing body temperature of chimps
are exponential and symmetrical, with an amplitude of 2.6-2.9?F
(2-3 AM - 2-3 PM) and a 24-hour mean of 99.0?F, or 98.7?F. The S.D. of the 17 daily means was 0.53?F; and
of the values at any single hour, 0.63'F....Thus, in the bulk of the species the temperature ranges daily from
37.5- to 39+?C whereas the ordinary range in man is 36.5 to 37.5?C. Low
values are similarly reported for several primitive primates.

some references: http://rspb.royalsocietypublishing.org/content/276/1672/3447  https://www.jstor.org/stable/1377087

Actually this study states a 0.35 degrees difference between a japanese and a malaysian, 36.95 and 37.3, and study referenced afterwards states states a 0.15 degree difference,

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929238/

https://www.ncbi.nlm.nih.gov/pubmed/20824480


Identifying mutations in a yeast strain Cells of a triple-mutant yeast strain (leu- his- trp-) were spread
either on minimal medium or on minimal medium supplemented with
various combinations of histidine, leucine, or tryptophan. The
cultures were grown at either 25C or 37C for 3 days. Colony numbers
in each plate were counted, and the data are listed in the following
table.

What kind of mutation most probably causes the his- phenotype?What
kind of mutation most probably causes the leu- phenotype?
A.Point mutation
B.missense mutation
c.nonsense mutation
d.conditional mutation
e.deletion mutation

My questions : What is the meaning of confluent in this context ? Can anyone give me a hint to solve this question ? I have no clue how to solve this.

For starters, you can just google "confluent".  It means that there are no colonies, but that the cells cover the whole plate.

So when you provide all three amino acids, the cells fill up the whole plate.  If you leave His out, but keep the plate at 25 degrees, the plate still fills up with cells, so the His- allele isn't hurting the cells at all at 25 degrees, but it's pretty nasty at 37 degrees.  That makes it conditional; the mutation only impairs His metabolism at some temperatures.

There is not a single cell which is surviving a lack of Leu, but there are some which are surviving the lack of Trp, and the lack of His at harmful temperatures.  Presumably, those are the small number which are lucky enough to acquire mutations which compensate for the original deleterious alleles, but NO cells were able to overcome the problem with the Leucine metabolism.  This suggests that the Leucine mutation might be a total deletion.


How does the drug MBC effect the depolymerization of microtubules in eukaryotic cells? I have tried to look for the mechanism of how methyl benzimidazol-2-yl-carbamate affects microtubules in eukaryotes, but what I found wasn't very useful:

Quilan et al 1980 assert that it acts by inhibiting polymerization of microtubules rather than by directly depolymerizing them.
In "The Cytoskeleton: A Target for Toxic Agents", it is mentioned that

  ..strains of Aspergillus that were resistant to the drug had a lower affinity for MBC in a binding assay, whereas super-sensitive strains had a higher affinity for the drug.

Any references would be appreciated.

In Summary: I would like to know how the drug MBC effects the depolymerization of microtubules in eukaryotic cells. I would also appreciate any scientific references.

Carbendazim inhibits microtubule polymerization by directly binding to tubulin, preventing subunits from interacting. Therefore, mytotic spindle malforms and potentially causes aneuploidy in affected cells. Mechanisms of resistance are often shown to be changes in membrane permeability to the compound.

CARBENDAZIM (addendum)


Are epigenetic changes involved in evolution? Evolution leads to phenotypic changes through changes in DNA such as mutations. Mutations are transmitted to offspring. Cumulative mutational changes across many generations may cause evolution and speciation.

As far as I know, epigenetic changes causes an individual to change in how it appears (phenotypic changes). In turn, epigenetic changes may be transmitted to offspring, just as DNA mutations can be.

Is epigenetics a factor in evolution?

To start I will repost some of an answer I have previously posted, which will explain what evolution is:

Evolution is simply a process of change.  It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection.

  "Evolution means change, change in the form and behaviour of organisms
  between generations. ... When members of a population breed and
  produce the next generation we can imagine a lineage of populations,
  made up of a series of populations through time. Each population is
  ancestral to the descendant population in the next generation: a
  lineage is an ancestor-descendent series of populations. Evolution is
  then change between generations within a population lineage." - Ridley,
  Evolution

Your Answer:

Evolution depends on the inheritance of information from the ancestral population to the descendant population. Much of the time we talk about information in the form of genetic variation, the information contained within the DNA. However, more and more we are realising that other forms of information transmission can occur, including epigenetic effects, and that these can contribute to evolution.

  "Epigenetic modifications are a bit like ornaments on a Christmas
  tree; the tree (the DNA sequence) is still the same, but the
  decorations (epigenetic modifications) change how it's perceived." ...

  "Over the past few years, several studies have compared the epigenetic
  modifications of our genome with that of other great apes, leading to
  an emerging picture of the importance of epigenetics in our recent
  evolutionary history." ...

  "The role of epigenetics in evolution (particularly primate evolution)
  is an active and exciting area of research..." - Nature Scitable


Why does NaCl react differently with a boiled potato and with a raw one Well my question is based on this question down below.

For those who don't speak german:

You have two potato slices one of them is boiled the other one is just raw.

Now you scatter some salt over both surfaces of the two different slices and wait about one hour.

After the time is over the salt on one potato isn't in his crystalline formation anymore.

So my question is why are behaving both slices different?

My guess is that the carbohydrates ( Starch ) reposition and the starchcores bind with H2O.
So the H2O binds with the NaCl?

I would really enjoy it when somebody could tell me the chemical reasons why this happens.

Maybe this passage is referring to this experiment?

The key missing from your description is that each potato is placed in water. When the cells are intact (unboiled), this causes water to flow into and out of the cells via osmosis: into the cells from the tray of water, and out from the cells into the salt. Once the cells are destroyed via boiling, there are no intact membranes to cross to osmosis does not occur and the salt remains undisturbed.


How deep underwater could you breathe using a tube which breaks the surface until the water pressure makes it impossible to inhale air? I'm struggling with a question asking how deep you can breathe underwater using a hollow reed before the water pressure makes it impossible to inhale. The question asked to use this data of maximal respiratory pressures:

The question also gave a hint that for every metre below the surface, hydrostatic pressure increases by 100 cm H2O.
I'm seriously lost on this question, from my research, all I could find was that a difference of approximately 50 cm H2O is needed in order to inhale, but I'm unsure if that is information I should deduce from the table instead of looking up. Even knowing that information, how would I then find out how deep that means you could breathe? Any help would be greatly appreciated.
Thanks

First, a sanity check.  Snorkeling isn't generally done at much depth, and this question reflects some subjective sense of that.
My guess (after much confusion) is the table they're providing is apparently the pressures that the subjects were able to apply, when striving to breathe in or out at various levels of "Lung Volume".  But what is "Lung Volume"?  Not Total Lung Capacity - is it Tidal Volume, Expiratory Reserve Capacity, something else?
If I read it that the person, at 22-54% "Lung Volume", can apply only 53 cm H2O of pressure differential while inhaling, that implies that at this depth of external pressure, they can't inhale.  (Oddly, if they lose the battle and go to 1%, the data says their ability to inhale is reduced!) In theory the fluid pressure of water or air on the body should be similarly positioned.
Even so, there are two things that make me doubt this.  First, the inability to inhale should be coupled with a greater ability to exhale.  So I still wonder if sort of shallow breathing might still be possible at the limit of the expiratory reserve, or even in the range of "residual volume", as the external pressure is opposed by connective tissue.  Second, the diaphragm and the external intercostal muscles are, well, muscles, so it should be possible that someone could train those muscles well and resist more pressure.


Do all cells of a plant contain chloroplasts? If the answer is no, then how do plant cells tell whether they need to keep chloroplasts or not? What kind of signals are used, and how are chloroplasts eliminated?

Not all cells of the plant contain chloroplasts, but they all contain some form of plastid. When the plant is its development state, they contain proplastids which may turn into chloroplasts if the cells are exposed to light. Other forms of plastids may play a role in storing lipids, amylum or proteins and they form because there is a lack of light (these are present mostly in roots). Chloroplasts are not eliminated from the cell.
 Here you have a helpful wikipedia image:

This is a very general explanation though and you should look more into hormones and specific triggers for the formation of chloroplasts.
Article talking about chloroplasts biogenesis


Role of Intermediate Filaments in cell - cell signalling A passage in my textbook mentions briefly that the role of intermediate filaments in the cytoskeleton is to enable cell to cell signalling by extending between special junctions and alowing cells to adhere to basement membrane

What does this mean?

There are desmosomes and gap junctions (cell-cell-contact), and hemidesmosomes (cell-basal membrane-contact) which enable a stable united cell structure. I'm not so aware with this topic, but I found some papers which may help you :)

Intermediate filament in cell architecture

Desmosomes and hemidesmosomes

Review on gap junctions

Blood-testis barrier and different cell-cell-contact structures


What is mold detection threshold in humans? I managed to find primary taste detection thresholds, e.g. for sweetness it's 1 part in 200 of sucrose in solution.

Recently I've noticed that I can detect mold smell/taste even if there are no signs of product getting spoiled.

What is the mold detection threshold in humans, and is that a dangerous amount?

It depends on the mold. For example, humans can smell octenol in ppb concentrations[1], presumably long before any toxic effects of this or other compounds produced by molds. Octenol is produced by many molds, always through breakdown of linoleic acid (part of many triglycerides, i.e., fatty oils present in most food).

Update: another example of a non-toxic mold is that causing cork taint. The responsible substances (trichloroanisoles, TCA) can be tasted by humans in wine at 2-4ng (nanograms) per liter wine.[2]

[1] M. J. Saxby: Food Taints and Off-Flavours., 2. ed., Springer 1995, ISBN 978-0-7514-0263-6, S. 210–212.

[2] http://schaechter.asmblog.org/schaechter/2018/07/tainted.html


Forward or Reverse Strand: Is there a difference when encoding genetic devices? Background:
In synthetic biology, and also in nature, there are lots of examples of genes in both the forward and reverse orientation. It seems in synthetic biology/bioengineering, most genetic devices are, by default, encoded on the forward strand unless there are concerns of readthrough from one expression unit to another, in which case one of the expression units is included on the reverse strand like below:

It also seems that genes are sometimes in the reverse orientation for no apparent reason, especially in plasmid backbones:

The Question:
My question is, ignoring issues of potential readthrough, does it matter which strand a genetic device is encoded on? So in the example below, would there be any difference between A and B, or does it not matter? Also, does whether it's on a plasmid compared to a genome matter? I'm specifically interested in bacteria here.

This seems like it should be a simple question to answer and I'm sure I'm just missing something, but I can't find anything about it.

First, I think you have misunderstood the concept of sense/antisense. These are defined individually for each gene, with the sense strand always referring to the coding (non-template) strand of a gene, and the antisense strand to its complement, the non-coding (template) strand. So in your plasmid example above, all genes are encoded by their respective sense strand, but which of the two strands that is sense for a given gene depends on its orientation. There is therefore no biologically meaningful sense/antisense concept for entire genomes, chromosomes or plasmids. Read more in the Wikipedia article on sense, and the answers to this SE Biology question.
Having said that, it should be clear that the expression cassettes pictured in figues A) and B) are completely identical. If you ignore the context around them (e.g. readthrough), their direction is irrelevant.

It also seems that genes are sometimes encoded on the reverse strand for no apparent reason, especially in plasmid backbones

Many commonly used plasmid backbones derive from vectors that date many decades back, to a time when cloning strategies were far from as flexible as today. Researchers were generally limited by the restriction sites occurring naturally in the DNA sequences. A gene's position and orientation with respect to its neighbouring genes might therefore be the simple result of lack of other cloning options - although I honestly doubt "wrong" orientation would even have been considered an issue. For an example you could read about plasmid pBR322 in this Wikipedia article, and references therein.


What species would this be? A common way to define species can be found on Wikipedia:

  A species is often defined as the largest group of organisms in which any two individuals of the appropriate sexes or mating types can produce fertile offspring

This got me thinking. Imagine the case where we have three "groups": A, B and C, where A and B cannot produce fertile offspring together (different species) but C can produce fertile offspring with both A and B.

Have this ever been observed? And how would you classify C?

What you describe is called a ring species. From wikipedia:

  In biology, a ring species is a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" population.1 Such non-breeding, though genetically connected, "end" populations may co-exist in the same region (sympatry) thus closing a "ring".

  Have this ever been observed?

While ring species is a classical theoretical concept, the cases of ring species is often open to some interpretation and limit case of what we want to call a ring species.

The question has been asked at Do ring species exist?, however the post is still left unanswered.

  And how would you classify C?

There is no obvious simple way to answer that question. The concept of ring species just shed light into the fact that the concept of species is an outdated concept and does not have a good formal definition. For much more discussion about the concept of species you should definitely have a look at the post How could humans have interbred with Neanderthals if we're a different species?.


Identification of Bug/Insect (with picture) What is this insect?

I’ve seen a lot of them indoors. The most distinctive characteristic is that single, orange dot in the middle of the back. The picture was taken in Louisiana, USA.

It is a cockroach, probably a German cockroach nymph.

Cockroaches are well-known pests. According to the Wikipedia link above, there are about 4600 species of cockroaches, 30 of them are associated with human habitats. Cockroaches are extremely resistant and are able to survive in a wide range of environmental conditions.

@PhysicalFatness pointed out that German cockroach nymphs look very much like your picture and it is likely the species that you've found. Don't be fooled by its name German cockroaches are found all over the world, not only in Germany.


Why is HPV vaccines targeted for preteens? Why is human papillomavirus products targeted to children before sexual activeness? Could all ages benefit from this vaccine even if they may have or have not contracted a form of HPV to prevent other forms of HPV?

https://okinawa.stripes.com/community-news/preteens-teens-target-audience-hpv-vaccine

I could not find anything where it says it is more effective on younger people vs older people.

A lot of sexually active adults carry one or another strain of HPV but most do not develop cancer. You can carry HPV — and spread it to others — without showing any symptoms yourself:

  HPV infections are so common that nearly all men and women will get at least one type of HPV at some point in their lives. Most people never know that they have been infected and may give HPV to a sex partner without knowing it. Nearly 80 million Americans are currently infected with some type of HPV. About 14 million people in the United States become newly infected each year.

There is less reason to give a vaccine to someone older, generally, who is almost certain to be infected with some form of HPV. A vaccination is not a broad cure, though it can provide some protection against infection from strains of HPV that someone is not already infected with:

  But the vaccine also offers some protection for HPV-positive women, reducing cervical lesions by 17% and genital warts by 35%. HPV-positive women usually aren't infected with all four of the targeted strains. In clinical trials, those infected with one or more of these strains before vaccination were protected against the remaining ones.

Pre-teens are unlikely to be infected with any forms of HPV, having no or much less sexual contact, and so they are the best candidates for being administered the vaccine.

This cohort will get the most protection from those strains that the vaccine protects against, strains which are most likely to cause relevant cancers.


What is the name of this yellow flower? India, It was growing outside.

April 2017

Center part of the flower giving me Heebie-jeebies.

I think this is Cosmos sulphureus which is also known as yellow cosmos or sulfur cosmos. See the image (from here) as comparision:

More information can be found here and here.


Are Young Girls Stronger than Young Boys? According to "common wisdom" the average man has, as a proportion of his body weight, 50% more muscle mass than the average woman. This is in addition to how the average man is several inches taller than the average woman and thus has a larger body mass to take that proportion out of.

Notice the above is phrased in terms of men and women as opposed to boys and girls. I am interested in how strength compares at a younger age. If we took the average ten-year-old boy and the average ten-year-old girl $-$ before the first growth spurt of puberty $-$ and compared their proportional muscle masses, how would they compare? Have any studies been carried out?

Looking for information online about this nets me a hundred accounts from men who remember how, as children, they lost every fight with their older sister. The problem here is that in any contest between siblings (twins excluded), the older sibling most likely has a height and mass advantage. So it's hard to say much about proportional muscle masses.

My guess is that if we took twins Bill and Roberta then they would have similar muscle-mass proportions up until about age 10. From then Roberta would have a growth spurt and increase proportional (as well as absolute) muscle mass due to extra testosterone (in addition to extra estrogen). A few years later Bill would have a growth spurt and increase proportional muscle mass to exceed Roberta's. But she would still be stronger than him, until he caught in terms of height.

Here's a study comparing performance in swimming. Before age 8, there's no difference; from age 11-12, there's some small difference, after age 13, there's a large difference.

https://www.eurekalert.org/pub_releases/2012-05/iu-wsg052512.php


Why a brain's hemisphere controls the opposite side of the body? As a physics student with very little understanding of biology, in a course about physics foundations diagnostic techniques I have come up with this question. I don't even know if it does make sense or not; in the latter case, please excuse me.

As far as I know, in the human brain the right hemisphere controls the motion of the left side of the body, while the left hemisphere controls the right side. Moreover, the part related to sight is on the back of the brain.

To me, it seems that there is a sort of opposition between the part of the body considered and the area of the brain that have to control it. Is this statement right? Only for human beings or also for animals? Are there any exception to this sort of pattern (if there is anyone)? Is there a logical reason to the fact that we show this characteristic and it couldn't be different from how it is?

"How" is easy to answer (signals from the right side of the body cross the midline and end up in the left cerebral hemisphere; answered well in a previous question). This pattern of wiring appears to have existed since bilateral symmetry first evolved.

"Why" is not a well-defined question; the possible evolutionary advantage gained by having cross-wiring is unclear.

To answer your explicit question: there is no "opposition" in any meaningful sense between the location of a sensory nerve on the body and the location at which the information is processed in the brain. There are a raft of visual areas in the neocortex, spanning from the back but extending forward. The areas that control eye movement are much more frontal ("frontal eye fields"). Before arriving in the neocortex, signals from the eyes pass through the dLGN, a nucleus in the thalamus which is a subcortical structure closer to the middle of the brain than the rear. This flow of visual information is similar across many (most? all?) mammals.


Why swordfish aren't put in the same family as Marlins? Why Swordfish (Xiphias gladius), which are very similar to Marlins, do not belong to the same family as Marlin - Istiophoridae?

Both has long bill or a sword in the upper jaw, both has (at least in some stage of life) a long sail along the back, both are predators and fast swimmers and both are of similar overall shape and size.

Moreover, as cladistics is prevailing over Linnean taxonomy, the ranks of family or superfamily are not essentially different, can we say that swordfish and marlins belong to the same clade which includes the two families Xiphiidae and Istiophoridae?

Why Swordfish (Xiphias gladius), which are very similar to Marlins, do not belong to the same family as Marlin - Istiophoridae?

The decision about what we call an order vs a family is very subjective. Someone decided that Istiophoriformes was an order containing the families Xiphiidae and Istiophoridae but someone else could have decided to call Istiophoriformes a family (although the name would have ended in -idae, then) and Xiphiidae and Istiophoridae subfamilies.

  [C]an we say that swordfish and marlins belong to the same clade which includes the two families Xiphiidae and Istiophoridae[?]

Yes, you can. This clade is the order of Istiophoriformes. You can hence say that swordfish and marlins are both Istiophoriformes. Or if you prefer, you can say that swordfish and marlins both belong to the order of Istiophoriformes.


Why might long telomeres be selected for in laboratory mice? In a recent episode of The Portal, Eric Weinstein sits down with his brother Bret Weinstein to discuss Bret's Reserve-Capacity Hypothesis. It's an incredible story of scientific discovery and and academic injustice.
One prediction of the hypothesis was that laboratory mice, known at the time to have abnormally long telomeres for their lifespan, were not a representative sample of the wild mouse population because the environment the lab mice were being bred in was selecting for longer telomeres. This had serious implications for drug safety testing.
My surface level understanding as a non-biologist from listening to the Podcast goes like this. Please point out any misunderstandings.
Antagonistic Pleiotropy Hypothesis for Senescence
George Williams predicted that pleiotropic (multi-purpose) genes which are advantageous early in life but detrimental later in life will be selected for in nature since organisms often die or reproduce long before the disadvantageous effects manifest themselves. This is an evolutionary theory for aging, which argues that trade-offs exist between early life and later life fitness. This effect was observed, but no gene had been known to be the cause. This was the "missing pleiotropy".
The Hayflick Limit
Telomeres are repeating, non-coding regions of DNA at the end of each chromosome which aid in cell division. Each division, the telomeres shorten. Telomeres are counters of sorts, which provide a hard limit (the Hayflick limit) to the number of divisions a cell can undergo. Any cell that started dividing uncontrollably (cancer) would eventually reach its Hayflick limit and die. Aging (senescence) is the manifestation of cells in an organism reaching their Hayflick limit.
The Reserve-Capacity Hypothesis
This is Bret Weinstein's work. The way I understand it is that Weinstein pointed out that the missing plyotropy was not a gene at all, but telomeres. Weinstein observed that there existed a trade-off which was reflected in telomere length. Long telomeres allow cells to repair themselves many more times, slowing the effects of aging, but simultaneously leave the organism vulnerable to cancer, as cells which begin to divide uncontrollably will never reach their Hayflick limit. The length of telomeres is the result of a trade-off between dying of cancer, or dying of old age.
The JAX Lab Scandal
One critical prediction of the Reserve-Capacity Hypothesis was that mice (which were at the time thought to have abnormally long telomeres for their lifespan) don't naturally have long telomeres. Instead, it was specifically the mice coming from the Jackson (JAX) Laboratory (which supplied a significant percentage of North America with mice) which had abnormally long telomeres. Since JAX Lab had economic incentive to breed as many mice as possible as quickly as possible, they were artificially introducing selective pressures on the mice. Namely, the pressure of breeding the mice early in their lives. This meant that any late-life disadvantages, such as susceptibility to cancer as a result of longer telomeres, were not playing an important role since the mice were bred well-before they were likely to develop cancer. Since telomeres are a non-coding region of the chromosome, variation can happen very rapidly (no need for the traditional timescales of Darwinian selection). Over time, long telomeres became dominant in the mice population, and so research being done on mice purchased from JAX lab concluded that mice had very long telomeres.
The primary gap in my understanding is the following. Why was it that longer telomeres were selected for? It is unclear to me how discounting the late-life disadvantages of long telomeres would result in long telomeres becoming dominant in population. If anything, telomere length should become irrelevant. If so, we'd see a wide distribution of telomere length. That is, unless longer telomeres provide benefits to organisms early in life. Is that the case? If not, how can we explain long telomeres becoming not just common, but dominant?

Their arguments for increased telomere length in lab mice are:

Rate of tumour formation is dependent on the number of cells within an organism. Additionally, tumours take time to form. Therefore, small animals that only need to reproduce early in life, like lab mice, are less prone to tumours and there is then less selective pressure favouring telomere shortening.
Senescence has a negative effect on reproductive success, even early in life, and there is therefore selective pressure favouring increased telomere length that reduces senescence.
While the lack of selection on senescence due to the short window for reproduction could have the opposite effect of reducing telomere length, point 2 is the dominant factor.

To be frank, this all sounds extremely speculative to me and the supporting evidence they did provide was not entirely convincing (though I am far from an expert in the field). Keep in mind that it’s a hypothesis only.

In case you don’t have access to their article, I quoted the relevant section below:

  The unusual telomere system of lab mice may be an unintended consequence of captive breeding. Retirement of breeders after 8 months eliminates selection on late-life effects. Tumor-forming mutations take time to occur, tumors take time to become lethal, and the likelihood of tumor initiation is presumably a function of the number of cells in the body, so in small bodied animals like mice, tumors may be rare and inflict minimal cost in the first eight months of life, even absent a telomeric fail-safe. Further, selection for sustained high reproductive output (beginning early and maintained for 8 months) should strongly favor a reduction in senescent effects occurring in that window. Selection acting to eliminate senescent effects and increase early reproductive output may tend to elongate telomeres. Because of the inextricable connection between tumor suppression and somatic maintenance, telomere elongation should dramatically increase the risk of eventual tumor formation, but any effects manifesting after the breeding cut-off will be selectively irrelevant. By our model, selection for early high rates of reproduction in the absence of selection for longevity or tumor suppression should produce long telomeres and a strong propensity for eventual tumor incidence. Despite diminished senescence, we expect these mice to have reduced maximum longevity compared to wild conspecifics. At all ages, lab mice (with elongated telomeres) should be more likely to die of tumors than wild mice. These mice should also be unusually resilient to somatic damage and show few signs of aging other than tumor formation.

  ...

  The hypothesis that an 8 month breeding cut-off should select for non-senescent, tumor prone mice seems paradoxical. One might expect the elimination of selection on late life effects to accelerate senescence, not retard it. But in lab mice, selection for high, sustained rates of breeding appears to be the dominant factor. The tumor fail-safe has effectively been turned off, condemning these animals to form tumors, but leaving an early-life window of reproduction within which there is minimal senescent decline.


Why do humans masturbate? Why does masturbating seem to be like an addiction?

What controls or initiates the urge to masturbate?

Is it good or bad or both and why is it so? I have heard guys who say that the do it regularly. Also there is a relaxing feeling; what generates that?

One word. DOPAMINE

See this article on Reward System and this one on Dopamine Those basically answer your question as to addiction, urge, and feelings of relaxation.

There is absolutely nothing wrong with masturbation, so long as you realize that it is a healthy expression of one's sexuality, that is observed, quite frequently, in our nearest relative, the Bonobo. There is no shortage of the study of primate masturbatory practices in the literature, and one could make a career out of its scientific study and analysis, so if you are interested in learning more, conducting a Google Scholar search on Primate Masturbation should give you literally years worth of reading material.

As for an actual addiction, it would only develop into a pathology if it became disruptive to one's life and was pursued at the exclusion of other basic activities.


Difference between Sphyraena obtusata and Sphyraena novaehollandiae "Striped barracuda" is the common name for both Sphyraena obtusata and the Sphyraena novaehollandiae.

Here's links to both fish species from fishesofausralia.net: S. novaehollandiae and S. obtusata

Are they the same fish just found in different parts of Australia, or are they completely different species? If they are different species, what is the difference between them?

I think you may have looked at these species too quickly.

They are in fact different species.

Sphyraena obtusata is referred to as the obtuse barracuda, the striped barracuda, or various other names that your linked website (fishesofausralia.net) provides:

  Dingo Fish, Obtuse Barracuda, Pike, Sennit, Short-finned Seapike, Short-finned Sea-pike, Short-jawed Sea-pike, Striped Sea Pike, Yellowstripe Barracuda, Yellowtail, Yellowtail Barracuda, Yellowtail Sennit

Sphyraena novaehollandiae, on the other hand, is referred to as the Australian barracuda, arrow barracuda, Australian sea pike, sea pike, snook, or shortfin barracuda.

Even your linked post doesn't provide "striped barracuda" as a common name for this species.

Differentiating the two species:

Your fishesofausralia.net links demonstrate these fish are found on different sides of Australia (S novaehollandiae in the south and S. obtusata in the North of Australia.

The Wikipedia articles for these fish (linked previously ion my answer) indicate that S. obtusata only reaches maximum lengths of 55cm, while S novaehollandiae can reach sizes exceeding 1 meter.

Both sources also list a number of additional color and morphological variations you can use to differentiate the two species.


Can DNA be denatured at acidic pH? Some say that DNA is denatured only at basic pH. And some say at both acidic and basic pH. So I want to know clearly why and how if DNA is also denatured by basic pH.

Alkaline denaturation neutralize the charge of acids but also cause hydrolysis of bases upon prolonged treatment. Strong bases will raise pH until the H+ shared between the N-base electronegative centers (N-H and O=) is stripped from the H-bond, effectively breaking them.

Organic solvents such as dimethyl sulfoxide and formamide, or high pH, could break the hydrogen bonding between DNA strands too. Low salt concentration could also denature DNA double-strands by removing ions that stabilize the negative charges on the two strands from each other.

Low pH (less than pH 1): both RNA and DNA hydrolyze (phosphodiester bonds break and the bases break off).

High pH (greater than pH 11): RNA hydrolyzes, DNA will denature but the phosphodieser backbone remains intact.

[salt]
Tm is sensitive to Na+ concentration.
Na+ acts to shield the negative charges of the sugar-phosophate backbone from interacting with one another. The repulsion between the negatively charged phosphate backbones is the major force destabilizing the double helix, therefore increasing Na+ concentration increases helix stability and decreasing Na+ concentration decreases helix stability.

References:

http://faculty.tru.ca/dnelson/courses/biol335/335notes/3recdna/4-hybrization/recDNA3a.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1367631/pdf/biophysj00681-0002.pdf


Could someone help me identify this insect from Malaysia? Could someone help me identify this insect? My grandfather went on holiday to Malaysia and found this interesting beetle it looks like and has been trying to find out what it is, he placed it in resin to preserve it and I was hoping someone might have the answer to what it could be. The beetle itself is about two inches long and is mostly a vibrant yellow. and sorry the picture is so blurry

That is Catacanthus incarnatus (Pentatomidae). http://cyy4993.blogspot.com/2012/11/stink-bug-pentatomidae-catacanthus_17.html
http://eol.org/pages/3685880/overview


Identification of South Indian plant I'm from South India and I'm having quite a fuss identifying this plant. It has totally transparent stems, and when I break them, water squeezes out. My local friend tells me that this was used in the olden days to clean slates. It has a bit fat stem. And another thing about this plant is that when you soak it in Ink, you can see the ink travelling up it. That's why it is so transparent.

I heard that it is locally called Mashithandu and I searched all  over the net for it, but can't find a name except that. I'm really sorry I can't add a photo. I'll see what I can do.

I presume you are talking about Peperomia pellucida. It is called  Mashithandu in Malayalam.

Reference: Wikipedia

You might like to go through this.

  Description

  Delicate, glabrous annual herbs; stems erect, 5-30 cm tall, pellucid,
  branched when well developed.

  Global Distribution

  Native of Tropical America; now Pantropical

  Indian distribution

  State - Kerala in all Districts


What is an epistasis group? I have been trying to wrap my head around the concept of epistasis for a couple of days now, and I think I understand it, at least at a basic level, but I still don't understand some of the ways that the term is used.

What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed? or is there more to it?

Also, what does it mean when genes are in the same epistasis group? I am currently studying the transcriptional up-regulation of PSY3 in yeast as a result of UV treatment. PSY3 codes for a protein that forms the Shu complex along with 3 other proteins. One paper I am reading states that PSY3, is in the same epistasis group as the three other genes that code for these other proteins. What does this mean?

What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed?

Yes.  Note that this does not say anything about mechanism. If A converts 1 to 2, and B converts 2 to 3, then A is epistatic to B, but A is also upstream of B.  In a signaling pathway, say B inhibits A and prevents it from signaling. A mutation in B allows A to signal. A mutation in A means there is no signaling. Mutations in both A and B means there is no signaling: A is epistatic to B, but A is downstream of B.

An epistasis group is a group of genes in the same pathway.  Knocking out any combination of these genes will not result in a more severe phenotype than knocking out the most "sensitive" of these genes (the single mutant with the most severe phenotype).


Do model species evolve away from Batesian mimics? Batesian mimics - palatable mimics of a poisonous species - are detrimental to the species they imitate. Predators learn which species are unpalatable by tasting some. If Batesian mimics are rare or nonexistent, few if any of these samples will be tasty and predators'll quickly learn to leave this species alone.  But if Batesian mimics are common, predators have good chance of being rewarded for attacking things that resemble the model species.  It would seem that an overabundance of mimics would create a condition for the model species to evolve to visually differenciate itself: is there any evidence that this occurs?

I have found some papers that support the hypothesis that an overabundance of Batesian mimics creates a condition for model species to evolve differentiating characteristics -- in particular,  Franks, D. W., G. D. Ruxton, et al. (2009). "Warning signals evolve to disengage Batesian mimics." Evolution 63(1): 256-267.

The authors argue that new conspicuous traits in unpalatable species evolve in response to mimicry, since a mimic that evolves conspicuousness without being a good-enough match pays full cost of conspicuousness without the benefit of its predator learning advantage.


Do skin mites reproduce on human face during night? I've seen this circulating on social networks:

I was wondering to what extent is it true. Do skin mites really get on the skin surface to reproduce? Why is it so?

Yes, it is true that these mites exist on healthy human skin, on >98% of people, no matter the country or hygiene.

However, I'm sorry to say that this photograph is not the follicle mite Demodex folliculorum. This image has been widely circulated around the internet as Demodex, but it is actually the head of a silkworm, Bombyx mori. The above version has been modified slightly from the original, but you can see the original here: https://www.sciencephoto.com/media/720736/view/silkworm-head-sem

And here is a zoomed out version of a silkworm: https://macrocritters.wordpress.com/2012/11/26/photographing-down-the-food-web-silkworms-bombyx-mori/

You can find a real close-up of Demodex here: https://www.sciencesource.com/archive/Demodex-folliculorum-(SEM)-SS2367855.html


What is this snail? (Location: Bangkok, Thailan; size: 3 cm long, 5 mm wide; color: mostly black) What is this snail? (Location: Bangkok, Thailan; size: 3 cm long, 5 mm wide; color: mostly black)

Video:  https://youtu.be/vxig5QOSoss

Possibly Macrochlamys indica or another species in the same genus, based on shell morphology.

Source


Why do people eat meat? My main question is why do people eat meat?
Can we not survive without meat?

I recently became a vegetarian and I have not yet felt any impact on my health. Can any one explain this phenomenon from the perspective of nutrition?

There are many reasons for why people eat meat. Some of them are to be discussed here and some of them have nothing to do with biology.

Reasons that have nothing to do with biology

There are many reasons that are not to be discussed on Biology.SE. These include cultural reasons, the reasons related to taste and appreciation, farming and availability, price and economy and of course for reason related to political ecology (incl. water and energy consumption of meat production).

Reasons that has to do with biology / medicine

We can talk about nutritional value though. According to a number of websites (sorry nothing peer reviewed; monitor.co.uk; rd.com; sparkpeople.com), people not eating meat may suffer from lack of

protein
iron
zinc
calcium
vitamin D
vitamin B12
omega–3 fatty acids

It is not impossible to get all of these nutrients without meats. However, when becoming vegetarian, some people need to be careful and rethink their diet to ensure not to suffer from the lack of these nutrients.


Population where most of the newborns die soon? Is there an ecological name to describe a population of organisms where most of the newborns die after birth without reproducing? The population as a whole keeps growing, however, because there are enough individuals that manage to reproduce.

Yes, we talk about r/K selection theory:

  In ecology, r/K selection theory relates to the selection of combinations of traits in an organism that trade off between quantity and quality of offspring. The focus upon either increased quantity of offspring at the expense of individual parental investment of r-strategists, or reduced quantity of offspring with a corresponding increased parental investment of K-strategists, varies widely, seemingly to promote success in particular environments.

The type of species you describe are the r type.

Please note the following potential confusions:

A species can vary its strategy through time and space

Species can change from K to r (and vice-versa) depending on the environment and number of individuals. Consider humans as an example.

The expression r/K selection theory can be misleading

The term "selection" in "r/K selection theory" can be a bit misleading as it refers more to a demographic reality (which has come to be due to selection pressures) but not to the selection process behind it.

Alternative meaning of 'r/K selection theory'

The terms r and K are sometimes used to mean whether a species has reached carrying capacity (K) or whether they are growing in number (r) which is not exactly the same as the interpretation of whether there is much parental investment in the species presented in the wikipedia article.

This second interpretation is actually closer to the origin of the terms r and K. The most common (and one of the simplest) equation of population growth through time is the logistic equation (see here for an easy explanation and also wiki > Population ecology )

$$\frac{dN}{dt} = rN \left( 1 - \frac{K}{N}\right) $$

, where $N$ is the population size, $t$ is time in generation, $r$ is the maximal growth rate and $K$ is the carrying capacity. On the graph above, $r$ represent the maximal slope (that is the maximal growth rate).

r selected species are those that have a growth rate as indicated at the center of the graph. K selected species are those that have a growth rate of 1 (no increase in $N$) as the ones that are at carrying capacity $K$.


The Relationship between Copper and Alzheimer's Disease I've been reading up about the research concerning the etiological factors behind Alzheimer's and I came across two papers - "Studies on Copper induced stability changes in DNA fragment (GCA ATC TAA TCC CTA): Relevance to Alzheimer’s disease" and "Copper interactions with DNA of chromatin and its role in neurodegenerative disorders." The issue I'm having is that the papers suggest that copper causes the DNA's double helix to unwind in some parts, and it causes it to coil more tightly in others (the fluorescence and circular dichroism research supports the latter).
My question is this: do high concentrations of copper cause DNA to unwind or coil more tightly?
If you could provide any help, I'd be very grateful, as I feel like I'm be missing something obvious.

I found your second reference online, which says

Hydrogen bonds are disrupted by the process of partial unwinding which induces structural changes such as loosening of base–base interaction, base tilting and destabilization of the DNA double helix leading to DNA denaturation [17]. The destabilization was due to most probable binding sites in DNA such as Cu2+ to N7 of guanine and N3 of cytosine in line with our present results and with the predictions of Eichhorn and Clark [18], [19].

With this in hand, we can Read The Friendly References.  #18 is on PMC and gets the first look - they say "perhaps the structure is"

The other references are less helpful for me right now - #17 is a paper from 1971 that's not online and never will be, and #19 talks about histone H1 blocking the copper interaction.
Now what I see here is only unwinding, and is dependent (as proposed) on the presence of G-C base pairs in the sequence.  So far from what I've seen, this is based at interactions at around 0.1 mM in in vitro studies, so I feel like it is possible a physiological situation could involve a completely different mechanism.
After writing the above, I found the other paper in Young Scientists Journal - it is quite a remarkable thing to consider.  The author is a 12th-grade student from Panama who was doing (among other things) a circular dichroism study and molecular docking with Discovery Studio 3.5.  Statistics is lacking and the experiments aren't very well integrated, and the model from the software, which doesn't agree with the image above (it doesn't bind a ring nitrogen in the cytosine), doesn't seem to be tested by the lab data.  Despite the sophistication of the software I'm afraid I'm about as skeptical as I was the first time.  Still, there is some Ph.D.-level thought there, using some methods that American undergraduates rarely access, conducted by a university in Panama with support from an Indian research institute.  Educationally, fascinating.
But I don't see much support for the interpretation in that paper that the DNA coils more tightly.  The fluorescence experiment suggests a competition between copper and ethidium bromide, but knowing what actually happens is another story.  The CD study ... well, some shifts are identified, one one way and one the other, but I don't see how they prove the DNA is coiling more.  But maybe I'm missing something!


What are some (bioinformatic) methods to characterize potentially novel gene transcripts? I am working with a few novel transcripts of genes- before I confirm their existence experimentally, I would like to perform some bioinformatic analysis. I have already considered coding potential, protein domain prediction, transcription factor binding sites, sequence homology, and RNA secondary structure (still a little unsure how to use this one). These transcripts were discovered using RNA-Seq. Are there any other elements of genes/confirmed transcripts that I should look for in the sequence of my transcripts and corresponding softwares? (I can find the software myself if necessary, but I have run out of characteristics to search for). I would like to characterize these transcripts structurally and functionally as completely as possible, including potential protein function, mRNA degradation, etc - some new features for what to look into would be appreciated.

It sounds like you have considered most of the obvious alternatives (and thank you for clarifying the question).  I suppose the first question in an alternatively spliced transcript with a retained intron is whether the open reading frame of the protein is maintained.  If there is a termination codon that now becomes in-frame due to the intron then the protein would ordinarily be truncated.  The mRNA could also get targeted for degradation due to the nonsense-mediated decay pathway (i.e., from introducing an early stop-codon).

If the alternatively-spliced transcript lacks any significant ORFs, or if there is an ORF but no suitable translation initiation codon then you have entered the realm of non-coding RNAs, of which there are two loose categories, microRNAs (there are several classes) or long non-coding RNAs.  most miRNAs have recognizable sequence motifs, may be contained in mir-Base, and may be complementary (in part) to a regulatory target elsewhere in the genome. lncRNAs are less well-defined. Perhaps the best criteria are transcripts that are stable enough to be detected, but lack noticeable protein coding features.  I don't even think there is a consensus on the minimum length of a transcript to be considered an lncRNA.

What sort of databases have you searched? For example the ancient dbEST contains all kinds of short cDNA reads from all over the planet, dating back to 1992 (or so).  Evolutionary conservation of exons and splice-sites, or reading frames can all be used to support the hypothesis that a transcribed region has a biological function.

For a really deep fishing expedition you can use tblastn, etc. to take a potential translated ORF and search all 6 conceptually translated reading frames of all the sequences in a database--it takes longer, and there can be many spurious matches that you have to search through, but if you are studying something that has never been annotated it might be worth considering.

RE: folding RNA (secondary structure) every sequence can be folded into some kind of structure (try it and see), but structurally conserved compact loops typically fall into one of a small class of selected families (like GNRY). Stems are easy to find, but if the single-stranded loop is huge, how likely is that structure to fold up in real time?

RE: TFBS not clear to me at all what you mean by this. Transcription factors bind dsDNA not ssRNA. There are families of protein domains that bind RNA but not typically with such sequence-specificity.  So unless this alternatively spliced transcript is being transcribed from some type of alternative promoter, I am not sure where you would even be looking for TFBS.  It's true that some large introns can indeed contain regulatory regions for the gene as a whole (cf. immunoglobulin heavy chain enhancer is conveniently stored in an intron), but it is not clear to me if that would have an affect when transcribed into RNA.

I do like your idea that a retained intron could now contain a binding site for a regulatory miRNA, but if I understand the theory this would lead to the transcript being degraded--so it would be more difficult to detect.


How much of the genetic differences between humans and chimpanzees are due to genetic drift? Both natural selection and genetic drift play a part in changing our DNA over time. Are there trustworthy estimates how much of the differences over the whole genome between us and chimpanzees are due to genetic drift and how much is due to natural selection?

The easiest way to track whether a particular protein-coding gene has diverged between two species because of drift or actively maintained selection is to look at the ratio of synonymous to nonsynonymous mutations within that gene. A synonymous mutation is one that doesn't change the identity of the amino acid within that protein; a nonsynonymous mutation is one that does. Synonymous mutations are neutral by definition; their presence gives us an idea of how much time has diverged and how frequently mutations in that protein coding region change over time.

A dN/dS (Nonsynonymous mutation to Synonymous mutation) ratio of 1 suggests that the primary driver of change between species is purely neutral change. That usually means that it doesn't matter what is going on with that protein and is a little unusual--I would primarily expect to see something like that in a gene that is on its way to becoming a pseudogene.

A ratio of less than one means that synonymous mutations are much more likely to persist in that region than nonsynonymous ones. This is usually a sign that purifying selection is happening--for whatever reason, it's important to the function of both species that those proteins stay relatively similar.

A ratio of more than 1 means that there is diverging or directional selection happening, and that that protein type is changing between the two species because selection is actively modifying one or both proteins.

Here is a paper specifically analyzing whole human and chimpanzee genomes using this metric.


Why are vaccines containing attenuated microorganisms preferable to those containing dead microorganisms instead? My teacher said it more closely resembles a real infection but I didn't get that.

It's not necessarily true that attenuated vaccines are "preferable" to killed vaccines. It's a case by case basis. In some cases one or the other simply isn't possible or practical. It may not be possible to make a vaccine that's attenuated enough, for example. Or a killed vaccine may not be effective.

Here are some pros and cons of attenuated vaccines:

more likely to follow the natural path of infection, so there might be more immunity at the specific site of infection. For example, attenuated vaccines against gut pathogens might drive gut-specific immunity.
Might replicate in the host so that the actual amount of antigen seen by the host is greater than the amount delivered -- so you can deliver a much smaller dose to get similar immunity
Might cause more inflammation. Inflammation can drive a much stronger immune response because the body "thinks" it's being attacked by a dangerous pathogen

Cons:

Might cause more inflammation. Inflammation can cause tissue damage or local pain
May be less safe. Replicating in the host may give the opportunity to mutate and become more dangerous
May be more fragile. A killed vaccine could be relatively temperature stable, while an attenuated vaccine might need to be kept in a very narrow temperature range so it doesn't die and become ineffective. That might make it difficult to use in, say, developing countries

There are many more points that could be made but the overall picture is that attenuated vaccines might be more effective but more dangerous. Attenuated vaccines that are used today have been shown to be safe as well as effective, and killed vaccines that are in use have been shown to be effective as well as safe, so these are concerns during development of new vaccines, not in use of present ones.


Why don't allergies cause fever? Allergy

To my understanding, an allergy is a hypersensitivity of the immune system causing a substance in the environment to be identified as pathogenic by the immune system while it is not pathogenic. During an allergic reaction, the immune system triggers histamine, which triggers an inflammatory response just as if the allergen was a pathogen. The resulting symptoms of an allergic response is similar to the symptoms of a cold but without fever.

Fever

To my understanding a fever is an increase in body temperature driven by the body through production of pyrogens, most often in response to a pathogen. This response might be adaptive for various reasons that I am not too interested in discussing here.

Question

According to NIH, an allergic response never causes a fever. Given that the fever is not directly caused by the pathogen but rather is caused by the body, why do allergies not cause fever?

The fact that allergies don't cause fever give me the weird impression that the immune system somewhat "understand" the allergen is not pathogenic otherwise the immune response would be the same in the case of an allergen or a pathogen.

Un-educated guess

Allergic responses implies the firing of IgE. IgE are typically involved in response to parasites such as helminths. Could it be that pathogens leading to an immune responses mediated via IgE never yield to fever. Why would it be the case?

Plasmodium falciparum (which causes malaria) is a pathogen who causes an immune response involving IgE (according to the wikipedia). Malaria's symptoms include high fever (according to Mayo Clinic). Now it would be possible that the pyrogen would be of external origin (not produced by the body but by the pathogen) or it is possible that several immunoglobulin are involved in response to P. falciparum. The same logic hold for Fasciola hepatica (an helminth; common liver fluke) who also causes fever and is who's infection lead to the firing of IgE.

The short answer seems to be that fevers help combat microbes (a term I take herein to include viruses for brevity), which aren't a part of the threat addressed in an allergic reaction. While there's not a full consensus on which benefits, if any, a fever brings to the response to microbes, both humans and other warm-blooded vertebrates fare better with infections when a fever is present.

Fevers appear to mobilise leukocytes and enhance their phagocytosis while suppressing endotoxin effects (see Craven, R and Hirnle, C. (2006). Fundamentals of nursing: Human health and function. Fourth edition. p. 1044) and proliferate T cells (see Lewis, SM, Heitkemper, MM, and Dirksen, SR. (2007). Medical-surgical nursing: Assessment and management of clinical problems. sixth edition. p. 212), rather than mobilising basophils.

Higher temperatures are also more damaging to at least some pathogenic cells than the body's own, as they are typically smaller with higher relative surface area. Note this also explains why fevers wouldn't be as natural a response to such large parasites as helminths. (Even their cells, being eukaryotic, are comparable to human cells.) It is unsurprising that IgE would be a more specialised response, found only in mammals.

On the subject of malarial fever, for which the pathogen is relatively large because it is eukaryotic, there is ongoing research into both the mechanism and function of this fever. It seems to be Plasmodium itself that creates and presumably benefits from the fever, not the host. I'll discuss the evidence in a moment, but note this means the "endogenous fevers follow suspected small pathogens" hypothesis is unthreatened.

According to this 2013 paper, the timing of such ruptures may (I stress may; the paper discusses the uncertainty around a number of ideas about this) serve the function of controlling the time at which the immune response is most active, so the reproductive cycle is unaffected. According to this 2007 paper, the malarial parasite's hemozoin causes the disease's characteristic fever following erythrocyte rupture. The same paper mentions that the timing of the fever has been used as a diagnostic criterion for malaria, and the 1927 Nobel Prize for Medicine was awarded for the now discontinued treatment of syphilis with a malaria-induced fever.