text:
Chart of intra-species genetic diversity across species / phyla?
I am looking for information on how genetic diversity within a species (not between species) differs between taxa. In other words: Is the "spread" in the genetic pool, if measured, for instance, in terms of single-nucleotide polymorphism (SNP), generally bigger / smaller for some groups of species than for others?
My ad-hoc idea is that species with a stronger phenotypic difference between individuals, like homo, should probably have a higher genetic diversity (higher rate of SNP) than those with lesser phenotypic variation, like, say, Orthoptera (grasshoppers etc.). But I couldn't find any statistics or research on this topic.
I am especially interested in data on far-related taxa. Ideally this would be a chart with comparative data for Sponges, Annelids, Arthropoda, Fish, Mammals (single representatives of these groups), or even Plants, Fungi, Archeae, Bacteria …
I do not look for information on the actual genome sequences, nor on biodiversity, but specifically on the genetic diversity within species from different phyla.
This is my first question here, thanks for you help!

I don't know any resource you can use right now, but one thing you'll need to be aware of is that genetic diversity generally correlates with (effective) population size. This means that species like insects should generally have higher genetic diversity than mammals just because there are more of them in a given population.

You can look at the Heterozygous SNP rates in genome-sequenced species, which is a measure of within species diversity.
You have an example in Figure 4 here:
https://genomebiology.biomedcentral.com/track/pdf/10.1186/s13059-016-1090-1
You can see in the figure that endangered species are plotted (most of them with poor genetic diversity).
Also, I am afraid that your starting hypothesis is not very good. Our species is very poor in genetic diversity and has little phenotypic variation. The human species went through several major bottlenecks during his evolutionary history that reduced their diversity. Even gorillas or giant pandas are more diverse than humans. You have a bias because you are human and are good at differentiating individuals from your own species.
Also a single representative from each group won't suffice as the differences can be huge inside a group. Additionally phenotypic variation is hard to measure in certain groups.
Sorry for being a bit negative

Yes, my ad-hoc hypothesis is probably wrong, as becoming clear after some more research. On the other hand, if including ethological traits into "phenotypic diversity", the grasshopper-human comparison will still hold. But no direct correlation with genetic diversity.
Figure 4 is part of what I am looking for, but it should be inter-phyla.
One runs into a bunch of problems when asking the question as I did, I see. Will try to unsnarl this a bit more when reading on.

Turns out this is in fact a subject in recent discussion: "Understanding why some species have more genetic diversity than others is central to the study of ecology and evolution, and carries potentially important implications for conservation biology. Yet not only does this question remain unresolved, it has largely fallen into disregard. With the rapid decrease in sequencing costs, we argue that it is time to revive it." http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001388 and some more.

I did not say it was not possible, or not interesting to do it. Simply that humans are not a diverse species. In fact the HSNP value is quite easy to compute from a genome, if it has not already been calculated by the genome consortium responsible of the assembly.


text:
Is "Virus" a part of Acaryote?
I am just a beginner of BIOLOGY as a Grade 7 student!
But the information which I got from my textbook and Internet has got me confused as MY TEXTBOOK SAID:-

Viruses are part of "Akaryote"

And 'Acaryote' (or 'Akaryote' or however 'Akaryocyte') is just a Smaller group of ORGANISM than Prokaryote. Example:- Blood (As said in Wikipedia)
Pic-1:- A VIRUS DECRIPTION BY BBC

(END OF PICTURE 1)

Akaryote is not used for a group of organisms in the way that prokaryotes and eukaryotes are used.  The word akaryote is not a common word, but when used it is a synonym for akaryocyte meaning "a cell that does not have a nucleus" and is used in the context of eukaryotes, in which cells normally do have a nucleus.  (It is not used in the context of a prokaryote, which does not have a nucleus but does have a cell, or in the context of a virus, which does not even have a cell.)
The diagrams in your question have confused two different things.  The first illustration is indeed a virus, as stated.  The remaining illustrations are not of a virus, though.  You may have thought they were visually similar, but they are not similar in the details.  The "fibres" may look like like "flagella", but they are different.  The virus is not a cell and has no cell membrane. Viruses are not prokaryotes.

Sorry, My mistake of Visual Identification, However I could not find any helpful INFORMATION about "Akaryote"...... Also thanks for helping....

source: Stack Exchange

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

sort: votes


text:
How much blood flows to female breasts?
How much of the entire blood in the body blood flows to the breast (while resting). If you know the percentage or absolute values , as well as the total cardiac output, I would appreciate it answers or referrals to publications or tables. Thanks.

Maybe this paper is relevant, but I don't have access to it.

This paper has an answer for a normal tissue in a patient with cancer. It is known that also blood flow of normal tissue increases near the presence of a cancerous tumor.

By resting do you mean supine or upright?

Resting = sitting on a chair.

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


text:
Size of Apatosaurus
What are the current and up-to-date estimates of the size of the big sauropod dinosaur Apatosaurus (the biggest species of it) in terms of mass range (weight) and total length? I prefer the answer in metric units.

From the wikipedia page on Apatosaurus:

Most size estimates are based on specimen CM 3018, the type specimen of A. louisae.
  In 1936 this was measured to be 21.8 m (72 ft), by measuring the vertebral column.[5]
Current estimates are similar, finding that the individual was 21–22.8 m (69–75 ft) long and had a mass of 16.4–22.4 t (16.1–22.0 long tons; 18.1–24.7 short tons).[6][7][8]
A 2015 study that estimated the mass of volumetric models of Dreadnoughtus, Apatosaurus, and Giraffatitan estimates CM 3018 at 21.8–38.2 t (21.5–37.6 long tons; 24.0–42.1 short tons), similar in mass to Dreadnoughtus.[9]
Past estimates have put the creature's mass as high as 35.0 t (34.4 long tons; 38.6 short tons).[6]
Some specimens of A. ajax (such as OMNH 1670) represent individuals 11–30% longer, suggesting masses twice that of CM 3018 or 32.7–72.6 t (32.2–71.5 long tons; 36.0–80.0 short tons), potentially rivalling the largest titanosaurs.[10]

"Osteology of Apatosaurus, with special references to specimens in the Carnegie Museum". Memoirs of the Carnegie Museum. 11 (4): 1–136, Gilmore, C.W. (1936).
"A new method to calculate allometric length-mass relationships of dinosaurs". Journal of Vertebrate Paleontology. 21 (1): 51–52, Seebacher, F. (2001).
"Giants and bizarres: body size of some southern South American Cretaceous dinosaurs" Historical Biology. 16 (2–4): 71–83, Mazzetta, G.V.; Christiansen, P.; Farina, R.A. (2004).
"Burly Gaits: Centers of mass, stability, and the trackways of sauropod dinosaurs". Journal of Vertebrate Paleontology. 26 (4): 907–921, Henderson, D.M. (2006).
"Downsizing a giant: re-evaluating Dreadnoughtus body mass". Biology Letters. 11 (6), Bates, K.T.; Falkingham, P.L.; Macaulay, S.; Brassey, C.; Maidment, S.C.R. (2015).
"A giant, skeletally immature individual of Apatosaurus from the Morrison Formation of Oklahoma" 61st Symposium on Vertebrate Palaeontology and Comparative Anatomy - Programme and Abstracts: 40–45, Wedel, M. (2013).

So if I understand correctly, the largest Apatosaurus was about 26-27 meters long and may have weighed 50+ metric tons.


text:
Brood Parasitism - Parasitism/Ammensalism/Commensalism?
Parasitism has the parasite benefitting while the host is harmed. In brood parasitism, the cuckoo lays its eggs in a crow's nest for incubation. How does this harm the host? Why is it not considered ammensalism?
If I see the fact, while laying its eggs, the cuckoo might break some of the crow's eggs, and in this way the crow gets harmed. Parasitism from here fits.
But, as the chicks grow, the cuckoo chicks protect the crow chicks from other birds or predators. Seeing this, yet commensalism fits.
So, if I have to finalise which species interaction brood parasitism comes under, what should I select?
And why is that interaction preferred over the other?

It's called brood parasitism because it's parasitism (and not commensalism/ammensalism). Because the Cuckoo benefits at the expense of crow (crow's time and heat energy, and the harm posed by hatched Cuckoo to the hatched crows)

As this question focuses only on crows as hosts, does not mention egg or chick eviction, and refers to the cuckoo chicks protecting the host chicks from predators, I think that OP is referring to a 2014 study in which carrion crows appeared to benefit from the presence of a cuckoo chick (from a non-evicting cuckoo species). I've posted more on this in my answer below.

The cuckoo chick hatches earlier and instinctively pushes the host eggs out of the nest. If you view this from the genetic perspective of the crow, it becomes the foster parent of offspring that does not carry its genes. The harm, therefore, is to the host's passing on of genes, rather than to the immediate health or well-being of the individual.
For more information see:

Brood parasite (Wikipedia)
The Ecology of Avian Brood Parasitism (Nature)

And it's not just the eggs - cuckoo chicks are also known to push live young out of the nest!

Various aspects of this question suggest that OP is not asking about cuckoo/host interactions in general, but about research published in 2014 which appeared to show carrion crows (Corvus corone corone) in an area of Northern Spain actually benefitting from the presence of a great spotted cuckoo chick (Clamator glandarius) in the nest.
Unlike other species of cuckoo, clamator glandarius chicks do not "evict" the host eggs and chicks by pushing them from the nest. Furthermore, they are actually notably smaller than the crow chicks, making it harder to compete with them for food and host-parental attention.
Based on a 16-year dataset of observations, the researchers found that the average number of crows successfully fledged in a parasitized nest was $1.584$, versus $1.379$ for an unparasitised nest, suggesting an advantage to the cuckoo chick's presence. This particular cuckoo species had other hosts in the region, notably magpies (Pica pica), and no such advantage was observed for magpie hosts.
When attacked, chicks of this species could secrete

a malodorous cloacal secretion ... a mix of caustic and repulsive compounds, dominated by acids, indoles, phenols, and several sulfur containing compounds ... that are known to repel mammals and birds

The researchers conjectured that this ability bestowed a degree of protection on the other chicks in the nest, by repulsing predators and causing them to abort their attacks prematurely. Experiments showed that crows, raptors and mammalian predators were more likely to avoid meat that had been treated with this substance.
Other experiments were carried out, such as introducing cuckoo chicks to unparasitised nests and observing the effect this had on crow chick fledging rates, which appeared to support the aforementioned findings.
Based on this, the researchers suggested that this relationship may be more mutualistic than parasitic. To quote the paper:

We believe that the outcome of this parasite-host interaction may depend on predator pressure and thus fluctuates among parasitism, commensalism, and mutualism. ... It has been advocated that interspecific interactions should not be strictly categorized as parasitism, commensalism, or mutualism (21), because costs and benefits for each partner may vary in space and time, producing variable outcomes depending on the environmental context.

However, these findings have yet to be replicated. In particular, a study was published in 2017 in which another research group studied great spotted cuckoo parasitism of magpie, blackbird and common crow nests in southern Spain. They had four years worth of data for the crows, and eight for the magpies. This group did not observe the same benefits in terms of predator repulsion, or in the average number of fledged crows.
With regards to the secretions, they noted:

Great spotted cuckoo nestlings do not excrete the malodorous secretion when they are scared in the nest (personal observation), as does happen with hoopoe (Upupa epops) nestlings that are capable of throwing their faeces and cloacal secretions directionally against the predator [35], but only when they are grabbed (personal observation).

this secretion did not protect parasitized blackbird nests

direct evidence of a predator releasing a cuckoo chick is also lacking today. During nearly 30 years of studying great spotted cuckoos, we have ... never found any injured cuckoo fledgling in either magpie or crow nests.

the protection of crow nestlings would occur only in the case that predators attack the cuckoo chick first, which presumably would happen only in a fraction of predation attempts.

They also criticised the experimental methodology, claiming that the relative developmental stage of the introduced cuckoo nestlings did not match that which would occur in the wild.
The autors of the original study wrote a response in which they put forward counterarguments to some criticisms (for example, the same size in terms of number of nests being smaller in some years than others). In the case of the introduced-cuckoo-chick experiments, I am not entirely convinced by the counterargument, but am definitely not an expert in this field.
The authors of both studies agreed that further research with more data on different populations was needed.
In the aforementioned response, the authors stated:

Interestingly, a positive effect of the presence of cuckoo chicks on magpie nest success was reported in a different population in southern Spain (Sierra Morena) where carrion crows are rare and are not an important predator of magpie nests

However, the 1998 paper they cited in which this was supposedly observed is not available online (not even behind a paywall!) and so I can't offer any opinion on this. I have, though, looked at some of the other papers that cite it and have not seen any reference to this beneficial effect.
In summary, there may, depending on further research, be evidence that this particular cuckoo/host relationship has commensalistic aspects which are more significant than the parasitic. Or ammensalistic, if the differences in crow chick survival rates are not statistically significant. But this is not guaranteed, and future research with other datasets may show that the relationship is mostly parasitic.
Sources:
Canestrari, D., Bolopo, D., Turlings, T. C., Röder, G., Marcos, J. M., & Baglione, V. (2014). From parasitism to mutualism: unexpected interactions between a cuckoo and its host. Science, 343(6177), 1350-1352.
Soler, M., de Neve, L., Roldán, M., Pérez-Contreras, T., & Soler, J. J. (2017). Great spotted cuckoo nestlings have no antipredatory effect on magpie or carrion crow host nests in southern Spain. PLOS ONE, 12(4), e0173080.
Canestrari, D., Bolopo, D., Turlings, T. C., Röder, G., Marcos, J. M., & Baglione, V. (2017). Formal comment to Soler et al.: Great spotted cuckoo nestlings have no antipredatory effect on magpie or carrion crow host nests in southern Spain. PLOS ONE, 12(9), e0184446.
The Sierra Morena paper I couldn't find online:
Arias-de-Reyna, L. (1998). Coevolution of the great spotted cuckoo and its hosts. In: Rothstein S. I., editor. Parasitic Birds and Their Hosts, Studies in Coevolution. Oxford Ornithology Series, 9, 129-142.


text:
Determining the Value of Inhibition constant
I am trying to understand how the inhibition constant is calculated for competitive inhibition.
$\frac{K^{app}}{V^{app}} = \frac{1+I/K_i}{V/K_m}$.
But often in secondary plots, $\frac{K^{app}}{V^{app}} $ vs Inhibitor concentration is plotted and the inhibition constant , $K_i$ is obtained from slope $1/K_i$. How is the slope equal to  $1/K_i$ from the above equation?
Could someone explain?


text:
How does the number of chromosomes evolve through generations?
Mitosis is a complex mechanism that, through mutations and crossover, determines how a chromosome is composed. But at that point, the number of chromosomes is already determined: how can this number evolve through generations? What mechanism is involved?

A mutation is a general term referring to any alteration of a nucleotidic sequence. It includes small mutations like indels (insertion or deletion of a single nucleotide) and substitutions, or bigger mutations such as e.g. chromosome fusions, whole chromosome duplications, Robertsonian translocation, whole genome duplications and gene deletions. Some of these bigger mutations can affect the number of chromosomes (and ploidy number).
Such of these mutations can typically be caused by the non-disjunction of homologous chromosomes during meiosis.
Most of these mutations are deleterious but some aren't and might eventually fix (fixation = reach a frequency of 1.0) in the population.
A very common example of such mutations in humans is the mutation that is causing the Down syndrome.

Note that I mainly recycled this answer of mine but as the question is phrased in a much more pleasant way, I did not want to mark it as a duplicate.

your answer is interesting, thanks. Do you have some source you can suggest to read?

It appears to me that very introductory source of information tend to neglect those types of "big mutations" (e.g. evo101) and after that you're only left with slightly more advanced source such as a good textbook or directly in the scientific literature....

... I am not sure what to point to like that. I would advice you to just have a look at the wikipedia entries of gene duplication, Robertsionian translocation and others and go into the scientific literature (you can use GoogleScholar to search in the scientific literature) if you have a more accurate, clearly defined question about it.

Sure, but when a mutation reduces - in one individual only - the number of chromosomes like it happened some time ago for humans (chr. 2 fusion), how can it pass into the germ line with a population having one mutant only and all other indiviuals with a different karyotype. Pathenogenesis being ruled out.


text:
White flower with spikes around base?

What type of flower is this?
Location : India

Where (country / region, ecosystem) did you find it? What is the approximate size? What did the rest of the plant look like (size, appearance of the leaves, branches, etc...)? What other info can you give us?

This does in fact look like the flower to the cactus species Selenicereus grandiflorus.

 Source: Wikimedia
According to "Indigenous Cactus biodiversity: A viable genetic resource to fulfill multiform needs under rainfed ecosystems"1, this plant is found in India:

Different varieties of the cactus are found in India which has immense ethnomedicinal value (Table 1). Selenicereus grandiflorus (with large sweet-scented night flowering flowers) and the Opuntia stricta are found in the wasteland as hedge plants

See here for a good image, and see here for a cool gif of one of these flowers blooming!

1. Rai, M., Singh, R.K., Sharma, P.C. and Singh, L.K., 2011. Indigenous Cactus biodiversity: A viable genetic resource to fulfill multiform needs under rainfed ecosystems.

This could be Selenicereus grandiflorus, the Queen of the Night.

Welcome & thanks for your post. Species ID answers should be accompanied by credible sources confirming that ID, a picture of the species from a credible source and background information confirming the species (geographical spread, habitat, ...)


text:
Describing the location of the thalamic adhesion in simple English
I'm trying to describe the location of the thalamic adhesion as part of a personal project. I can't reference pictures, and I need to be as precise as possible without using convenient anatomical terms (e.g., dorsal, superior, etc.).
I have to use plain and simple English, with a consideration for people who speak English as a second language. My approach is to describe its location relative to more prominent and easily recognized body parts (e.g., bones and organs on the face or side of the head).
In every English construction I've tried, I first start by describing it as being located in the middle of the head. Then I describe its location in reference to common body parts on the transverse and coronal planes.
Most X-ray pictures I've found are only somewhat helpful to me here, because they're a sagittal cutaway of the head but they don't include the ear. Based on the X-rays, I'm confident that it's located at about the same level as the eyebrow ridge on the transverse plane.
The big problem I keep running into here, is that almost every drawing and rendering I find on the internet seems to put the thalamus in different locations on the coronal plane. This makes it pretty hard for me to find a precise coronal location for the thalamic adhesion.
In some of them it seems to be where the tragus of the ear meets the mandible. Some of them draw it further forward, more towards the mandible. In other illustrations it's drawn further back, almost directly above the helix of the ear.
I'm not a physician and I can't remember how many years ago it was that I took an anatomy and physiology class. So my question is, where is the thalamic adhesion actually located in the human body on the coronal plane? Is it in line with the tragus, or the ear canal, or some part of the mandible, or does it vary from person to person?

Here are two possible translations of the above into simple English constructions:

The "thalamic adhesion" is in the middle of the head, as high as the eyebrow ridge, and as far back as the ear canal
The "thalamic adhesion" is in the middle of the head, as high as the eyebrow ridge, and as far back as the temple

Secondary question: could anyone with a more expert knowledge of human anatomy suggest better constructions?


text:
NAG, FUC molecules in PDB files
In some proteins (such as 4ZXB, 6CE9 which are respectively apo and halo forms of insulin receptors), I see ligands such as FUC (ALPHA-L-FUCOSE) and NAG(N-Acetylglucosamine). No matter which paper I checked I see no explanation for these ligands and therefore I assume they have to do with the experimental procedure but I do not quite understand what is their role. Do they stabilize a particular state of the protein? Note that the proteins above are determined by different methods the first one X-ray crystallography and the second by electron microscopy. I have no technical knowledge about the neither method so any input or link to a paper that actually explains them would be appreciated.
Thanks

The insulin receptor is a glycoprotein. This is discussed, albeit briefly, in both papers for the structures you mentioned and the glycosylation is visible in the structures themselves. You can get more info in the following paper, among others:
Sparrow LG, Lawrence MC, Gorman JJ, Strike PM, Robinson CP, McKern NM, Ward CW. 2008. N-linked glycans of the human insulin receptor and their distribution over the crystal structure. Proteins 71(1):426-439.

Yes this is the right answer. However I would make the following point (which you are welcome to incorporate). The PDB entry page visualizes manose, fucose and N-acetyl glucosamine as individual sugars. The paper you cite involves painstaking chemical analysis to show how the sugars are linked together into glycans (GlcNAc2Man6, GlcNAc4Man3Gal2Fuc etc.) and where they are linked to the protein. This emphases that the interpretation of X-ray crystal structures assumes linear polypeptide chains, but has no basis for assumptions on sugars, and the resolution is insufficient for this.

Thanks, since I was particularly interested in the insulin protein I will select this as the correct answer. As a side note to anyone who is interested this article discusses possible functional role of glycosylation for insulin: 1- https://www.sciencedirect.com/science/article/pii/S0167488900001099
2-http://www.jbc.org/content/274/32/22813.full

Apologia
This addresses the general case, rather than the particular case of the insulin receptor, which is answered by @canadianer.
The General Problem of unexpected ligands in PDB structures
In preparing a relation database of about 400 protein structures I encountered the problem of distinguishing ligands that were substrates or cofactors of the enzyme from those that were not. And, believe me, the latter were widespread (and a real pain). In some cases it was obvious that the ‘ligand’ was the buffer (often MES) in which the protein was dissolved or ions such as sulphate. In the case of sugars, I assumed that the latter were present to aid crystalization. That view seems to be supported — in some cases at least — by a review by McPherson and Gavira. In a list of eight categories of additives that are used in protein crystallization they include:

(v) Osmolytes, co-solvents and cosmotropes are compounds that exert their effects at relatively high concentrations, 1 M or more, and include a wide range of molecules such as sucrose, trehalose and other sugars, proline, TMAO, glycine, betaine, taurine, sarcosine and a host of others. The effect of their inclusion in the mother liquor is to stabilize (or destabilize) the native conformation of the protein by altering the interaction of the surface of the protein with water, or by altering the hydration layer and possibly the structured waters.

Example
As an example I cite the seven molecules of glycerol in 1B6G (shown below), a haloalkane dehalogenase from the bacterium, Xanthobacter autotrophicus. Although certain, usually pathogenic, bacteria do have glycosylation pathways, there is no suggestion that this is the case here, as indicated by the nature of the triose and the fact that the crystallization was performed in a glycerol solution:

Subsequently, the crystal was equilibrated for 0.5 h in a solution containing 70% ammonium sulfate and 100 mM MES buffer pH 5.0 and was then soaked for 3 h at room tempera- ture in 10 mM 1-chloropentane, 70% ammonium sulfate and 100 mM citrate buffer pH 5.0. A solution of 30%(w/v) PEG 6000, 20%(v/v) glycerol and 100 mM citrate pH 5.0 was applied as cryoprotectant during data collection.

Haloalkane dehalogenase, 1B6G. The glycerol molecules (grey and red) are shown in space-filling mode. (The yellow and red molecule is sulphate, the green one a chloride ion.)


text:
Inhibitory effect of GABA through GABA(A) receptors
Over at Wikipedia, the following is written in the article about GABA(A) receptors:

"Upon activation, the GABA(A) receptor selectively conducts Cl− through its pore. Cl- will flow out of the cell if the internal voltage is less than resting potential and Cl- will flow in if it is more than resting potential. This causes an inhibitory effect on neurotransmission by diminishing the chance of a successful action potential occurring." (https://en.wikipedia.org/wiki/GABAA_receptor, Accessed: 22 May 2018)

Based on my understanding, if an action potential is to be inhibited, the internal voltage of the neuron needs to be decreased further away from the voltage at which the neuron's voltage-gated sodium channels open up.
With this in mind, I take issue with the statement Cl- will flow out of the cell if the internal voltage is less than resting potential.... If the internal voltage is less than the resting potential, and the Cl- flows out from the cell, then the internal voltage will increase, hence coming closer to the action potential.
This would increase the probability of reaching an action potential, not decrease it, wouldn't it?
My Question: Does Wikipedia have it wrong, or is there something I haven't understood?

Great question! This apparent contradiction has puzzled many neuroscience students before you.
Short Answer:
This is often called "shunting inhibition," in particular when excitatory and inhibitory conductances are out on dendrites.
Longer Answer:
The part that is wrong is this (emphasis mine):

the internal voltage will increase, hence coming closer to the action potential. This would increase the probability of reaching an action potential, not decrease it, wouldn't it?

The idea that "hyperpolarization is inhibitory, depolarization is excitatory" is only partly true. It is very important to also consider what the spike threshold is, and to think in terms of reversal potential for a given ion channel (or more generically we can just call it a 'conductance'), and then you can revise the statement to say this:

Conductances with reversal potential greater than spike threshold are excitatory, conductances with reversal potential less than spike threshold are inhibitory.

Most often, chloride-based channels fit into the second statement: their reversal potential is less than the spike threshold.
How Shunting Inhibition Works:
Any time you open a channel, you will shift the membrane potential towards the reversal potential for that channel. The amount of current that flows through a channel depends on the 'driving force': the difference in voltage from the reversal potential.
Let's consider a fairly typical textbook cell, with a spike threshold at -50mV, a resting potential of -65mV, and a chloride reversal at -60mV.
If the cell is at rest, and you open chloride channels (such as with GABA via GABA-A receptors), the resulting flow of current will tend to push the membrane potential towards -60mV, so the cell 'depolarizes'. However, no matter how big of a chloride conductance you open, you will never pass -60mV, so you will never reach spike threshold.
If, in that same cell, you instead opened AMPA channels, with a reversal of around 0mV, you also get depolarization, but in this case as you open more AMPA channels you can potentially depolarize the cell all the way to 0mV. Of course, unless you have blocked sodium channels you will get an action potential before you reach that point, but that's the key: you will cross threshold, therefore we call it excitatory.
Now let's consider a third case where we open both AMPA channels and GABA-A channels. As long as the membrane potential is <-60mV, both channels contribute to depolarization. However, as soon as the membrane potential is >-60mV, chloride ions will start flowing into the cell. We call this "shunting" inhibition because if you look at the sum current flow in the cell, it will look small, because you have chloride ions coming in at the same time as sodium ions, resulting in little change of the membrane potential despite lots of ions moving.
The result is that GABA-A channels, even if they can depolarize a cell that is at rest, will act to prevent the cell from depolarizing far enough to reach threshold. It's important to consider the dynamics of the membrane potential, rather than thinking of the membrane potential as something that is simply added or subtracted to instantaneously.
Important Caveats:
Ion concentrations matter! If chloride concentrations are not 'typical' or if the spike threshold is more negative than in a 'typical' textbook cell, then chloride conductances can indeed be excitatory! In fact, excitatory GABAergic transmission is important are certain stages of development. If cells have too much chloride in them, this can also cause GABAergic transmission to become excitatory (or at least limit the efficacy of the inhibition), and this can lead to epilepsy (see Cohen et al. 2002).
There can also be a time window where GABAergic transmission is excitatory even in a typical cell: this is the period where the GABA-A channels have closed, but the membrane remains slightly depolarized and has not returned to rest. Excitation that arrives during this time will sum with the residual depolarization, and there are no open GABA-A channels to 'shunt' the current.

Alger, B. E., & Nicoll, R. A. (1979). GABA-mediated biphasic inhibitory responses in hippocampus. Nature, 281(5729), 315.
Cohen, I., Navarro, V., Clemenceau, S., Baulac, M., & Miles, R. (2002). On the origin of interictal activity in human temporal lobe epilepsy in vitro. Science, 298(5597), 1418-1421.
Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.


text:
The role of GC content in promoting or hindering transcription
This is quite a specific question, and I'm hoping someone might be able to assist in a literature hunt I've been engaged in for ages.
I study some long bacterial operons, and have noticed that the GC% content at the 3' end drops significantly compared to the beginning of the operon.
I vaguely recall hearing (I can't remember if it was from a paper or a lecture or something), that lower GC (higher AT) content can promote transcription. This sounds plausible to me since it promotes strand separation (this is how replicon origins are often defined), but I've tried several times to find a paper that might demonstrate/attest to this. The hypothesis therefore, is that the distal ends of the operon might have lower GC in order to enhance transcription as the influence of the 5' UTR promotor sequences etc being to wane over a distance.
Has anyone ever come across such a paper or has any information to confirm or deny this? Information to the contrary (e.g. high GC reduces transcription) would also suffice.

Why would you think that transcription would be controlled at the 3' end of an operon? Surely all that it could do there is help termination. I don't understand what you mean in molecular terms about the influence of the promotor sequences begining (?) to wane. The promotor promotes binding of RNA polymerase, that's all. And the promotor sequences are not part of the  5'UTR (untranslated region of the mRNA) as they are not transcribed into mRNA. Have you compared different operons in your bacterium? The problem with GC content is that this varies drastically among bacteria.

What makes you think that bacteria do not modulate transcription along the transcript? The influence of a promoter sequence is essentially strongest nearest to it due to the processivity (or lack of) of the RNA polymerase. Yes I have compared multiple equivalent operant across various related bacteria and this is a consistent trend. I believe it has some significance as bacteria have mechanisms such as transcript elongation to assist in transcribing very long sequences. That is, at least, my conjecture. I am positive I’ve heard of this as a phenomenon before now...

Now you mention it I have heard that there was a problem with reading long sequences, although whether this was transcription or translation I don't remember and can't find it. But I would be wary of the simplistic GC = stronger base pairing therefore more difficult to separate idea. There was expectation that thermophillic bacteria would have higher GC contents, but they don't, and high-GC genomes like those of the herpes simplex virus manage as well as the related low-GC varicella zosta.

This paper suggests the opposite in mammalian cells. Obviously, gene regulation is quite different in prokaryotes, so don't know how much confidence you want to put into that one.
This paper suggests more of the same, but includes some caveats related to prokaryotes that may pique your interest. They do a pretty in-depth dive of GC content near genes from many different species, but I haven't read it closely enough to give a good breakdown.


text:
Neurones and putting on clothes (Pacinian Corpuscle)
If I put on clothes, a gentle pressure is applied to the Pacinian corpuscles in the skin, causing Na+ ion channels to open and an action potential to be initiated - hence I feel the clothes on my skin.
However, I was reading that after prolonged time, the action potentials are no longer generated unless there is another change in pressure as the clothes again move over the surface over the skin.
I'm confused why. The reason I am given is that the Na+ ion channels remain open so a resting potential cannot be established, but I can't see how this contributes to the effect.
Can someone explain why?


text:
Why is hydrogen sulphide being generated on Caribbean beaches?
Once again, there has been a massive influx of Sargassum weed in the Caribbean. It is coming ashore on Atlantic facing beaches and forming piles up to 3m deep. As it dries and decays, hydrogen sulphide is being emitted. Why?

It would seem from a quick perusal of the literature that this is caused by sulphate-reducing micro-organisms. To quote from the eponymous Wikipedia article:

Sulfate occurs widely in seawater, sediment, or water rich in decaying organic material. Sulfate-reducing microorganisms are common in anaerobic environments where they aid in the degradation of organic materials.

which is consistent with the situation described.
In biochemical terms, these anaerobic bacteria are using sulphate rather than oxygen as the final electron acceptor (oxidizing agent) in the elctron transport chain which generates ATP through the chemiosmotic mechanism. The reaction for the reduction of the sulphate to hydrogen sulphide (dissimilatory sulphate reduction), according to the Wikipedia article already quoted, is:

A simple way of thinking about this is that in both aerobic and anaerobic respiration the oxidizing agent itself becomes reduced. Whereas oxygen is reduced to H2O, sulphate is reduced to H2S.

Thanks. I think you’re right. That suggests that agitation might stop formation of the gas.

Decomposing plants in fresh water also generate H2S. Anaerobic bacteria in deep underground strata generate H2S. , Also, sometimes in home water wells pumping water from shallow strata. The darn bacteria are everywhere.

What’s the best way to stop the process? Add oxygen (air)?

@Dave No, remove the rotting stuff.

@Dave — I personally wouldn’t know, but if you could arrange to fly me out to the Caribbean I would do my best to help. ;-)

It piles up to 2m deep at the high water mark and forms in a mat over 100m out to sea. The dogs can walk on it! If you clear a section of beach it refills at the next tide.


text:
Genes and Intelligence
Assuming that intelligence has a genetic component,
• do we know which genes contribute to it?
and, if so,
• can we predict intelligence from genomic analysis?

I'm voting to close this question as off-topic because it concerns a construct — Genetic IQ — that has no meaning, certainly no biological meaning.

@David Questions about predicting phenotypes from genotypes are perfectly valid and on-topic questions about biology.

@Eff — Remind me what "phenotype" the poster was asking about.

@David IQ. If you read this question--with respect for the fact that laymen will have trouble formulating their questions in very precise terms--OP is asking whether we can predict a person's IQ from their genotype. This is a problem actual biologists (specifically, geneticists) work on, so clearly it is a problem that is relevant to biologists.

@Eff — This is not a site for laymen, but for "biology researchers, academics, and students". My whole point was that the "phenotype" in the question was something referred to as "Genetic IQ" which is meaningless. Further IQ is not a phenotype and by its nature cannot be measured at birth. Intelligence is different. You appear to think that the question means "Assuming that intelligence has a genetic component, do we know which genes contribute to it, and can we predict intelligence from genomic analysis?", so I have edited it, but it is a duplicate.

Please cite your sources when you say that "IQ is not a phenotype and by its nature cannot be measured at birth". According to most definitions of the word "phenotype", it includes not only "structural" traits observable at birth, but also developmental processes, biochemical and physiological properties, behavior, and the products of behavior.

A few words on genomic prediction
No complex trait is 100% heritable, hence no prediction based entirely on DNA would ever be perfect. With that said, predictive genomics is progressing at a quite amazing rate right now. So while predictions can be nowhere near perfect, it is getting possible to make DNA predictions that correlate substantially with observed values.
The genes that correlate with phenotypic differences are found using genome-wide association studies (GWAS). The total effects are then aggregated up to what is called a polygenic score.
A success story --  Height
Height is highly heritable, meaning that much of the phenotypic variance (although not 100%) is due to genetic differences. Height is also highly polygenic -- it's a trait influenced by many genes, each of small effect.
Many variants that correlate with height have now been found. Polygenic scores of height correlate higher than ~0.60 with observed height. DNA predictions are generally within a few centimeters of true height (Lello, Avery, Tellier, Vazquez, de los Campos, Hsu, 2018). According to an interview with Stephen Hsu, one of the authors of this paper and co-founder of the company Genomic Prediction, they can correctly predict the height ordering of siblings within the same family 80-90% of the time (source). So based purely on DNA, can we say which of two siblings are going to be taller than the other? Not perfectly, but with decent reliably, yes.
This is about as good as predictions of complex traits can be based on current methods. There are a few principal reasons that correlations are not higher (even though it is quite impressive already in its own right). First, as I said, complex traits are not 100% heritable and therefore predictions are not expected to ever be perfect. Second, current GWAS are typically based on SNPs which are common gene variants. Rarer gene variants are expected to contribute to the variance and their effects are still needed to be uncovered. Third, only additive effects are taken into account, not gene-by-gene interactions.
Genetic IQ Prediction?
IQ, like height, is a heritable trait and is highly polygenic.
There are several approaches to finding gene variants correlated with IQ, however they can broadly be categorized into two. The most obvious approach is to simply give people intelligence tests and get their DNA. The problem with this is that it is difficult to get large samples with good intelligence tests. When this approach is used, usually a very short (say, 2 min) intelligence test is used. The second approach is to use a proxy phenotype. With this approach, the variable years of educational attainment has been used to good success, and has been shown to have a high genetic correlation with intelligence ($r_g \approx 0.7$).
Many variants that are associated with intelligence or educational attainment have been found, see e.g. (Lee et al, 2018; Savage et al, 2018). While many variants are known, IQ is not as well understood as height, and current SNP predictors correlate about ~0.3 with observed IQ (See e.g. Allegrini et al, 2018). This correlation is bound to increase in the coming few years.
Further Information
If you want a simple introduction to what can be read from the genome so far, there is a TED talk on this subject, TED2016: How to read a genome and build a human being. Although, major improvements have already been made in the years since 2016. For anyone that is more interested in the mathematical techniques used for prediction and the underlying theory, I recommend this talk by Stephen Hsu if you're further interested in genomic prediction of complex traits. I also recommend reading this review by Robert Plomin and Sophie von Stumm to get an easily understandable overview of the current state of knowledge on the subject.
References
Lello, Avery, Tellier, Vazquez, de los Campus, Hsu (2018). Accurate Genomic Prediction of Human Height. DOI: https://doi.org/10.1534/genetics.118.301267
Marty Nemko (2018). The Future of In-Vitro Fertilization and Gene Editing. Psychology Today Link.
 Lee, ..., Cesarini (2018). Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals. DOI: https://doi.org/10.1038/s41588-018-0147-3
Savage, ..., Posthuma (2018). Genome-wide association meta-analysis in 269,867 individuals identifies new genetic and functional links to intelligence. DOI: https://doi.org/10.1038/s41588-018-0152-6
Allegrini, Selzam, Rimfeld, von Stumm, Pingault, Plomin (2018). Genomic prediction of cognitive traits in childhood and adolescence. DOI: https://doi.org/10.1101/418210
Sabatini (2016). How to read a genome and build a human being. TED2016 Link to Talk.
Hsu (2018). Genomic Prediction of Complex Traits. Youtube Link to Talk.
Plomin, von Stumm (2018). The new genetics of intelligence. DOI: https://doi.org/10.1038/nrg.2017.104

This answer is clearly better than mine! +1

IQ typically has a relatively high heritability (see this post). Please have a look at this post to understand the concept of heritability.
In order to know what loci (QTL as the trait of interest is quantitative) are associated with a specific trait of interest, one must perform a GWAS The studies listed in the first pots linked above do not involve GWAS but only some kind of parent-offspring regression or twin studies to estimate heritability. From these studies, one cannot infer anything about a person's IQ from its genome.
GWAS studies on IQ do exist though (reviewed in Pfiffer 2015). It would be possible from one to make predictions and compute confidence intervals as well of someone's intelligence based on their genome, yes. I doubt anyone ever wrote such algorithm though. Without having such algorithm in front of one's eyes, it is impossible to tell, whether the confidence intervals are going to be very wide or very narrow though.

Why do you say you would need Bayesian statistics to get predictions?

To get a confidence interval at least. Or maybe one could use resampling but then you need to re compute the GWAS plenty of time which should take forever. I did not think this through though but it does not sound like easy statistics to me. The details of how to compute this confidence interval is not really on topic with the question but if you have some thoughts, I'll be happy to hear them for curiosity.

I was mostly just curious. I didn't think that Bayesian GWAS was done that much, because of the slowness in MCMC sampling vs. fast matrix algebra for "frequentist" GWAS. The traditional way will yield intervals as well, but probably too wide.

The Pfiffer paper compares IQ and genetic traits between distinct countries and ethnicities rather than IQ for single people as outlined in question above.

In order to make predictions for a single individual, you need to know the association between loci and the trait of interest through a GWAS. None of the cited paper offer an algorithm to make such prediction from a single person but one who would want to develop such algorithms will need access to this type of GWAS.

No, because the trait you describe does not exist
Your question betrays a common misunderstanding of how genetics and the environment interact in order to produce complex phenotypes. In fact, every biological trait is 100% genetic and 100% environmental. Don't believe me? Try teaching algebra to your cat, or see what height someone is after you've dropped them into the sun.
The only sense in which you have an "IQ you were born with" is the measurable IQ of a newborn child which I'm guessing this comes out as 0. Instead your IQ is a result of continuous interaction between genes and environment. You can say that at the end of process, across the population, 70% (say) of observed variation is explicable by genetic variation but this does not mean that you got 70 points of IQ from your genes and 30 points from the environment. The whole score is attributable to an interaction between the two. There is no "null" environment in which you would observe pure genetics, nor does it follow that increasing the range of environments encountered across your sample will increase the proportion of variation explicable by the environment. A gene that has no effect on IQ in one environment may have a marked effect in a different environment and you'd only discover this by varying the environment so both are encountered.
So, there is no trait "genetic IQ" to predict from someone's DNA, even if we had perfect knowledge of the link between genes and intelligence. Which we don't.

What I meant by "genetic IQ" was "What a person's IQ would be assuming optimal environmental conditions".

@Thomas That's not a meaningful concept.

@Thomas To expand on that: there is no way of knowing what the optimal environmental conditions would be, or that there actually exists a peak environment, and if it exists it will almost certainly be completely different for different backgrounds.

I notice that the question was substantially edited some six months after I posted this answer: the original asked "is it possible to tell a person's genetic IQ (the IQ he/she was born with) just by examining his/her DNA?"

IQ is pretty much like muscle strength, in the sense that you may have the right combination of genes that would give you extra strong muscles but the environmental factors do play an essential role as well.
Nutrition, training etc will have a profound effect on the development of your muscles. You cannot predict the effect a priori.
For IQ, it is the same thing. On one extreme you may have genetically-linked developmental diseases, physically impairing the normal brain functions, i/e/ negatively affects your IQ.
In most of the cases however, the effects of genetics on IQ is shadowed by the actual "brain training" you get during your life, by nutrition, and by other environmental factors.
So, yes, IQ is influenced by the underlying genetics.
Yes, in some extreme cases you can predict a very strong detrimental effect of some genes/mutations on the IQ.
For most of the cases, it's very hard to predict and genetics alone would not be enough to do so.


text:
How is it possible to breathe perfluorocarbon?
I have heard of liquid breathing, where an organism, usually a person, would be breathing in perfluorocarbon. Now I looked up perfluorocarbon on Wikipedia and I noticed, no oxygen at all, but fluorine that would rather bind to the molecules inside you and kill you. I mean, fluorine is electronegative enough to oxidize oxygen. So why doesn't perfluorocarbon fluoridate every oxygen molecule in your body preventing your cells from working and form calcium fluoride in your bones?
How would a person not be killed by breathing perfluorocarbon? Is oxygen more soluble in perfluorocarbon? Does perfluorocarbon not even get into the blood and instead stay in the lungs? And even then, why wouldn't the oxygen coming in be turned into oxygen fluoride? Is it simply because oxygen fluoride has such a short half-life, especially at body temperature that it never forms in significant enough amounts? But even then you would still be breathing out fluorine gas of which some will come back in the next breath. Fluorine gas is toxic because it is such a powerful oxidizer that it will oxidize anything.

At a guess, the fluorine in such molecules is in a stable enough state that it doesn't bind to haemoglobin. Perfluorocarbons have very high gas solubility. Perfluoromethylcyclohexane is one commonly studied for its gas solubility and potential use as an oxygen delivery system. There's a paper on this, but it's paywalled unfortunately.

Fluorine (or any atom) that's bound in a molecule has very different properties from the pure element.  Consider common salt, composed of sodium, a highly-reactive metal that spontaneously bursts into flame on contact with water, and chlorine, a poisonous gas used in chemical warfare (WWI).  Yet the combination is necessary for life.  Or the fluorine atoms in such things as toothpaste & non-stick cookware, or any number of rocks: https://en.wikipedia.org/wiki/Category:Fluorine_minerals

I think that's a chemistry.stack quesiton... Toxic chemicals are absorbed differently depending on their organic chemistry compatibility with the body... you can hold 200g of pure mercury in your hand without any risk of death, all day, but the lethal dose of certain mercury compounds is 1 drop for a minute, because pure mercury is not absorbed, whereas certain organic mercury compounds are so reactive that they can't even by synthesized without killing the researchers.

In liquid breathing systems the perfluorocarbons are simply an inert carrier for dissolved oxygen. It turns out that oxygen and other atmospheric gasses readily dissolve in perfluorocarbons without chemically reacting with them. Some perfluorocarbons can carry over 300 times as much oxygen as the equivalent amount of water. Perfluorocarbons are incredibly stable under conditions compatible with life, they aren't being broken down into free fluorine in you lungs or blood, or reacting with your tissues much at all. The perfluorocarbons don't cross the lung-blood interface in significant amounts.


text:
Scaling of Ca2+/biochemical signals with dendritic spine size?
I am looking for references that discuss the scaling of biochemical signals in dendritic spines with spine size/synaptic strength. A recent paper (Walker et al. 2017) reports attenuation of NMDA receptor Ca2+ signal with increasing spine size, consistent with a scenario where increase in synaptic efficacy (AMPAR/NMDAR conductance) is overcompensated by spine volume expansion. However, it is not clear to me if this trend is also reflected in the activation of downstream biochemical signals like calmodulin (CaM) or CaM-dependent enzymes. This relates to the issue of how the threshold for plasticity might be regulated as a function of synapse strength/spine size. Would be very interested in knowing if this kind of data has been reported in the literature.


text:
Is antivenom fatal?
Antivenom is used for curing snake bites. Is it fatal when used without being bitten by a snake?

1. Synopsis
I'd like to preface this by saying don't randomly use medicines without a doctor's advice. It's fairly unlikely antivenom would cause you any harm but in some cases, antivenom could be dangerous and even lethal. You have to consider possible allergic reactions and the route of administration. In any case, it would be a stupid idea to blithely inject yourself with antivenom for no reason, so why run the risk?
2. Introduction and Mechanism
Antivenom is made of a type of protein called an antibody. Antivenom acts by chemically binding to the animal's venom in such a way that the venom is blocked from binding to anything in your body. This prevents the venom from causing any damage. In fact antibodies typically bind very specifically, so they wouldn't usually bind to anything other than the venom itself. Hence, it's unlikely that antivenom would bind to anything in your body or cause any off-target effects if they were injected into your body.
3. Anaphylaxis
But antibodies are all proteins, and your body will be skeptical about any foreign protein since it could signal a pathogen. Hence, an injection of antivenom could cause an immune reaction and possibly lead to anaphylaxis. Anaphylaxis is potentially fatal, and it wouldn't be easy to know whether your body will have a reaction to the antivenom so basically keep random proteins out of your bloodstream.
4. Route of Administration
The way you introduce the antivenom to the body will have an impact on its effect. Consider what happens when you eat something. Your body passes the food from your mouth to your stomach, then liver and so on. At each step, the food is processed and broken down. In fact, chemicals like proteins are broken up during digestion, so they typically lose their effects. Hence, the effect of the antivenom will depend on where in this chain it enters the body, which determines how much it's broken down. An intravenous injection of the antivenom could have strong effects that you might be safe from, if you eat the antivenom. This is similar to the adage that you can potentially eat a snake's venom and not get harmed.
This is the reason antibody-based drugs are typically injected. By avoiding proteolysis of the antibody, it retains its shape and can successfully bind to its epitope.
5. Addendum
Your use of the word "cure" in the title is arguably slightly suspect. Antivenom doesn't stop or reverse the effects of venom that's already bound to chemicals in your body, antivenom just stops more venom binding.

“antibodies typically bind very specifically” — Tell that to biologists trying to optimise antibodies for ChIP, they’ll be delighted to hear that their hard work is unnecessary!

Aside: use multiple #s at the beginning of a line to introduce a heading, rather than bold plus two spaces at the end. This makes the formatting more uniform, and also makes the answer’s structure easier machine-readable. E.g. use ###1. Synopsis: instead of **Synopsis:**␣␣.

Hi, @KonradRudolph. Thanks for the note about formatting (I'd wondered about doing it that way but was slightly put off by the large line-break). Also, that's quite interesting about ChIP, I'd not read much about that before! I'd mostly encountered Ab specificity in regards to biologics and the immune sys (where Abs bind sufficiently specifically). Presumably the issue for ChIP is nonspecific binding, which undermines your data since you don't know whether you're binding to the protein of interest?

Precisely: ChIP assays are highly variable in quality depending on the binding specificity of the antibody. Antibody optimisation aims to improve this but is often costly and time-consuming. I’ve seen researchers come to opposite conclusions on specific research questions because they’ve used different, less specific antibodies (an example from my own research: the behaviour of pol III driven transcription).

Anti-venoms are not fatal. They are also ideally not fatal even if administered without any snake-bite, provided the anti-venom has been approved for clinical use by the pharmaceutical regulatory board for the country in question. World-wide, the Food & Drug Admin. (FDA of the USA) standard of phases of clinical trials is generally used or followed.
Anti-venoms become fatal if the person given the drug develops a hypersensitivity reaction to the drug, that is why a skin test using a small amount of the drug is injected intradermally on the forearm is conducted prior to giving the full dose of the drug. This way, toxicity is minimized, usually by not giving the drug when a positive test is unanimously declared by clinic staff.
Simplistically, a good rule of thumb to consider is that all drugs without exception are potentially toxic. That is why drugs are considered double-edged swords. Having accepted that, first, a drug should not cause someone to be sick if given to a healthy person. The related reasoning goes that if a drug causes a healthy person to be sick, then the more a sick person given the drug will more likely feel sick, i.e. 'sicker' than previously when he had no drug treatment. That is embodied in the Phase I clinical trial, where it is implied but not stated the Hippocratic oath 'First do no harm.' Hence, the subjects for that phase are (classically) generally healthy college students. By phase II, (classically) sick patients are added to the test population. By phase III, usually more hospitalised patients are included. By phase IV, generally out-patients become enrolled in the study, and so on.
For the drug company to recoup its investment in drug development, then a suitable sponsor agreement may be undertaken to administer the drug for free, and also to keep the drug industry afloat to develop more drugs.
Well-known snake venoms are phospholipases. Lipases are enzymes that can specifically target the lipid bi-layer of cell membranes of tissues and cause them to disrupt. Most anti-venoms are also enzymes that destroy these foreign lipases, and their toxicity may lie in their ability to disrupt our own lipases needed for critical bodily functions.

I'm not sure whether "destroy these foreign lipases" is the best description since the enzymes are still intact, albeit not functional. The mechanism of antibody-based inhibitors is to bind to the enzyme, such that the enzyme can no longer catalyze any reactions. It would be more like blocking the barrel of a gun, as opposed to destroying the gun itself.


text:
Can Programmable Cell Death (PCD) be engineered in a bacterium like E. coli?
I am reading a paper which says :
Messages not received after a certain time can be considered lost, as bacteria carrying them will suicide.
I even read some paper which says about PCD like this, but it just tells about a mechanism of Toxin and Anti-toxin.
My question: is there a reference which talks about genetically modifying E. coli bacteria (i.e. introducing a plasmid in it) which will cause cell death of the bacterium after a certain time. In short, we decide the life time of a bacterium after which it just commits suicide.


text:
Where can I find the pZ189vector plasmid vector sequence?
I need this sequence since it was used in this paper https://onlinelibrary.wiley.com/doi/pdf/10.1002/em.1046. They say that the plasmid was prepared as in this paper http://www.jbc.org/content/271/16/9637/F1.expansion.html (see figure below)

However, they do not seem to be reporting the sequence of the pZ189 vector. Does anybody know where can I find this sequence?

Did a search on NCBI and found a list of nucleotides. Maybe you need one of these https://www.ncbi.nlm.nih.gov/nuccore/?term=pZ189

Turns out the sequence is not actually written down anywhere. I asked one of the original authors of the plasmid (not the paper above) and he said that nobody ever did it because at the time when the plasmid was used it would have been a laborious task with little utility. Bummer :(
He also said that plasmid pSP189 is sort of the same but much more efficient and what it does, and is also more studied, with the sequence freely available around the internet.


text:
How to know which residues belong to the variable or constant regions of a Fab (fragment antibody)?
I have a fragment of antibody (Fab) structure, and I know its amino acid sequences of its heavy chain and light chain. As each chain of Fab can be divided into variable and constant regions, how can I know which residues belong to the variable or constant regions?
I can of course look at its 3-D structure in pymol, but it is difficult to know the belonging of residues between the variable and constant regions.

This link clearly shows how to identify the CDR regions based on its amino acid sequence. Is there a similar way to differentiate variable and constant regions?

The CDR is the variable region. I'm not quite sure what you're asking.

The CDR is only part of the variable region, i.e. the CDR is only part of the VH, VL. Could you please remove the downvote? Complementarity-determining regions (CDRs) are part of the variable chains

I stand corrected. I did not downvote, but I will upvote.

thank you! It is really frustrating to be downvoted without knowing the reason....


text:
What is the minimum number of clades necessary to partition Vertebrates while maintaining the classical groups of Birds, Mammals, and Amphibians?
At school I was taught the Linnaean view of vertebrate life - that vertebrate animals consisted of 5 distinct groups: mammals, birds, reptiles, amphibians, fish.
I learned later however that this was phylogenetically inaccurate, with birds being 'closer related' to crocodiles than other reptiles are, for example.
As such I am curious - since the idea of these groupings is so strong in popular conceptions of animals:
What is the minimum number of clades we would need in order to partition 'Vertebrates', maintaining 'Mammals', 'Amphibians', and 'Birds' as clades?

@Remi.b By completely partition I mean, every member of vertebrates belongs to one of the clades, and the clades are disjoint; by minimum I mean make the remaining clades as large as possible given the constraint Birds, Mammals, Amphibians are already clades. e.g. Crocodilians is 1 clade (considering smaller clades e.g. Crocodiles, Alligators & Caimans just increases the amount we need to consider, therefore not minimum), and it cannot be extended to form a larger clade as this would be (at least) 'Archosaurs', and hence absorb 'Birds', breaking one of the conditions.

Oh I got it now $\ddot \smile$. Here is the beginning of the tree of vertebrates and as you can see there are already quite of few branches that will need named to "completely partition the clade of vertebrates". One could just screen through tolweb.org (or some other similar ressource) and count.

Phylogenetic taxonomy of the Vertebrates (mun.ca) has the following graphic (14 clades total, minimum of 12 collapsing Amphibia):

Here, what was preivously 'Fish' (the paraphyletic group of non-tetrapod vertebrates) becomes 6 clades, and 'Reptiles' (the paraphyletic  group of non-avian Sauropsids) becomes 3.
It seems the question is equivalent to asking "what is the minimum number of clades necessary to partition Vertebrates while maintaining 'birds' as a clade?".

Related: https://biology.stackexchange.com/questions/88511/is-a-lion-a-bony-fish


text:
Why do scabs itch?
I have noticed that scabs formed over wounds itch a lot.
And if the scab comes off then the skin rarely completely heals and a scar is left.
Assuming scabs are important for the healing of skin ,shouldn't the scabs not itch?
Since they itch,we sometimes scratch them off which is detrimental to skin health and also can lead to infections.
If they wouldn't have itched, most people wouldn't scratch them off thus ensuring better health for the organism.

Part of this is due to the immune response to such an injury, which causes some amount of inflammation leading to histamine release - the introduction of this paper has a nice overview. In addition, mechanical stress on nearby nerves due to collagen fibers being reformed may increase the feeling of itch. The sensations of pain and itch are at least partially connected - there are pathways that are specific for each but also some that are shared. This is why pain can actually inhibit itch in some cases - like when you have a mosquito bite and slap it or apply a very hot wetted cloth to it.
This article gives a decent layman's overview of the connection between the two sensations. The sensation of itch still isn't fully understood, and there remains controversy as to how deeply it's actually tied to pain.

Shouldn't there be systems in place to damp this feeling cause it'd be beneficial to the organism if he doesn't scratch the scab?


text:
The information carried by nerve signals
Action potentials carry nerve signals in individual neurons and somehow encode information. My question is if it is possible to read that information carried by the nerve signal and feed it into a computer to understand what information it contains?

Neural info is contained in spike trains, mainly in terms of spike frequency and related parameters. These spike trains in individual neurons can be measured by techniques like patch clamp and Ca2+ imaging. These techniques are all pretty sophisticated and computer assisted for sure.
However, by recording of action potentials in e.g. the optic nerve, we cannot  possibly know what the person is seeing. Nonetheless, by cleverly mapping responses of conglomerates of neurons we can make estimates of what the information carried in the nerve fibers mean. For example:

Mapping the responses of an ensemble of place neurons in the hippocampus has been successfully used to predict where a mouse is exactly located in a maze (Guger et al., 2011);
Gross potentials measures with EEG can be used to move artificial limbs, as shown in physically handicapped people. In essence, by mapping out the responses of motor areas in the brain, it can be predicted where a person is thinking their limb is moving.

Reference
- Guger et al., Front Neurosci (2011); 5 85


text:
Difference between Genus, Genus sp. and Genus spp
What is the difference between the three following sentences?

There is significant increase in Bifidobacterium
There is significant increase in Bifidobacterium sp.
There is significant increase in Bifidobacterium spp.

Of course, this could be applied to any genus.

https://en.m.wikipedia.org/wiki/Species#Abbreviations

Is this homework?

Wikipedia:
Books and articles sometimes intentionally do not identify species fully and use the abbreviation "sp." in the singular or "spp." (standing for species pluralis, the Latin for multiple species) in the plural in place of the specific name or epithet (e.g. Canis sp.) This commonly occurs when authors are confident that some individuals belong to a particular genus but are not sure to which exact species they belong, as is common in paleontology. Authors may also use "spp." as a short way of saying that something applies to many species within a genus, but not to all. If scientists mean that something applies to all species within a genus, they use the genus name without the specific name or epithet. The names of genera and species are usually printed in italics. Abbreviations such as "sp." should not be italicised. When a species identity is not clear a specialist may use "cf." before the epithet to indicate that confirmation is required. The abbreviations "nr." (near) or "aff." (affine) may be used when the identity is unclear but when the species appears to be similar to the species mentioned after.


text:
RNA polymerase and DNA helicase
Is DNA helicase or RNA polymerase responsible for breaking the hydrogen bond between the 2 strands during transcription for eukaryotic cells? My textbook (WJEC Biology for AS level) says it is DNA helicase that breaks the hydrogen bonds while RNA polymerase catalyses the formation of bonds between RNA nucleotides.

The enzyme DNA helicase breaks the hydrogen bonds between the bases in a specific region of the DNA molecule. This causes the two strands to separate and unwind, exposing nucleotide bases. The enzyme RNA polymerase binds to the template strand of DNA at the beginning of the sequence to be copied.

However, when I searched online, for example on https://en.wikiversity.org/wiki/Effect_of_hydrogen_bond_on_RNA

Transcription can be explained easily in 4 or 5 simple steps, each moving like a wave along the DNA. RNA polymerase unwinds/"unzips" the DNA by breaking the hydrogen bonds between complementary nucleotides. RNA nucleotides are paired with complementary DNA bases. RNA sugar-phosphate backbone forms with assistance from RNA polymerase.

Then do RNA polymerase break hydrogen bonds? If RNA polymerase can break hydrogen bonds between strands then what is the role of DNA helicase in the transcription process?

Good. I was answering the question while you were updating your answer, but I hope it clarifies things. Read the section of Berg et al. carefully. Successful text books are big earners for publishers, who put a great deal of effort checking each new edition. So you are likely to get a clearer account from such texts. The only problem is fast-moving fields where the material goes out of date. Wikipedia entries can be a dog's breakfast.

Disclaimer
As I have pointed out in my comment, it is not clear whether the sources mentioned relate to eukaryotes or prokaryotes, assuming they are correct. I am a translation man, rather than a transcription man, and so am answering this from the 2002 edition of Berg et al. ‘Biochemistry’, as I happen to have a copy of my own (a freebie from when I was still teaching) and this edition is freely available online. List members with more expertise in this area are encouraged to post comments to correct any errors in my answer or supply updates.
Answer

in neither prokaryotes nor eukaryotes is the DNA helicase that operates during DNA replication involved in transcription although other proteins necessary for transcription have DNA helicase activity.
In prokaryotes it appears that the RNA polymerase holoenzyme (made up of just four subunits) is responsible for unwinding about 17 base-pairs of template DNA. Quoting from Section 28.1.3:

Each bound polymerase molecule unwinds a 17-bp segment of DNA, which corresponds to 1.6 turns of B-DNA helix

There may be some ambiguity caused by the description of how this value was determined experimentally as it involved addition of topoisomerase II. However it is clear from discussion elsewhere that this is an enzyme of DNA replication and is not involved in transcription.
In eukaryotes transcription is much more complex, involving separate polymerases for different classes of RNA product and a variety of auxiliary transcription factors in the case of RNA polymerase II, which transcribes mRNA. According to Section 28.2.4:

The TATA box of DNA binds to the concave surface of TBP [the TATA-box-binding protein]. This binding induces large conformational changes in the bound DNA. The double helix is substantially unwound to widen its minor groove, enabling it to make extensive contact with the antiparallel β strands on the concave side of TBP.

So the initial recognition of the TATA box causes some unwinding. However the major player appears to be transcription factor TFIIF:

an ATP-dependent helicase that initially separates the DNA duplex for the polymerase


text:
What is this bird - sound attached - (Atlanta Georgia)?
We live in Atlanta Georgia (northern suburb) & this bird starts singing in the middle of the night !!
And goes on for almost 2 hours without stopping.
Here is the link to it :
https://drive.google.com/open?id=0B3WzrpCj4uKeQ3l5MnJPY1RfcUpiVzkxRHBsWEN4RnYtTlNB
Any way to politely ask him/her to stop singing at night ? :)
Would highly appreciate any help in this regard !

It sounds like a Chuck-will's-widow; click the "sound" icon in that link for the song. They're native to Georgia and sing interminably at night, so the story checks out.

Thanks ! You are correct ! Now I just need to find out how to put it to sleep at night. Since it sleeps on ground, maybe I can do something..


text:
Major effects on cells grown with 5% FBS supplemented media instead of 10% FBS?
I maintain a few cell lines in the laboratory (industrial R&D) that I use regularly for experiments. I realized today that the media i prepared for the week on monday was only supplemented with 50 mL of FBS into 1 L of DMEM, instead of the usual 100 mL that i usually do. I was in a hurry and absentmindedly didn't add the second 50 mL autopipettor's worth.
My cells are fine morphologically but I think they're growing a bit slower than usual, my guess is due to the 1/2 concentration of all the FBS growth factors, etc. Are there any other effects that would be pronounced in these?
I understand that it will be apples to oranges to do compare results with these cells to, say, an experiment done with a batch of cells grown in complete (10% FBS supplemented) media.

If you were to run a flow-based viability assay (annexin V, live/dead fixable dyes, 7-AAD) or dual-fluorescence count (like acridine orange/propidium iodide, popular method as of late), you might find that more cells are undergoing apoptosis, or an increase in dead cells. I say this because trypan blue often overestimates viability. Your most pronounced effect should simply be a reduction in viable cells or a slower growth curve if you take those data points. Otherwise you'd need to run some test (fair example).
The problem being, these observations vary wildly based on what cell line you're using, lot-to-lot variability of the serum, and reagent handling. For example, the serum was heat-inactivated improperly, medium was degraded, bad lot of serum, and so forth. So take this as a generalization and a good reason to validate your serum lots.


text:
Difference between AjuA and ajuA in biosynthesis
I cannot for the life of me figure this out. In the following figure, you can find ajuA and AjuA for example.
I do understand that the lower-case ones are the genes. The arrows indicate the direction of transcription. However, what is the difference to the upper-case AjuA? The text speaks of subunits. How are the two related? When do I speak of ajuA and when would I be talking about AjuA?
I would also be happy if you could point me in the direction of some literature about the basics of this kind of notation.
PS: I do understand the mechanisms of the biosynthetic route and am familiar with the different domains in the modules as well as PKS and NRPS modules.

It's just the nomenclature:

Bacteria: Gene symbols are typically composed of three lower-case, italicized letters that serve as an abbreviation of the process or pathway in which the gene product is involved (e.g., rpo genes encode RNA polymerase). To distinguish among different [but related genes], the abbreviation is followed by an upper-case letter (e.g., the rpoB gene encodes the β subunit of RNA polymerase). Protein symbols are not italicized, and the first letter is upper-case (e.g., RpoB).

[source]
You can check out the Wikipedia article on Gene Nomenclature for more information.

But what is the relationship between gene and protein symbols? Can they be used interchangeably? The paper talks about AjuK containing a module, while "genes ajuK and ajuL encode the first two biosynthetic proteins". Does that mean, the gene ajuK for example encodes the protein AjuK, which in turn does biosynthetic stuff?

@basseur "Does that mean, the gene ajuK for example encodes the protein AjuK, which in turn does biosynthetic stuff?" Without reading the paper, yes that's what it sounds like.


text:
Names and abbreviations in biology
After one year in college, I am quite surprised with the number of different abbreviations used in biology for the same thing.
I wonder if there are any rules for naming something new in biology, for example new genes, or if it is just up to the researchers without restriction?  If there are rules, how did the confusion arise?

Can you provide examples?

What do you mean? This is not about examples mg! :D That wasnt a point of this question.

I have made some further modifications to the question to include more explicitly the obvious concern of the original poster that different abbreviations are used for the same thing. I have also extended it to the actual names, because the problem is in the name itself. In the case of gene symbols these sometimes are, in fact names rather than abbreviations, for example bacterial genes named A, B, C etc for a particular operon when their individual functions are unknown. Finally, I think the poster wished to know how the confused situation had arisen. I shall add my own answer about that.

Elsewhere on SE Biology I have answered a related question regarding enzyme names. Here I will restrict myself to genes, as it seems that this is the main concern of the poster. (In talking about ‘abbreviations’ I think he is referring to what are generally termed gene ‘symbols’.) The answer from @KarlKjer addressed current recommendations regarding gene nomenclature; mine addresses the causes of the current confusion.
Summary

Rules (actually recommendations) did not appear until a late stage in
the development of the field of genetics, when the problem was
already there and there was a need to do something about it.
Historically in animal systems the naming of new genes tended to
relate to mutant phenotypes as this was how they were discovered. The function of the gene that had been mutated was generally unknown.
Sometimes different mutants of the same gene caused different
phenotypes, either because of severity of damage to the protein, use
of animals from a different development stage, or different growth
conditions for bacteria. These mutants appeared to be of different genes, which
were given different names.
Sometimes the same gene was discovered at about the same time by
different workers and given different names in the laboratory while work was in progress and, hence, on publication.
Later it became possible in some cases to identify the products of
genes for which there was no clear mutant phenotype — perhaps just
lethality — and one method of naming was on the basis of the size of the
protein, preceded by the letter ‘p’ (e.g. p63)
The current trend is to try to rename genes according to the function
of their products, where these are known, i.e. to replace the name of a
mutant phenotype by the name of an enzyme or structural protein.
The implementation of such rules or recommendations is imperfect,
depending on the cooperation of authors and editors.

Illustration using some Drosophila genes
I shall use Drosophila melanogaster (the fruit fly) to provide some illustratations of the history of genetic nomenclature, because this was the organism used by Thomas Hunt Morgan (he of the centimorgan) to perform genetic studies after the rediscovery of Mendel’s work in 1900.  His laboratory was responsible for the discovery in 1910 of the first Drosophila mutant, a spontaneous sex-linked mutant that resulted in males having eyes that were white, rather than the normal red. The gene responsible for this mutant was named white, initiating the custom of naming genes after their mutant phenotype. (Drosophila gene names became italicized by convention.) What else could they have done? Not only was the protein product of this gene unknown, the whole idea of genes encoding proteins did not yet exist. The abbreviation (symbol) for this gene was merely w. Clearly, nobody anticipated that another 17,000 genes would follow, or suggested that a committee on gene nomenclature should be set up.
It is interesting to note that the product of the white gene was not identified until almost 90 years later. In 1999 it was established that this was a member of the ABC transporter family, responsible for bringing  into cells the guanine and tryptophan  needed to make the red pigment so characteristic of the eye of the wild-type Drosophila. The human version of white was identified roughly contemporaneously by sequence homology, and although it was initially referred to as hW (human homologue of white) is now named according to its gene product: ATP-binding cassette sub-family G member 1 (ABCG1). Its function in humans — who only have red eyes in flash photographs — is in lipid transport.
The era of of molecular genetics in the late twentieth century brought an avalanche of new genes, many not associated with a particular phenotype. The culture — accepted by scientific journals — was that if you discovered a new gene you had the right to name it as you pleased. A generation of young scientists were pleased to chose names that reflected twentieth century, rather than classical, culture. Flip through the names of Drosophila genes (try the autocomplete here) and you will find alien, bazooka, cactus, Dorothy, ether a go-go all the way to zucchini. Nor was it only the Drosophila geneticists that were responsible for this. The hedgehog segmentation gene, discovered in Drosophila, has three human homologues. One of these was named ‘sonic hedgehog’, which I am informed is the protagonist of a children’s video game. O tempora, o mores!
A couple of final points will be made to illustrate the problems of nomenclatue of Drosophila genes. Several other mutations of the white gene have been observed which have different phenotypes (e.g. result in different eye colour). This is because they involve insertions into the gene rather than its complete deletion. This also illustrates one historic difficulty that could result in several names for the same gene. The other point is that many of the genes identified by genome sequencing, at least initially, were associated with no mutant phenotype and had no known function, and were so named simply be an accession number (CG1234 etc.). As functions emerged they would be renamed. And an example of the nomenclature situation can be seen in the NCBI entry for Drosophila gene TfIIS (RNA polymerase II elongation factor):

Also known as: BG:DS00929.12; br52; CG3710; Dmel\CG3710; DmS-II; DmSII; l(2)35cF; l(2)35Cf; l(2)br52; l35Cf; RnpSII; TFIIS; TFIISA; TFS-II

Regarding the hedgehog gene, the name stems from the appearance of the larva of the mutant larva, which, like the animal, is covered with fine hairs (ZPA property of hedgehog). The original mappers of the fruit fly genes were German (Nüsslein-Volhard and Wieschaus from Tübingen). So they initially gave some genes German name, mostly from the appearance of the mutant (knirps, krüppel, and spitz) and some in English (shavenbaby, buttonhead, faint little ball). They got the Nobel in 1995 for this I believe. No, not the Nobel in Literature.

@AlainPannetier — Yes, I realize that many of the 'amusing' names were related to appearance, and that this was extremely important work. And my experience in Germany (I had a sabbatical there and speak the language) suggests that German scientists would have been unlikely to name genes after video games characters. But thanks for the comment, and I don't think it harms to have a little history for the younger scientists. Indeed my objective in posting was to show that these irritations of nomenclature arise from the way science is actually done.

There are rules. Both genes and proteins are regulated in their formats, and standardized in terms of capitalization and italics. Different species have different rules. So for example SHH is a human gene, and Shh is the homologue in mouse.
You can find these rules here: https://www.genenames.org/about/guidelines and read about them here: https://en.wikipedia.org/wiki/Gene_nomenclature
Also, amino acid abbreviations are standardized in both one and three letter forms. Also, things like restriction enzymes are given as the first letter of the genus, and then the first two letters of the species epithet, such as EcoR1 from E. coli. Note that since it comes from a Linnaean species (in Latin) it is italicized. Other enzymes like Taq polymerase, come from species names, and follow similar guidelines.

One reason why some genes have several different names is because they have been discovered several times by different teams in different species.
For instance mice Int1 being Wg of the fruit fly.  Each team name their discovered genes independently and they eventually realise they're the same (homologous).
This was quite common before biologists understood/accepted the universality of homeobox genes.


text:
How are the helices of MscL gating "attached"?
I'm attempting to model the mechanosensitive channels of large conductance (MscL) in E. coli for finite element analysis purposes. I have a number of papers where this has been done, and one shows the modelling with van der Waals forces (as seems logical), but is it known how/where these forces exist?
For references, two papers I'm using have videos and pictures:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0183822#sec013 (see the movies S1 & S2)
https://www.cell.com/action/showFullTextImages?pii=S0006-3495%2806%2971838-0

What do you mean by "how/where these forces exist?"

Well, the N-terminus is connected to the TM1, which is connected to the TM2, which is connected to the C-terminus... how are they connected?

There are two types of interactions: bonded and non-bonded. There are two types of non-bonded interactions: electrostatic and non-electrostatic. Electrostatic (also known as 'polar') interactions are usually modeled using Coulombic potential energy equation; non-electrostatic (also known as 'non-polar' or 'van der Waals') interactions are usually modeled using Lennard-Jones potential energy equation.

Thank you @MartinKlvana, if you put that as an answer I'll vote it. It's exactly what I was looking for.

It is the combination of intra- and inter-molecular interactions that determines the conformation of the protein.
There are two types of interactions: bonded and non-bonded. There are two types of non-bonded interactions: electrostatic and non-electrostatic. Electrostatic (also known as 'polar') interactions are usually modeled using Coulombic potential energy equation; non-electrostatic (also known as 'non-polar' or 'van der Waals') interactions are usually modeled using Lennard-Jones potential energy equation.


text:
Are there any pairs of animal species that regularly prey on other?
I don't mean cannibalism within a single species - I mean, are they are any pairs of species A and B such that members of species A regularly prey on members of species B, and also members of species B regularly prey on members of species A? I'm considering adults preying on other adults of the other species, not on individuals early in their life cycle.

Caiman and Anacondas - though each hunts the other at a stage of development when the hunter is larger.1 2
Occasionally this occurs with Orcas and Sharks.3
Some species of shark3
Spiders and mantids4
Alligators and catfish (catfish prey on infant alligators)
Many species of predatory fish
Some species of constrictor and venomous snake.
Some frogs and Epomis circumscriptus / Epomis dejeani5
Some amphipods6
In Antiquity, hominids and lions7 8
Big cats preying on eachother, among other large predators:

Carnivores eat a variety of vertebrates: e.g. desert coyotes eat … carnivores (roadrunners, reptiles, and mammals)… Carnivorous mammals often overlap substantially in diet (30). Many “readily prey on other carnivores” (125), e.g. tigers prey on bears (black, brown, and sloth bears), dogs, wolves, lynx, and badgers (125): leopards prey on lions, cheetahs, wild dogs, and spotted hyenas (also raptors, crocodiles, and pythons; …
Leopards are mutual predators with lions, spotted hyenas, tigers, large raptorial birds, crocodiles, and pythons…

The Ecology and Evolution of Intraguild Predation: Potential Competitors That Eat Each Other

A python will eat an alligator:

Source:  http://www.miamibeach411.com/news/python-snakes
and an alligator will eat a python:

Source:  https://www.palmbeachpost.com/news/gator-chows-down-python-florida-golf-course/9HUGKYz7j3qF1BGJwc2RUL/


text:
DRD4 genes and their connections to Dopamine 2 subtype
I am trying to find out how the DRD4 gene correlates with the dopamine 2 family subtype receptor in the brain. Does a certain amount of methylation of DRD4 affect how much Dopamine is present in the brain?


text:
Why do humans have digestive system present at front and kidneys back?
Outlet of digestive system is present at back of the body but its digestive system at front.
Outlet of urinary system is present at front of the body but its system present at back.
Why do humans have digestive system present at front and kidneys back?

Rather, I'd think of both the digestive and urinary systems as occurring top-down and inward-out, because gravity helps.

Teleologically, one can say the kidneys are fragile and need to be protected from trauma, which does actually occut in the relative safety of the lower ribs and spinat support structure. The GI tract, on the other hand, would be too restricted in the retroperitoneum; it needs to be able to expand (food, gasses, etc.) Realistically, because it evolved that way; all vertebrates have the same basic anatomy (basic, not specific.)

I don't claim to have the full answer to why these organs are located in the way they are, but I think these factors have an influence on the anatomy:
1- The urinary system's link with the reproductive system in male mammals: The male reproductive system outlet needs to be located as far to the front as possible in a 4 legged mammal to facilitate sexual function, forcing the urinary system to follow
2- The kidneys are very fragile and need to be protected by the thick back muscles and partly under the rib cage. They would be too vulnerable at the front
3- The urinary system is generally sterile of bacteria, and so is the reproductive system in males, and partially in females. The digestive system isn't sterile in both. The outlet of the digestive system can't be in the front of the genitals in a male as this will increase the risk of urinary infections overall and also genital infections after mating. It can't be in between the urinary and reproductive outlets for the same reason, so it has to be located behind both to cause the least interference with their functions

Please provide support for your answer.


text:
Lifeless Lake in Siberia
There is a lake in Siberia called Lake Pustoye. No life exists in the lake. There are no fishes and no plants and even trees around the lake die . No birds even visit this lake .The lake even has bubbles in it like champagne .The water has been tested and there is nothing in the water that makes it harmful to life.  It even tastes like champagne and yet life cannot exist in it .Fish were introduced into the lake but they quickly died off . So why can't any life form survive in this lake ?

Can you give links with evidence that The water has been tested and there is nothing in the water that makes it harmful to life?  I.e. not just the claim that this has been done, but some specifics saying who has done it, and what they've found? Otherwise, this looks like just another click-bait made-up claim.

Yeah a I agree with Iayork a claim like that needs some serious sourcing otherwise you can assume it is wrong.

Assuming the claim is supported. perhaps the water is saturated with volcanic gasses, like Lake Nyos in Africa: https://en.wikipedia.org/wiki/Lake_Nyos  That would account for the bubbles and possibly the absence of animal life, though I can't see why it would affect plants or microorganisms.

The article said that supposedly several countries around the world have tested the water and found nothing harmful about it . Also if there is no vegetation or other life forms then how did they expect the fish to survive that they attempted to introduce into the lake . What would the fish have ate ?

If you google" Lake Pustoye Mystery" the very first link on the page "The Secret of the Siberian Pond" will take you to the article @iayork

@PeterU You understand that that article is completely devoid of facts, right? It makes claims about 'large numbers of scientists", "experts", and "specialists", but gives absolutely no information on who they are, where they're located, what they are specialists in, what they looked for, and what they found. It's classic click-bait vagueness and obfuscation. If that's all you have, I'm voting to close this question as "Unclear what you're asking", since you have no actual facts to discuss.

Pubmed, which includes over 28 million peer-reviewed articles, has 0 instances of "Pustoye" in it, suggesting that no experts have actually looked at the lake.

And finally, The Geographical Journal, Vol. 19 (1902) refers to villagers living on Lake Pustoye who "make a comfortable living by fishing", which suggests the lake is far from empty.  I think this is some kind of misunderstanding (perhaps based on a translation of the name) that has been mindlessly parroted by the gullible and sensationalist.

Sounds like carbon dioxide, it seeps up from an under ground source. At high levels it will kill all normal life. There is at least one lake in Africa that has this  CO2 saturation. There was a program on TV a few years ago about it. There is some unusual circulation and out gassing but I forgot the mechanisms..CO2 would explain the "tastes like champagne" .

So I guess that is the reason that my Doctor said that I shouldn't believe what Doctor google says, lol . So in other words you are saying that villagers are fishing in this lake, which would mean that the article is false ? @iayork

@iayork - it sounds all like an excellent answer. Combine the comments (mind to include the links) and et voila?

If the water is bubbly and taste like  champagne, it means that the water is saturated with carbon dioxide, and has a pH of about 3. the water probably kills everything (plant, animals and most bacteria) around it by carbon dioxide poisoning and very acidic water.

I am more curious if something can survive in the lake. Lake Pustoye has actually been tested and scientists have found nothing wrong at all with the water, and when they saw that the lake had bubbles and tested those too, again they found nothing, so they did a few tests. First they put the least demanding fish in the lake but soon found that they all died, they tried the same thing with aquatic plants, those just rotted away. They just straight up labeled it as a dangerous lake due to nothing being able to survive in it, what I am personally curious about is if a tardigrade, aka water bears

https://www.researchgate.net/publication/200464654
This is a detailed comparison between two lakes in the Trans-Volga region in Russia, one of them being Lake Pustoye. I'm not sure if the Lake Pustoye in this article is the same lake being referred to by the op as it isn't in Siberia and there's no mention of champagne-like water, but it does bear the same name and has a curious lack of fish. The authors found that while there is an absence of fish, there is by no means an absence of life in the waters of Pustoye. In the article, they catalog the seasonal shifts of biodiversity in the waters of both lakes. The pH was observed to be low in Lake Pustoye which they implicated to be the likely cause for the lack of fish, though they indicated that more research would be needed to determine the exact cause of the acidification.

Impressive detective work, Sherlock. +1

Pustoye, or Пустое, means empty. It's not an uncommon name for a lake. This is certainly not the one the apocryphal story is about.  Search Озеро Пустое in google maps and you'll find many of them.