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Are humans getting taller, shorter, staying the same height?
This post stems from this question, and specifically this article, which was provided within a response.
From what I gathered, the article attempts to make a correlation between the size of a creature and the length of its gestation period, with there being a linear, positive correlation.
This then led me to the question of, have homo sapiens more or less maintained the same [average] height since the advent of our species? In my searches I was able to find a few articles (e.g., here), however, they mostly only consider height changes within the past 100-200 years. Ideally, I would like to know if there have been significant changes (>13 cm) in average height for homo sapiens over the past 150,000 to 200,000 years.

I think that getting a global mean human height is nigh impossible.

Yeah, I agree with kmm. However, You could probably find heights of specific genetic groups (can't remember the word for them) over time a bit easier.

This is not an answer: There has been a significant change in average height in Swedish males between 1850 (167.4 cm) and 2004 (180.2 cm). The reason we know this is the compulsory draft conscription and the records kept. To my mind mind the reason is probably changes in nutrition and health care. I would guess that the introduction of farming about 10000 years ago (take or add a few thousand years) increased human population and probably changed average height. My guess is that it initially decreased average height.


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DNA Analysis (AncestryDNA)
A recent1 AncestryDNA commercial highlights a customer who discovered that she was 26% Native American.

Credit: ancestry.com/dna
You can see the full commercial here.
My question is, how can this be?
What combination of parents' race lineage would dictate that a person is 26% Native American (or any other race for that matter), and how many generations back would one have to go to achieve these numbers?

1. Recent to me, I don't watch much television.

These tests don't actually tell your ancestry, there is no way for a genetic test to do that because there is too much genetic variation among populations, as well as between.
Instead, the test is reporting, based on the polymorphisms observed, an estimate of their ancestry based on sharing those polymorphisms with others from a group. How do you know what polymorphisms an Asian or Native American has? Well, you do tests on a bunch of Asians and a bunch of Native Americans and use the similarities between them compared to other groups to form a 'profile' for that group. However, even an individual with a perfect geographical pedigree can share polymorphisms with other ethnic groups.
Wikipedia has a section on this:

Many companies offer a percentage breakdown by ethnicity or region. Generally the world is specified into about 20-25 regions, and the approximate percentage of DNA inherited from each is stated. This is usually done by comparing the frequency of each Autosomal DNA marker tested to many population groups.[2] The reliability of this type of test is dependent on comparative population size, the number of markers tested, the ancestry informative value of the SNPs tested, and the degree of admixture in the person tested. Earlier ethnicity estimates were often wildly inaccurate, but their accuracies have since improved greatly. Usually the results at the continental level are accurate, but more specific assertions of the test may turn out to be incorrect. For example, Europeans often receive an exaggerated proportion of Scandinavian.[10] Testing companies will often regularly update their ethnicity estimate, changing an individual's ethnicity estimate.

In summary: ethnicity testing is at best to satisfy a curiosity. There is no way that genetic testing can identify your geneology perfectly, and in fact it is pretty meaningless to do so, because interbreeding between geographically distinct populations happens all the time.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Mathematical Biology Jobs/Prospects?
I'm a junior math major starting to take his first courses in Algebra, Analysis, Topology, Nonlinear and Partial Differential Equations, etc.
I am just considering my career options at this point and somebody told be biotech/biology could have some interesting work. So I have come here to hear some advice if that is okay! Is there anything highly mathematical about the search for anti-aging or achieving the whole "biologically immortal" thing? I just don't know about any of this stuff so please inform me :)
PS: I also know Prob/Stats at a decently advanced level. So there's that too. Thanks!!

Off course you can! Here are career paths for you as per my limited knowledge:

BioStats

There are lot of applications in this domain. For example in Microarray Gene Expression or Proteomics analysis (for example, this paper).

Bioinformatics

Sequence alignments use common techniques like Dynamic Programming, Probabilistic or Heuristic methods, etc.

Computational Biology

There are lot of applications like Lagrangian and Eulerian Mechanics (Computational Anatomy), Computational Phylogenetics (Computational Evolutionary Biology), etc.

Systems Biology - In Systems Biology, you can have applications in:

1-) Probability and Hypothesis Testing - usually used to find associations between genes (Ref: S. Krawetz (ed.), Bioinformatics for Systems Biology, DOI 10.1007/978-1-59745-440-7_8, Chapter 8)
2-) Stochastic Modelling of Biological Patterns - ODEs,PDEs (applied to lot of problems), Markov Chains, HMM, PSSM are common mathematical implementations in this domain.
3-) Population Genetics - uses Statistical models (for example Genetic Distance), exponential equations (for example, Cumulative Effect of Mutation)
P.S: Here are some tools you might be interested in:
1-) Bioconductor - one of the main reasons why R is preferred language by BioStatisticians.
2-) BioPython
Wish you best of luck with your career!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Help identifying winged, moth-like creature
I noticed this moth (?) on my sofa yesterday. It matched the color of the sofa, so it was pretty hard to see. It's about an inch long, with a yellow body and light brown wings. I think it's a T. bisselliella. I'm from Kerala, South India.

The wings:

This is not a Clothing moth, they are not so yellow and are much smaller, about 7-10 mm (1/3 inch). Please add a picture of the wings if possible, and rhe location it was found, that will make it easier to identify.

Try bugguide.net they are really good at this.

@futurebird We're really good at this too. ;)

I'm quite certain that this is an owlet moth that belongs to the species Asota caricae. It has the nickname "Tiger Moth", and is commonly found in the tropics of India.
I would like to note though that your first picture is somewhat misleading, just from where the flash washes the color so much. Because of this, I decided to more heavily rely on the second image than the first, which exhibits orange instead of yellow.

This is it, but the eyes weren't this blue and the legs were pretty different.

@AravindSuresh I'm gald to hear it :) Regarding the eye color, I believe the specific camera used changed the purple to a blue. See here for a discussion of this effect. As for the legs, I think they look fairly similar.. can you tell me what you think looks different between the two? Just trying to refine my identification process. Thanks :)

The legs were not this gray, and not this big. Almost not this scary. But this is it anyway, I think the one I saw was younger than the one in the photo.


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Are baby centipedes poisonous like the adults?
I know that centipedes have an appendage called "poison claw".But I am not sure if the same is there in the baby centipedes and if its functional like that of the adults.
So are baby centipedes poisonous like the adult?


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Can one refer to pieces of proteins produced by enzymatic digestion as "enzymatic lysates"?
A Russian text I'm translating says this:

The location of post-translational modification (PTM) sites was determined using the “bottom-up” approach commonly used in this field. In accordance with this approach, enzymatic lysates from each of the studied MAB batches were separated using a reversed-phase chromatography column at high pressure (UHPLC), and peptide maps were plotted.

Can one refer to pieces of proteins produced by enzymatic digestion as enzymatic lysates? Or will lysates always imply that a biological cell has been destroyed?
The text I'm translating does not refer to cells being destroyed. The proteins in question are monoclonal antibodies present in drugs (solutions, tablets), therefore no cell destruction is involved.
I'm unsure whether to retain this word, "lysates", or use "digests" instead.
Here's an excerpt from the original Russian text:

Идентификация положений РТМ проводилось по общепринятому в отрасли подходу «снизу-вверх». В соответствии с этим подходом, ферментативные лизаты каждой исследуемой серии МАТ разделяли на обращенно-фазовой хроматографической колонке при высоком давление (УВЭЖХ) с получением пептидных карт.

Digests would ok or maybe hydrolysates. Incidentally for monoclonal antibodies I think mAb, not MAB, is probably standard usage.


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Reference for most up to date sport physiology
I currently have

Exercise Physiology Nutrition Energy And Human Performance, 7th Edition, 2012, McArdle et al.

as my reference book for Exercise physiology. However, based on a question I recently asked here on this very same board, I realise the book sometimes takes shortcuts and does not provide a complete explanation. Plus, the structure is sometimes a bit difficult or not to my liking.
I saw that the 8th edition (2014) has been issued. I don't know if it is significantly different from the edition I have.
Would someone have another solid reference for Exercise physiology? I am particularly interested in the energy pathways and their training.


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How long can one go with necrosis?
In general, when a limb dies, how long does it take before it falls off? Can you go years with a black and useless limb, or does it just.. fall off right away?

I feel like a study on the mechanics/pathology of gangrene could help here. But I am not an expert in this field but that is where I would start.

As it is the question cannot be answered, many variables play a role, such as where in the limb the necrosis started, what is the cause, health condition, age, etc. etc..


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Why do women go through menstruation?
I do understand that the female has to prepare for possible fertilization and make sure that the egg is of the best quality, so they try to remove aged egga from the uterine. However why cant the body just simply get rid of the egg not the uterine lining?  Maybe like reabsorb the egg or pass them out as waste? I mean its extremely energy consuming etc and it would be an evolutionary disadvantage since many other mammals dont go through menses.


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Are there predefined implantation sites in mammalian uterus?
  I do surgical embryo transfer of genetically modified (microinjected) mouse embryos (at 1 or 2 cell stage). As most of the constructs are new, we expect that it may affect birth rate. In case there are no or very low number of pups born we try to investigate at what stage the problem occurs. I dissect the embryo recipients on day 21(+48 hrs to make sure that we don't sacrifice a mouse that is late to litter down). Sometimes I find dark, gelly, regularly interspaced structures on the mesenterial side of the uterus. Initially, I thought them to be implantation sites of the embryos that have been subsequently resorbed for some reason. Until I found similar structures in mice that haven't been mated with male. My question is: are there anatomically predefined sites in an uterus that embryos can invade? Are my dissections just a waste of time and yield no valuable data?

I haven't been able to verify this, but if the gelly on the outside of the uterus looks at all like endometrial tissue, might you be seeing mice with endometriosis? In humans, there are no special implanttation sites, just highly probable to low probability. The embryo can implant anywhere it "touches down". Where it implants does influence the probability of carrying to term, though.

Hi, It is inside the uterine horn's wall, where placentas are formed. It seems to be connected to the blood vessel branches. Basically it looks very structured and be there for the purpose. I dissected one of this thinghs and it looks (100x magnification) like very dense capillary network.

Ah, thanks. I know of no similar anatomical structures in humans. It's strange, though, that you find them only on some female mice (is that correct?) I, too, in your place would have thought them influenced by the embryo(s), since the embryo has the ability to alter the architecture of it's implantation site, especially with regard to vascularization. Odd to find them on non-mated mice. I wish I could help.

Just had a thought; when you find them in unmated mice, look at the ovaries for visible corpus lutea. It may be anatomically normal but cyclical.

I started to believe that it is anatomical feature. The problem is that I talked to many people including vet surgeon, people doing research on embryology etc and nobody gave me the clear answer.

Keep an open mind. You might have made a discovery. :)


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Aerobic respiration
I read a sentence in my biology book while i was reading respiration chapter.  i wasnot able to understand it. It was in the process of oxidative phosphorylation"
"as the proton pass through channel their electrical potential energy is used to synthesise ATP in a process called CHemiosmosis" Can anyone plz explain that from where this energy came in proton and how is it transfered during facilitated diffusion.!


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Are enzyme inhibitors only a possibility?
I take 3 medications that metabolize by the same liver enzyme cyp2d6. A drug interaction checker told me that on or two of the medications i take may slow metabolism of another by altering drug metabolism. Ive had no side effects or interactions from this combination of drugs. Ive also read of people being on the same combination of drugs with no problems. If a drug is considered an enzyme inhibitor, is it a definite that it will slow metabolism and raise blood levels of another drug, or is this just a possibility?
Thanks for any feedback

The interaction checker is flagging those drugs for a physician/pharmacist to monitor and make a treatment decision on. It does not mean "people that take these two drugs will die immediately." It might mean "people that take these two drugs together are more likely to see rare side effects" or "people that take these two drugs together might have a lower blood pressure on average" - without more information you can't know.

It is unlikely that any of the drugs are enzyme inhibitors.  Generally the drugs can interact by competing for the use of the CYP2D6 enzymes for the period needed for enzymatic activity (usually quite short for each molecule of a drug or other compound, other than inhibitors).

My main question is that the interaction checker states that two drugs i take may or can alter the metabolism of a third drug i take. To me this means only a possibility, and won't necessarily happen. Hence, using the words may and can. Is this the way others here understand this?


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Fluffy creature
Can anyone help identify this little creature?  It was found in Gulf Shores, Al., USA. Approx. size 2-3 inches (5-7,5 cm)

What is its size?

Maybe 2-3 inches long, looked like it had guinea pig fur

This is a caterpillar of a moth from the Genus Megalopyge.
Here is another picture for comparison (the species here is M. opercularis, also known as "puss caterpillar"):

Another one:

And here is an imago (adult), also M. opercularis:

Good god, that is a very fluffy moth.

The moths are called "Flannel Moths" for a very good reason ...


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What is the correct classification of population groups of homo sapiens?
The classification system of the United States census into various races of humans is a bad way to classify population groups of humans, because both East Asians and South Asians are classified the same, yet they look different and are genetically distinct. So, has anyone proposed a more scientifically accurate classification of population groups of homo sapiens?

Basically all the genetic variation of humans is inside the native african populations.  A norwegian and a australian native are more closely related  to each other than two random native Africans are. So the only accurate way to do it would not only group those two asians together but also group them with europeans and native americans. If you split people up enough to get two groups of "asians" then you end up with more than a hundred races the vast majority of whom would be split among the native african populations.
Humans have very low genetic diversity in the first place, and most of our diversity is within our populations not between them, so splitting us up does not make a lot of sense. We end up doing it mostly on superficial variations.
Source


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Insect Identification needed
I found this sitting on my window, could not understand what it is. Any help would be appreciated.

Where did you find it?

Size and location would help a lot!

size - 3 inches max and location is Rajarhat. It can fly. Is their any moth that comes similer? Its my guess though.

It is a moth, maybe Miresa clarissa but not sure, so not an answer.

@anongoodnurce Thanks. I checked several other pics of this insect and the pic I clicked. Its almost looked the same and most probably the ans you have provided is correct.


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Phenotype-Genotype for multi-hybrid crosses
It's generally easy to figure out genotype and phenotype frequencies using a Punnett square for monohybrid and Dihybrid crosses. But what about situations involving 5 or 6 traits? Is there a simpler way to get about this?
As a sample problem:
If we have two organisms crossed, one with genotype AaBBcCddEe and the other with genotype aaBBccDdEe (lowercase is recessive and upper case is dominant), how many individuals would have the genotype AaBBCcDdEE?

In my opinion, the easier way is dealing with each trait separately, as if it was a simple monohybrid cross, and writing down each result:

Aa x aa → $\frac{1}{2}$ Aa;
BB x BB → 1 BB;
Cc x cc → $\frac{1}{2}$ Cc;
dd x Dd → $\frac{1}{2}$ Dd;
Ee x Ee → $\frac{1}{4}$ EE;

Now, simply multiply all the results:
$\frac{1}{2} * 1 * \frac{1}{2} * \frac{1}{2} * \frac{1}{4}$ → $\frac{1}{32}$
I don't know about your country, but in my country of birth all secondary books have a chapter for monohybrid cross and another chapter for dihybrid cross. I don't like that, it creates a nonexistent separation and it makes (some) students memorize concepts. Linkage apart, I like to say to my students to do not mind about dihybrid, trihybrid, tetrahybrid etc crosses, just treat them as individual monohybrid crosses combined.


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Why do (many) humans like carbonated drinks?
Many/most humans like certain types of food/drink because of the psychological/physiological responses we have to consuming them. Some examples:

We like sugar because it is very energy-rich (and is relatively scarce in nature).
We like salt because it is one of the essential building blocks of our cells.

But why do we like drinking carbonated drinks? (Soda drinks like Cola, Fanta, Tonic, Dr. Pepper, etc. but also sparkling wine, cider, champagne) Except in some very rare, special springs, carbonated water does not occur in nature. Why do we like drinking it so much?

Effervescence is fun. Pop rocks, Fizzies, etc.

@anongoodnurse Yes, but why do we like it?

Because it's fun. Why do you like swinging when you're a kid?

@anongoodnurse That's circular reasoning. I like swinging (and still do :D) because of the adrenaline rush caused by the point of weightlessness when the swing is at its highest point, as well as the speed at which you can move forwards and backwards. I do agree with you that many preferences are mostly psychological, rather than physical (and thus a lot harder to quantify), but "it's fun because it's fun" is not an explanation at all. :)

Of course it is. I just didn't go into all the reasons it was fun. It's the condensed version.


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What hold and inject pressure to be used in microinjection?
I am planning to set up micro-injection apparatus in our lab. Normally what hold and inject pressures are used to inject DNA in fly embryo? I couldn't find in any literature as far as I've come across.

It depends on volume that you want to inject and the width of your needle! Try to optimize the pressure by measuring the volume that you inject in mineral oil (I use grid in the objective to measure the drop size). You will decrease the volume by decreasing the injection pressure, of course. I work with zebrafish embryos so I am not sure if it is the same since it's in the water, but for DNA injection (1-2 nL) I normally use Hold Pressure 2 kPa and Injection Pressure 20-30 kPa.

That sounds similar to what I was using. We pulled our own micropipettes from borosilicate glass though, so had total control of the size. Edit I think we used 40kPa for 50 microseconds maybe, or milliseconds, whichever sounds more normal.

@Tamara Spika, I standardized the parameters (Micropipette size, inject and hold pressure) according to my need. But most of the time, when I try to inject in mineral oil, the water does not come out. I mean, the needle gets clogged. Do u have any idea about how to solve it?

@Mosquitoman Did you try to increase the pressure (like 10 fold) and press  once just to clear your needle and then try to inject again?


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Rabies in spiders - is it possible?
What if we inject rabies virus into an insect body, like spider or a bee, will it contract rabies as humans, cats, dogs, racoons or bats do?

Rabies is a viral disease that causes inflammation of the brain. It is adapted to the nervous systems of vertebrates particularly mammals. Arthropods are too different for lyssaviruses to survive in their body.

I'd like to ask you a question since I have not enough knowledge of biology and also assuming you'd like to speculate a bit. So the virus enters the body of a spider (let's take a spider as a example) and then what? To put it more metaphorically, the lyssvirus looks around, realizes the host is not a mammal and disappears? I'd like to know how it goes with lyssaviruses, but (to anyone) take it as an invitation to a discussion.


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What fruit did I just accidentally buy?
I live in Oxford, in the United Kingdom, in a part of the city with a vibrant multicultural community. My local corner shop has an excellent selection of spices, pulses, and obscure and vegetables fruit that mostly tends to be from the region of Pakistan and India, and only labelled (illegibly) in a language that I do not speak.
I've just bought a fruit I thought at first inspection was an unripe mango -- previously they have had excellent, cheap, small alphonso mangos for sale that I'm rather partial to. I'm completely wrong, however, for I've bought something about the size of my fist with striking white seeds that taste very peppery, a green coat, and somewhat sour flesh. It floats in water, and the skin exuded a slightly sticky, partially white gummy substance when I removed it from the bag. It's not particularly soft to touch. The seeds look a bit wrinkly, and are not hard at all to touch. The flesh has a consistency of an apple.

I can't for the life of me identify it! I'd love to know any suggestions! Thank you!

Looks like a papaya that isn't ripe yet. Being said, if you already cut it in half it probably isn't going to ripen any further. A ripe papaya has pink/orange flesh and the seeds turn black.

Yep -- with a bit more googling, I think that's exactly right. I had absolutely no idea that unripe papaya had white seeds -- I had assumed that they were black from the beginning. Thank you!


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Gibbs free energy and entropy in enzyme catalysis
In enzyme catalysis, the formation of the enzyme-substrate complex causes a reduction in the entropy of the system. If entropy reduces, the gibbs free energy will become less negative. How then is enzyme catalysis favorable? Are there any other factors that off-set this?

Enthalpy.......

And is it impossible to decrease the entropy of a molecule? And does an enzyme reaction stop with the formation of the ES complex? And what exactly is the second law of thermodynamics?

As @canadianer hinted, the answer is enthalpy.
ΔG = ΔH - TΔS
For binding to be a spontaneous process ΔG must be negative. If the binding of a ligand to a protein decreases system entropy then ΔS is negative and the entropy term -TΔS is positive. However ligand binding involves the formation of various protein-ligand interactions (hydrogen bonds, ionic interactions, van der Waals interactions) all of which make a negative contribution to the change in enthalpy, so ΔH is negative. If |ΔH| > |TΔS| then ΔG will be negative.
This simplified account ignores the parallel changes taking place due to the ligand 'dissociating' from the solvent.


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What kind of eye strain causes an visual aurora effect?
When I have done too much reading on the PC sometimes I feel a tickling sensation inside my eyeball. At first I didn't even notice the tickle, however my eye would start to see blurred in one area, and a growing halo of yellow blue orange stars grows outwards from one place in my visual field. the shape is not very round, it growns like a mycelium shape, where the border is very bright with stars and lights.
So the effect resembles a mushroom growth ebbing slowly outwards from a point over the space of 30-45 minutes, where my vision in one eye becomes overcome with a blurring effect and a flashing colored araura, and an annoying tickling/electrical effect inside the eyeball. it can be more or less pronounced, and sometimes I can barely read anything up to 1 hour afterwards, and after 2 hours it has returned to normal.
I have 9.5/10 visual acuity, and this started occuring every few months since I was 33.
I can't find what I am experiencing, all the eye disorders and symptoms seem to describe different issues than what i have.
What can it be?

That's called a scintillating scotoma, and it should be present in both eyes (cover one eye when it's happening and see if it isn't the same in the other.) Look it up. It's a kind of a migraine. It's not serious (honest), but you should let your doctor know you're having them. I have them too. I think they're fascinating.

Thanks that's a very good answer, if you write it as the answer i'll mark it as true.

We're not supposed to answer medical questions. :(

I'll have to check if it is unilateral and if my irises are the same size afterwards. I found a page which sais that some versions can be caused in the retina: https://www.reviewofoptometry.com/article/visual-aura--and-scotomas-what-do-they-indicate there's masses of pictures of scintillating scotoma on the image search too. thanks again.

most ocular migraines can't be medicated and they are more "trippy" than than noxious. It's also a neuroscience and optical quesiton. anyways, the answer helped a lot with knowledge.

They are trippy to me as well. They are treatable if serious enough. I can't read without great difficulty when I get one. Luckily, it never happened to me at work!


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Will a sandwich assay work with a GST 26 antibody/protein?
I have a GST 26 kda antibody, and want to use it in a sandwich lateral flow assay. Are there enough epitope regions for both antibodies to bind to the protein?

This is completely dependent on the type of antibody you are using and the epitope specificity of that antibody (or antibodies). Because you haven't given any more detail, it's very hard to give you a definitive answer.
GST is known to dimerise, so even a monoclonal antibody might work in your sandwich assay, as long as the (identical) epitopes are far enough apart in the dimeric structure to allow two antibodies to bind.
If you're dealing with a polyclonal antibody mixture, then your chances are better. But even still, you won't know until you try it.


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How do you consider an organism to be a new species?
How do you consider an organism to be a new species? Can a new parthenogenetic organism be considered as a new species?

The answers here https://biology.stackexchange.com/q/34594/107 cover species concepts.

There are various hypotheses and concepts proposed to define a species, but no definitive answer. Mostly a combination of these concepts are used because each hypothesis has exceptions. Classification is constantly being debated, reevaluated, and changed as we learn more. Some of the most notable definitions are:
The is the biological species concept in which Ernst Mayr defines a species as actually or potentially interbreeding populations that are reproductive isolated from other groups and produce viable, fertile offspring. But this doesn't by definition exclude hybridization between species, but often hybridization does not produce viable or fertile offspring. (This definition doesn't work with parthenogenesis. Also, hybridization is accepted as a mechanism that can lead to speciation, most notably seen in plants, where the hybrid offspring can interbreed with other hybrids, but are not able to reproduce with their parental species.)
There is also the morphological species concept which uses morphology and body features to classify organisms, which is more useful when there is little population information available, such as for fossils. But this can result in one sexually dimorphic species being classified as two. (The eclectus parrot was initially classified as two species because the males are green, while females are red.)
In the phylogenetic species concept Willi Hennig defines a species as the smallest group of individuals sharing one common ancestor and a set of fixed heritable differences to make up one phylogenetic branch. Genomics is often used to define this. There is debate that this method creates "taxonomic inflation" and creates more species than necessary because different populations may be able to interbreed, are not reproductively isolated, but are genetically differentiated enough due to local adaptation.
The ecological species concept defines species by their environmental niche--organisms that look, act, and share similar life history patterns. This definition includes parthenogenic species as a separate species from its non-parthenogenic relatives.
(It becomes much more complicated when trying to classify prokaryotes and viruses because mutation occurs at a much higher rate and many of the above definitions cannot be effective applied.)
Ultimately, yes, there are various accepted species that reproduce only by parthenogenesis (like the mentioned New Mexico whiptail lizard), and parthenogenesis can be a defining factor which separates them from a sexually reproducing counterpart species that is similar in morphology, niche, and evolutionary history.
Information comes from courses and textbooks from my Ecology & Evolutionary Biology major within the last year.

A quick look in the Wikipedia article for parthenogenesis gives an example of New Mexico whiptail (Cnemidophorus neomexicanus).
It is a hybrid between the little striped whiptail (C. inornatus) and the western whiptail (C. tigris). It reproduces through parthenogenesis - there are only females from these species and they lay unfertilized eggs.
The answer to your question is obviously: yes, a new parthenogenetic organism can be considered as a new species.
However the taxonomy undergoes continuous changes and what has been a subspecies might be later classified as a species or vice versa. There are no clear and unambiguous criteria deciding when a new discovered organism is a species on its own.
Generally speaking if the individuals of a population can reproduce and have offspring resembling their parents, but can't reproduce with individuals of other populations resulting in reproductive able offspring, then they are considered to be a species. Although there are many exceptions and no strict rules.


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Why do some armadillos roll into a ball while others don't?
My question is pretty simple that why do some species of armadillos (like three-banded) roll into a ball, while others don't?

Para 4

@Tytoalba Thanks! and Yes I know that, perhaps I haven't been able to word my question properly. I am more interested to know about why they were evolved this way (to have less plates, etc.)


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What is the first recorded unambiguous case of childhood cancer?
I can't seem to find any references to childhood cancer going far back. I am asking for the first verifiable instance of childhood cancer.

Kindly add some references as well

What? ..........

Verified how..?

"Cancer" is a huge range of diseases. Some are not uncommon in children. Others are rare/undocumented. This question is unclear or too broad until it is narrowed down.

Osteosarcoma is mostly a disease of teenagers and it leaves characteristic changes in the bone.  Sometimes archaeologists find such bones.
I found this

Malignant primary bone tumours were very rare in antiquity and
  continue to be rare in modern populations. The earliest known case
  affected a male Celt (about 800–600 BC) who was about 15 years old and
  lived in what is now Switzerland.1 The lesion is a neoformed bone mass
  at the level of the metaphysis of the humerus, whose gross pathology
  and radiographic aspect are consistent with a possible osteosarcoma or
  chondrosarcoma. A few additional cases of malignant primary bone
  tumours have been mentioned in literature. A possible osteosarcoma of
  the pelvis has been reported in a young individual from Ancient Egypt,
  dating to about 250 AD,92 and a well-documented case of osteosarcoma,
  with the typical radiographic “sunburst” pattern, has been observed in
  the femur of a native Peruvian dating to 800 BP (Fig. 4).93 Possible
  additional cases of osteosarcoma have been reported in a young female
  femur from the prehistoric population of Oahu in Hawaii,94 in a
  zygomatic bone from the French Middle Ages,95 in a 17th century
  mandible from West Virginia,96 in a young male from the Saxon
  necropolis of Standlake, England97 and in medieval skulls from the
  Czech Republic98 and France.99

http://onlinelibrary.wiley.com/doi/10.1002/ijc.20610/full
But if you want "described" meaning a contemporary of the child wrote down what he saw, I found this by John Abernathy in 1804.

from https://archive.org/details/surgicalobservat1804aber
Surgical observations : containing a classification of tumours, with cases to illustrate the history of each species : an account of diseases which strikingly resemble the venereal disease : and various cases illustrative of different surgical subjects
by Abernethy, John, 1764-1831
Percival Pott was an English surgeon who is remembered for his realization that the job of chimney sweeping puts men at risk for development of scrotal cancer.  Mostly these were grown men but among cases described was an 8 year old; this in 1808.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1037746/?page=3
I am pleased that my find in Abernathy's and Pott's works predates the earliest listed in this 1937 review of pediatric cancer, which gives a date of 1819 for description of tumors in the eye of a 3 year old.
[Dargeon, J Pediatrics 1937].   Dr Dargeon did not have Google.
  (http://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S0022347639800415/first-page-pdf)
ADDENDUM:  An earlier find yet:
from http://onlinelibrary.wiley.com/doi/10.1002/cncr.25000/full
A note from history: the first printed case reports of cancer.
Hajdu SI. Cancer. 2010 May 15;116(10):2493-8. doi: 10.1002/cncr.25000.
He describes the work of Theophilus Boneti, whom in 1700 published a book of many hundreds of case reports accumulated from the previous 150 years.  Included was a case of retinoblastoma (I could not tell what year it was from):

In the fourth case, the patient was a 5-year-old girl who presented
  with a fungous (soft) tumor of the right eye. After a short period of
  observation, a similar tumor was detected in the left eye. Both tumors
  invaded the meninges with adhesion to the brain. Boneti did not say
  so, but this youngster must have had bilateral retinoblastoma.

That puts the earliest solid description of a cancer in a child at 1700.


text:
Praying mantis identification
I found this praying mantis in Bangalore, India. It is around 6 cms in length and has a distinct marking on the forelimbs. Can I know the species ?

@charles, There's another angle. I'm pretty sure it is a mantis and in fact according to a taxonomical key that I found, I think it may belong to the genus 'Hestiasula' . I'm just waiting for a specific confirmation.

.. according to a taxonomical key that I found, I think it may belong to the genus 'Hestiasula'.

You're absolutely correct! This is of the species Hestiasula brunneriana, and is belongs to a group of praying mantis that are referred to as "Boxer mantises", due to their enlarged raptorial forelegs, of which are used for communication.
And though I can't quite tell, but at first glance this appears to be a female, due to what seems to be a longer than not abdomen; a female will only have 6 segments, whereas a male will have 8, however, the segments belonging to the female will be longer than that of the males. If you can somehow get an underbelly image, a much more definitive statement can be made.
The following image accurately matches your aerial image:

And then here's an image that demonstrates those distinct black markings on the raptorial forelegs:

Thank you @charles . Could you please upload the link to the key that you found. I would find it pretty useful for future reference. Thanks again.

@AdDate I used this image index, provided by the Indian Council of Agricultural Research, which is accompanied with taxonomic details.


text:
Why do we drink clean water
Most of the street/feral animals (cats, dogs, cows, some wild animals too) drink tap water or dirty water, but it doesnt seem to affect them. So, why do humans drink pure water?

We can drink dirty water, and have through much of history (until we discovered fermentation and later, sanitation). Dirty water is bad for you regardless though. That's part of why we live to 80+ these days, but died younger in the past. You'd probably find you'd be even more ill from drinking unclean water nowadays vs several hundreds/thousands of years back (in the West at least) since our levels of hygiene have reduced our immunity to many of the nasties in dirty water

@JoeHealey - Or, many of the nasties in the water now weren't yet invented by man. It's not only bacteria that pollutes.


text:
Enzyme kinetics at the chemical level
I am stumped by two questions:

Why do we take only the initial 10%(or may be 9.99999....%) of S conversion as the rate of the enzyme reaction. why not more than 10%?
Why doesn't the velocity keep on increasing linearly until the Vmax is reached (as all the S molecules get exhausted)

Research and attempts to answer:
Why v0's 10%?

Steady state kinetics apply when the [ES] is constant, on reaching 10% [P] (for a uni uni reaction) the backward reaction increases, increasing the [ES]?
On reaching 10% conversion the rate decreases, so we measure the optimum activity.

Why doesn't the velocity increase linearly until all the molecules are used up?

Since an enzyme's turnover number (kcat) is constant...
...

Disclaimer :

'have put two Qs together.
Didn't find relevant Q on BioSE.

related

For 2. Think A. about the importance of MM kinetics, which was to establish that the reactions were catalysed by a single active site on the enzyme. Simple non-enzymic chemical kinetics would, instead, predict an order proportional to the product of concs of reactants. B. About the interaction of a substrate with the active site and why this has a hyperbolic shape. Consider collisions between entities (here a substrate and active site) to understand the hyperbola. 1 is trivial.

@AlanBoyd — But the answer to that question, despite its votes and acceptance is unsatisfactory. It does not explain why the curve is hyperbolic rather than linear.

@David 'trivial' is a subjective comment, which in itself is trivial according to what BioSE is for ('... biology researchers, academics, and students.') When there's a Q there's either an answer or it is yet to be unraveled.

Hint. Read sections 8.3.1 and 8.4 (start) of Berg online. Oh, and I don't know why you have a fixation on 10%. It's the initial velocity while the rate is linear, whatever that % may be.

You write: "Why doesn't the velocity increase linearly until all the molecules are used up?" Which molecules? The substrate? What other molecules are involved? Think!

I have decided to answer your second question. I now notice that your question says "…Vmax is reached (as all the S molecules get exhausted)". That's your basic misconception. It is the enzyme molecules that are saturated. You are adding more and more substrate to less and less effect — it can't be the substrate that is exhausted!

For a user with a high reputation you have been rather quiet in reponse to the answers suggested. Did either of them solve your problem? If so you might consider accepting the one that did. If not, perhaps you could explain the problem you still have.

The answer to the first part of your question is that we don't take the initial 10% of a progress curve (velocity vs time) as a measure of activity, but we measure the initial rate of the reaction.  We do this by drawing a tangent at the origin.
It is merely a 'rule of thumb' that progress curves are practically linear provided that not more than 10% of substrate has been used up. If there is significant slowing down before 10% is used up - and there may be if the substrate concentration is way below Km value - then it is not valid to draw a line through the points: we must draw the tangent to the curve. That is, it is not acceptable to take the average rate during the first 10% of the progress curve.
For this reason it is desirable to use as sensitive a method as possible when measuring an enzymic rate, and to never rely on a single time point (as is common in radioactive assays) without sufficient controls to justify that it it is the initial rate, and not the average rate (or something else) that is being measured.
The reason we measure initial rates is that is makes things simpler on two fronts.
Firstly, the decrease in rate with time of an enzymic reaction may be due to many factors: product may be inhibiting the reaction, the reverse reaction may become important, the enzyme or substrate may be unstable. It is only during the initial rate period that conditions are accurately known, and such  effects may be legitimately ignored. It was Michaelis and Menten that first realized the importance of measuring initial rates, and of the great simplification principle that ensued, in enzyme kinetics. (see Cornish-Bowden, 2004).
Secondly, the rate laws themselves are greatly simplified.  Provided that eo << So (the initial enzyme concentration is very much less than the initial substrate concentration), we may take the So as being equal to the substrate concentration and 'plug in' this value into our rate law (such as the Michaelis-Menten equation), and ignore the effect of time on the value of S.  In addtion, we can set all product terms to zero. This can greatly simplify things.
For example, the rate law for a reversible single-substrate mechanism (see here) is the following:
$$ v = {
  {{{V_{max}^f}\over{K_{m}^s}}\ S\ -{{V_{max}^r}\over{K_{m}^p}}\ P }\over{1 + {{S}\over{K_{m}^s}} + {{P}\over{K_{m}^p}}}}\ \ \ \ \ (1)$$
This one is not as complicated as it looks: we have just defined a Km and Vmax for the forward and reverse directions. But let's set product to zero:
$$ v_i = {
  {{{V_{max}^f}\over{K_{m}^s}}\ S_o\ }\over{1 + {{S_o}\over{K_{m}^s}} }}\ \ \ \ \ = \ \ \ {{V_{max}^f S_o}\over{{K_{m}^s} + S_o}}\ \ \ \ (2)$$
We now obtain the familiar Michaelis-Menten Equation (where $v_i$ is the intial velocity).
The second part of your question is more fundamental. I'll take it to mean the following. Why does an enzymic reaction not follow second-order kinetics at all substrate concentrations? Why doesn't doubling the substrate always double the rate (as is often the case in chemical kinetics)? A. J. Brown in 1902 suggested that the reason for this is the formation of an enzyme-substrate complex and that at sufficiently high substrate concentration all the enzyme would exist in such a complex and the enzyme would become 'saturated'. The formation of an enzyme-substrate complex, of course,  is now a cornerstone of enzyme kinetics. One of the early key pieces of evidence for an enzyme-substrate complex was the observation that an enzyme is much more heat-stable in the presence of its substrate than in its absence.
Finally, it is probably worth pointing out that some enzyme operate way below Km values and at 'physiological' concentration of substrates do obey (to all intents and purposes) second-order kinetics. Catalase, for example, has a Km for hydrogen peroxide of about 1 Molar (Ogura, 1955), and one assumes that physiological concentrations never reach this level. (We need to be a little careful about catalase, however: it is one of the few enzymes that is inactivated by substrate).
A great reference on enzyme assays is the following:

Principles of enzyme assay and kinetic studies by K. F. Tipton in Enzyme Assays: A practical approach

For an introduction to enzyme kinetics, and the early history of enzymology, I like the following:

Cornish-Bowden (2004) Fundamentals of Enzyme Kinetics 3rd Edn. Portland Press, London.

This answer is far too complex to be comprehensible to a student who is obviously doing a first course in enzymology as part of a general biological sciences degree and is asking very basic of questions. Recommending she read Tipton or Cornish-Bowden is absurd. The answer to her question at the level she requires can be found in the Berg reference in my comment. It would have been better to let her read that (it is on line) and learn for herself.

No, she's just starting enzyme kinetics and her question, though understandable, is a poor addition to SE Biology. I've seen the subjects she has been asking questions on over the last year and have a shrewd guess as to her background. I think it's wise to try to establish first what the poster is asking before writing over 700 words with two equations in which the terms are not even defined. I surmise that you have never taught university students if you imagine that they will even buy a biochemistry text such as Berg when doing a broad biology course, never mind advanced texts.

Her answer is correct but shows only that she has learned the reactions of glycolysis and gluconeogenesis, not that she knows anything of kinetics or even the thermodynamics involved in the irreversible reactions. What Berg is trying to do is provide a visual way for the beginner to think about simple kinetic constants and, most important, that the saturation curve indicates the existance of an ES complex, the kinetics of which validate this. Many students, lacking chemical kinetics, do not understand the significance of the hyperbola, which is the point that needs explaining to them. I may.

The kinetics of enzyme catalysed reactions is a specialized area of biochemistry. It was historically important when much less was known about enzymes and the tools for studying them were limited. Why, then does it retain a place in contemporary text books? I would suggest that it illustrates how many of our ideas of enzymes and their reactions were developed, and that on a more mundane level it provides a cheap basis for laboratory experiments where students can encounter some of the pitfalls of experimental science and also learn to test ideas numerically.
For the average innumerate contemporary student of biology struggling with the Michaelis–Menten equation it can be easy to miss what I regard as the most important concept that this illustrates. This is that the kinetic analysis of simple enzymes supported…

…a model of the enzyme in which the substrate bound and the reaction
occurred at a specific site — the active site.

How does it do this? To understand that one must first contrast these enzyme kinetics with those of uncatalysed chemical reactions. It is assumed that chemical reactions occur due to the collisions of the reacting molecule. Depending on the reaction, the rate (r) of a chemical reaction and will be proportional to some power (n) of the concentration of the  reactant(s) (S):
r = k[S]n
and the ‘order of the reaction’ is n — often 1 or 2 (first and second order). (k is the rate constant, which reflects how this proportionality is manifested in different cases.)
What this means is that if one plots r (product per time) against the concentration of the reactant one gets a line of a particular shape (linear or curvilinear — see below) in which the rate continues to increase as the concentration of reactants increase (assuming the formation of product is small in comparison).

[Taken from Askiitians]
In contrast, the rate of enzymic reactions (velocity v) reach a maximum (Vmax), approaching this asymptotically as shown. (This is for a fixed amount of enzyme, as shown for an enzyme obeying simple Michaelis–Menten kinetics.)

The existence of a Vmax is consistent with the idea of a single (or small finite number of) active sites on the enzyme — when all enzyme molecules are saturated (all functioning) increasing the concentration of reactant (substrate) can provoke no further increase in rate.
Finally to the poster’s question (or at least the part that is most interesting conceptually): Why is this maximum velocity approached asymptotically? To appreciate this one should be aware of the disparity in numbers of molecules of reactant and enzyme — for glucose at 5mM and hexokinase at 20µM this is about 250 to 1. As the concentration of reactant is increased the number of ‘free’ enzyme molecules will decrease and a corresponding greater number of reactant molecules will be needed to produce a successful collision with, and binding to, the active site. This effect is small initially, but becomes successively more severe, so that in practice Vmax is never  reached and has to be calculated by extrapolation.
And however much the purists may object, the two kinetic constants that emerge from numerical analysis — KM and kcat — illuminate for the student two key aspects of the catalytic site. These are that it has a particular binding affinity (which may vary for different substrates) and that it has an intrinsic catalytic capability. So for those who wish to learn to walk before they can run, I recommend section 8.4 of Berg et al., which can be read online.
Addendum
And the answer to the first ‘boring’ part of the question is shown in the insert added to the second figure.The kinetic analysis is only valid if you consider the initial velocity (for which you have presumably been given the arbitrary figure of 10%) while the rate is linear with time. (There are various practical reasons linearity is lost with time — removal of substrate, back reaction as products build up, denaturation of the enzyme etc.)

Having given the poster time to think about it, I decided to post an answer to the conceptually interesting part of the question because the second question recently that does not seem to understand it, and it is generally taken for granted in texts. I suppose it needs a numerical explanation, but I didn't want to get bogged down in whether it was a hyperbola or not. I just wanted to get over the idea of why this kind of phenomenon has this sort of curve.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
What is the reproductive success of a biting mosquito?
Female mosquito can lay ~50-100 eggs in each batch. It takes some time between the hatch and until the time the female mosquito bits. During this time many of them will die.
What is the average percentage of the eggs that mature (in other words, if a female mosquito lays one hundred eggs, how many of them will become grown females that bite)?

The amount (percentage) of eggs to mature varies greatly and depends on many factors and off course varies by season.
The correct (but not really satisfying) answer is that from every 100 eggs, between 0 and 100 eggs will mature. On average, this number is greater than 1 (otherwise the species would go extinct), and much smaller than 100 (otherwise the world would drown in mosquitoes). Because the question doesn't include the complete lifecycle, it is not exactly 1, but greater than 1.
Some explanation
Mosquitoes lay eggs in water, and the larvae are easy prey for predatory invertebrates (larvae of dragonflies, beetles etc.) and fish. Many mosquito species choose small, isolated waters (like small pools and plant-pots) where there is likely to be little predation. This however carries a risk: these waters often dry out (reproductive succes 0%), offer little resources (reproductive succes low) and offer no shelter against an unforseen predator (reproductive succes low). If they choose wisely however, reproductive succes can be very high. Because of this large variation, an average number is really not so informative.

I think the number has to be almost exactly 1 (not more than 1) for the population to remain stable. And that's 1 maturing egg for the entire life of the female, not 1 per batch nor 1 per 100 eggs. See my answer for more details.

@Stephen_Thomas The question is not about the complete lifecycle, so it must be greater than one.

So suppose the answer is 2. Then, for every batch, 2 females would reach maturity (and, we're assuming, breed). And for a complete lifecycle of, say, 5 egg-laying batches, 10 females would reach maturity. In that case the mosquito population would grow 10-fold at each generation. Clearly that can't be correct.

Ah, I get it now. My answer is indeed incorrect.


text:
Cold water sour taste
Recently I underwent a wisdom tooth extraction, and while there is still numbness I have observed something peculiar. If I drink cold water, it tastes sour, however the same effect is not observed with room temperature water or hotter. What is causing this effect?

Interesting question , this reminds me of miraculin which makes us perceive sour as sweet. Maybe something like that is happening in your case.

My guess (hence not an answer) is that the regional block also affected your tongue and taste buds; signals might just have gotten crossed.

An interesting effect to note is that distilled water tastes very sweet.

Here is an educated guess: firstly the typical dental anesthetic is lidocaine which tastes very bitter. Secondly, a bitter taste if often misclassified as sour. Thirdly, sensory thresholds (the amount of a compound required to detect its taste) is temperature dependent and lower at cooler temperatures. In other words, I assume that drinking cold water made you able to detect small remaining traces of bitter lidocaine that were too small to detect at warmer temperatures, and that you misclassified as sour.
Wei, Y., Nedley, M. P., Bhaduri, S. B., Bredzinski, X., & Boddu, S. H. (2015). Masking the bitter taste of injectable lidocaine HCl formulation for dental procedures. AAPS PharmSciTech, 16(2), 455-465.
https://www.sensorysociety.org/knowledge/sspwiki/Pages/Sour-Bitter%20Confusion.aspx
McBurney, D. H., Collings, V. B., & Glanz, L. M. (1973). Temperature dependence of human taste responses. Physiology & Behavior, 11(1), 89-94.

what  type of time interval might you expect that persistence. This question was asked roughly 2 months after the extraction i  believe

Hum, ok. Then definitely not remaining traces of lidocaine. I assumed it was few hours after extraction.


text:
Sensitivity Along Digestive Tract
Suppose you swallowed a little capsule with a blunt poker which had
some impulse of force applied every few seconds.  What would be the
sensitivity ordering (of lips, mouth, throat, esophagus, stomach,
duodenum, jejunum, ilium, colon, rectum, anus)?
Does sensitivity just fall to a minimum in the middle of the digestive
tract and increase again to the exit, or are there any other extremum
(e.g., at the ilium-colon interface) along the way?  I'm guessing
people could infer the answer by looking at the density of nerve cells
along this route, but I couldn't find any comparable scientific data
in my quick internet searches.

Let's be clear do you want only perceivable sensibility or non perceivable sensitivity?

I want perceivable sensibility. In the experiment, the person would be ranking how well he/she feels the periodic poking (and for a bonus, I might ask if it feels good or feels painful). It's still subjective, but the best experiment I could think of.

This is such an artificial scenario, I'm wondering why it would matter? Different parts of the GI tract are innervated for different things/reasons.


text:
what is the poison in chinaberry?
I was trying to look up what the poison in Chinaberry is, however, with the exception of a couple related compounds was able to find no information on the poison. What chemical makes up the Chinaberry poison, and what is this chemical's concentration and LD50, if known?
Edit: The Chinaberry I am referring to is Melia azedarach

Which chinaberry do you mean? https://en.wikipedia.org/wiki/Chinaberry_(disambiguation)

@jamesqf I am referring to Melia azedarach, I was not aware that there are multiple plants by that name.

The toxin is Meliatoxin, in a class of toxins called tetranortriterpenes.
I found this here.  Bold emphasis mine.
https://wagwalking.com/condition/chinaberry-tree-poisoning

What is Chinaberry Poisoning? The chinaberry tree is a member of the
mahogany family that is native to Australia, China, and India. These
deciduous trees sprout delicate light purple flowers in the spring,
which develop into yellow, berry-like fruits in the summer. They were
transported to North America in the early 1800’s as an ornamental
plant, but has escaped into the environment and is considered an
invasive species in several southern states. It produces a potent
insecticide which utilizes a tetranortriterpene neurotoxin known as
meliatoxin. This insecticide is found throughout the plant’s bark,
leaves, and flowers but is found in the highest concentrations in the
ripe fruit. If you suspect that your pet has consumed any of this
plant, contact your veterinarian immediately. The chinaberry tree, or
Melia azedarach, is a deciduous tree that produces a potent
insecticide which utilizes a neurotoxin that can prove detrimental to
your pet if ingested. Symptoms of Chinaberry Poisoning in Dogs
Symptoms of chinaberry tree poisoning occur most often from eating the
ripe fruit, however, the bark, leaves, and flowers also contain
smaller amounts of the toxic substances. Symptoms usually begin within
just two to four hours from ingestion. Abdominal pain Blood in stool
Colic Constipation Death Depression Diarrhea         Excessive
drooling Heart attack Hyperactivity Lack of coordination Loss of
appetite Muscle rigidity Seizures Slowed heart rate Stupor Vomiting
Weakness Types
The scientific name for the chinaberry tree is Melia
azedarach, and it belongs in the mahogany family.

From another source
http://www.sciencedirect.com/science/article/pii/0031942283830398

Toxic tetranortriterpenes of the fruit of Melia azedarach . .Peter >B.Oelrichs. Michael W.Hill. Peter J.Vallely. John K.MacLeod. .Tadeusz >F.Molinski
Show more https://doi.org/10.1016/0031-9422(83)83039-8Get rights and
content Abstract Four new tetranortriterpenes, meliatoxins A1, A2, B1
and B2 have been isolated and identified as toxic constituents of the
fruit of Melia azedarach L. var. australasica. Toxicity and
pathological results confirm that the meliatoxins are responsible for
most but not all of the symptoms resulting from the ingestion of whole
fruit.


text:
Question to the color scientists
I have a question.
if you look at these two spectral diagrams (SPDs) from two different televisions that is calibrated to the same white point (D65) 6500K with a spectrometer.
The problem is that white still looks different to the eye here.
why does white look different is my question.
Television1
(pictures from avsforum)

Television2

A logical explanation would be great as i trying to figure out whats causing it.
is it the spectral power differences that causing it or is it the different distribution of the GREEN and RED with its more narrow peaks on television1 that causes it?
what i can see and what i understand is that Television1s spectral power will produce a more natural light as its more close to the warm light from an incandescent bulb.
Television2 reminds more of an typical LED lamp that we all know have a more harsh and poor light.

First: What is TV in this context? Then: LED lights are not necessarily cold, they can be produced in almost all color temps you want to have.

Tv=Television and ok cold is maybe the wrong term. poor and harsh is the right description.

The difference between both images can by explained with the spektrum. The upper one lacks most of the colors between green and red (more or less) while the lower one is more complete here. Both also differ in green.

Thanks for the input but i think its more about the different energy of Green and Red on the first television thats makes the difference. higher energy for Green and Red compared to Blue should make whites "look" more warm..while television 2 only has high energy for Blue it will give whites a more cold tone.  i have already captured the differences on whites with an DSLR camera but the differences on photo is not the same as i see them.. the camera sensor picks up the correct white for television 1 but not for television 2 for some reason.

i have already captured the differences on whites with an DSLR camera but the differences on photo is not the same as i see them.. the camera sensor picks up the correct white for television 1 but not for television 2 for some reason.. here is the differences for white with similar televisions models but not the exact ones from these photos..television 1 to the left..whites "looks" correct on the photo but white on television 2 looks too much Blue/Green. http://privat.bahnhof.se/wb192876/500M%20B7_2.jpg

it has nothing to do with computer graphics. where do you think its related to graphics from a computer?.. its more about how our eyes see light and colors different compared to spectrometers and cameras.

This is probably caused by the imperfection and/or mismatch between what your eye thinks white and the calibration device's white...color perception from spectrum can be nonlinear and have individual variations.

A simple observation: whilte points are a single dimension: temperature.  Color itself is a 3 valued thing (for human eyes).  Thus it will always be possible to have two colors with the same temperature.  Color temp is more useful if your source is blackbody.

After more reading and information its quite simple.
our eyes picks up the energy from the primary colors.
if a television has higher BLUE energy than RED and GREEN that picture will have a blueish cold look to it even if its calibrated to D65
the SPD from television nr1 has higher energy for GREEN and RED and so whites on this television will look more warm and less blue.
how distinct and separate the cones are can also matter here.
television nr1 has no clear separation between GREEN and RED while television nr1 has.


text:
Can a human actually be "frightened to death?"
I've been watching some classic horror movies as of late, and a trope I see in many of them is where a person will see the big bad monster and "die of fright." I'm curious, for the average person, could this happen? Or would it require a prior medical condition of some kind?

The people whom this happens to consider themselves average people.
The thought is that catecholamine surge caused by the event triggers some predisposition to cardiac arrhythmia - maybe inherited, maybe due to medicines.  People predisposed to this sort of arrhythmia probably do not know that is the case, and consider themselves to be average people.  It would seem that the victims of this are not average and have some sort of predisposition to that problem.  There is a lot of interest in figuring out who there people are in advance - not in the context of being frightening to death but in the context of SUDEP - sudden death in epilepsy.  Epileptic people sometimes just die, presumably for cardiac reasons, but there is no way of knowing who among this large group is at risk.
In the following abstract the frightening thing is being restrained.  Other circumstances that produce a catecholamine surge can do it too.
https://www.ncbi.nlm.nih.gov/pubmed/25628339

Med Sci Law. 2016 Apr;56(2):85-90. doi: 10.1177/0025802414568483. Epub
  2015 Jan 26. Sudden cardiac death with stress and restraint: The
  association with sudden adult death syndrome, cardiomyopathy and
  coronary artery disease.
Krexi L1, Georgiou R2, Krexi D1, Sheppard MN3. Author information
  Abstract OBJECTIVE: The aim of this study was to report on sudden
  cardiac death (SCD) during or immediately after a stressful event in a
  predominately young cohort. METHODS: This study used retrospective
  non-case-controlled analysis. A total of 110 cases of SCD in relation
  to a stressful event such as altercation (45%), physical restraint
  (31%) in police custody (10%), exams/school/job stress (7.27%),
  receiving bad news (4%), or a car accident without injuries (2.73%)
  were retrospectively investigated. The majority of the subjects
  experiencing SCD were male (80.91%). The mean age was 36 ± 16 years
  (range 5-82 years). Twenty-three cases (20.91%) were psychiatric
  patients on antipsychotic medication. RESULTS: Fifty-three per cent of
  cases died with a negative autopsy and a morphologically normal heart,
  indicating sudden adult death which is linked to cardiac
  channelopathies predisposing to stress-induced SCD. Cardiomyopathy was
  found in 16 (14.5%) patients and coronary artery pathology in 19 (17%)
  patients, with atherosclerosis predominating in older patients.
  CONCLUSIONS: This study highlights SCD during psychological stress,
  mostly in young males where the sudden death occurred in the absence
  of structural heart disease. This may reflect the proarrhythmic
  potential of high catecholamines on the structurally normal heart in
  those genetically predisposed because of cardiac channelopathy.
  Structural cardiomyopathies and coronary artery disease also feature
  prominently. Cases of SCD associated with altercation and restraint
  receive mass media attention especially when police/other governmental
  bodies are involved. This study highlights the rare but important risk
  of SCD associated with psychological stress and restraint in
  morphologically normal hearts and the importance of an expert cardiac
  opinion where prolonged criminal investigations and medico-legal
  issues often ensue.

I guess by "average" I mean average health

Edit that quote. Please. better yet, summarize in your own words what's important, then support it with a snippit. This is too much copypasta. Also, how does the abstract support your comment about restraint?

If I edit a quote it is not a quote any more.  I summarize in my own words at the top.   As regards restraint, the question was about being frightened but the persons suffering sudden death underwent a range of catecholamine-inducing events including non-scary ones.  I suppose the car accident would be frightening also.


text:
Identify this insect - unknown location
Please help identify this insect - genus, species and anything interesting about it.
(Part of this old thread.)

The link is broken...

yes, the link isn't working. so i don't know if the link would have explained that this and your other question is about computer modeled insects. https://www.cgtrader.com/3d-models/animals/insect/insect-collection-vol-2 i'd think that's kind of important to know!

It is a beetle of the genus Eudicella.
There are several species and some look quite similar, they are from tropical Africa.

which would you pick for species identification?

Eudicella gralli would be my guess but I do not know enough the group to be 100% sure.


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Identify this insect - beetle (?)
Please help identify this insect - genus, species and anything interesting about it. (Species of beetle?)
Old link - please vote to un-delete it https://biology.stackexchange.com/questions/64042/can-you-identify-these-insects?

That's a red rhinoceros beetle. Although, "red rhinoceros beetle" is not the correct name. I'm simply observing that it is red, and that it is a rhinoceros beetle. So, according to wikipedia: suborder Dynastinae. Do an image search for "red rhinoceros beetle" and you'll stuff that looks quite similar. Searching google for that specific image show's that it is a 3d printed model. The list of bugs in list of 3d printed models includes something called "Rozenkever". Which is remarkably similar to "Red Beetle" in German.
Golofa porteri perhaps

Here is a gallery of this 3d printed beetle. Also, the artist of that beetle is from Belgium, so the translation makes sense.

Is there any way we can get this down to the species identification? the missing link from above, long story short, the artist sent these files to me without proper naming for an entomology app I'm developing. https://biology.stackexchange.com/questions/64042/can-you-identify-these-insects?

golofa porteri seems likely then.

@Charles Translation makes no sense at all. Rozenkever is Dutch, not German and means "rose beetle", not "red beetle". Your link shows an image, with the name "Meikever", meaning "May beetle". However, this is not a meikever Melolontha melolontha.


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Visual maps of the neuronal membrane
There are lots of visual maps of the brain as a whole, especially the cortex, that show the distribution of "features" over a two-dimensional map, e.g. the Brodman areas (their morphology and their functions), or the cortical homunculi.
What I would like to literally see - on a quite different level of resolution - are density distributions of some "items" over the membrane of some prototypical neurons, especially:

excitatory synapses
inhibitory synapses (mainly on the soma?)
vesicles (not in, but near the membrane)
receptors (not only at and near synapses?)
the different ion channels
electrical synapses
sodium–potassium pumps

So my question is for instructive graphical displays of such distributions, may it be in an article, on a website, or in a book.
(I assume that none of the items above is distributed evenly. But maybe some are on a specific type of neuron?)

I can easily answer about excitatory synapses and perhaps about receptors, and some ion channels but your question is too broad and I'm afraid any answer is going to be too lengthy. Please consider breaking it up.

Why not breaking up answers? I am not especially interested in one of the "items", any single example is welcome (but of course I would appreciate as many as possible - this would allow for comparisons and detecting of correlations). At other StackExchange sites such questions are called "big list" question and are rather well-liked.

With biology, though, there is bound to be nuance involved. So, a whole discussion is required for any of the 'items'. Furthermore, when you ask about categories such as 'receptors' or 'ion channels' which each have numerous members you are expanding the scope of the question (and the answer) substantially. Lastly, you are not asking for just a list but rather the full distribution of each category on a cell, which requires more than just mentioning a single number.

In fact I am only asking for (samples of existing) "instructive graphical displays". If there aren't any: what a pity! If there is only one:I would be happy to see it. (I cannot see, which discussions are required to answer my question. Am I too naive?)

Also, this website's guidelines suggest to ask and answer specific questions (https://biology.stackexchange.com/help/how-to-answer), and for good reasons, I think. Making a thread tractable facilitates both answering and perusing.

Please tell me, what is unspecific about my question? In which respect is it vague? (I admit it is broad, because it allows for a lot of answers. This makes it a "big list" question. But what is bad about "big list" questions?)

For example, answering about excitatory synapses would require me to discuss how they were measured with sufficient detail that someone could evaluate what I would present. There are some technicalities that are important in those studies. It would also require me to mention in which cells their distribution was evaluated. Additionally, and based on the previous comments, it would be necessary to present the two contrasting theories and how they take this evidence into account. All these would be required in my view in order to give a comprehensive answer, just for this part of your question.

Let us continue this discussion in chat.


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How does coconut form?
I've seen that at the earlier stage coconut is filed with water and, as time passes, the water inside the coconut escapes and a thick layer of white substance forms.
Is the water converted into that white substance?

There is no water escaping from the coconut seed. The transformation of coconut water into coconut meat is explained by the development of the endosperm.
What happens is that, after the (double) fertilization, the endosperm of the coconut forms by nuclear division without cellular division, that is, without the formation of cell walls. This is called nuclear endosperm. According to the Wikipedia link above:

Nuclear endosperm formation → where repeated free-nuclear divisions take place; if a cell wall is formed it will form after free-nuclear divisions. Commonly referred to as liquid endosperm. Coconut water is an example of this. (emphasis mine)

So, in an oversimplification, think about the coconut water as the cytoplasm of a single, huge cell, full of hundreds of nuclei.
After some time, cell walls surrounding the nuclei start to form. This is what we call cellular endosperm. According to the same link:

Cellular endosperm formation → where a cell-wall formation is coincident with nuclear divisions. Coconut meat is cellular endosperm. (emphasis mine)

Therefore, in the coconut, the endosperm is initially nuclear (coconut water) and, after some time, becomes cellular (coconut meat).
According to Abraham and Mathew (1963):

Cellular endosperm development becomes visible in nuts about 6 months old, at which stage a thin coating of jelly-like endosperm tissue is seen around the periphery of the large embryo-sac cavity.

This image shows those two tipes of endosperm (and helobial endosperm as well):

Source:

ABRAHAM, A. and MATHEW, P. (1963). Cytology of Coconut Endosperm. Annals of Botany, 27(3), pp.505-512.


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What is a proper software to do GWAS analysis of tuberculosiis VCFs and phenotype data?
What is a proper software to do GWAS analysis of tuberculosis VCFs and phenotype data? Need a software which will accept VCF file and phenotype data as an input and produce genome wide association with a report generation.

Have you tried https://omictools.com/gwas-category ?

thx, need 1 or two most relevant can`t experiment with a 100 of them

Analysis of GWAS data generally requires quite a bit of data cleaning, as well as imputation, and the structuring of covariates. These are typically done on unix based clusters with some expertise in bioinformatics and are hardware resource intensive unless the number of subjects is very low.


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Is far Infrared heaters in the market truly producing healthy far Infrared and is it practical to install them at home?
I read few blogs and websites about far infrared heaters and all are very possible about this new technology. I bought one of the heaters as a test and find quite impressive also.
However, I am concern about long term health effect. I know, there is no health effect of far infrared but the Heater that is producing infrared, is it truly producing only far infrared?
This business is not regulated so What Type of test (or certificate) the heater has to pass before coming in the market?
I am planning to install this heaters in my whole apartment, anyone has experience to live in a flat/house with far infrared heater? if then can you please share your experience? Is it medically healthy?
Thank you very much.

Far infrared is also known as thermal radiation. It is less harmful to the human body than red light and blue light. If you are under a cloudy sky and it is hot, say 30 degrees, that is how harmful thermal radiation is to the body.
The hight you climb up the electromagnetic spectrum, from radio waves to thermal waves to light waves to UV Xrays and Gamma rays, the more they can interfere with atoms and molecules, because they can disrupt bonds, ionize, and so forth.
So IR can only heat the body and can't ionize or disrupt the body.
Far infrared is the heat you feel when you are far away from a fire and the heat travels towards you without air transport. Near infrared is the heat you feel closer to the radiator, and that which causes convection nearest to the heat source, it gets absorbed faster by the air.
Insulation is most important for heating, as more than 50 percent of heating is lost through the ceiling. modern buildings in the west have high roof insulation standards.
oil heaters tend to absorb near infrared and reflect it back as far infrared better.
I think that the smaller and hotter the source, the nearer thermal wavs it produces, and the larger and less hot surfaces can make more far infrared.
It sounds like a lot of marketing terms.
Oil heaters are traditionally very efficient. I had one which i bought a bit rusty for 15 euros and it has lasted 5 years. the only issue with oil heaters is that they can eventually leak when very worn or less strongly welded.
microwaves are less HF than thermal, and they have not been associated with any health risks either even from phones used all day beside the ear.
You can think of far infrared as the warmth that is reflected from a hot wall heated by the sun. It is one of the least dangerous forms of radiation.
you may consider investing in a HPS lamp of 600 or 1000w because it produces 90 percent heat from that, and also vast amounts of light which are good for mental biology and good for growing tomatos and strawberries in the middle of winter. because they go in a ventilated area under a table in the house, the also radiate well. of all kinds of radiators, i prefer by far sitting under a hot lamp with a summer hat tending plants in the middle of winter, it's definitely hot. A 600W lamp can produce about 200 tomatos, 100 strawberries and 20 peppers and some melons/beans etc, in the winter months.

Thanks for your wonderful reply. I am not using far infrared heater outside though. I will use inside in my house to get heat in this coming winter. more or less 16 hours i will get heat from these heaters. I am a small child. My main concern is on her health. These heaters are cheap and feels comfortable. just i am concert about longer term effect. In UK I haven't seen any far infrared heating system. I wonder why?

hot tea is also full of radiation. so how is an IR heater made... some electricity passes through some flat metal zigzags of a larger surface area than a normal heat and the heat is therefore lower on a larger surface. that's all it is. you generate far infrared inside your own body, about 50W of it. it is radiation because you emit heat. it's safe, probably better than a cheaper heater, both are safer for your child than pesticides on fruit, factory foods and excessive cleanliness, none of which are healthy, 100 degrees radiators are as healthy as standing beside a hot pan of water.

Thank you very much. I am using FI heater now and feel really comfortable at home and cheaper heating.


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What happens to the cut-out introns from a pre-mRNA?
Once the spliceosome has cut out the introns from a pre-mRNA they are said to be degraded. What does that mean and is that happening in the cytosol? Can the nucleotides be used for something else within the cell?

Yes. Ribonucleases (RNAses) break down the spliced RNA strands back into mononucleotides, and these building blocks can be reused.
They will be broken down into nucleotide monophosphates, so they will have to be re-phosphorylated to triphosphates before they can be reused for transcription.
Here are a couple of reasonable reviews of the mechanisms:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177198
Note: this one also mentions that sometimes introns are not fully degraded to single nucleotides, but instead can serve as signaling molecules.
http://www.sciencedirect.com/science/article/pii/S0092867409000671

Not just signalling, some are ribozymes. Group I ans II introns are good examples.

Another use for a spliced out intronic piece of RNA is as noncoding RNA. Here's an example which include pre-mRNA also transcribing microRNAs.
http://www.nature.com/nrm/journal/v10/n2/fig_tab/nrm2632_F1.html?foxtrotcallback=true


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What does metal-dependent mean?
I was reading about Cas1 and Cas2 and came across this excerpt:

...Cas2 was identified as a metal-dependent endoribonuclease that cleaves ssRNA or dsDNA...

What does metal-dependent mean in this context?

What is the source of this quote?

Here, http://www.cell.com/cell/fulltext/S0092-8674(15)01321-5 it's (the quote) at the beggining

It means that these enzymes need a metal ion as a co-factor for their function. This metal ion is typically bound somewhere near or in the active center and helps stabilizing transition states.
Without these metals, these enzymes cannot function properly, that's why chelating agents are used in protein or DNA preparations to inhibit their function.
References

Information available at cut rates: structure and mechanism of
ribonucleases.
The Role of Metals in Enzyme Activity


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How big is the change in proteins due to alternative splicing?
How different can the proteins be that are coded from the same DNA-sequence but undergoe alternative splicing?
What I am trying to wrap my head around is why we are so fixated with the DNA-sequences and what they are coding for, if the outcome can differ a lot due to alternative splicing.

For your first question, They can vary dramatically.
I did not originally post as a formal answer because my statement below is hard to cite a source and would therefore be somewhat subjective, although I am pretty confident in the assertion. It is based on my own experience in both GWAS and EWAS literature reading. My research concerns methods for analysis of such data.
To answer your second question, the main focus has shifted from genetic variation (still done though) to expression variation and epigenetic variation. The expression research focuses exactly on the type of issue you are discussing with alternative splicing, and this is largely possible because of the decrease of the cost of RNAseq. We aren't as fixated on sequence anymore; the advent of GWAS, once thought to be a panacea for the explanation of disease susceptibility has only ended up explaining a fraction of genetic heritability estimates. Not to say it isn't focused on, just in the context of other types of variation and environmental exposures.


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Drinking and eating ability of infants soon after birth
How do infants know how to eat, drink without being taught? How do they get this ability soon after birth?

It's called instinctual behavior. And they have very, very many abilities after birth: the ability to swim (rudimentarily, not like Michael Phelps), take steps on a hard surface, to cry, to open their eyes, etc., etc.

These are just reflexes which are executed involuntarily, they need not to be learned , but are present naturally in the neural circuitry.


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Preparation of dihydroxyacetone phosphate from glycerine by fermentation
I read on Wikipedia that
dihydroxyacetone (DHA) can be obtained from fermentation of glycerin. I would like to obtain dihydydroxyacetone phosphate (DHAP) for a science experiment but, since I'm 15, I cannot purchase it.
So I'm gonna have to make some if I want it.
With that being said, how do I properly ferment it, and how do I phosphorylate it? (I have phosphoric acid at home, maybe that would do the trick...)

I'm not convinced DHAP is easy to obtain by a fermentative process: it's an intermediary of glycolysis, so it's probably not accumulated.


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Indicators of Ras binding domain (RBD) activity in Ras effector proteins?
Ras family based small GTPase proteins usually have a Ras binding domain (RBD) in their effector downstream proteins like Raf. Roughly Ras proteins cycle between active(GTP-bound situation) and inactive(GDP-bound) states. So what information is passed onto RBD when Ras protein is active in a Ras:Raf complex. It is well known that Switch-I , Switch-II root mean square fluctuations(RMSF) of inactive Ras protein is very high. In the active Ras case the Switch-I RMSF falls by making that loop rigid.
So my question is that is there any observables like RMSF of RBD region indicate the "activity" of effector molecule(like that of Raf). In other words how do I understand that the RBD region is active/inactive (say from simulation perspective or experimental perspective) ?
Please suggest me any related references or links.


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What is this plant with pink flowers and maple tree shaped leaves?
This plant goes in my front yard in morning sun in the interior of British Columbia.

It has green leaves initially and then they curl brown and turn yellow. It gets water weekly but not lots. Is it okay to divide this plant to thin it out?

It's a Japanese Anemone (Anemone hupehensis); if I had to guess, I'd guess it was the cultivar "Robustissima".

I used to grow these when I had gardens. Absolutely you can divide them! Wait until the spring if you can; if you have to divide in the fall, wait as long as you can to do so.

What kind of climate can these grow in? I really like them..

I love them; they're easy to grow , they last long, the seedheads are charming, and they're hardy perennials. What's not to like? They're hardy in zones 4 - 8.

thanks so much for figuring it out for us.  It is beautiful and looks like the hot location in the garden means it needs more water so the leaves don't turn brown.


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Energy transfer from P680 to oxygen-evolving complex
This topic is confusing me.
As I understand it, in the PS2, photons are used to split water into molecular oxygen + protons and electrons in the oxygen-evolving complex. To do this, a photon is used to excite an electron in the P680, this electron is then released to go through the electron transport chain and somehow the oxygen-evolving complex gets energy from it to make water endure a "photochemical reaction" as described in my biology book.
But how the electron can transfer its energy to the oxygen-evolving complex if it went directly to the electron transport chain? how the energy produced in the P680 transported to the Oxygen-evolving complex?
I would appreciate simple terms as I'm still a college student.

You have to think the other way around: don't pay attention to where the electron from P680 is going.
Instead of that, pay attention to this fact: after PSII absorbs a photon and triggers the loss of an electron from a P680 chlorophyll a molecule, this P680 has now an electron deficit. That is, this P680 has lost one electron.
This P680 without one electron is now called P680+. And here comes the important information, which answers your question: According to Lodish (2002),

P680+, the photochemically oxidized reaction-center chlorophyll of PSII, is the strongest biological oxidant known. (emphasis mine)

And that explains what (thermodynamically) drives O2-evolving complex (still according to Lodish, 2002):

The reduction potential of P680+ is more positive than that of water, and thus it can oxidize water to give O2 and H+ ions. (emphasis mine)

I hope those terms are simple enough for you. Finally, for better understanding all this, have a look at the concept of reduction potential (which, as a college student, I believe you have to study).

Source:

Lodish, H. (2002). Molecular cell biology. 4th ed. New York, N.Y.: Freeman.


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World population pyramid since 1800
I am interested in understanding how the global population pyramid has changed in the last couple of centuries.
I have two questions:
1) Has this been calculated? Are there estimates of population pyramids from the 19th century? Or from the beginning of 20th century? The earliest I have seen is 1950 (below).
2) If it hasn't been done, how can I construct it? It should be possible to model the population dynamics using birth and death rates (I would be surprised if this hasn't been done, as it has many applications outside of demography - e.g. economics).

I'm voting to close this question as off-topic because it is not a question about Biology in the terms of SE Biology.

@David: I have edited the question to emphasise the population dynamics aspect. Similar questions have received answers, e.g. here: https://biology.stackexchange.com/questions/36715/what-is-the-percentage-of-people-living-in-england-in-1500-ad-whose-lineage-is-s?rq=1

Also this one here: https://biology.stackexchange.com/questions/32981/human-population-growth-where-can-i-find-the-data?rq=1

Just because people answer questions that are not about biology sets no precedent. The site is adminstered by its users and not everything that should be is caught. I just call them as I see them. It will take another four like-minded reviewers to put your question on hold. They may not materialize.

Makes sense. Let's see how the others see it. And I would be of course happy to migrate the question elsewhere if anyone has ideas of a better fit.

Global seems like quite a far fetch to find out for one of us. It's therefore a research question, you would find out by searching for as old pyramids as you can find for various population types in the past and present and making an estimate of totally un-industrial types versus transition and modern types.

I am voting to close because it is a question of geography, not Biology.

@EOO The first post you link is clearly about population biology. The post you linked (which I asked), I agree, is arguably more about geography than biology.


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DNA replication, why complex
When the DNA replicates, it first attaches RNA since the DNA polymerase can't attach DNA in the 3' end. Why the replication is happened this way?
If the DNA polymerase can attach DNA from the 3', the replication process will be much simpler.
Is there a special reason for this?