text:
Tree identification in the Caribbean
I live in Puerto Rico and I'm trying to identify this tree and if possible how to kill it since it is infested with termites.
https://i.sstatic.net/2TfN5.jpg
Tree

Closer view of flowers and leaves. The rectangles on the floor are about 3mm x 6mm.

Seed pod

Hi Rick. Please copy your images directly into your post. Linking to external photos is not appropriate for our site due to the propensity for such photos to later become unavailable. Posts should be complete in and of themselves. [Edit] your post to include these photos, update with some measurements, and please provide more specifics about location/habitat. We'll be happy to try to help at that point. (see here for more guidelines). Thanks.

Google lense I.D. Program works on nearly all european and north american trees, bark and flowers, and many tropical ones. try it...

Google lense said either Saussurea obvallata or eucalyptus... I doubt it is.

@aliential I STRONGLY disagree with your statement about Google Lens, as it is, in my experience, patently false. From what level of botanical expertise are you coming from? The issue with such programs is that users are typically not equipped in any way to recognize/challenge the accuracy of results. I have only tested Lens out of curiosity for accuracy, and my personal take is that it is rarely accurate when it comes to IDing organisms (e.g., trees). Complicating this matter is that many species are no longer differentiated based on easily-identifiable gross morphological characteristics.

First discovery was a photo of a golden egg bug...100% ok was amazed. Second task was a split gill mushroom... 100%... then monkshood... 100% correct, and lense also manages various leaves and flowers, especially horticulture and unique patternings. I had very high accuracy for  common and morphologically peculiar and specific photos. Yes it though this pages photos are a mantis... awful. But the images are blurred... i recommend trying lense on certain types of targets like flowers and fruits, it can be very worth the 10 seconds of time involved. Try lense on photo of g egg bug.

Also, it got dogwood the first time and i read that Oetsi had dogwood arrows. That ID took me only 10 seconds. The photos have to be very identifying and only for well documented easy  species.

The photos of this tree indicate that it is a horseradish-tree (Moringa oleifera). See https://rngr.net/publications/common-trees-of-puerto-rico-and-the-virgin-islands as well as google searches of that species. Killing the tree will do nothing to eradicate the termites as they will just move onto another source of food.

Thanks for answering this question! We appreciate when new users with expert knowledge begin answering questions! Please update your post, however, to include more information about why your ID is correct. Given the propensity for external links to go defunct, we ask that your answer here can adequately stand on its own in explaining both the correct answer and your rationale. Support as a link is fine (and citing/linking sources is preferred/required), but please capture some of the relevant detail from your external source in your post itself. Thanks!


text:
What are the marker enzymes for Nucleus, Ribosomes and cell membrane?
Are there any marker enzymes present for ribosomes, nucleus and cell membrane. For mitochondria there are many, for lysosome it's cathepsin. I read about the marker enzymes of most of the other cellular components, but no information is there on these three.
If no marker enzymes are present then how are ribosomes, nucleus and cell membrane are identified.
I am specifically looking for marker enzymes which can help identify the pellet component after subcellular fractionation.

Why are specifically interested in marker enzymes? And could it be any enzymtically active proteins or are you looking for which activity can easily be measured? Ribosomes are catalytically active (ribo-)enzymes themselves and aren't actual compartments of the cell like all of the other things. The plasma membrane and nucleus are much more heterogeneous than mitochondria or lysosomes so they are usually identified by other markers than enzymes.

You need to describe the experimental procedure in which you need to check for these components. You can see nuclei and membranes under a microscope, and ribosomes are characterized by their components (look them up to see what these are), but I imagine that this may not be what you want. I suspect there is some incorrect premise underlying your question, but without the detail we cannot point it out.

source: Stack Exchange

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

sort: votes


text:
Can caffeine act as viagra
Recently I studied that cAMP which is a 2° messenger can cause various physiolocal changes under the action of proper hormones. Now cAMP is degraded by phosphodiesterase and this ceases the actions. Viagra drugs like sildenafil are phophodiesterase inhibitors and therefore prolong cAMP action. Also caffeine inhibits phosphodiesterase and therefore it should cause a similar phenomenon. But does it actually happen? Or some other mechanism stop it from happening. What are those mechanisms?

Is sildenafil a "phophodiesterase inhibitor"? Or is it a specific inhibitor of a particular phophodiesterase? If the latter, which one? How potent is it vs. caffeine?

To put it in everyday terms: caffeine raises blood pressure, and this is pretty much the same effect as that of viagra, just less specific and less long-lasting.

Didn't realize this Q only had DVs... given the amount of totally crap questions here that somehow get a lot of upvotes, this one was treated rather harshly... I mean we know the answer because it was actually investigated and published, so it wasn't a totally outlandish Q to consider.

Not much luck there. Although caffeine, sildenafil and cGMP share a basic ring structure, the specificity and potency of caffeine for PDE5 is rather underwhelming:

On the basis of comparative IC50 values, the potency of sildenafil is about 1 million times higher than that of caffeine (Corbin and Francis, 1999).

This is a lot of coffee.

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


text:
Redheads and pain receptors
I remember reading this in a biology textbook, and decided to do a little digging. Redheads have a lower sensitivity to some pain and a higher sensitivity to other compared to people of other colored hair.
Sciencenordic.com and webmd.com note that redheads have a higher sensitivity of pain when it comes to dentistry, yet can tolerate more pain subcutaneously. According to the Journal of the American Dental Association, redheads require more anesthesia due to some mutation in the MC1R gene. What mutation could account for this difference, could this be a point mutation or nonsense mutation?
Source: http://www.webmd.com/pain-management/features/whats-your-pain-tolerance?page=2
http://sciencenordic.com/redheads-feel-different-kind-pain

I think it's best to break this question up in to two parts:

What mutations account for red hair and fair skin in humans
How might these same mutations affect pain sensation

MC1R variants & red hair
The MC1R gene encodes a transmembrane receptor protein (belonging to a very common family of receptors), called melanocortin 1 receptor. It also has another name describing its best known role in the body: 'alpha melanocyte stimulating hormone receptor'.
This receptor binds ligands - both agonists and an antagonist - outside the cell, and passes signals to the pigment-producing pathways in melanocytes; activation favours eumelanin (brown) production over pheomelanin (red).
Common MC1R variants are all single point mutations which cause an amino acid substitution and reduce/impair the normal function of the receptor - i.e. loss-of-function mutations. E.g. Arg151Cys, Arg160Trp, Asp294His, the most common variants in european red-heads probably arose ~80,000ya in a eurasian population, and have a reduced ability to activate adenylate cyclase inside the cell.
How & why could the same mutations affect pain sensation?
Genetic linkage, or dual role of MC1R?
Firstly, it is possible that MC1R variants are linked to a mutation at a separate nearby gene; the two making a haplotype.

In this diagram, mutation A might be a red-hair MC1R mutant, and mutation B might be some other pain-sensitivity mutant. Through random effects on small populations, group Hg B might have 'seeded' the european population, say; meaning that the two mutations are inherited together in that population. If the two loci are very near, their linkage is less likely to be disturbed by recombination.
This is an obvious possibility whenever two seemingly unrelated traits co-occur.
However, there's good reason to believe that this case is due to a dual-role of MC1R...
Arguments against linkage; for dual role of MC1R: The existence of many different haplotypes in redheads argues against linkage, if this pain sensitivity effect is found across all/many redhead haplotypes, and not in wildtype MC1R europeans.

Indeed, this study shows that europeans with 2 MC1R mutant variants (homozygote or compound-heterozygote) have increased pain tolerance to electric shocks compared to people with 1 or more functional copies of MC1R. The second panel shows that a mu-opiod analgesic (morphine) has greater effect on those with no functional MC1R. The effect coincides with presence of functional MC1R, not a particular haplogroup.
MC1R is also expressed in a region of the midbrain responsible for pain modulation. This region produces endogenous opioids to control pain. As far as I can gather, researchers are trying to work out what exactly it does there.
The study by Mogil et al suggests MC1R in the brain somehow counteracts pain inhibition by the opioid receptors, and so MC1R mutant redheads have more effective ex/endogenous opioid pain inhibition, which reduces noxious pain.
This study found that redheads are slightly less susceptible to pain-sensitisation by capsaicin.
Whereas this study found a contradictory result, that redheads are more sensitive to thermal pain and that lidocaine is less effective for them. (This study didn't genotype the subjects, and red-hair may be caused by mutations in other genes.)
Overall, the number of subjects in these studies (both humans and mice) is fairly small; and the science of MCR pain modulation seems early-days.
But at least we can answer your question: the mutations apparently responsible for red hair and altered pain sensitivity are amino acid substitutions in MC1R causing loss-of-function variants.
The fact that MC1R probably has totally different roles in the brain and in the skin is an interesting general point of biology.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288200/ < about the evolution of MC1R mutant variants.
http://www.ncbi.nlm.nih.gov/pubmed/10403794/ < about the mechanism of loss-of-function
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1736101/pdf/v042p00583.pdf < evidence of increased pain tolerance & greater morphine effectiveness
http://www.scandinavianjournalpain.com/article/S1877-8860%2810%2900111-4/abstract < evidence of resistance to hyperalgesia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692342/ < evidence of decreased pain tolerance & lesser lidocaine effectiveness

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


text:
What causes the line patterns in the palm of the hand?
The line patterns on the hand are unique to each individual, but what causes these lines and re they advantageous in anyway?

Is this a homework question?

The lines on the hand are known as flexion creases, and they exist because in their absence, the skin will stretch outwards when the palm is closed due to the decreased surface area of the closed palm, causing problems with gripping.
Developmental disorders such as Down Syndrome often cause there to be only one palm line, known as the simian crease, as shown on the left.

I don't think this answers the entire question that was posed by the OP.

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


text:
What is the significance of 9+2 arrangement in flagella?
Why eukaryotic flagella have 9+2 arrangement .? What is the significance?  a 9+0  flagella should have worked the same way .

What do you mean by 'normal flagella'?


text:
How is flagellar movement controlled?
How does a cell control the movement of flagella? Both the rotatory movements and sideways movements helps the cell to move. How are these flagellar movements controlled ? It is through the regulation of the proteins flagellin and tubulin? I want to know the mechanism for both prokaryotic and eukaryotic flagella ?

No its not a homework question I know the rules of homework questions

Can you expand a little bit: What do you mean by how are they controlled? Response to stimulus or the biomechanical aspects? Note that the bacterial flagella is different from the eukaryotic flagella. Please clarify which one you are interested in.


text:
Animals in predicting disasters..!
I have been working on a project related to how different animals help in predicting natural disasters. But google searches and news only give evidence where animals showed some signs before disasters. But I am really interested to know what special sense they have due to which they can predict disasters early like earthquakes and tsunamis.
Particularly about the following animals -

Flamingos
Dogs
Elephants
Cats
Weasels
Bees
Bats
Snakes
Horses
Cows
Sharks

If anyone can suggest a book related to this or any website please mention .

Animals do not have any special sense which allows them to predict earthquakes or similar disasters, but humans do have an ability believe most anything they hear, or, especially, see written down.

I googled it and read it in a book . This site is for clearing misconception isn't it . Thanks for help

ReReading your question, I realize I probably misunderstood it. Your question is definitely opinion based. You should first find a claim that a given animal has some kind of supersensory power and then ask whether it is true on skeptics.SE

@Pi5 then please cite your sources in your question so we can evaluate them. Just because you read something on the internet or in a book doesn't mean it's true, unfortunately. Google "chemtrails" for an example.

The question is currently too broad and your list of species is rather unexpected!
Important Concepts
You probably want to learn about the concept of bioindicators

Bioindicators are a species that can be used to monitor the health of an environment or ecosystem. They are any biological species or group of species whose function, population, or status can reveal the qualitative status of the environment. One example of a group of bio-indicators are the copepods and other small water crustaceans that are present in many water bodies. Such organisms can be monitored for changes (biochemical, physiological, or behavioural) that may indicate a problem within their ecosystem. Bio indicators can tell us about the cumulative effects of different pollutants in the ecosystem and about how long a problem may have been present, which physical and chemical testing cannot.1

You also probably want to hear about ecotoxicology

Ecotoxicology is the study of the effects of toxic chemicals on biological organisms, especially at the population, community, ecosystem level. Ecotoxicology is a multidisciplinary field, which integrates toxicology and ecology.

I would advice that you read more on bioindicators and ecotoxicology.
Why is the question too broad?
If you are interested freshwater toxicity you will probably be interested copepods (as stated above). If you are interested in soil toxicity you will probably be interested in Collembola (see here). The question is currently too broad.
You should first address these questions to narrow down your question

What disaster are you interested in?
What kind of ecosystem are you interested in?

Why is the list of species unexpected
Typically, cats and horses are probably the worst bioindicators one could think of as their survival depend mostly on humans care and not so much on the environment.
It is unclear too why you are only interest in animal species.


text:
Small Pimple like structure in lips?
Is this some  kind of disease ? I saw this in one of my family member
Usually it is totally not visible  but whenever the lips are stretched they are seen


text:
Organ and Bone Marrow Transplantation?
In organ transplantation the transplant is rejected by the body's immune system , but is it possible if along with organ transplant if bone marrow transplantation is carried out from the same donor , then will the Cell Mediated immunity still reject the graft ?

As Mowgli pointed out, a bone marrow transplant involves destroying the patient's own immune system with radiation and, essentially, replacing it with a new one from the bone marrow donor. If you did a double kidney/bone marrow transplant from Alice into Bob, then Bob's new immune system (which is the same as Alice's) would recognize the new kidney from Alice as self (because it is) and not attack it. Yay!
The problem is that, to the new immune system, all the rest of Bob appears to be non-self and will get attacked. This is called Graft-versus-host disease and is at least as serious a problem as organ rejection.

"The problem is that, to the new immune system, all the rest of Bob appears to be non-self and will get attacked. This is called Graft-versus-host disease and is at least as serious a problem as organ rejection": What do you think of this https://biology.stackexchange.com/questions/79881/could-bone-marrow-transplants-be-used-to-prevent-tissue-rejection-of-trans-speci as a fix for that, introduce both patient & body donors cells to the pig fetus then transplant it's bone marrow?

Bone marrow transplant requires to first destroy the pre-existing immune system with chemotherapy and/or radiations. So essentially you would not have the first immune system and my guess is that yes, in theory, it would work.
However, double-grafting an artificially immunocompromised patient (who clearly suffers from another severe pathology, if they need an organ graft in the first place) would be extremely risky as it would exponentially increase the risk and mangnitude of post-operation complications, and I think no surgeon in their right mind would ever take such risk.


text:
Identification of a moth

It is from Bangladesh. Is it hawk moth? I am not sure. Please help.

Looks like a small Sukhoi plane :P. Jokes apart, this doesn't look like a hawk moth. I know that this moth is from Bangladesh since you mentioned that in other posts but it better to always keep your question complete with all necessary information.

Do you have think this picture is enough for visually identify it (at least at genus level)? Otherwise I gotta hunt this guy :P

It looks like a Hesperiidae (Skipper), not a hawk moth (Sphingidae). There are more than 3500 species of skippers worldwide though, and I don't know what species this is. However, I'm sure that somebody who knows butterflies in Bangladesh could identify this to the genus level.
One suggestion/guess/starting point might be Baoris pagana, but this is merely based on a quick glance at skippers found in India.

(picture from http://www.ifoundbutterflies.org/)


text:
What is the name of this plant, from Bangladesh?

This is a small plant from my backyard. I have found the flower closes in the evening.


text:
Is Bramble (blackberry bush) carnivorous?
I have come across this video which put forth the hypothesis that bramble actually qualifies as a carnivorous plant.  The observations that have led to the hypothesis are:
1. Sheep getting caught frequently in bramble
2. Sheep will die  without human intervention.
3. The rotting corpse of the sheep will nourish the plant for many days.
4. The thorns angle inward -- supposedly evidence for adaptation that helps trap prey animal.
I agree , on the surface it looks plain silly but that is a reflexive reaction, not an argument.  Is this a plausible hypothesis? If not , please give reasons.

Could you provide more information about why this plant may be carnivorous?

Are you using the word 'carnivorous' as meaning "meat eating"? What is the (unstated) hypothesis that the plant is carnivorous? ("The plant is carnivorous" is not a hypothesis. It is a conclusion.) Please do not simply link to a video; summarizing the relevant content is more likely to get you a good answer. Thanks.

@anongoodnurse: There are also some of us for whom video is not a good way of conveying information.  Even if I chose to spend my time watching, the amount of information I'd retain would be significantly less than if it was presented as text.

@jamesqf I understand your point, but in that case we would have to present information always in many different ways to provide for all types of learners. For me, a mp3 file with spoken word, please.

Voted to reopen and flagged. Thanks for the edit!

@skymningen: But StackExchange is fundamentally based on the written word.

Even if the adaptations to tangle were well supported, brambles would still not be carnivorous.
Carnivorous plants release digestive enzymes to digest their prey or have other adaptations specifically to pull nutrients from the things they kill. Brambles would have to rely on something else to rot the carcass and pick up whatever trace nutrients that get released into the soil like any other plant. Brambles tendency to tangle could just as easily be a defensive adaptation meant to encourage herbivores to avoid it. Without any specific adaptations to uptake the nutrients from killed animals, classifying them as carnivorous would be premature.

This is really more of a comment than an answer, but I'd challenge most of those premises.
1) Sheep getting caught.  But (AFAIK) wooly sheep are the (recent, in evolutionary terms) product of human breeding.  Blackberries &c wouldn't have had time to evolve specific mechanisms to trap them.  Most animals have relatively slick hair (or none, as with humans), and don't get trapped.
2) Domestic sheep don't really exist in the wild, do they?  So there almost always will be human intervention.
3) Does rotting meat provide needed nutrition to the plant?  I grow blackberries & raspberries, and they seem to do just fine without dead critters.
4) But if you spend time in places where blackberries or other brambles grow wild in some profusion (western Oregon, for instance), you do not notice (or at least I never have) an abundance of dead critters in the bushes. (Addendum: and dead critters of significant size, say larger than a rabbit, tend to be noticable, especially when you hike with dogs :-))
So I have to conclude that there's something wrong with this claim.

I had a farm so cluttered by brambles that I considered calling it Bramble Hill. My goats loved to eat brambles (I think they're well known for it), and, as you said, slick hair means no problem. Never lost a goat to brambles nor found any dead animals amongst them.

I saw the same video and thought it was interesting. While others who didn't bother to watch the video might miss a few interesting points.
Video link
https://youtu.be/RuzLXxbGc4c
It was pointed out that the thorns didn't stick straight out defensively as many thorns do, but rather raked back, thus grabbing and making it difficult to pull away.
Based on this article, it appears it would be more appropriate to call bramble "Protocarnivorous".
https://en.m.wikipedia.org/wiki/Protocarnivorous_plant


text:
Are erythrocytes lysed during alpha hemolysis?
Wikipedia says:

When alpha hemolysis (α-hemolysis) is present, the agar under the colony is dark and greenish. Streptococcus pneumoniae and a group of oral streptococci (Streptococcus viridans or viridans streptococci) display alpha hemolysis. This is sometimes called green hemolysis because of the color change in the agar. Other synonymous terms are incomplete hemolysis and partial hemolysis. Alpha hemolysis is caused by hydrogen peroxide produced by the bacterium, oxidizing hemoglobin to green methemoglobin.

From this it seems that in alpha hemolysis , it's not the lysis that's the defining event rather the chemical change of the hemoglobin molecule.
Wikipedia states:

Beta hemolysis (β-hemolysis), sometimes called complete hemolysis, is a complete lysis of red cells in the media around and under the colonies: the area appears lightened (yellow) and transparent.

I am unsure of the reason for color change (blood agar plate) in beta hemolysis, my guess it's due to diffusion as I have found no mention of chemical change in hemoglobin molecule anywhere (yet).
So far my position is chemical change in hemoglobin without lysis is alpha hemolysis and lysis followed by diffusion of the hemoglobin molecule is beta hemolysis. Problem is my support is shaky at best.

Alphahemolysis simply oxidizes hemoglobin to methemoglobin and causes a color change on blood-agar. The RBC membrane is left in tact as far as I know. If you look at a picture of the 3 types of hemolysis, you will see that there is no zone of clearing in the alphahemolysis plate. Compare that to the obvious zone of clearance observed on the betahemolysis plate, in which complete lysis occurs. Here is a nice picture

Anaerobic condition and CO production

Hemolytic and nonhemolytic bacteria were incubated aerobically and anaerobically with the following substrates: erythrocytes, hemoglobin, myoglobin, cytochrome c, hematin, iron hematoporphyrin, copper hematoporphyrin, protoporphyrin, and bilirubin. After 18 hr at 37 C the evolved CO was measured by gas chromatography. None of the bacteria formed CO anaerobically.

CO and alpha hemolysis

Because our two strains of S. mitis differed with regard to H202 production and hemolysis, we also compared an H20 2-producing strain of Streptococcus faecalis with a peroxide-negative mutant, kindly supplied by Beulah Gray Holmes. In both cases the H20 2-producing organisms generated alpha hemolysis and formed CO from heme compounds, whereas the peroxide-negative bacteria did not demonstrate alpha hemolysis or CO formation. If, in alpha hemolysis, hemoglobin is converted into a green pigment without lysis of the red cell membrane, then the failure of this pigment to diffuse away from the colony would be explained.

Color change in beta-hemolysis can be explained with diffusion of content from lysed erythrocyte.

All six strains of bacteria that formed hemolytic zones on blood agar plates also produced CO from erythrocytes, and conversely the four strains that were nonhemolytic did not make CO. Despite this concordance, it appears that the formation of beta-hemolytic zones around colonies grown on blood agar plates does not depend on hemoglobin catabolism. Thus, prominent beta-hemolytic zones were formed under anaerobic conditions that prevented CO formation. Also, hemolysis but not CO formation was produced by sterile filtrates of the extracellular products from beta-hemolytic bacteria.
Clear zones resembling beta hemolysis can
  be produced by simply freeze-thawing a spot
  on a blood agar plate and then waiting a day
  for hemoglobin to diffuse away from the lysed
  cells. Although hemolytic B. cereus grown on
  aerobic hemoglobin agar plates gradually produced
  diffuse color changes, the discrete zones
  observed on plates with sheep erythrocytes
  were absent.

http://jb.asm.org/content/112/3/1310.full.pdf+html


text:
Why is traditional rank based taxomomy considered by some as logically inconsistent with phylogenetic knowledge?
Following is from wikpedia:

Under the traditional nomenclature codes, such as the International
  Code of Zoological Nomenclature and the International Code of
  Nomenclature for algae, fungi, and plants, taxa that are not
  explicitly associated with a rank cannot be formally named, because
  the application of a name to a taxon is based on both a type and a
  rank. The requirement for a rank is a major difference between
  traditional and phylogenetic nomenclature. It has several
  consequences: it limits the number of nested levels at which names can
  be applied; it causes the endings of names to change if a group has
  its rank changed, even if it has precisely the same members (i.e. the
  same circumscription); and it is logically inconsistent with all taxa
  being monophyletic.
Especially in recent decades (due to advances in phylogenetics),
  taxonomists have named many "nested" taxa (i.e. taxa which are
  contained inside other taxa). No system of nomenclature attempts to
  name every clade; this would be particularly difficult in traditional
  nomenclature since every named taxon must be given a lower rank than
  any named taxon in which it is nested, so the number of names that can
  be assigned in a nested set of taxa can be no greater than the number
  of generally recognized ranks. Gauthier et al. (1988)[6] suggested
  that, if Reptilia is assigned its traditional rank of class, then a
  phylogenetic classification has to assign the rank of genus to
  Aves.[7] In such a classification, all ~12,000 known species of extant
  and extinct birds would then have to be incorporated into this genus.

What is the precise meaning of "it is logically inconsistent with all taxa being monophyletic"?

I've changed your title, removing the "please explain". This could be included in almost every title, and though it may seem polite, it is an impediment to readers finding out what question you are asking.

Maybe your should also put your question in the discussion page corresponding to the wikipedia article you cite.

You can find discussions of problems with rank-based taxonomy in light of phylogenetics in Ereshefsky 1994, de Queiroz 1996 and Ereshefsky 2002. To summarize, the main problems they identify are:

It's hard to define what exactly an "order", "family" or "genus" is; in particular, taxa at the same rank aren't always comparable. For example, order Hymenoptera, which evolved 250 million years ago and consists of over 150,000 species, with order Carnivora, which evolved 42 million years ago and consists of "over 280 species".
Not enough ranks: NCBI recognizes 29 higher taxa for Homo sapiens. That would require dozens of sub-and-super ranks to render into Linnaean taxonomy.
Names based on ranks: current nomenclature allows certain ranks to be identified by their ending, for example names ending in "-ini" refer to tribes (e.g. Hominini, Canini). If one of these tribes turns out to be non-monophyletic, it may have to be moved to a higher or lower rank to keep its monophyly -- which would have to be renamed, increasing confusion.
Redundant taxa: take division Ginkgophyta. It contains a single class, the delightfully named Ginkgoopsida, which contains a single order, Ginkgoales. In the Linnaean hierarchy, each of these taxa contains the next one along, but in terms of monophyly, they are exactly identical to each other, as they share exactly the same most recent ancestor.


text:
Pelleting bacterial cells using centrifugation and getting proteins in the supernatant
Do significant amount of proteins from cells find their way in supernatant during pelleting? If the answer is yes then I see two ways in which protein can be in the supernatant
.
1) Through lysis during pelleting
2) Through leakage of protein from cells during pelleting
if significant amount of lysis occur during pelleting then obviously protein will be there in the supernatant due to lysis alone. However, If most cells (like 98%-99%) remain intact  then only by leakage significant amount of protein can be in the supernatant. Both way can also contribute. Which is the case?

I don't have an answer, but secreted proteins will be in the supernatant.

@canadianer I know. But here I am interested in the protein that are inside the cell and are forced outside so to speak by the process of pelleting.

Have you actually seen intracellular proteins in the supernatant after centrifugation that weren't there before?

@canadianer No. Someone suggested that possibility.


text:
What's the name of this bug from Toronto, Canada?

It's about 3 millimetres in length. Found on September 10, 2015.

It's a moth fly. They're cute fuzzy little things. Most people consider them pests.

An annoying and troublesome pest that concerns numerous homeowners is the moth fly, also commonly known as the drain fly, filter fly, or sewage fly. Moth flies are frequently found indoors on windows, sinks and walls.

They're often found around sink drains because the eggs and larvae survive on the biofilm in your, well, drains.

This IS a Moth Fly (Family Psychodidae), but the heavily-patterned wings and their posture at rest argue against the genus Psychoda; the pale spots at the wing margins suggest Clogmia albipunctata (Williston, 1893) which has been extending its northern range limits (half a century ago, this species and Toronto mentioned in the same sentence would have been considered a likely misidentification; this diptera.info thread discusses two localities for that species that are even further north -- Clallam and Grant Counties in Washington).


text:
DNA methylation on the forward vs reverse strand?
I'm wondering if there are meant to be differences in DNA methylation between the forward and the reverse strand of the gene? I'm wondering because in primer design for bisulfite pyrosequencing one might only design primers for the forward strand. Should this matter for human/mouse DNA?
cheers and thanks in advance for any advice.

In most tissues, close to 100% of DNA methylation occurs at CpG sites. This provides a straightforward mechanism for epigenetic inheritance. Since C and G are complementary, both strands have the CpG site at the same locus and methylation is either present on both strands or on neither. During replication, each daughter DNA molecule inherits a parent strand with the (un)methylated CpG sites. Enzymes can recognise when there is asymmetrical CpG methylation and subsequently methylate the new strand where required. So, for CpG sites, both strands are methylated or not.
In embryonic and induced stem cells, however, ~25% of the total methylation occurs at non-CpG sites (especially CpA). Thus, methylation at a specific locus would only occur on one strand. As far as I know, how/if this methylation pattern is inherited has not yet been elucidated. Furthermore, this type of methylation occurs throughout the chromosome and is particularly high in exons whereas CpG methylation generally occurs upstream of a transcription start site.

There is also a phenomena called hemimethylation where one of strand is methylated while the other one is unmethylated or vice versa. There have been various research questions associated with hemimethylation, you can find more about it in here: http://nathansheffield.com/wordpress/what-is-hemimethylated-dna/

Recent work showing functional role of hemimethylation: http://science.sciencemag.org/content/359/6380/1166


text:
Why in some cells is GTP made in citric acid cycle and in some ATP?
In many  animals GTP is produced in citric acid cycle. While in  plants,bacteria and some animals ATP is produced. Why is this so ? What is the advantage ?

This step is catalyzed by succinyl-CoA synthase which has two different isoforms- one which produces GTP while the other produced ATP.
It seems from this study that predominantly anabolic tissues prefer the GTP-producing form whereas the predominantly catabolic tissues use the ATP-producing from.
In the same paper they discuss that GTP is important for protein synthesis and it is also involved in production of phospho-enolpyruvate by PEP-carboxykinase in mitochondria; therefore playing an important role in anabolic processes.


text:
Stopping the effect of hormone
Many hormones released by endocrine organs travel down in the blood and bind to specific receptors on the target cells. What then breaks that binding of the molecule with the receptor ? ( thus inactivating further stimulation of the target cell )

The binding is reversible typically; part of the potency of a drug is ow well and for how long it binds to its target. There's a natural equilibrium of binding and dissociation. Many drugs, once bound to their cognate receptor, cause a down regulation of their cognate receptor on the target cell. The bound/activated downstream signalling pathways may be inhibited by ubiquitination of the downstream signals themselves or upregulation of antagonists etc. The hormone itself has a half life, which is very important, thus levels naturally decrease and for some hormones this is incredibly rapid. Levels may decrease due to breakdown or excretion. Increase of binding hormones may decrease free hormone thus it's effect also.

Nice answer ! What is down regulation ?

The number of receptors on cells are regulated by sometimes thousands of things. Often the hormone that activates a receptor in addition to its normal effects, also causes the numbers of its own receptors to go down. This is down regulation which prevents against too much of a hormone over a long period of time.

Another point: even if a receptor is not downregulated or inactivated, certain signaling and gene regulatory circuits can prevent prolonged response.


text:
Utilising Mycorrhizal Association
We know that mycorrhizal association helps the plant to absorb nutrients.
Why can't this association be exploited in agriculture ?
Can't we add spores of the specific fungi to specific plant and enjoy the benefit of this association as we would not have to add many fertilizers ?( We could add organic manure whose main drawback is the time it takes to release nutrients. The fungi could probably solve the problem.)

Mycorrhizal fungi are often used in small-scale agriculture for just that reason.  If you search mycorrhizae on amazon they sell it by the tub.  I think its especially used in organic gardening for just what you said, the slightly less-processed organic fertilizers are harder to take up by plants without their mycorrhizae partners.
I'm not sure about how widespread the practice of applying mycorrhizae is in large-scale non-organic farming.  Judging by how big of a problem fertilizer runoff is, my guess is that a lot of companies have decided that their bottom line is best served by just swamping everything with artificial fertilizers.  I'm not sure how mycorrhizae is produced either, it might really be prohibitively expensive to scale production of it up that much.


text:
Reassociation of DNA
What is the order in which this DNA samples would would reassociate ?
e.coli DNA
plasmid DNA
viral DNA
satellite DNA
DNA-RNA hybrid
This is a homework question and I have not been given any information about the condition in which they are reassociated.

RNA-DNA hybrids have a higher thermodynamic stability compared to DNA-DNA hybrids (deltaG(hybridization)) is low. However that doesn't really mean they will form faster. Just that the equilibrium is towards association.

The rate is determined by the size and complexity of the sequence. Short, non-repetitive sequences should re-associate (at a given r.t.p.) faster than longer, repetitive DNA.
I'm guessing that that is what this question is getting at.


text:
What decides whether a lysogenic cycle or a lytic cycle will take place?
A virus can either participate in a lysogenic cycle or a lytic cycle. What decides that?

This is a broad subject which is well covered in many articles available on the internet. Before posting to this site you are expected to do some research on a topic — see "How do I ask a good question?". That is why I have voted to close this question, despite its age. Others please take note.

It depends on a few factors, such as how many phages infected the cell, whether or not the cell is in good growth conditions, and so on. If the cell is in stress or has low amounts of nutrients, the lysogenic pathway is typically activated.
The underlying mechanism has to do with a protein cascade involving either the cro or cI protein that is encoded by the virus. The cI protein is a repressor, and it will prevent the lytic genes from being transcribed. By default the virus will transcribe the lytic genes, so they must be repressed for lysogeny to occur. Similarly, cro is also a transcriptional repressor. The two proteins work in opposition to each other. cro binds to an operator, oR3, that is involved in repressing cI, which may prevent cI from being expressed and thus preventing it from repressing lytic genes (however the importance of this is debatable because if you replace oR3, the cell can apparently still lyse).
There are numerous other proteins, such as N and Q, that are involved. The N protein has to be transcribed by the polymerase ‘anti-terminating’, or reading through a termination signal. This will happen more frequently when the protein RNase III is present at high concentrations. The N protein is a lytic regulator. Thus, when there are high amounts of RNase III there will be more N expressed which leads to the lytic cycle. RNase III is not a viral protein. It is a host protein and the host expresses more of it when nutrients are abundant. This is how the virus is able to ‘sense’ if nutrients are high enough to enter the lytic cycle.
The whole system is way more complicated but this is it in a nutshell.
http://www.annualreviews.org/doi/full/10.1146/annurev.genet.39.073003.113656

The term “lysogenic” implies that prophages are capable of giving rise to active phages that lyse their host cells.  This occurs when the viral genome exits the bacterial chromosome and initiates the lytic cycle.  The triggers for this switch-over are usually environmental factors such as mutagens (e.g. radiation and presence of certain chemicals)

Welcome to SE Biology. Here we're looking for answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Please read the help on "How do I write a good answer?". All you have done is state what lysogeny means and made a vague one-line statement of the factors usually involved.


text:
Reason behind formation of different shapes of cell
I have always wondered how cells are modified to give them a specific shape. On what specific part of a cell does gene regulation act  for giving the shape ?

Are you interested in the specific mechanisms of cytoskeletal remodelling or simply asking what portions of the cell give a cell its shape?

Cell shape is dictated by the cytoskeletal arrangement. There are both intrinsic and extrinsic factors that control cell shape.
Extrinsic factors consist of environmental factors such as extracellular matrix. Rho-GTPases relay the environmental signal to the cells to cause cytoskeletal rearrangement.
Intrinsic factors are basically the stable transcriptomic identity (a gene regulatory programme) which determine a cell shape. I personally don't have an idea about what genes give an intrinsic cell shape. For e.g. why does hela cell look different from HEK cell in the same type of cell culture plate under same conditions (even at low densities where there is no neighbor effect).

What is the meaning of Rho-GTPase , hela and HEK cell ?

Rho-GTPase is a protein which relays extracellular cues to the cell and causes cytoskeletal rearrangement. HeLa and HEK are commonly used animal cell lines (check wikipedia enries on these)


text:
Insect that has evolved to recognize carnivorous plants
Obviously in a biome consisting of high density of carnivorous plants any insect that can recognize these plants or at least recognize organs associated with carnivory will get fitness advantage. So it seems a very natural thing to evolve from insects point of view. Has it happenned? If yes, what are some of the examples? If not, why it hasn't happened?


text:
Identification of an insect from Bangladesh
This is a video of the insect. Sorry, I don't have any still photograph.
Location: Savar, Bangladesh.
I've been suggested by an insect photographer that it is a caddisfly.
EDIT: Here are two images from the video


text:
What is the function of epiglottis?
The last time I came across this question was when I was in high school. And the explanation I was given is that epiglottis works like a valve, it prevents foods from getting into the windpipe. Still, if I google the majority of the top results agree with this answer.
Recently I got interested in rabbit anatomy after I bought a pair as pets. I learned they are "obligate nose breathers due to their epiglottis positioned rostrally to the soft palate". Then I tried to revise my understanding of epiglottis and that let to some sources that claim that epiglottis is not essential for swallowing. For example:

It was at one time thought that the epiglottis acted as " the lid of
  the larynx"; it was supposed that during deglutition it fell back like
  a flap over the laryngeal aperture in order to prevent ingress of food
  or water. This erroneous view as dispelled by Stuart, who proved that
  during swallowing the epiglottis actually moved forwards, to be
  squeezed between the base of the tongue and the rest of the larynx.
  This view cannot be disputed by anyone capable of judging, and the
  truth of it is borne out when observing a patient whose epiglottis has
  been almost entirely destroyed by lupus, but whose powers of
  swallowing remains unaffected.

Negus, VE (1927). "The Function of the Epiglottis". Journal of Anatomy.

Controversy has continued for well over 100 years regarding the role
  of the epiglottis in deglutition. We describe the effect of isolated
  epiglottectomy on swallowing success in a case series of 3 adult human
  subjects with isolated epiglottectomy due to trauma, surgery, or
  cancerous erosion. The patients were 42, 51, and 70 years of age, and
  swallowing was analyzed objectively with videofluoroscopy. All
  subjects exhibited successful swallowing with all food types: thin
  liquid, puree, and solid food. Specifically, the patient with
  traumatic epiglottectomy exhibited rapid swallowing success, the
  patient with surgical epiglottectomy exhibited a short period of
  dysphagia due to postoperative edema, followed by swallowing success,
  and the patient with epiglottectomy due to cancerous erosion of the
  entire epiglottis exhibited long-term adaptation, with successful
  swallowing maintained. We conclude that the epiglottis is not
  essential for successful swallowing in humans, because individuals
  can readily adapt to isolated epiglottectomy and avoid tracheal
  aspiration.

Leder, Steven B et al. “Epiglottis is not essential for successful swallowing in humans.” The Annals of otology, rhinology, and laryngology vol. 119,12 (2010): 795-8.
Judging from google searches and Wikipedia entry on the topic it seems the dominant view is: epiglottis prevents food from getting into the trachea. But many research like the ones  I have mentioned above says that people can swallow without epiglottis. How to make sense of these apparently contradictory claims?
Edit: My question is not the same as the question suggested. The suggested question seeks the function of "hyoepiglottic ligament" which is a ligament that connects epiglottis "to the upper border of the body of the hyoid bone". My question is related to the function of epiglottis itself in the background of contradictory claims found in the literature.

@tyersome No it doesn't. I have added the reason in the OP.

@tyersome As the user who asked the question you proposed as dupe, I can say that this post is clearly asking a different question and should not be closed. (this is akin to comparing the function of the knee and the funciton of the MCL ligament or to comparing the function of the lungs vs the function of the trachea)

AhmedAbdullah and @theforestecologist — Ok, close vote withdrawn.

You are right, The main function of the epiglottis is to seal off the windpipe during eating, so that food is not accidentally inhaled.(quote from here).
It's a flat shield of cartilage, which is obviously an efficient valve, It's a valve between the trachea and the esophagus.
It lets lions to eat a pound of meat without choking on their prey. It lets humans drink tea without coughing on their buddies.
Information stating that it's "possible" to eat without an epiglottis doesn't imply that it's "efficient and safe", and contradicts medical interventions where they use a piece of ear cartilage to build a new epiglottis.
Survival didn't encourage the "possibility to eat"... it has made animals very robust and efficient at it. Herbivores can spend most of their day eating, and are often attacked while they are eating and drinking. Carnivores also have reasons for efficient swallowing, big carnivores can eat many pounds of meat very fast while fending off competition from hyenas and other predators.
Sleep apnea patients have their epiglottis modified to give room to breathe at night, and they risk choking and aspiration for a while, although they can adapt because they keep some of the cartilage, so they still have a valve.
Different animals have different breathing habits, with some being obligate nose breathers, including human babies of under 6 months and up to 6 years. That's because the epiglottis either contacts the trachea or it leaves space there.

I would strongly advise refraining from using healthline.com as a source of "reputable" information (read here). Healthline.com competes with equally non-reputable WebMD and is associated with additional non-reputable medical websites such as Yahoo! Health and DoctorOz.com.  --------- More reputable sources could include the CDC, medlineplus.gov, mayoclinic.org, or actually reporting from primary literature  (try searching PubMed).

You also make a number of claims throughout your post that are not supported (e.g., ear cartilage procedures, feeding efficiency of animals, sleep apnea patients and adaptation to treatments, and breathing habits). Please update your post with support for these claims. Thanks!


text:
Identify this frog from Bangladesh
Description: About 5-6 in long
Time: March,2019 (summer)
Location: (Alutila Cave) Khagrachari, Bangladesh

Pleae provide approximate size of the specimen and time of year (month and season if possible). Thanks.

Thanks for the updates. +1 for the post. Hope you get an answer! :)


text:
Is there animal other than human that can recognize distal causes?
We know animals can recognize proximate causes. For example, if animal A hits animal B and injures it then usually animal B is able to associate animal A with his injury. From our everyday experience with pets and other animals we know that. What about distal causes? Proximate causes are not always the most appropriate causes, sometimes distal causes are more appropriate to identify the responsible agents. Let's modify the previous hypothetical example by bringing another animal, animal C: Animal C pushes animal B so that animal A hits animal B and injures it. If animal B is capable of recognizing distal causes, it'll associate animal C with his  injury (not animal B which is the proximate cause of the injury).

I don't know about your example, but would you consider a bird using a piece of bread to lure fish a distal cause? So if the fish looks for more bread it knows its to eat fish.

@Cell but it doesn't show that the bird is consciously doing that. the behavior you mentioned can be hard-wired in the bird brain so  the bird can carry out that behavior without having the general cognitive capability of recognizing distal causes.

How can using bread (a human invention) as lure be hard-wired? Or putting off eating the bread for immediate nourishment for bigger gains?

@Cell Actual baiting behavior can be specific hard-wired adaptation and the fish may develop the flexibility to use x,y,z as baits . I am not entirely dismissing it as a possible answer to my question. If the fish does it out of its general intelligence then of course it qualifies as "recognition of distal causes". Is there any evidence that it's not hardwired behavior?

What about when my dog brings me his leash to push me to take him out? Dogs do recognize distal causes.


text:
Are phylogenetic tree construction algorithms any different than general clustering algorithms?
I suspect the answer is no. But I don't know enough to be sure that that is the case. Of course phylogenetic tree construction uses biological knowledge, e.g special distance metrics, but does it brings anything new at the level of clustering agorithm (e.g hierarchical, neighbor-joining etc).

Not all methods are based on distance matrices. There are methods based on  parsimony, others on maximum likelihood, and others taking MCMC approaches. Even with methods based on distance matrices, there are complications that are specific to phylogenetic (e.g. the cluster need to be rooted somehow, sometimes a network is a better descriptor of the relationship among lineages than a tree). Now, cluster algorithms is a very broad field of knowledge and I am not sure whether all cluster algorithms are based on distance matrices.

One difference is that phylogenetic tree construction algorithms will typically try to jointly estimate the tree and the transition parameters.  A general clustering algorithm might assume that a difference in one feature would make the same contribution to 'distance' between clusters as a difference in another feature. In phylogenetic tree construction, it is explicit that not all differences between taxa represent the same evolutionary distance between taxa, and the parameters governing the distribution of distance/difference may be jointly estimated with the tree.


text:
Is there a limit on how big a free living unicellular mono-nuclear organism can be?
When I looked for the largest protozoan I've found the name Syringammina fragilissima. According to wikipedia " .. Syringammina fragilissima, is among the largest known coenocytes, reaching up to 20 centimetres (7.9 in) in diameter." The catch is it is multi-nucleated organism, not exactly what I had in mind. The reason I am interested in the upper limit of the size of the free living unicellular organism is because I want to have a sense of the limitation of single center has in emitting and receiving information across a large span of space. My interest is not about non-compartmentalization (as in the case of multi-nucleated unicellularity)  rather about single center.

There are individual neurons in multicellular organisms that are meters long with a single nucleus. Certainly they are nothing near spherical, but just something to think about.

I have edited the title to only include free living organism. Apparently a too specialised and dependent cell can become very large. :)


text:
Can a brown recluse bite lead to diabetes?
Ok, I realize that this question may seem crazy at first glance. I would agree. Also, this does deal with a medical diagnosis, however, as I'm more concerned with the explanation behind it, I figured it fit in this category the best. Feel free to move this question (or suggest a better bit) if this is incorrect. On to the question...
Apparently (according to a friend of mine) this person woke up in the morning, could barely move, had a bite-like sore/mark and went to the hospital. Doctor said it was a brown recluse bite and as a result of the incident, this person now has Type 1 diabetes.
It really doesn't matter how (the result is still living with diabetes), but I'm fascinated by this incident and, being neither an expert on spider nor diabetes, I would like to know if this is plausible and, if so, how?
I realize that (1) approximately 80% of brown recluse bites are misdiagnosed and (2) I will never have access to their medical records, but let's operate under the assumption that this was as reported.
From what I've been able to find, in very rare cases, brown recluse venom can result in viscerocutaneous lexoscelism, which may lead to acute kidney failure... but through my research, I can't seem to link that to diabetes (the converse is easy, as diabetes is one of the leading causes of kidney failure).

What (if anything) am I missing?
Is there another response to Lexosceles toxin that can lead to diabetes?
If this isn't possible, what could be an explanation that would cause diabetes but look like a brown recluse bite to a doctor?

This may be better suited for skeptics SE. Wild speculation: antibodies against spider venom are cross reactive.

Hmm...I was debating between the two, however, this seems like a more focused community, with more activity. I've added it to that SE too. Forgive me for my lack of biology knowledge (I'm a physics/CS guy), but what do you mean by "cross reactive"?

@canadianer I think it's better here though, because I wasn't able to find anything on google to support it, so it would be more of a question for a biologist/researcher.... just imo.

https://en.m.wikipedia.org/wiki/Cross-reactivity … https://en.m.wikipedia.org/wiki/Molecular_mimicry

Islet beta cells were shown to undergo apoptosis in a sphingomyelinase-dependent manner in the presence of amyloid peptides like IAPP, article here. Looks interesting, but I'm no expert! Would anyone like to weigh in?

As I am uncertain what type of spider bite my daughter had for sure there were 3 spider bites on her rear while sleeping. As a result of these bites taking a toll on her system she later developed type 1 diabetes. She was 1 1/2 when she was bitten and now 15 living with this terrible disease all behind a spider munching on her. I say that because she had 3 bites in total all of which were filled with puss and have left scars in the effected areas. So yes venom from a spider bite CAN and DOES lead to type 1 diabetes, my baby is a living testimony to that fact. I would so love for someone to fin


text:
What are the most efficient heat exchange sites on the human body?
Where on the body would be the best place to achieve the greatest cooling effect with a "cooling undergarment"?  Concentrated over the kidneys, groin, inside the wrists, back of the neck?

@Charles yes, the suit's internal conditions would be the same; however, the external mechanics of radiating heat into space vs. into an atmosphere would not.  And no, I'm not asking "the best way to maintain a cool internal suit environment"; rather, I'm asking what points on the body are the best for heat exchange.

Gentlemen, the space suit, the environment, and the actor/astronaut is irrelevant.  The relevant question is "what points on the body are the best for heat exchange".

@Charles OK well it sure looks to me like the question asks what are the places on the body that would be the most effective to keep it cool inside a poorly-ventilated suit worn by an actor. The OP lists some locations, and wonders if these are the right ones or not. To me the question is simple and clear. It could be that mentioning space suits is a little distracting. It was brought up as background (how the OP got to this question) but it may not be helping the question about cooling an actor in a costume.

@Charles William'Scott'Baker is the OP.

@William'Scott'Baker asking questions in a new SE with lower rep has "special challenges". There's always someone who thinks they see an "easy mark". I liked your original question :) Anyway you might add back that it's for maintaining a healthy temperature in a suit for an actor with poor ventilation (rather than a patient undergoing Deep hypothermic circulatory arrest for example)

@Charles I have already deleted some of them.

the one i know, is our skin via sweat-evaporation.

@TanzeelAshraf are you literally saying that the answer to "where on a body" is "the skin"?  Aye cheers mate, my guess was injecting ice water in the liver.  :-)

Based on hte thermal maps from this paper it appears the most consistent place would be the along the spine on the back, with a small "V" like split near the neck. since this is where the most heat is radiation it is the place the most heat can removed. Oddly the neck appears to vary quite a bit in its cooling capacity, this may be a result of different muscle mass.
This does make sense physiologically since it is both the core of the body and he closest you can get to the largest blood vessels for the entire body, the abdominal aorta. It should also be consistent for males and females for this reason, even in the obese those portions of the body stay relatively uninsulated.
although according to trails for and with cooling vests and hyperthermia, no one part of the body can cool the entire body very quickly or consistently (the bodies own responses fight you on this) although it certainly helps with comfort.

From personal experience, the best places to put a cooler (at maximum metabolic load) are across the back and over the neck and head.
Good candidate areas for a heat sink or exchanger:
Any region where large volume per unit time of blood travels close to the skin. Some dinosaurs are thought to have cycled blood through spiny fins on their back to cool down (obviously this works for non-dinosaurs too, and even better if the blood vessels in the fin are pressurized (see Are there any known examples of animals with air-conditioner type cooling? ).
Regions where a lot of metabolic activity takes place, including muscles in active use and "brown fat" (see https://www.webmd.com/diet/features/the-truth-about-fat)


text:
How increased potassium intake increases sodium excretion?
"K+ antagonises the biological effects of Na+". I have been reading the same many times without any explanation. How actually (mechanism) K+ helps excretion of Na+?, their interactions? And eventually lowers blood pressure?

That's because cell membrane could have a protein, called Na/K pump who's able to regulate the level of Sodium/Calcium using the energy gained by the hydrolysis of a phosphate bond from ATP.


text:
Disease causing variants and Hardy-Weinberg Equilibrium
Is it true that many disease causing variants/mutations do not follow Hardy Weinberg Equilibrium?  If so, then please elaborate on why this may be true (or not) and provide examples.
I am interested in single-gene disorders or those linked with single nucleotide variants.  I was told that many disease causing variants/mutations do not follow Hardy Weinberg Equilibrium, but I cannot find any documentation showing this (so I am looking for a reference on this matter).  In particular, I have considered Huntington's disease, Sickle cell anaemia and Hemophilia, but have not found any special relationships with these diseases and HWE.
Thank you.

Welcome to Biology.SE. Homework questions are considered off-topic unless the OP shows attempts of answering its own question.

This is not a homework question. I am a research data analyst proposing a bioinformatics model and I imagine the answer to this question will be helpful to my work.  I have done much searching, even considering HWE along with single-gene disorders such as Huntington's disease, Sickle cell anaemia and Hemophilia. I turned to StackExchange because my searches have proved unfruitful thus far. Thank you.

Ok, I retracted my close vote!

@user918804 in that case, please [edit] your question and add more details as to what you've already looked at, what you've learned, and what exactly you're still having problems with. Citations would also be helpful. The more detailed a question, the better the chances of getting a good detailed answer.

Hardy-Weinberg law makes a series of assumptions. One of them is the absence of selective effects. As you talk about disease, this assumption of neutrality is obviously not met.
At the moment of fecundation
Imagine for example that at the moment of the fecundation, the genotypes AA, Aa and aa are at Hardy-Weinberg equilibrium. Let x be the frequency of the allele A at the moment of fecundation, the frequencies of the genotypes AA, Aa and aa are $x^2$, $2x(1-x)$ and $(1-x)^2$, respectively.
After selection
As all genotypes aa die off, you're left with the A allele being at frequency $y=2x^2 + x(1-x)=x(1+x)$ and the frequencies of the genotypes AA, Aa and aa are $\frac{x^2}{x^2 + 2x(1-x)}=\frac{2x-2}{x-2}$, $\frac{2x(1-x)}{x^2 + 2x(1-x)}=\frac{x}{2-x}$, and $0$, respectively.
Expressing the genotype frequencies in terms of the new allele frequency
You can as well plug $y$ into those genotype frequencies to get the expression in terms of the genotype frequencies at birth ($y$; after selection). It gives you $\frac{1-\sqrt{4 y+1}}{\sqrt{4 y+1}-5}$, $\frac{2 \left(\sqrt{4 y+1}-3\right)}{\sqrt{4 y+1}-5}$ and $0$ for the genotypes AA, Aa and aa respectively. So, obviously, it is not at Hardy-Weinberg equilibrium.
Assumptions
You can make some more interesting calculations by leaving out the assumptions that all aa genotypes die at birth and you could use a Leslie matrix to describe the probability for an individual of each genotype to make to the next age. I also assumed that the a is completely recessive. You might want to release this assumption as well by computing the death of a fraction of the Aa genotypes.

I welcome the readers to double check my calculations.

I think the real surprising effect is the rather high frequency of the sickness causing alleles. For sickle cell anemia there is a well-known explanation, but I am wondering about Huntington Chorea.

In the case of sickle cell anemia, there is a positive selection effect of the illness causing gene variant: Heterozygous gene carriers have some immunity against malaria. Therefore, sickle cell anemia is quite frequent in malaria affected regions of the world.


text:
Do deaf people sleep better?
Since deaf people can't hear, is relaxing and falling asleep easier for them? In general, do they sleep better than hearing people?
Of course some hearing people have no trouble getting to sleep, but others awaken whenever they hear a sound.

I'm voting to close this question as off-topic because it's not biology

@rg255 - since when are sleep and sensation not Biology?

ok perhaps better to say I think it is trivial, does not deal with any kind of biological question or problem, and is unlikely to be of interest to the target audience (students, academics and active researchers)

You must also consider the reason for the condition. Are they deaf because of something mechanical in the ear? Something neurological? Maybe even psychosomatic? I would postulate that the total lack of one sense from birth would have no discernable effect on sleep patterns. As well, I would think that induced heading loss would harm sleep, because of the likely depression to go with loss of hearing.

Let's firstly differentiate deafness - profoundly impaired ability to hear, and other states where the subjects can still hear at different degrees.
Secondly, differentiate the congenital deafness & infantile hearing loss and hearing loss in adults who previously had normal hearing.
The subjects with congenital and very early infantile hearing loss would have better sleep characteristics (this state will affect psychological state in a lesser degree than one acquired in more mature & "conscious" state), while persons who have lost their normal hearing would have abnormal sleep patterns at least in the period when they have just realized that they are going to lose their hearing. After this "preliminary" period, the sleep pattern should be dependent on the person's psychological status and other similar factors.
Many persons will mention that while using ear plugs they feel that their sleep is better comparing with "un-plugged" sleep.
sources

Characteristics of sleep in deafness. Rev Neurol. 1998 Jun;26(154).
Non-scientific source.

Please pay attention that scientific sources are scarce, thus take the answer as one of limited evidence.


text:
Can a cell completely lose the ability to undergo apoptosis?
What I mean is - can a super-cancer cell completely lose the ability to kill itself, losing all apoptosis-related mechanisms and becoming eternally resistant to any drug that tries to induce apoptosis directly or indirectly.

It's not so much that a cancerous cell loses "the ability to kill itself". Rather, many cancers occur because there is a relative lack of inhibition of apoptosis. Many cancer drugs try to un-inhibit these apoptosis mechanisms. I think it is unlikely that a cell would be "resistant to any drug"; the problem with cancer treatment is that the drugs often kill healthy cells too, and there is a limit on the dose that can be given while keeping the patient alive. This may give the impression that the cancer is resistant, but it may just mean that the drug dose is too low.

Try reading The Hallmarks of Cancer and The Hallmarks of Cancer: The Next Generation by Hanahan and Weinberg. Both are Cell Reviews.


text:
Raising two legs together while lying on bed
Let's do some exercise(duh!)
Ok so lie on the bed. Lift your left leg. Put it down. Lift your right leg.Put it down. Easy?
Now lift your left leg and without putting it down, lift your right leg. Easy ? No.
Now try to lift both the legs together. Easy ? No.
My question : What is the anatomical reason ( arrangement of muscles around the bones etc.) which makes it difficult ?

I don't know if this is relevant, but with one leg down, we actually push against the bed while raising the other to increase the upward normal force and to shift the normal force toe-wards to maintain stability. This cannot be done if both legs are in air.

@SatwikPasani If your reasoning is correct, it would be interesting to know whether people with only one leg are able to raise their leg easily.

I suspect it is just physics. Each of your legs makes up about 1/6 of body mass, leaving about 2/3 of your mass superior to your hips.
Raising one leg requires action of the hip flexors (i.e., iliopsoas complex) but also activity in the anterior abdominal wall muscles (rectus abdominis, obliques) and back muscles to stabilize your abdomen. To raise the other leg simultaneously, you recruit the ipsilateral hip flexors. But, importantly, you probably have already maximally recruited most of your abdominal and back muscles.
Imagine the body as a lever system. With one leg raised, you have 1/6 of body mass balanced against 2/3. With both legs up, you have 1/3 vs. 2/3 and with potentially increased torque, because your legs are long (a force acting at a larger distance). The muscle forces to stabilize that must be larger, but the additional muscles are not there.
I can raise both legs with difficulty (admittedly, $n=1$).


text:
Are abrasions considered closed wounds?
A closed wound is one where skin is intact and underlying tissue is not exposed to the environment.
Abrasion is an erosion of skin usually due to sheering force. In most cases the dermis is intact and the injury is superficial limited to epidermis. Abrasions heal without scarring by epithelialization.
Are abrasions considered closed wounds? I would think they are open wounds as the underlying tissue (which would be dermis in this case) are exposed to the environment. Please state the reason why they are classified into whatever group.

I beg to differ... I have a lot scrapes that have scarred.

The definition of closed and open wounds is variable. In histopathological terms (i.e. looking under a microscope) it is usually defined that a wound where the dermis is affected is open. In this case an abrasion is an open wound. This puts it in the same class as cuts (incisional/lacerations), tears and punctures. Closed wounds on the other hand are when the dermis isn't affected, such as in a haematoma (blood collection under the skin) or crush injury (extreme force typically for a long period of time) and contusions (i.e. bruises).
Medically they may be divided by management. Where open wounds are wounds which are likely to be contaminated and need thorough cleaning and may need antibiotic cover whereas closed wounds are ones that are very unlikely to be. In this case, abrasions may be considered a relatively closed wound as not all the protective layers of the skin have been breached (the dermis is not completely breached). Thus the physical barriers are relatively intact and continue to offer us defense against bacteria and organisms.

Thanks for the answer, so as long as the skin is not breached the wound is considered closed

Updated the answer to include pathological definitions :)

authors: Σπύρος Μαυρίκας


text:
Death Psychology

Why do we sympathize in general when we see something or someone dying even if we personally don't know it/them?
Is there any species which sympathize with the death of its own species?
Is there any species which sympathize with the death of other species?

It's considered a requisite on biology.se that at least some research is carried out and presented with your question. Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

This question seems to be off-topic in biology unless more technical details are included. I think CogSci.SE would be suitable for this question.

Thanks for pointing out. I have submitted a migration request

@CRags - migration is often performed only with rockstar questions. As you haven't had any upvotes whatsoever I suggest cross posting.

@ChrisStronks do I close the question here?

@CRags - nope, just leave it as is, or close it if you wish of course


text:
How was the origin of CTVT parasitic cancer determined?
The wikipedia article on CTVT says that the tumor cell has 57-64 chromosome while a normal dog has 78 chromosomes. Similarly while all chromosomes in dogs except the X and Y chromosomes are acrocentric, many of the CTVT chromosomes are sub-metacentric or metacentric. Reference is given for the data in Wikipedia though a subscription is needed to view the referred articles themselves, so I was unable to confirm the data. (Wikipedia is sufficient for me, though popular opinion seem otherwise)
In addition there seems to be numerous (in the order of thousands) differences in sequences.

Their study showed that the cancer cells all originated from a common ancestor cell, not from the dogs themselves. Comparisons of the cancer DNA with dog DNA from reference samples held by the US Kennel Club and Crufts showed that it most likely originated at least 250 years ago from a wolf or an "old" Asian dog breed such as a husky or Shih Tzu, and spread like wildfire thereafter.

This was taken from Riddle of Infectious Dog Cancer Solved.

How is the conclusion arrived at in cases like this in general? What percentage / degree of genetic similarity is needed to identify something as belonging to a specific species?
How was the conclusion arrived at in this specific case? (I know I am greedy!)

I don't quite understand what (or maybe better why) you're asking. If Wikipedia is sufficient for you, why do you want more information?

Because what I am asking is not there in Wikipedia

"How is the conclusion arrived at in cases like this in general?" The same way it was in this case, by DNA analysis. It's in your article.

I am asking how DNA was analysed? Especially when there is such gross deviation in chromosome number and structure. Why are you being so antagnostic? Are you fed up with me because I disagreed with you? Lol, it's a free world and a person can disagree with anything!!

I'm not being antagonistic. You stated that you rely on Wiki. That's fine, then did you read about DNA analysis on Wikipedia? DNA analysis doesn't mean comparing chromosomes. It means looking at, for example, histocompatability loci. In the case of your tumor, mitochondrial DNA was very useful. My questions are usually a prompt to improve questions with a bit of research. The answer is in your article. If that's not helpful, you can do a bit of research to let us know what, exactly, you know or don't know, so we don't need to write a chapter on DNA analysis and guess at what you're asking.

@anongoodnurse OK, will read the article again and try to refine my question. Thanks for the pointer

@anongoodnurse after reading different articles I could not find how the genetic matching was done, if you would be kind enough to provide a link I would be grateful.

Your answer to your titular question, How was the origin of CTVT parasitic cancer determined? is that cytogenic studies were done on the tumors. It arose in dogs and was logically assumed to be of dog origin, and was first characterized in 1876. The tumor cells were/are characterized by a rearranged karyotype, which is similar in tumors from in different parts of the world. (1969) Thus it was postulated that that the transmissible agent causing the CTVT is the tumor cell itself and that all worldwide CTVT have a clonal origin. (1985)
Your later question states:

What percentage / degree of genetic similarity is needed to identify something as belonging to a specific species?

When a tumor arises in an animal (say a dog), it is automatically assumed that the cancerous cells, regardless of their ploidy, arose from that animal (in this case, a dog), not a different animal. Not all animals have had their entire genome sequenced, so this question as stated isn't answerable (although the genome of the dog has been completely sequenced). And certainly, not all tumor cell lines have been completely sequenced. The assumption of origin is made by looking at certain genes (e.g. histocompatibility genes) and others known to be species specific.
Since there are relatively few transmissible cancers (that is, where the cancer itself acts as the infectious agent), this is still a safe assumption. While I'm fairly confident more transmissible cancers will be found, I'm also fairly confident that they will be species specific, because in order to escape detection, they will need to be recognized immunologically as "self", as they must survive in the host at least long enough to be transmitted.
This is the case with canine transmissible venereal tumor (CTVT). It is also the case with the contagious tumor Tasmanian Devil face tumor disease (DFTD). Just as with the canine infectious cancer, DFTD cells in different individuals have identical, complex chromosomal rearrangements and are genetically identical to each other but different to the host devil.

Spread of such an infectious cell line between unrelated individuals should be prevented by major histocompatibility complex (MHC) Class I antigens on the surface of the tumour cell, as Class I molecules play a key role in self/non-self-recognition. The recent emergence of the tumor (transmitted by biting) in the endangered marsupial Tasmanian devil (Sarcophilus harrisii) is an unfortunate exception. In the Tasmanian devil, the tumor is very aggressive and kills the host.

In the case of canine transmissible venereal tumor (CTVT), it was shown about five decades ago to be the same dog tumor being spread from dog to dog. The earliest studies were based on histological studies and karyotyping. Paraffin-embedded tumor samples still exist. More recently, with genetic analysis, it is possible to perform much more sophisticated testing on the tumor DNA.

The transmissible agent causing canine transmissible venereal tumor (CTVT) is thought to be the tumor cell itself. To test this hypothesis, we analyzed genetic markers including major histocompatibility (MHC) genes, microsatellites, and mitochondrial DNA (mtDNA) in naturally occurring tumors and matched blood samples. In each case, the tumor is genetically distinct from its host. Moreover, tumors collected from 40 dogs in 5 continents are derived from a single neoplastic clone that has diverged into two subclades. Phylogenetic analyses indicate that CTVT most likely originated from a wolf or an East Asian breed of dog between 200 and 2500 years ago. Although CTVT is highly aneuploid, it has a remarkably stable genotype.

Your quote

likely originated at least 250 years ago from a wolf or an "old" Asian dog breed such as a husky or Shih Tzu...

Has been disputed. Estimates vary widely, from 11,000 years to 250 years.
Canine TVT: Evolution of Somatic Tumour Cell as Transmissible Parasites
MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer
Clonal Origin and Evolution of a Transmissible Cancer

@CRags - Are you an editor? Perhaps you can update the Wikipedia article to reflect the new information?

ok, will do today later @anongoodnurse


text:
How does Tylenol relieve pain without making me drowsy?
So I have a crown that popped out and has been killing me, I've lived on a steady diet of Tylenol since it popped out. I've noticed that aside from killing most of the pain from the tooth, the tylenol hasn't made me particularly drowsy, which to my understanding was how most pain killers work. If it doesn't just put me to sleep, how does tylenol work to numb pain?

Opiate pain killers or pain killers that act on opioid receptors have a different mechanism of action than NSAIDs. They tend to act as receptor agonists which exert their effect on the CNS (oxycodone as an example). Opioid receptors are associated with analgesia, CNS depression, sedation, etc. Tylenol on the other hand is thought to exert its effect by downmodulating cyclooxygenase, and therefore inhibiting the production of prostaglandins like H2, which is a precursor to lots of pro-inflammatory compounds.


text:
Do Tumor-Infiltrating T Cells Experience Any Prolonged Effects Due To Hypoxia After They Return To Normoxia?
Adoptive cell transfer (ACT) therapy using tumor-inflitrating lymphocytes (TIL) is at the cutting edge of immuno-oncology treatments involving metastatic melanoma and other indications (1). The idea is that at some point during the growth of a tumor, some T cells attempted to mount an immune response, extravasated and got into the tumor, but they became overwhelmed and exhausted. The therapy itself involves taking these cells out from some excised tumor, reversing their condition and since they're already neo-antigen specific from having attempted an attack on that cancer: Expand them, put them back in the patient, let them hit the tumor much harder than before.
Not only do you need to reverse exhaustion in the TIL, but you also need to have the right population of T cells to get the best response. The factors involved are beyond this question, and so I'll get to the point.
In the tumor environment, the T cells become exhausted and their expression profile changes (2). It makes them more prone to apoptosis and they lose effector functions like GranzymeB production. You can tell how this is problematic. My suspicion is that in the tumor the T cells may become hypoxic, and what we know is that in the oxygen-sensing pathway, hypoxia inducible factors exert their effect. Normally, these should be kept in check by inhibiting proteins if they get produced under normoxia:

And so to my question:
After prolonged exposure to hypoxia, are there any regulatory or transcriptional changes that after prolonged return to normoxia render either of HIF1α or HIF2α active where they would normally be repressed?
Whether I just need a fresh set of eyes or the data just doesn't exist, I haven't necessarily found it obviously. I'd like to know if there's a remnant hypoxia-like regulation framework that remains after O2 gets back to normal that affect pathways like mTORC1/2. Thanks if advance for any insights!

It seems like you've made up a hypothesis with no evidence, and rather than actually look for evidence for the hypothesis you're charging down the pathway and asking about hypothetical recovery from hypothetical effects of hypothetical problems.  Why not actually try to validate your model before asking about far-downstream effects?

@iayork It seems that way when I type things up (I miss a lot), but it's established that the T cells we're getting out of these tumors are in bad shape due to many factors including hypoxia, and that HIF very much modulates T cell responses (1) (2). If there's even a mundane tidbit I'm missing while I trudge through tons of papers, however, it will be great to find out.

Have you actually looked at HIF1α/HIF1α-Pro-OH levels in your TILs compared to circulating T cells with the same or similar surface markers, then made the same comparison after culturing TILs under normoxia for some period of time?

Alternatively, you could label the cells, then do an adoptive transfer of extracted TILs into non-tumor-bearing mice and follow them that way, if you're afraid that ex vivo culture might muddle the picture too much.

@MattDMo Just because it's not on our project list, I haven't run any such tests. We also don't work with mice (that's a collaborators' job). I'd like to do something similar, however, at some point in the future. I'm just looking for data that exists so i can come at the issue from the correct angles.


text:
Identifying Some Kind Of Fossil
This was found off the coast of Ireland by a friend of mine. The running gag is it's some kind of fetish or totem and should be immediately discarded, but we're interested in whether it's perhaps a coronal section of a fish skull, a bivalve or something else entirely. Many thanks to anyone participating!
Attachments :
Image-1

(higher resolution)
Image-2

(higher resolution)
Image-3

higher resolution

Mostly speculation on my part but the patterns and configuration look like a sand dollar to me. Likely a species in the order Clypeasteroida.

I've shared a link of this to the EarthScience.SE chat room to see if we can get some geologist eyes on this as well.

looks like the fossil Brachiopod

The best page on the web to find fossil ID experts is: Fossil ID - The Fossil Forum ... There was a molar ID on this forum some time ago, and the fossil forum guys knew what it was the same day.

Coronal cross section of a fish skull to me!

I know this is quite old - but those two oval marks could be limpet home scars

I don't know what kind of fossil is this. But, I can help you with link to website called FossilID, here you just have to fill a submission form and Expert paleontologists will answer you and help you identify this one. Here's the link: https://form.jotform.com/221665322452047 Also, you can try downloading an app called Digital Atlas of Ancient Life. Available both on Apple App Store and Play Store. If you want you can use other online services.

looks like part of an echinoid aka sea urchin skeleton. there is a huge variety of shapes and patterns, especially when you start looking at fossil ones.

Archaeocyatha cross section fossil.


text:
Is there a correlation between total neurons and intelligence?
Thanks for looking.
First off, I am not a biologist, just a curious layman, so I apologize in advance if this isn't a "good" question.  Please don't downvote me into oblivion.
I read today that the human brain has about 100 billion neurons and that got me wondering: is that number pretty standard for everyone or does someone like say,
Einstein, have many more neurons than this daft poster.
Question
Is there a correlation between total neuron count and intelligence, or does intelligence depend more on the way neurons are used--or some other factor like previous experience--rather than their total count?
Can this question be answered?
There are two very valid points-of-view posted as answers below, but it sounds like we simply don't have a solid answer to this question at this point in time, so I hesitate to select a "correct" answer.

See this too: http://skeptics.stackexchange.com/q/2948/19552

@Cornelius--Thanks.  I wasn't aware of that subdomain of SE.  Although, is it really the same question?  It seems like more neurons would equal more brain mass.  I truly don't know--not trying to be sarcastic or anything.  Thanks again.

@Cornelius--One other thought--if what the OP says on that post is true, it would seem that mass has no correlation to intelligence and, by extension, maybe neuron count doesn't either.  Wonder if that means we all have the capacity to be an Einstein?

somewhat related what is an effective metric for the complexity of a neural net / [cogsci.se]

we can't measure no of neurons precisely 2) we don't know exactly what "intelligence" is 3) walking is more difficult for brain than solving riddles (https://en.wikipedia.org/wiki/Moravec%27s_paradox)

Totally agree with point 2 of @Mithoron comment.

There are an estimated 100 billion neurons within the human brain. In general a minor variation in the number of neurons should not effect individuals too much, however when there is a more significant loss, such as brain injury or in some forms of dementia cognitive abilities do decline. So in this sense yes the number of neurons does relate to intelligence. However this variation is not what accounts for general variation of intelligence in the population.

Unlike a computer, the speed at which any brain can perform a computation is related to the number of synapses it goes through. This means fewer synapses in series correlate with decreased reaction time.
An example of fewer neurons correlating with a decrease in reaction time is exemplified in sensory neurons. All sensory nerve cell bodies are all located in the dorsal ganglia of the spine. Only projections from single nerve cells here reach our tissues. Furthermore, it's only in ganglia, nuclei, and the cortex that we see additional nerve cells. This is because each nerve cell in series introduces latency.
Latency in our sensory and motor circuits is very important to survival. Our intelligence is limited by a pressure to have a desirable reaction time. Reaction time does correlate intelligence. This is why tests of the sort are timed.
There is another factor in intelligence relating to number of neurons: An increase in grey matter means an increase in white matter. There has been some speculation that humans have nearly reached the limit of our cognitive ability, as our ability to store white matter has been reached.
We seem to be occupying the intelligence Goldilocks zone where reaction time, energy consumption, white matter are all in near optimal balance. It's the balance of these things, the sophistication of the circuits themselves that determine intelligence, not neuron count.
Here's a news link about running out of room for white matter
Here's a study which correlates perception time with reaction time

There is perhaps a trade-off between speed and functional complexity, since synapses are the sites of 'learning' and signal processing, by combining or subtracting, or applying conditional logic to different inputs to the next neuron in a pathway. We have many different neural pathways whose form suits their 'job', carrying out very different tasks - the anatomy of a reflex pathways looks nothing like a visual info-motor control network.
The nervous system is fascinating and curious!

I know of no correlation between number of neurons in cortex and intelligence. This question is fraught with controversy because there has been very little work on it but much speculation. Some have suggested that the connectivity between neurons is what is important rather than the number which is logically possible but remains to be supported by definitive evidence.

there is no question there is a rough correlation between neuron count and intelligence capability in a general way from looking at the biological species "spectrum" outside of humans. see wikipedia list of animals by number of neurons. eg in wide differences such as comparing insects vs primates etcetera. there is also a rough correlation of neuron count with body mass and total cell count in animals. however within a single species, small variations in neuron count probably do not have much effect on overall intelligence. also it is known that homo neanderthalensis, the ~30k yr precursor to [homo sapiens] had a larger brain cavity and therefore presumably more neurons but apparently less intellectual capacity than homo sapiens, possibly one factor in its extinction due to competitive evolutionary pressures. even various gorilla species have larger brain mass and conceivably correspondingly larger amounts of neurons (under a rough assumption that neuron density per mass would not vary strongly).
it is also thought that brain size has been affected by evolutionary pressure wrt smaller skull size which has to comfortably fit through the birth canal as a constraint. another aspect to study is the enteric nervous system in the human which has a large number of neurons but does not seem to exhibit a large measurable "intelligence" in the classic sense of guiding the animal behavior, but conceivably uses significant processing to manage gastrointestinal control.
another aspect of the question to consider: programmed cell death in the developing nervous system. large numbers of neurons die during normal natal development in "critical windows" and this seems to show that biologically, total number of neurons is apparently not a key measure or controller of intelligence (otherwise evolutionary pressures would tend to decrease this). the nervous system appears to grow "extra" neurons more than "necessary" for smooth functioning of the human organism.

Homo neanderthalensis was not an ancestor of Homo sapiens. It is discussed, if H.n. is a sideline of the H.sapiens line. They lived around the same time. See here for some details.

ok good pt; however this all still applies even if neanderthalensis was a relative. quoting the start of your article "There is some debate as to whether they were a distinct species of the Homo genus (Homo neanderthalensis) or a subspecies of Homo sapiens." another funky point from "how has our brain evolved": "With some evolutionary irony, the past 10,000 years of human existence actually shrank our brains." thought to be due to decreased nutrition.