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Why did the face of human species changed so much during the course of its evolution?
I recently watched this video which showed the evolution of facial features of the modern man
https://youtu.be/-69K7E0UlBI
I'm wondering what evolutionary advantage did we get by having our face from this-

(reconstruction of the face of Australopithecus)
To this-

(Homo sapien sapien)
"In other words for what advantage did nature selected our present face?"

Just curious, but it's there some kind of juxtaposition going on here? Is that to be the Robert Downey Jr of Australopithecus??

There are many things going into the evolution of our face. It is not as simple as discussing a single trait. Your question is therefore quite broad. So I will just pick up three different traits and talk a little bit about them. Those traits are

hairs
size of the jaw
cranial capacity

As I will only say a few words, you will have to look for more advanced information by yourself if you want to deepen your knowledge.
But first, let me make a few other comments
A few comments
Panselectionist view of evolution
When you say what advantage did nature selected our present face?, you seem to assume that any evolutionary had to be brought about via a selective pressures. Yet, there is so much more to evolution than just natural selection. Not every trait has been selected for (otherwise we would not have any genetic disease). There is for example genetic drift who is also a very important evolutionary force.
On this subject, you might want to have a look at the paragraph Did you say Natural Selection? of this answer to Why don't mammals have more than 4 limbs? and to Why do some bad traits evolve, and good ones don't?
Accuracy of your Australopithecus's face
In the reconstruction of the appearance of a extinct lineage, there is always some part of artistic representation to fill the gap of what we don't know. One should investigate the exact method used to recreate this image before assuming that Australopithecus looked exactly like that.
For more information have a look at In reconstructions, how are various shapes of facial features determined from skull only?
On top of that, please note that there is variation in faces within a species. This is true for Homo sapiens today and it was true for other great ape lineage. More importantly, there were at least 6 species of Australopithecus (see wiki > Australopithecus).
Human species or hominini lineage?
Your question is

Why did the face of human species changed so much during the course of its evolution?

When we say "human species", we typically refer to H. sapiens (or even H. sapiens sapiens). Based on your images, you seem to rather ask about the evolution of faces in the hominini lineage and not only in H. sapiens as Australopithecus is not the same species as us. Australopithecus is actually a genus (other than Homo) containing several species.
Evolution of a few facial traits
Hairs
We've lost plenty of hairs! Have a look at the post Why did humans lose their fur? to understand why.
Size of the jaw
Here is a timeline of evolution of hominini

As you can see, Australopithecus did not know how to cook. They did not know how to control fire. The first to have a good control of fire were probably Homo erectus.
By cooking, we pre-digest our food, leaving much less work for our digestive system, including the physical mastication performed by our jaws and teeth. As a consequence our jaws reduced in size (Wrangham and Conklin-Brittain 2003, Lucas et al. 2006; See also this book from Lucas).
Size of the brain
H. sapiens cranium is about 3 times the size of Australipithecus cranium (Leigh 1992 and Smith et al. 1995).
Cooking allowed us to save much energy, which could then be used for higher cognitive abilities. Without cooking, it is likely that our brain would never has gotten to the size it has today. Our brain consumes about 20% of our energy today (which is very unusual if you compare to other species). Cooking therefore also lead to an increase in brain size.

When I have to scroll, and then scroll some more, I'm always anticipating on seeing a small red box at the bottom. I'm curious though, can you provide any literature on, "By cooking, we pre-digest our food, leaving much less work for our digestive system, including the physical mastication. As a consequence our jaws reduced in size."? Specifically, the sentence in bold. Thanks.

It is a pretty common claim. It was easy to find evidence. I added two papers and a book as reference in the text. Thanks

The most unusual features of the human face on a purely visual basis is our nose and our chin.
OUr chin has been hotly debated I know of no less than five separate hypothesis about its development. The leading idea based on current evidence points to the chen being a side effect of our shrinking faces and therefore jaws at the same time we are increasing our reliance on speech, the need to keep the the jaw braced at the same time we did not 'want' our throat or tongue to be smaller, the chin is a side effect of how the jaw grows under these constraints in early  development. Oddly fetal chimps have something similar to a chin.
The nose is a bit easier it appears to be a response to our ancestors both growing larger brains (pushing the sinus forward) at the same time we are moving into drier climates, the nasal passage keeps the air you inhale humid enough to not damage your lungs. So the nasal passage needed to be larger (or at least not get smaller) at the same time the face is getting smaller and the brain is squeezing out the sinuses. The solution is a protruding nose.

Almost all the muscle groups around the eyes nose and cheeks are primarily for communicating, so the face has developed into a communication organ, it is a highly varied organ with more muscles than the hand. 43 muscles in the face, and 34 muscles in the hand. Mostly the facial muscles are unconsciously triggered by emotional states, not by physical necessity. Our subconcious also reacts faster and more primitavely to facial emotional expressions than it does to logical processes that require concious awareness and reasoning. i.e. when a human sees an angry face in his peripheral vision or centrally, his nervous system reacts faster than he can actually turn his eyes to observe the face directly, and he will become aware of the fact after he has reacted.
The human climate range and population size is huge, so the differences are on par with other primates that have divided 2500 grandfathers (generations) ago, we have very distinct populations from Australia to Africa. Secondly, humans have selectively bred with non-human species such as Denisovan and Neanderthal species. Bushmen are not part Neanderthal, and Papuans are part Denisovan, and the rest of us have neanderthal genes.
Primates have a tendency to develop facial display features, faces are more important for primate communication than in felines for example. many primates also have bald cheeks and chins, which is uncommon for mammals. We have bald faces and more muscle groups in our face than many other animals.
Primates have red, blue, pink, white, colors on the face, mustaches, maturation protrusions, whereas felines, squirrels, bears, don't often have face specific displays, perhaps camouflage, except for example the lion.
2-3 of the animals at the end are not primates, see if you can guess which ones:

One theory suggested by my human ecology professor at Oxford posits that 4 legged primates communicate sexually by displaying and looking at each other's sexual organs, because they are at the same level as the head.
The theory states that humans use strong eye and face contact to communicate sexually, instead of smelling and so the mouth has come to symbolize the sexual organs in communication, and so have other facial features.


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Why women have high Erythrocyte sedimentation rate?
Why ESR (Erythrocyte sedimentation rate)
1. higher in women
2. increases with age
3. increases in pregnancy, infection, malignancies
what I thought so far : since women are menstruating so there shall be some blood loss and this might be related to that.
For age I have no clue and in pregnancy might be related to fact the mass of rbc increases during pregnancy.
But is that right ? and what about  2 and 3 ?

I have already shown an attempt at the question

source: Stack Exchange

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

sort: votes


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Opening coverslip package
I feel pretty silly for asking this but I don't want to damage these coverslips.
I just ordered a 100ct box of coverslips and see no way to open them without destroying the container they are in. How are these little boxes typically opened? It seems smooth and sealed on all sides.

Looking at the container from the side, it's probably a situation like this:

There might be some clear plastic wrap around the entire thing as well that you would need to cut/break.

Thanks! I ended up using a knife to pry it open, turns out my fingernails weren't enough was all.

@Dilo You're welcome! Often times I can grasp both ends with just my fingers and pull them apart but it depends on how tight the fit is.

@Diio Thanks! I know how the package was built, but it just won't budge. I think it formed some kind of a vacuum. Pushing the cap up with a knife equally on all sides opened it, and subsequent opening is much, much easier.

Thanks for this posting. I was getting worried about my sanity. I pressed a knife edge hard on one of the sides, effectively cutting some plastic off. After that it opened w/o any trouble.

@peterd You're very welcome.

Basically the same answer, just explained differently... The top lifts off.  There is a tiny lip around the bottom edge (all four sides opposite the label). It's just a matter of getting a grip well enough to slide the top and bottom apart. (See diagram in last post, just imagine it vertically)
Thank you to the previous poster.

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

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


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What's the cause of the scars on these cherries?
These cherries have some scars. Are they coming from a disease? Is it correct to call them "Cherry scabs"?
Here's the photo:  -

U think those happened way before the cherrie were ripened, else the lack of acid would have made them rot from exposure, so I don't know why they would split at that stage, considering they usually split from excess rain.

Are they coming from a disease?

No, this appears to be a combination of rain damage and pests. If a disease were present, much more of the cherry would suffer, there would be signs of rotting, and, the damage wouldn't solely be so superficial, as is the case in your posted images.
Consider the next few images which demonstrate the effects that various diseases have on a cherry, and notice how much more detrimental [and different] the impact.
Bitter Rot (Colletrotrichum gloeosporioides & C. acutatum)

Brown Rot (Monolinia fructicola)

Alternaria Rot (Alternaria sp.)

There are other [equally common] diseases of cherry trees (Prunus sp.), including cherry spot leaf, black knot, silver leaf, and PNRSV, however, in pretty much all of these cases too, there's no modification to the cherry fruit (excluding extreme circumstances, as is the case with spot leaf, I believe).
Instead, as mentioned, one major cause of the damage is rain. Just before harvest, when the cherry is at it's greatest [and possibly maximum] volume, rain that's absorbed through the surface of the cherry causes the cherry to further enlarge, which ultimately splits the cuticle (skin). The result is the following:

For more information on cherry splitting/cracking:

Fruit Splitting (Cracking) – What causes it and can we do anything about it?
Fruit Split In Cherries: Learn Why Cherry Fruits Split Open
A Review of Cherry Fruit Cracking
Story: Stone fruit and the summerfruit industry
Cherry Weather Worries

Given the irregularities of scarring on some of the cherries, I also suggest that insects and/or birds scratched/ate away at them. Consider the following images that illustrate the kind of damage that birds & wasps cause when feeding on cherries, and notice the similarities to those in your images.
bird damage

wasp damage

This, in combination with the rain, is most likely what caused damage to your cherries.

Is it correct to call them "Cherry scabs"?

I just call it scarring, and I believe many other people do too. I'm not sure if there's a specific term for fruit damage that's then been "scabbed" over. If someone knows of a term for this, please provide in a comment and I will supplement my response with it. Thank you.

While continuing to research this topic, specifically when attempting to find alternative reasons that could explain this kind of damage, I did ran across this article which talks about wind damage, and provides an image that slightly resembles the markings on your cherries. I'm still heavily convinced though that your cherries suffered their damage from rain & pests.

This answer has a lot of "beliefs" and "suggestions" - we prefer referenced answers at Biology.SE for all but the most basic questions.

I'll add the sources I used, and will change my verbiage to be more definitive. I would have done this already but I answered from my phone. Thanks.

Maybe just adding a source for the images may help a lot. For the moment, the only thing that could make us thing the scarring on the images are due to rain is  the title that you gave to the image.

@BryanKrause Proper edits have been made. Thanks again.

My cherries look quite similar with the rain affected ones that you linked. It's just that mine are darker and the cracks are wider. However, fruit diseases doesn't always make them rot, for example apple scab, sooty blotch and flyspeck - or avocado scab - https://en.wikipedia.org/wiki/Apple_scab - https://commons.wikimedia.org/wiki/Category:Avocado_scabs

@Fructibus In the case of cherries, most every disease [of cherry trees] either rots the cherry, or the fruit isn't affected at all. That being said, what may be true for apples [and other fruit] isn't necessarily true for cherries, and vise versa.


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Human genetic diversity in Africa in comparison with the rest of the world
Background
The claim ...

Most of the genetic diversity in humans is in Africa

... is quite common. On Biology.SE, it is easy to find posts that make this claim. Consider for example:

Do humans have enough biological differences to be grouped into races or subspecies?
How do we know the human species arose in Africa?
What is the correct classification of population groups of homo sapiens?

Question

Is the claim true?
What fraction of the total genetic diversity is present in Africa?

I understand that the term genetic diversity is often used in a vague sense. Please make sure to explain what statistics has been considered in the study you would refer to when giving estimates of what fraction of the genetic diversity is found in Africa. Note that I am not asking "why is it true?" but only "is it true"?

I would love to know the source for this claim. My money is on it not being true.

Here is a tree based on mitochondrial DNA variations in human populations.
van Oven M, Kayser M.  Hum Mutat. 2009 Feb;30(2):E386-94.
Updated comprehensive phylogenetic tree of global human mitochondrial DNA variation.

Looking at genetic distance between populations via mitochondria DNA, all nonafricans are descended from a founder in one mtDNA group (L3).  All the other L groups are African populations: L0 is the San people, L1 is Mbenga pygmies, L5 is Mbuti pygmies, and the others are other African groups.
If one considers each L haplogroup to represent genetic variation then 5/6 (83%) of human genetic variation is from African populations.
From a different source looking at genetics differently   A map of human genome variation from population scale sequencing Nature. 2010 Oct 28; 467(7319): 1061–1073

Populations with African ancestry contributed the largest number of
  variants and contained the highest fraction of novel variants,
  reflecting the greater diversity in African populations. For example,
  63% of novel SNPs in the low coverage project and 76% in the exon
  project were discovered in the African populations, compared to 20%
  and 33% in the European ancestry populations for the exon and low
  coverage projects respectively.

I've found two papers that provide some information on this, but no definitive answer.
The 1000 Genomes Project Consortium (2015) analysed whole genomes and found that "28% of novel variants" were found in African individuals. Novel variants were mostly (>99.9%) single nucleotide polymorphisms or short indels. This table has full count of all variants. However, 26% of the genomes were African, while African's make up ~16% of the world population, so these numbers cannot be extrapolated to the whole world. Another problem is that the samples were not taken from geographically dispersed people (figure 1).

Figure 1. Proportion of genetic variations shared in different populations.
Evidence for greater African genetic diversity is presented by Stephens et al (2001), though they look at North Americans from different ethnic groups which isn't ideal. They found many more unique SNPs in African-Americans than other ethnic groups.

Figure 2. SNPs in Americans of different ethnic groups.Population codes are AF, African-American; AS, Asian; CA, Caucasian; and HL, Hispanic-Latino.
I haven't been able to find the claim that most human genetic variation exists in Africa being made in the literature, though Africa is characterised as having high genetic diversity, e.g. here. I'm sure I've heard this claim outside of Stackexchange though.
My review of the literature definitely isn't comprehensive, so if anyone finds anything else feel free to add it.

Thanks that was already helpful. I had to check the original paper to make sure this weird 3D, Excel look alike graph was indeed from a peer-reviewed journal (journal: Science)!

Two new studies, the result of the human genome project, examined the genetic diversity of over 1,000 individuals from 51 population groups all over the world.6, 7 As in previous studies, peoples of Africa were the most genetically diverse. However, these studies also determined that those from the Middle East were the second most genetically diverse.
  difficult to interpret

http://www.godandscience.org/apologetics/humans_out_of_africa.html
I think it means that Africa contains 150,000-500k years of human heritage in a wide base of population, whereas the base for the rest of the world is narrower... same as if you had 10 colors of cats in one enclosure, and only 3 colors of cats moved into the park across the road and bred there.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067985/
Consistent with the “Out of Africa” model of modern human origins, analyses of genetic data indicate that Africans have higher levels of genetic diversity than non-Africans (Cann et al. 1987, 2002; Tishkoff et al. 1998; Marth et al. 2004).


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Why aren't human babies considered larvae?
I've seen people who are anti-baby describe babies, or children in general, as human larvae. This is generally done in order to make them seem weird. While I feel like this statement is wrong, I can't quite put my finger on exactly why.
Many definitions of "larva" specify that they must metamorphosize, or go through significant morphological changes on the path to adulthood. However, tadpoles gradually change form, rather than metamorphosizing, and hemimetabolic insects have larval instars that aren't substantially different from adults, aside from being sexually immature and smaller. "Sexually immature and smaller", of course, also describes babies fairly well.
Unfortunately, I'm no biologist and my knowledge of what defines animal young as larval vs. non-larval is rudimentary, at best, so I'm not sure if there's a more precise definition of "larva" than the one I found on wikipedia, which would disqualify human babies. What traits differentiate larva from non-larva, and which of those traits to babies lack?

I'm voting to close this question as off-topic because it’s a not about biology but semantics.

For animals with a clear larval stage, the presence of such a stage indicates that there is a metamorphosis, a change in body morphology at some point in development.
Metamorphosis does not necessarily refer to an 'instant' transformation or one that requires a pupation step or something similar; gradual change can still be metamorphosis, as long as there is a clear 'before' and 'after.'
Human infants, on the other hand, don't go through much of a metamorphosis: sure, they grow quite a bit, but their general body plan does not change. Contrast this with insects, or your tadpole example, and it is clear there are major body plan changes from larvae to adult stages.
The Wikipedia page on larvae describes the characteristics of larvae fairly clearly. Like most traits in biology that vary across taxa, you are likely to find some intermediate creatures where the presence of a larval stage is somewhat controversial or depends on opinion. There could be a difference of opinion on how much of a change is sufficient to describe a juvenile form as a larvae. Humans don't have a postnatal stage that approaches that potential boundary.
The part in your question about people who are "anti-baby" sounds a bit judgmental, but I think what you are describing is just a phrasing meant to be somewhat humorous and to evoke images of "gross" larvae; I wouldn't take that for any biological meaning and I wouldn't focus your time on proving it "wrong" - the actual difference of opinion you have is something entirely different.

Children certainly are not human larvae biologically, for the reasons explained in the accepted answer.
However, calling children larvae is a metaphor that refers to child's mental and social development rather than morphological. Stepping back and looking at a kid as human larva can give adults important insight:

A larva has entirely different needs and capabilities than imago. Adults sometimes forget that.
Important milestones of development (walking, talking, social training, adolescence) resemble instars: behavior and needs of a kid at given milestone have little in common with needs at previous stage.
The purpose of a larva is to molt into adult form. Which is something that many parents tend to forget: that the only purpose of their kid is to grow into a functioning adult eventually.
Actions of the larva make no sense for the imago, and imago can't be held responsible for it's previous instar actions. That's somehow a trope for family embarrassing teens/young adults with things they've done as kids. Larva analogy helps to deal with such situations and memories.

This analogy is anti-baby only used in context against babies. In some parenting books, this analogy is used to help parents understand their children better. The only inherently bad thing about it I can think of is exploiting some people's aversion to insects in general and larvae in particular.


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Can anyone help me identify this insect?
I'm trying to identify the insect below that I found in Edmonton, Alberta, Canada. Any help would be appreciated.

Where was it found?

Edmonton AB, Canada

Also, what type of environement was it found in? Forest, grass, in the basement, etc...?

it was flying in my garage while the door where open. I assume it's terrestrial but I'm not 100% sure

This a long-horned caddisfly (gallery), which belongs to the superfamily Leptoceridae, though, due to a combination of the quality of your image, as well as limited available resources online, I'm currently not able to confidently suggest a genus or species. At any rate, here are a few pictures of various caddisfly that resemble the characteristics of your posted insect.

Unkown genus & species

Ceraclea dissimilis

Ceraclea sp.

Ceraclea slossonae

From where the majority of what I believe to be the closest matches mostly all belong to the genus Ceraclea, I am currently leaning towards that, however, I will continue to search for further validation.


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If alcohol is a depressant, why does it makes certain people more hyperactive?
Alcohol is by traditional definition a depressant from what I have been taught, ergo it shows down CNS responses.
However, why does alcohol then make some people act out and be more energetic than when they don't drink?

These types of reactions in pharmacology in general are called paradoxical effects.
The main effect of alcohol on the CNS is the potentiation of GABA receptors. GABA receptors are (mostly) inhibitory receptors in the CNS, so potentiation of GABA receptors mostly decreases brain activity by increasing inhibition.
However, you can distinguish between neural inhibition and behavioral inhibition. Some brain regions, like the prefrontal cortex, seem to primarily have inhibitory effects on behavior. That is, usually prefrontal cortex is active when suppressing actions. If you were to suppress the prefrontal cortex, you would get the opposite effect on behavior. When there is "inhibition of inhibition" the term often used is "disinhibition."
It isn't yet clear why exactly alcohol leads to behavioral disinhibition at lower doses, but this is one possible mechanism. In general, U-shaped dose-response curves are quite common in neuroscience, so alcohol isn't all that unusual in that sense.

Most people experience some stimulating effects from alcohol in small doses. Drinking alcohol, often a person finds increased talkatively, feelings of energy, and desire for action. In small to moderate doses of alcohol, the initial effects of alcohol act like a stimulant. However, alcohol is actually in the depressant class of drug types. Alcohol, like sedatives and tranquilizers, actually slows down activity in the central nervous system. To be more specific, it slows down the activity in the GABA receptors of our brains. The slowing of these systems is responsible for the relaxing quality produced by alcohol. The slowing of the central nervous system is also responsible for the lowered reaction time and dissociation.
Look at this wikipedia article: https://en.wikipedia.org/wiki/Short-term_effects_of_alcohol_consumption

" slows down the activity in the GABA receptors of our brains" - ehhh... that statement is misleading at best, completely wrong at worst. Ethanol potentiates GABA-A receptors through multiple kinetic effects; the only thing you could describe it as 'slowing' possibly is the time to close, but that's not by an actual kinetic slowing.


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Why is the chemical of an hexose not sufficient to ID the molecule?
Here is the homework question I have to answer to

The Chemical formula C6H12O6 can mean any number of different hexose sugars that share the same chemical formula. To tell the hexoses apart, you would need to see their structural formula. This is because they are ___________ of each other

My thoughts are ...

Welcome to Biology.SE. Your question is off-topic because 1) It is more of a chemistry question than a biology question and 2) homework questions are off-topic unless you've shown your attempt at solving it.

The format of your question is not great. Just to show you what a good format is, I edited your post. Of course, as it is a homework question, I can't fill up for you what your thoughts on the question is. Good luck

@Justin The question is saying that, based on the specific notation being used to represent this molecule, i.e., by expressing the molecule using its chemical formula, it's not possible to distinguish different hexose sugars (sugars with six carbons) from each other simply by considering their chemical formula. Instead, you would need to use structural formula notation. The reason why you need to do this is because different molecules that have the same chemical formula, but different structural configurations, are considered to be _______ of each other.


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Species of dinosaur with longest fossile record (no birds!)
There were many species of dinosaurs and many got extinct long before the whole clade disappeared. I am wondering which species has shown the longest fossile record. Since birds descend from dinosaurs, I excluded that case to preclude the easy answer! I fully understand the vagueness of my question, stemming from the uncertainties associated with the definition of species but I would think that at least some ballpark could be estimated?

If there's any validity to this article, perhaps one of these?

Dinosaur biostratigraphy makes it not possible to answer your question through all of history. 8Ma is the highest longevity species I found in a biostratigraphy table. Dinosaurs are faster evolving than crocodilians who have 1/3rd as big a genome as a mouse and 1/6th that of a shark. Adaptive genus existed for 5-30 million years, and well known clades exist for 20-500 Ma.

The most complete geological formations often only cover small spans of history. Generally you will find that paleontologists have few species, and more often groups and genus represented by 10-20 species fragments.

The Hell Creek Formation covers 2 million years of history, and has revealed 400 species, of turtles, dinosaurs, metatherians, mammals, turtles, and a very rich image of life at that time, and 90 percent of the geological time scale is represented by only a fragments of fossils.
So, you won't find a good answer for species, perhaps the best way to find out the longest lived genus (i.e. like a dragonfly, all species are in the same family) is by doing some google tricks:
For genus i can find this:
Plateosaurus 214–204 Ma
Thyreophorans group 199.6–66 Ma
Gryposaurus genus  84-73 Ma
Plesiosaurus genus 199.6–175.6 Ma
Gorgonopsians 265–252 Ma
Dimetrodon 295–272 Ma
Carcharodontosaurus 112-93
Pterosaur 228–66 Ma
Mussaurus : 215–203 Ma
Lesothosaurus : 199–189 Ma
Spinosaurus : 112-93
Kronosaurus genus 125–99 Ma
scorpion 430–0 Ma.
Dragonfly     325–0 Ma
brittle star 499Ma-present
crocodilians 200-0
some shark genus: 100-0
snapping tortoise 100-0
horeshoe crab 455-0
nautilus 488-0
Fossil fields are incomplete, so the HellCreek time period is very well represented with lots of tyranosaurus, and other time periods are incomplete.
Animals with small genotypes Crocodiles and turtles evolve very slowly, and it gives you an idea of evolution speeds prior to the arrival of mammals, who seem can adapt faster than all previous larte animals.
crocodiles have less than 1/3 of the genes of a mouse and a human
tortoises have 2/3rds and so do horseshoe crabs
dragonfly have 1/6th the genome size of a mouse
sharks have twice as big genome


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What does a wing shake in crickets indicate?
What does it mean when a male cricket (Acheta domesticus) shakes its wings towards another male cricket? Is this an act of aggressiveness?

Could you elaborate a bit what you mean with shaking its wings? You mean chirping?


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What is mean by the term "an organism's genotype is its specific combination of alleles for a given gene"?

an organism's genotype is its specific combination of alleles for a given gene

What is meant by this? Is it talking about heterozygous and homozygous (like GG or Gg) or is it talking about the nuclear bases?
Thanks

I'm voting to close this question as off-topic because there is no source given for the fragment quoted.

From wikipedia

An Allele is a variant form of a given gene.

Let's consider a simplified example. There is a gene for eye color and there are different alleles at this gene. The allele for blue eye, the allele for brown eye etc...
In a diploid (see ploidy) individual (humans are diploid), we have two copies of each gene (exception of sex chromosomes). Let's imagine, at a givne gene, there are 3 possible alleles called A, B and C. The possible combinations are
AA
AB
AC
BB
BC
CC

The genotype of an individual for a given gene (I should say locus for the sake of generality) is called the genotype of an individual.

Is it talking about heterozygous and homozygous[?]

The terms "homozygous" or "heterozygous" are adjectives to define whether, in a diploid genotype, the same allele is found on both haplotypes or not. In the above examples, 3 genotypes are homozygous (AA, BB and CC) and 3 genotypes are heterozygous (AB,AC and BC).

[I]s it talking about the nuclear bases?

For two alleles to be different, they must differ in their sequence of nuclear bases of course.

Alleles are different versions of the same gene; they have different nucleotide sequences. Which versions of each gene an organism gets defines its genotype.
Zygosity (heterozygous/homozygous) is a related idea. When creatures have more than one copy of a chromosome (e.g. one from each parent) the alleles of each gene on each chromosome may be the same (homozygous) or different (heterozygous).


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Transpiration Process
During periods of rain/showers, does the transpiration process in plants slow down as a result of an equilibrium of water in the interior and on exterior of a plants foliage?


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Is this an ectopic beat?
First of all, I am unclear as to whether the answer to this question is a matter of fact or of opinion.
Nevertheless, I hope to find the answer.
In the image below, is the green beat considered ectopic?

What do you think, and why?

For reference: a normal P QRS from an EKG

from https://www.healio.com/cardiology/learn-the-heart/ecg-review/ecg-interpretation-tutorial/qrs-complex
The question and the different looking beat: one cannot say it is ectopic because the strip represents some sort of atrial arrhythmia.  Atrial fibrillation is the most common of these.  The beats are not regularly spaced and there is no sign of a P wave (the one produced by the atrium).
From link

Atrial Fibrillation occurs when multiple electrical impulses occur
  within within the atria. This chaotic electrical activity results in a
  chaotic wave form between the QRS complexes. P waves are absent. They
  are replaced by lower case "f" waves. No P waves means there is no PR
  interval measurement. This rapid electrical activity overwhelms the AV
  node causing impulses to enter the ventricular conduction system at
  irregular points. This results in irregular R to R intervals.

"Ectopic" beat suggests there is a regular beat going on and some rogue beat elbows its way in.  In A fib they are all rogue beats - "multiple electrical impulses".  The one you see is not in structure different from the rest - there is a T for every QRS and so they are all coming from the atrium.  It is just that with that beat the S wave is deeper.  Maybe because it is so close to the T?   I bet if you ran that strip a while you would see others comparably deep.
I am betting this is homework.  What exactly is the question?

Thanks for your assistance Will.  I had the assumption that even in atrial fibrillation, there is some ventricular rhythm to be studied, given by the RR intervals of suitably "normal" beats.  Essentially I was wondering whether the size of the beat would qualify it as "not-normal," meaning not part of the intrinsic ventricular rhythm, if any.

And you are right in predicting that there are more beats with the same S-depth as the green one, though they are fairly sparse.

this isn't biology, this is medicine. go to the medicine stack exchange

Beats coming from within the ventricle look different - wide weird QRS.  Google up PVC or premature ventricular contraction to see a common type.

@4DNeuron This post is considered as on-topic. Please see here for further details. Also, there are tags that directly support the topic of this question, so I don't see a problem.

Just to be clear, this is not AFib. March it out. (That's one of the first things to learn when studying EKG's: "march it out". It's tedious but instructive.) You'll see a pattern impossible with AFib. It's a crappy EKG tracing, but information is there. There is, however, an atrial problem.

@Will - Also, "ectopic beat" does not equal "PVC".


text:
What is the most primitive organism that can die of aging?
I know that simple organisms containing of just few cells have no mechanism of dying because of aging. I guess, they typically die due to being out of food or due to becoming someone else's food.
Leaving aside the numerous theories of what can be the origin of such phenomenon as aging, I'm asking a simple question: what is the most primitive organism known so far which has the feature of aging and (as a consequence) dying, even if the environment is perfect?

I feel it's essentially a dupe of question mentioned by Remi, as OP could easily call bacteria simplest organisms.

The adjective primitive is undefined, at least when comparing extant species. We have all gone through almost 4 billions years of evolution.
I would suspect you would consider a bacteria quite primitive though, so note that bacteria appears to age (see Do bacteria die of old age?).


text:
Which extinct creatures were most genetically distant from everything alive today?
The more distant the common ancestor of two creatures the more genetically distinct the creatures will be. For example I am more genetically distinct from a mushroom than an ant. I am more genetically distinct from an ant than a fox. Etc.
Extinction in the deep past has cut off some evolutionary branches. Which extinct creatures (including all living organisms) were most genetically distinct (alien) from living creatures today?

I vote for the Edicaran fauna.

from http://ediacaran.blogspot.com/2008/11/introduction-to-ediacaran-fauna.html
from en.wikipedia.org/wiki/Ediacaran_biota

Most macroscopic fossils are morphologically distinct from later
  life-forms: they resemble discs, tubes, mud-filled bags or quilted
  mattresses. Due to the difficulty of deducing evolutionary
  relationships among these organisms, some palaeontologists have
  suggested that these represent completely extinct lineages that do not
  resemble any living organism. One palaeontologist proposed a separate
  kingdom level category Vendozoa (now renamed Vendobionta)[8] in the
  Linnaean hierarchy for the Ediacaran biota. If these enigmatic
  organisms left no descendants, their strange forms might be seen as a
  "failed experiment" in multicellular life, with later multicellular
  life evolving independently from unrelated single-celled organisms.[9]

No-one can say what the DNA of the Edicaran organisms were, or whether they were related to what came after.  Apparently these fossils do not resemble the fossils of the subsequent Cambrian or much of anything else.  The triskelion fossil I put in here looked the coolest to me.  If they were a "failed experiment" or some sort of false start on multicellular life, they might have been totally alien.

I think this works for Eukaryotes. But I wonder if there are bacteria that are further still. Though, It could be hard to tell.

Stromatolites are fossils of bacteria colonies.  Some people think the edicaran fauna is the same sort of thing.

The very first ones to go extinct would be the most genetically distant; at that distance, the issue becomes more "how do you define life?" or "how do you define a species?" to get the actual most distant. Overall, it sounds like an interesting question, but it really isn't: extinction isn't special, it's the norm. There are most certainly extinct organisms or pre-organisms of some level of development that never contributed to the existing life on earth and have no descendants or relatives.

The first to go extinct could have been a part of a family or genus that still exists today. So, this isn't just about who went extinct first?

@futurebird No, it's certainly not. The first life to go extinct would have been relatives of the very earliest life to exist; these would also be the most genetically distinct, because everything since then is more genetically related than anything extant now is to the first life to exist.

that make sense do we know anything about these organisms?


text:
Why E.Coli get bigger if they replicate faster?
When E. Coli divide faster, they tend to have larger volumes. If the same cells are grown in a poorer medium, they'll have longer replication cycles and shrink. What is the explanation of this phenomenon?
Refs.
http://book.bionumbers.org/how-many-ribosomes-are-in-a-cell/
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0023126

@Charles I don't think the answer is so simple. How do you justify the implication more nutrients --> larger matured cell? Faster growth might just mean that the cell divides faster, so the average volume need not change. There are other examples with mammalian cells, I'll post them here.

@Charles You are correct. I meant cell division rate, not growth rate.

@becko If you could, please specify the kind of cell(s) you're talking about. So far, this has only been shown to apply to E. coli, given the article you provided.

Rapidly dividing bacteria contain more than one bacterial chromosome, and often more than two. The chromosomes take large amount of space in the cytoplasm and also attach to the cytoplasmic membrane. More chromosomal DNA requires larger cytoplasmic surface area; larger surface, larger volume.

This is interesting. Is there published research pursuing this line of thought?

Cooper & Helmstetter (1968) J Mol Biol 31(3): 519-540. ". . . multiple replication forks during rapid growth [of Escherichia coli] . . ."
https://www.ncbi.nlm.nih.gov/pubmed/4866337
And many papers since then; for example, recently: Khan et al. (2016) Genetics 202(3): 945-960.
https://www.ncbi.nlm.nih.gov/pubmed/26801182

THanks, but that paper does not mention volume explicitly. I had read some stuff about the multiple forks of the plasmids in bacteria, but did not relate it to volume. Do you happen to know any paper where this connection is pursued?

"The average dimensions of cells of Escherichia coli and other bacteria change markedly with changes in growth rate (20), but it has been noted that two parameters appear to remain relatively constant throughout: the ratio of cell mass to number of copies of the chromosome origin at the time of initiation of DNA replication" -- Donachie & Begg (1989) J Bacteriol 171(9): 4633-4639. https://www.ncbi.nlm.nih.gov/pubmed/2670889

Thanks again! That looks more directly related. I'll read this one and hopefully find some keywords that will allow me to find more recent stuff.

Here's one way to think about this. The key question is "how does the cell decide when to divide"?
You can imagine there are two major mechanisms:

The cell needs to accomplish some task that takes more or less a constant amount of time (DNA replication may be a close example). After that's done it can divide
The cell needs to accumulate a certain amount of biomass to grow to a certain size (protein synthesis is closer to this). When it gets there, it can divide.

(1) is often called the "timer" hypothesis and (2) the "sizer" hypothesis.
If (1) was true, then cells would grow at the same rate regardless of the medium. If (2) was true, then all cells would always have the same size regardless of the medium. Neither statement is true, so the truth is some combination of both effects.
However, under the timer hypothesis, larger cell size with faster growth rate comes out naturally, since the cell size will be determined by the amount of biomass that can accumulate during the constant time. So as long as there is some aspect of "waiting for something that takes a certain amount of time", you will get a positive correlation between size and growth rate.
Now this is an extremely naive explanation. In fact, not all bacteria show this correlation. There are also models other than "timer" and "sizer" -- e.g. here's an "adder" model that also explains the size effect.
Google "cell size control in bacteria" for a ton more papers.

The timer model explains a correlation between biomass production per unit time (units of mass / time) and cell size. It does not explain the correlation between doubling time (units 1 / time) and cell size.

I think this is a misconception. Biomass production rate is also in units of 1/time (exponential growth). More biomass produces biomass faster. In your model (linear biomass, exponential cell number), cells would get smaller over time in constant conditions.


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Why is Mus Musculus a good model organism?
I'm reading through a number of articles that use partial hepatectomy in Mus Musculus to study the mechanisms for liver regeneration (1, 2, 3). I have no doubt that a better understanding of hepatocyte regeneration mechanisms will allow scientists to discover/create new theurapetic targets that would improve liver regeneration in mice. However, these articles seem to imply that the results of the research will be applicable to liver regeneration in humans as well.
What makes Mus Musculus a good model organism? I'm inclined to think that some mouse genes might have homological human genes; is there more to that? Bonus points for answers that would show how research on non-coding RNAs, as compared to protein-coding genes, in mice would apply to humans.

"I'm inclined to think" that you should do a little research before posting if you don't know the extent of the genetic similarity among mammals. And what species would you expect experiments on liver regeneration to be performed? Homo Sapiens? Finally this is not a quiz show and you can only award points by accepting or up voting an answer. We don't do bonus points here.

@David "bonus points" was a figure of speech. I would gladly rephrase the question as a resource recommendation one. Go-to sources such as Model organism didn't help much, and, as an outsider to biology, I know no better sources. Finally, thanks for taking your time to explain the downvote.

Your question certainly needs revising because (1) it is unclear what you are asking (2) part is based on a false premise. First, you do not define model organism. Do you mean "why do scientists work on mice?" or "why is mouse a model organism for liver regeneration in humans?". Second your "thought inclinations" do not take into account that scientists have been studying liver regeneration in rodents since the middle of the last century, at which time nothing was known about non-coding (or coding) RNAs, and little about protein sequences. You should find out for yourself what is known now.

Mice are mammals, like humans, so their proteins tend to show more homology with human proteins than non-mammalian options. They are also actually more closely related to humans than cats or dogs due to the relatively recent (~80 million year) separation of lineages that led to modern rodents and primates.
Mice breed fairly quickly year-round and have relatively large litters. Laboratory strains are also quite tolerant of research lab conditions.
Mice are inexpensive to keep: they are small, require little food and care, etc.
People tend to have less opposition to research in mice due to their status as pest species.
Many genetic tools are available for mice, which makes them better models for the next generation of science, which means there are more genetic tools available for the generation that follows, etc. There are now many specialized mouse lines, some for particular diseases, some for particular techniques, etc.
Mice are well-studied, so experiments in mice can be easily compared to other experiments, and there are a lot of standards for protocols. Most experiments are done on inbred mice, which have the advantage of being nearly genetically identical to each other, so experiments done in different labs are done in (nearly) genetically identical subjects which can help with reproducibility and comparisons across studies (though there are also downsides to inbred animals; see below).
None of these factors make mice perfect model organisms. Many successful experiments and treatments in mice have not translated to human outcomes. Laboratory mice are typically highly inbred and may display characteristics thought to be "normal" that are actually the result of genetic drift, founder effects, etc. These can include preferences for alcohol, tendencies toward obesity, poor immune systems compared to wild mice, etc. Some get particular tumors early. Some have seizures. Some lab mice are blind at birth or shortly after. Others have hearing problems.
References

Abolins, S. R., Pocock, M. J., Hafalla, J. C., Riley, E. M., & Viney, M. E. (2011). Measures of immune function of wild mice, Mus musculus. Molecular Ecology, 20(5), 881-892.
Beck, J. A., Lloyd, S., Hafezparast, M., Lennon-Pierce, M., Eppig, J. T., Festing, M. F., & Fisher, E. M. (2000). Genealogies of mouse inbred strains. Nature genetics, 24(1), 23.
Battey, J., Jordan, E., Cox, D., & Dove, W. (1999). An action plan for mouse genomics. Nature genetics, 21(1), 73-75.
Gordon, J. W., Scangos, G. A., Plotkin, D. J., Barbosa, J. A., & Ruddle, F. H. (1980). Genetic transformation of mouse embryos by microinjection of purified DNA. Proceedings of the National Academy of Sciences, 77(12), 7380-7384.
Justice, M. J., & Dhillon, P. (2016). Using the mouse to model human disease: increasing validity and reproducibility.
Kurien, B. T., Gross, T., & Scofield, R. H. (2005). Barbering in mice: a model for trichotillomania. Bmj, 331(7531), 1503-1505.
Lynch, V. J. (2009). Use with caution: Developmental systems divergence and potential pitfalls of animal models. The Yale journal of biology and medicine, 82(2), 53.
Martin, B., Ji, S., Maudsley, S., & Mattson, M. P. (2010). “Control” laboratory rodents are metabolically morbid: why it matters. Proceedings of the National Academy of Sciences, 107(14), 6127-6133.

You could also add that it is relatively easy to produce inbred strains that will be more likely to show consistent experimental results.

@David I don't know if mice are particularly easy to produce inbred strains compared to others species, though I'd happily add a reference if that's the case for some reason. I did add a section on the advantages of standardized inbred strains since I spent a paragraph describing the disadvantages.

I don't have a reference. It must be easier than in rats (or mice are easier to breed) because there are so many more cited in the literature. Perhaps I should have said more are available. The other mundane factor is how much tissue you need and can obtain from the organism. Don't try isolating erythropoietin from fruit flies (even assuming they have it).

Understood. My experience in using both mice and rats is that there just as many "wild type" inbred strains of rats as of mice, at least as would be expected by each of their prevalence as research animals. The huge numbers of available mouse strains are mostly on the same several inbred backgrounds, and that's just because of all the available genetic tools for mice to generate mutants and transgenic animals.


text:
Why there is such low diversity of higher plants in sea?
I think it could be because of mycorrhiza or maybe because of the problem with flowering and seeds.
But really, I don't know.
edit:
by higher plants I meant Embryophytes

Welcome to Biology.SE. The concept of higher / more evolved lineages is undefined. You should probably just name what lineage you call "higher plants". Maybe you meant Angiosperm or Embryophytes, ...?

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


text:
What kind of spider is this please?

What type of spider is this PLEASE. My friend found it in her home. She has 3 boys under 10yrs old and people are telling her its a wolf spider i really dont think it is. Please help

It looks similar to a fishing spider. Please let us know your locale so we can make a more accurate determination.

We need to know the region, and also the size of this spider.

If you are in the US there are very few spiders that bite unprovoked. It looks more like a wolf than a brown recluse. (one of the few possibly dangerous US spiders, still needs to be provoked)

https://entomology.ca.uky.edu/ef631 can you get a better photo of the eyes please?

but they look like non recluse eyes to me.

It looks like a Wolf spider to me, probably one of the Tigrosa (formerly Hogna and Allocosa) species.  The narrow central line on the 'head', and what appears to be a blocky dark central mark at the front of the abdomen, are what I would expect.  I can't tell if the appearance of bands on the legs is real or an artifact of the light and photograph.  Oh, yes - these spiders are quite harmless (to humans, anyway), like almost all spiders.  They can give you a bite if you force them to, but I've handled them a lot and have never been bitten.  I would expect it to hurt a bit like a wasp sting, though.


text:
What is the role of Cl-, H+ and Malic Acid in stomatal opening and closing?
I understand that K+ influx brings in water making the guard cell turgid. This opens stomata. What is the role of other molecules/ions in this?


text:
Can a mathematical function be assigned to ECG diagram?
This is a 12 lead electeocardiogram of a 26 year old male:
This is the graph of function $5sin(7x)sin(.5x)cos(3.25x)$
 This graph look quite similar to the ECG diagram.After sketching this graph, I thought whether ECG diagram could be assigned roughly to a mathematical function.
Question: Has anyone ever tried to even roughly assign the diagram to a mathematical function? Is it even possible?

"Has anyone ever tried to even roughly assign the diagram to a mathematical function?" Yes, it was done before, using Fourier series (kind of what you have in your graph). The result is far from beautiful, see here: https://www.intmath.com/fourier-series/ecg-fourier-quartic-plusT.pdf. And here a detailed explanation: https://www.intmath.com/blog/mathematics/math-of-ecgs-fourier-series-4281

The links are broken or I can't open them from my android

Fourier series was my first guess, too. Is there any particular reason you would like to do that? I'm asking because if fitting is your concern, wavelet decomposition may be easier to work with. By the way, the links work for me.

@Mockingbird the links are up.

Yes, this would require Fourier series, in which case you would then desire to establish the number of terms needed to best fit your data, and, at the same time, find the value for each term's coefficient. If you have the raw data, you can upload to it Wolfram alpha and it will generate a function that fits. For example, WA can generate a function for Obama's signature; #26 on the list.

I recommend checking out this Mathematics.SE post, which nicely outlines Fourier series.

I’m voting to close this question because it's not about biology.

Yes a function could be assigned to an ECG diagram. I don't know if that would be helpful in any kind of research. Anyway I believe that from a mathematical point of view that if you manage to include all the equations shown in the picture into a single one you should get what you are looking for.

I have not made the diagram it was taken from this paper https://www.researchgate.net/publication/286584223_Design_of_a_synthetic_ECG_signal_based_on_the_Fourier_series by Radana Kahankova.

I was a high school back then when I asked this question. Obviously I had no emphasis on the graphical analysis being useful. haha

Try this:
$f(x)=-20(e^{\left(\operatorname{mod}\left(x-10,\ 20\right)-10\right)}*(e^{5\left(\operatorname{mod}\left(x-10,\ 20\right)-10\right)}-57*e^{4\left(\operatorname{mod}\left(x-10,\ 20\right)-10\right)}+302*e^{3\left(\operatorname{mod}\left(x-10,\ 20\right)-10\right)}-302*e^{2\left(\operatorname{mod}\left(x-10,\ 20\right)-10\right)}+57*e^{\left(\operatorname{mod}\left(x-10,\ 20\right)-10\right)}-1))/(e^{\left(\operatorname{mod}\left(x-10,\ 20\right)-10\right)}+1)^7$

Er, how does anyone know whether this is right or not?

Just copy the tex and paste it here: https://www.desmos.com/calculator

To be clear, there is really no biological reason to do this. ECGs are not collections of these sorts of functions. Fitting something like this is just a curiosity and gives you no understanding that you can't find in the original signal.

@Amad I see what you did here. You ploted a graph that slightly resenbles an ECG (Only QRST). Appreciate your intend to answer but I am afraid this is not what the author of the question's looking for.

@BryanKrause Haha I was a teenager back then when I asked this question and had no interest in the biological importance of the graphical analysis

@Mockingbird Yeah, that's kind of what I figured, I'm just going to close it. It's effectively a variant of https://math.stackexchange.com/questions/54506/is-this-batman-equation-for-real which is also closed over at Math.SE.


text:
Are ion channels/resistancies in Rall's model voltage-independent or not?
In the description of the electrical circuit that models a piece of membrane

in Rall's Scholarpedia article on Ralls model, I read:

"[...] this conductance [$G_e$] is zero under resting conditions, but
  is turned on by an excitatory synaptic input. [...] this conductance
  is [$G_i$] zero under resting conditions, but is turned on by
  inhibitory synaptic input."

Does this mean, Rall is assuming voltage-dependent ion channels? Or why does he stress, that the conductances can (or even must) be turned on and off?
From an electrical point of you, I would guess, that the three resistancy-battery pairs can be replaced by one such pair that would not be voltage-dependent, and maybe even the battery is not needed, as in cable theory:

Or would Rall's model not work anymore, then? This doesn't get clear to me, and would not have been stressed by the author. (Later in his article, Rall doesn't mention $G_r$, $G_e$, $G_i$ anymore, but talks only about membrane resistance $r_m$.)

Is it clear for you that the switch for those conductances turning on or off is synaptic transmission? Channels at the synapse will only conduct ions when a neurotransmitter binds on them. $G_e$ and $G_i$ could be replaced by a single element, except we know that excitatory and inhibitory synapses exist and may be active at different times and in different places of the cell. So you need them there if you try to describe further attributes in more complicated models (timing, localization). $G_r$ I guess cannot be fused with the other conductances as it is always on.

Yes, this is clear for me, but I didn't want to think of the initial creation of the potentials but only how the travel and spread (driven and controlled by membrane capitance and resistance). The conductances then will not be turned on and off by neurotransmitters but by the traveling potentials themselves. This means: I am only interested in voltage-gated but not in ligand-gated ion channels. (The initial potentials at time t=0 may just be "given".)

Then Rall's model is not appropriate for your purposes. Once $G_e$ and $G_i$ are turned on there is no additional voltage modulation - synaptic transmission is their only purpose. His is a 'passive' model, as we call it, and you seem to be interested in 'active' models.

@vkehayas: In this question I actually was interested in passive transport. Thanks to your explanations I now understand: that travel and spread of EPSPs - once initiated - is controlled solely by $C_m$, $G_r$, and $E_r$ - the other conductances are just off. And they are not voltage- but ligand-gated channels, so won't be influenced by passing-by potentials, right?

Mostly correct. The passive diffusion is described by the cable equation $$\frac{1}{r_l}\frac{\partial^2 V}{\partial X^2} = c_m\frac{\partial V}{\partial T}+\frac{V}{r_m}$$ Each compartment like the one you showed is assumed to be connected to its neighbours with $r_l$.

If you are interested in passive diffusion and not just membrane potential generation in a dendritic compartment, then you need to look at the cable equation:
$$\frac{1}{r_l}\frac{\partial^2 V}{\partial X^2} = c_m\frac{\partial V}{\partial T}+\frac{V}{r_m}$$
Here, every compartment is connected in series with resistances $r_l$.
We define the length constant as
$$ \lambda = \sqrt{\frac{r_m}{r_l}}  $$
and the time constant as
$$ \tau = r_mc_m$$
Then the equation can be re-written as:
$$\lambda^2\frac{\partial^2 V}{\partial X^2} = \tau\frac{\partial V}{\partial T}+V$$
The reason $G_e, G_i$ are not mentioned when talking about diffusion along the dendrite is that they are only involved in the generation of voltage $V$ in the compartment.

I added the corrections based on your comments.

I deleted the comments.

Final remark: the ion channels that are responsible for $G_r$, resp. $r_m$ are the leak channels, right?

Not quite. The diameter of the process comes into play: https://en.wikipedia.org/wiki/Cable_theory#Deriving_the_cable_equation

OK, $G_r$, resp. $R_m$ depend solely on physical properties of the leak channels, but $r_m = R_m/2\pi a$ also depends on the diameter $a$. Now I got the picture!

Wouldn't a natural refinement of Rall's model be simply to consider the voltage-gated (dendritic spike generating) ion channels during (otherwise passive) transport, instead of just neglecting them or switching them off (like the ligand-gated channels, that are described by $G_e$ and $G_i$)?

They simply were not known to exist and/or be implicated in dendritic processing when Rall's model was first formulated. For the rest, you may want to ask a new question.


text:
Differences that are too small to see
Consider two identical pieces of paper.
Scenario 1: On both something is drawn in black ink. If the difference between the areas covered in black ink is sufficiently small, I cannot see the difference between the two drawings.
Scenario 2: Now imagine that the same parts are covered with ink, but their color differs. Again, if the difference is sufficiently small, I cannot see the difference.
Firstly: what causes this? I am aware of the terminology of just-noticeable differences/limina, but do not understand precisely what causes them. Is there some discretization of continuous signals going on that causes `nearby signals' to be treated the same way?
Secondly: one person may have better vision than another, but are there physical constraints that are the same for any two persons and that imply that if the difference in scenario 1 or 2 is sufficiently small, no two persons will be able to see a difference?
Addenda: I phrased the question informally by not defining what a `small difference' is, trusting/hoping that this does not lead to confusion. If desired, such statements can be made precise by adopting appropriate distance functions. In scenario 1, one way to measure distance between two areas covered in ink could be to use the Hausdorff distance; likewise, one way to measure the distance between colors in the second scenario could depend on the difference in responsivity of the three types of cone cells.

I am having problems understanding your question. Would it be possible to add an image for your example? Also note that you may increase your chances of getting an answer over at cogsci.stackexchange.com.

Thanks, I will give the cogsci site a try as well. Two concrete examples: load a digital image into your computer, change just the colour of a single pixel. This is typically not a difference you can see. Likewise, it is not clear at first sight whether the strings 0000000000 and 00000000000 are identical. Why exactly can we not see small differences?


text:
Use of progesterone in preventing ovulation?
I have heard that progesterone in contraceptive pills or interuterine devices have been known to prevent ovulation. How is this possible since the LH and FSH are only affected by oestrogen not progesterone (am i wrong?)  Also,  my textbook says hormonal intrauterine devices contain progesterone to lessen uterine lining but doesnt the uterine get maintained by progesterone ?
Edit : I have yet to receive a satisfactory answer... Help anyone?

I'm voting to close as homework because explanations on how progesterone pills work are freely available from many sources, and as such it doesn't seem like this answer was very well researched.

@BryanKrause I have already done research on contraceptove pills but could not find any website specifically explaining how progesterone inhibits pregnancy

Did you try wikipedia?

When progesterone alone is used as a contraceptive it is assumed that the oestrogen level is endogenously maintained by the follicular cells.

Yes mainly oestrogen and only little does progesterone inhibits LH or FSH secretion.
LH surge is the principle stimulator of ovulation.

However,experimental work has suggested that immediately before the LH surge occurs, there is probably a sudden depression of estrogen...and this might be ...that leads to LH surge
  [source: Textbook of medical physiology A South Asian Edition- Guyton & Hall]

If progesterone or progesterone-oestrogen combinations be given before ovulation then feed back inhibition of LH surge occurs.This would lead to contraception by anovulation.

Progesterone is only known to proliferate the endometrial lining.

However, administration of progesterone or oestrogen -progesterone combinations after ovulatory phase helps to achieve high concentration of these hormones ,much before the normal time required to attain peak levels due to endogenous secretions alone.
This helps to depress the FSH -LH secretion by feedback inhibition very quickly causing involution of the corpus luteum and early shedding of the endometrium termed as breakthrough bleeding
REFERENCE:

reference site
Textbook of Medical Physiology A South Asian Edition-Guyton & Hall

This might and must be known to you that progesterone is known as the pregnancy hormones as it maintains the endometrial lining to Slough off  the  baby along with the corpus luteum (strata functionalis) and thus maintaining the pregnancy   and as far as the contraceptive pills and IUDs' are concerned they contain PROGESTIN i.e synthetic progesterone which inhibits LH production and hence anovulation  which is a type of we can say contraception  (prevention ) from pregnancy ;)÷

This answer needs citations and editing for English usage/grammar; there are randomly capitalized words, very unclear wording leading to incorrect statements, etc. It doesn't meet the standards of an answer on Biology.SE.


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Negative Phototropism In Plants
Why does the root of a plant go away from the sun? The shoot goes towards the sun, why does the root go away from it?

What do you think would happen to the direction the roots would grow, if the light source was below the plant?

@GabrielFair I don't know sir thats why I am asking the question. If I were to guess, it goes away because it wants water and sunlight evaporates it.

can someone please answer

All you have to do is read the wikipedia page for phototropism. https://en.wikipedia.org/wiki/Phototropism

The roots respond to gravity, not to light.  They display what is called a geotropism (aka gravitropism).  It has nothing to do with the light..  The roots grow TOWARD the force of gravity so the roots exhibit positive geotropism.   The stem grows AWAY from the force of gravity so it exhibits negative geotropism.   Think about a tree planted on a hill.
Phototropism is a plant's response to light.  It has nothing to do with the direction of room growth.  The stem may lean toward the sun (because of it's positive phototropism) but will still grow upward because of its negative geotropism.
**If the light was below the plant, the roots would still grow downward.

This is a good answer, though we prefer answers here at Biology.SE to include some citations to support statements and encourage further reading.


text:
Measuring depolarizations over the membrane
Measuring the rest potential of a membrane is relatively easy and straight forward: put one electrode inside the neuron, the other one (the "counter electrode") outside the neuron.
Because everything is at equilibrium (steady state), it's not important where exactly inside the neuron you place the first electrode, and even less important where outside the neuron you place the counter electrode: in the extracellular fluid next to the neuron or inside a container filled with extracellular fluid placed anywhere. One may even connect the other electrode to the ground (a lightning rod), if one does it consistently (over all measurements).
But now consider you want to measure the spread of depolarization along the membrane by measuring the membrane potential at two different locations of the membrane: You place one electrode underneath the membrane at point $p_1$ (and its counter electrode to the ground). And you place another electrode underneath the membrane at point $p_2$ (and its counter electrode to the ground).
Now it seems possibly important where exactly inside the neuron you place the two electrodes: the distance from the membrane might make a significant difference. (But maybe not.)
What probably would make a significant difference: Since the ionic compositions of the extracellular fluid in the vicinity of $p_1$ and $p_2$ will differ, it might be important to connect the counter electrodes not to the ground (or to some volume of normal extracellular fluid) but to corresponding points $p_1'$, $p_2'$ directly opposite to $p_1$, $p_2$ on the other side of the membrane.
I emphasized might be important because in practice it may be not important. That's what my question is for:

Is it OK, even for the measurement of the dynamics of depolarizations,
  to connect the counter electrodes to the ground (if only
  consistently). What would be the difference in the measured voltages,
  and can these be determinstically be cancelled out?

It is extremely important where you put your electrode when measuring such delicate structures as dendrites (which is when you want to compare voltage changes between two parts of a neuron). That is why you put your electrode inside the dendrite. Each recording electrode has its own ground that goes inside the bath, i.e. outside the neural tissue. Alternatively, you can observe fluorescence changes of a calcium or voltage dependent indicator that you have introduced inside them.
https://www.janelia.org/sites/default/files/Labs/Spruston%20Lab/Stuart_Spruston_2015.pdf

That's what I presumed: I put two electrodes inside the dendrite. But where to put their respective "counter electrodes"? Or do I use only two electrodes (both inside the dendrite), the second being the counter electrode of the first? But how to take measurements at three, four, many points on the membrane?

The ground goes inside the bath, i.e. outside the tissue. I am not sure I've seen any paper with more than three recording electrodes, but of course I cannot exclude that it exists. A 'usual' setup is having one electrode in the soma and one or two more electrodes on the dendrite. Needless to say, these are very challenging recordings and very few labs in the world are able to perform them. That is why fluorescence imaging of activity is becoming more popular, despite its limitations.

I've edited my answer to address your comment.

Llinás in  his "I of the vortex", p.9 evoked the following picture: "[The membrane voltage] may oscillate in a manner similar to the traveling, sinusoidal waves that we see as gentle ripples in calm water, and are weakly chaotic." What you say ("no paper with more than three recording electrodes") means - not surprisingly - that we will probably never see these ripples measured - but only simulated. (Do you know a reference for such a simulation?)

(I already asked this here: https://biology.stackexchange.com/questions/65550/visual-maps-of-the-neuronal-membrane - without explicitly mentioning membrane potentials, being another kind of "item").

@HansStricker Llinas is almost certainly referring to temporal oscillations (since that's what his whole book is about), i.e. plotting voltage versus time. The analogy to ripples is just that, an analogy.


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What are the major differences between good study habits for biology vs mathematics?
I'm a math prof. But, I've always loved reading about biology (the paleobiology of microbes and some small animals mostly) it's my hobby but I want to learn more maybe take a course. My longer term goal would be to be able to be of better assistance to my online friends who are biologists who are always asking me to help with the statistics in their papers. (I have been able to help, but I feel like I could do better)
When I study math, I aim to be able to identify and prove all major results from memory, state all definitions, and solve new problems and proofs. I have a process it works.
But with biology I often find that there are multiple definitions or there are big differences between textbook content and studies. It's really upsetting. I understand why this is true, that's just the nature of science, but I don't understand how to best navigate when a topic has multiple interpretations that are all possibly true. I get really hung up on not being able to find one definition for some terms.
Should novices and students stick to textbooks and "widely accepted" definitions? Or should one make and effort to keep up with the most recent research and learn to live with the ambiguity?
I can take one course for free at my university each term. Should I start with 101? Or can I do that through self-study and start with something more specialized?
What is a good self-study book?
My only science background is a few newtonian physics courses.
I'm kind of scared to go to the biology department and ask. Biologists are really intimidating when you teach something simple and clear like math.

Possible duplicate of Introductory biology text for an outsider

Every field is different! I am not sure if anyone could give much more advice. In general, the existence of several different definitions in the literature rarely causes any trouble in practice. Often enough, authors care about defining the terms they are using when dealing with terms that has been defined in several different ways.

It is always a bit scary to start a studying an entire new field. The teaching philosophy may differ from what we're used to, same goes with the type of mental effort but in the end, it always work out. Don't be intimidated by your fellow biologists. Most biologists are quite literate on a number of side fields (typically, data analysis, math, computer science, chemistry, ...), they will understand how lost one can be when starting to learn a new field.

Part of your question might be more on-topic on Academia.SE but I'm not sure they will be able to give much more advice. Good luck!

I don't think this question would be well-received on Academia, it doesn't really fit their scope of on-topic questions. In general, StackExchange isn't really intended for opinion-type questions like this.

I started in cell and molecular biology, but moved to applied math and computer science, so perhaps I can give my thoughts.
Personally, I found that biology learning was more about big ideas and visualization. The first is because biology has an extraordinary amount of details (e.g. Molecular signaling pathways, biochemical properties of different molecules, the location of different foramen in certain fossils, etc...), so it is truly impossible to remember them all. You should focus on learning what to look up, not what is actually occurring. Something you work on will be gradually memorized on its own, so don't spend effort memorizing things you can look up (you're not an undergrad :) ). So don't remember that histone acetyltransferases use acetyl-coa to act upon the NH3+ groups of lysines. Just remember that those enzymes modify chromatin in a way that alters transcription, thus changing the cell and its behavior. The second (visualization) is because it is very hard to understand biology without pictures! So use them, not text (no kobayashi and nomizu style). Mathematicians like symbols but (at least in the molecular case) there are too many of them (and they are mostly useless names... e.g. P53). Much of biology is about seeing  visual results (blots, fossils, medical images,...) and interpreting them.
Note that (I think) the first suggestion is harder in biology than in math, because math partitions naturally into theorems, corollaries, lemmas, and their applications (roughly in order of importance of what you need to know :) ). Biology as a field is more of a fast moving chaos of  observations and changing inferences. But of course there is a constantly growing core of the field that is not in flux.
One good thing about biology is that one can be an expert in one area but know little about most others. Math is a little more intertwined. So there's no need to read a "general bio" book. Just read an intro book to your target topic (e.g. Ecology, evolution, cell bio, molecular biophysics, bioinformatics ...). They will cover the relevant parts of other fields, usually. I know genetics experts who know basically nothing about cell trafficking for example. But you will definitely need some background to read the latest literature (i.e. Don't skip straight to Cell papers).
One issue that occurs throughout science, but also in math, is that learning is a process of improving models. In math, we might start with linear algebra, then basic manifolds, and eventually with, say, finsler spaces. In physics, we go from Newton to Einstein. In biology, we start with a basic model and set of rules, but gradually add exceptions and details to it. I think this is where much confusion can arise, because things that were correct in the simplified model might be wrong in the better, more complex one.
Also, models are being updated at an insane rate in biology. Often that means that previous models were wrong (though the evidence underpinning them is not); hence definitions and results might change over time! Science improves over time, and this is a good thing. Of course, in math, once something has been proved, it will never change. (Although definitions, or at least notation, in math can be very inconsistent too). Of course, if there are inconsistent definitions, you can ask here and see what people think. I will agree that biologists are less concerned about detailed rigor than being correct overall. Generally scientists will either define such things themselves or cite a reference with their chosen definition.
My suggestion for your question is to learn the basic widely accepted definitions first, then go to the literature. Often it is the case that different groups think different things. Most likely, one or both will be proven wrong eventually. Each paper is likely to be internally consistent; the only ambiguity is usually in areas where no one knows the correct answer or interpretation. Two groups in conflict usually have reasonable hypotheses consistent with the evidence, and if they can't decide how to mesh their ideas, probably we can't either. So don't worry about it too much.
So when a topic has multiple interpretations that are possibly true, use your math background and consider it from a Bayesian perspective :) most likely all the interpretations are at least partly true, and have some non zero probability of being true. And as you read more papers, update your posterior. :)
Also, don't worry about talking to biologists (as the other commenter states). In fact, among the sciences and engineering fields, my opinion is that biologists are on average the friendliest and least arrogant :)

Biology is the most vocabulary intensive science to learn. You are learning a lot of new terms all the time because biology is a very descriptive science. With my students I recommend flash cards, mnemonics, word banks, basically the same tricks you might use to learn a new language. Additionally draw things, a lot, and encourage your teacher to sketch things. Biological concepts are often tiered or interwoven enough that even simple diagrams can make it much easier to understand.
as you said definition are not set, basically different branches of biology will use slightly different definitions, (defining species based on ability to interbreed works ok with animals but is useless for bacteria for instance.) you are not seeing changes in definition with new research as much as you are seeing different working definitions for different branches. For the purposes of a class the exact definition is less important than the concept. think of the difference between a book and a pamphlet, you cant really say where one stops and the other starts on the spectrum of printed media but you are relatively sure most of the time which one you are looking at. As much as I don't like recommending it wikipedia often has very nuanced descriptions of biological terms which can also be helpful.
One important concept in biology is that almost everything lies on a continuum or spectrum, very few things are truly discrete. Organisms don't exist in discrete categories we invent those categories to make it easier for us as humans to think and talk about them, which works fine on the large scale but can get very blurry on the more detailed scale.  Because of this terms are often vague on the macroscale but get get more precise as you get more specialized. (this is why there are no less than eight separate definitions of species, how would you define it in fossils for instance) It also means that even basic concepts often have several conditions/assumptions that have to be true before they even apply. The fact that almost everything in biology is conditional is a big impediment to understanding when you first start.
There is an old joke in biology that there is an exception to every rule including this one. This is because biology constantly comes back to the real world for its information, it is focused on description and prediction less proofs. Even in a single organism there are so many interactions on so many levels that generalized rules simple fail to predict details ( for a comparison, imagine trying to do calculations when you are only allowed one significant digit).
I definitely recommend starting with the basics, this is important in any science, jumping right into more specialized classes is like trying to learn quadratics without understanding basic algebra, you are just making it harder on yourself. In biology it is especially bad becasue you hit a wall of terminology which biology needs just to keep from describing things as "that squishy grey bit squirts the yellow stuff on the red pastey stuff"
If you are truly very focused on math, mathematical/theoretical biology may be the most interesting as it is concerned with describing biology in mathematical ways. But really the advent of computers has led to a huge surge in applying mathematics to biology, because the complex equations are now practical. But it is important you have a basic understanding of biology first, if for no other reason than to get past the terminology/jargon wall. On the upside biologists know that terminology is an issue so they often have resources to help, that is why so many biological terms are laid out on wikipedia. Additionally a basic grasp of latin root words can be a big help, since so many biological terms use latin roots (originally to make it easier but now when no one speaks latin it makes it harder)
now an obligatory comic.


text:
Inoculating agar plates with microbes suspended in sterilised water?
We were having a problem with our experiment (culturing microbes on homemade nutri agar) so we decided to change our set-up. It already cost us quite some money. So, we saw this procedure. Can anyone tell if this is legit? Thank you!

You have more chance of a useful answer if you include brief outline of your original protocol and your problems.

What kind of bacteria are you using? 2. I prefer to store my Petri dishes at room temperature. If they are contaminated at least I can see it. If contaminated Petri dishes are stored in the fridge, you'll see the contaminant only after inoculating your strain

Replace "microbes" with "bacteria."

It would be great if you could provide more information with regards to what you have done already and what the problems were that you observed. That being said, yes, the "protocol" you found should work.
I am assuming that this is some kind of homework / school project so you don't actually need to know what organisms you are inoculating with and at what levels.
One thing I would recommend is that when you take your swab sample, wet your swab by dipping it into the sterilised water first and then swab a predefined area of about 10cm x 10cm (4in x 4in) very thoroughly before putting the swab back into the test tube. Once back in the test tubes make sure that you swirl the swab around for a sufficient length of time (~30s) and press the swab against the inside of the test tube to allow as much liquid as possible to run out of the swab. The last step is important in order to maximise the yield of bacteria, yeasts and moulds that you might find in your sample.


text:
What is the evolutionary advantage of telescopic generations vs normal pregnancy with more young?
There are a small number of organisms, so far I'm aware only of mites and aphids, which practice telescopic generations, where the a female is pregnant with a daughter that is, itself, already pregnant, meaning the adult is carrying two generations within itself.
I'm trying to better understand the evolutionary advantage of this, specifically when compared to the 'normal' evolutionary strategy of non-telescopic generations but giving birth to more young.
In both cases, telescopic generations vs increased young, the mother invests the same amount of resources towards the pregnancy, be it through multiple daughters or fewer daughters but a head start on granddaughters.  At first glance it would seem this would make both strategies about equal in reproductive success.
In the case of mites which reproduce sexually, by mating in the womb, I can see one potential advantage of increased genetic diversity...presuming there is any noticeable difference between phenotype of grandchildren in a species that practices serial obligatory incest.  Since I'm not certain how large a difference in phenotype children can be expected to have after genes have mostly homogenized I'm not certain how large an advantage this may actually offer, if any.  It also doesn't explain the advantage in the case of aphids which are clonal when practicing telescopic generations
So, there any other reasons I'm missing for why telescopic generations would be preferable to birthing more daughters?

Do you mean telescopic generations? Just as an advice, note that long posts without sections tend to be discouraging for users and few people really read them (I did not read your post for example, I only reacted to the title).

@Remi.b yes you are correct, I have corrected my terminology.  I've also shortened the question at your suggestion, I'll just presume anyone who knows enough to give a useful answer will understand what I mean about increased genetic diversity ;)


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Classification and differences between homologous, homoplastic, analogous, derived and ancestral traits?
My question is contextualised for basic phylogeny knowledge. Here is my understanding: similar or identical traits between any two species, at the basic level, can be either homologous, meaning the trait is developed from a common ancestor, or homoplastic, meaning that the trait was independently developed.
Homologous traits can be either ancestral or derived, and derived traits are a subset of ancestral traits as derived traits need to be from the most recent common ancestor.
Homoplastic traits can be analogous, meaning they developed independently without any common ancestor or commmon initial trait, or can be traits that arose due to convergence, where species with the same (distance/close) ancestor independently developed the traits.
Please evaluate whether my understanding is correct.

As a complement to the other answer: homoplasy and analogy are not synonyms, but not for the reason described in your question.
According to Ridley (2011):

Analogy: A term mainly not used in this edition of the text, but close in meaning to homoplasy. That is, a character shared by a set of species but not present in their common ancestor — a convergently evolved character. Some biologists distinguish between homoplasies and analogies. (emphases mine)

Most of books on phylogenetic systematics treat analogy as a special case of homoplasy. A good explanation can be found, surprisingly (because he was not a systematicist), in Stephen J. Gould's last book (2002):

We now encounter the logical dilemma that underlies nearly all our extensive and lamentable confusion on this issue. Homoplasy and analogy might strike us, at first, as fully synonymous, for both invoke natural selection as the source of separate evolution for similar structures in two lineages. This synonymy certainly applies for convergence. But homoplasy comes in two flavors: parallelism and convergence — with parallelism as the historical root (in Lankester's original definition of homoplasy), but only convergence carrying the full flavor of synonymy [...] Unfortunately, a common error of human thinking leads us to define broad and variable categories by their clearest extreme cases. Thus, many scientists have assumed that all homoplasy, whether by parallelism or by convergence, must originate entirely for functional reasons, and not at all by constraint.

Therefore, all analogies are homoplasies, but not all homoplasies are analogies. As suggested by @Remi.b in the comments:

In short, an analogy is a homoplasy caused by convergent evolution. However, a homoplasy not caused by convergent evolution is not an analogy.

Sources:

Gould, S. (2002). The structure of evolutionary theory. Cambridge (Mass.): Harvard University Press.
Ridley, M. (2011). Evolution. Malden, Mass. [u.a.]: Blackwell.

I'm not sure I understand the difference. homoplasy comes in two flavors. I suppose one of them would correspond to an analogy but I don't think the quote says which one. Is a homoplasy due to convergent evolution an analogy while an homoplasy due to parallel evolution is not an analogy?

Yes, exactly. It's called just homoplasy, without being called analogy.

Ok, I get it. You might want to add something like In short, an analogy is a homoplasy caused by convergent evolution but an homoplasy not caused by convergent evolution is not an analogy. because I personally had to read Gould's text 3 times before finding This synonymy certainly applies for convergence, which is the key in knowing what is an analogy. +1

@Remi.b Indeed, Gould's text makes sense if I copy/paste all of it, which is (for that section) some 5 or 6 paragraphs. I thought that it'd be a wall of text, too much for the answer. I'll edit it with your suggestion.

@user98937 here at Stack Exchange the OP (you) can accept any answer he/she wants, and the accepted answer is nobody's business except OP's. That's out of discussion. However, I'd like to ask you to accept the other answer, because this one is just a complement to that other one.

This vocabulary is common in textbook but not in the peer-reviewed literature
First please note that while those terms are often used in intro class to evolutionary biology, they are actually rarely used in the peer-reviewed literature.
No trait value is fundamentally derived / ancestral
Note also that any given set of shared trait could be called ancestral or derived depending on the size of the tree that you consider. A trait is therefore not fundamentally ancestral / derived, it depends upon what other trait value you compare it to. Per consequence, it would easier to have a tree under our eyes to discuss these terms.
Note that there is one exception to that. Traits that are shared with LUCA are fundamentally ancestral!
Two states in different lineages can be fundamentally homologous / homoplastic
In general, when we are interest in a given trait, we display a tree so that all homologous trait states appear ancestral. While it is true that homoplastic trait state are necessarily derived when shown, homologous trait state can be shown as derived from a yet more ancestral trait state.
Analogy vs homoplasy
Many think of an analogy as a synonym of homoplasy. However, have a look at @GerardoFurtado's answer for the subtle difference between the two.


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What type of Insect Egg is this?
Can you please tell me what type of insect eggs these are? I found them in the corners of my office kitchen behind boxes and cardboard. Found them in between the broom bristles. Found them along the edge of the wall. There are quite a few of them.
If you could please provide me some tips on how to avoid getting these eggs or killing off the main insect would be helpful.

I doubt they're eggs, but possibly larvae. Call an exterminator.

These are probably cockroach cases, or oothecae, that may contain up to 50 eggs, depending on species.

It looks like they are oothecaes of German cockroaches.
You can read more about baby cockroaches here.

I think these are cockroach oothecae. These are small casings that contain many eggs.

Quoting from wikipedia

Female cockroaches are sometimes seen carrying egg cases on the end of their abdomens; the German cockroach holds about 30 to 40 long, thin eggs in a case called an ootheca. She drops the capsule prior to hatching, though live births do occur in rare instances. The egg capsule may take more than five hours to lay and is initially bright white in color. The eggs are hatched from the combined pressure of the hatchlings gulping air. The hatchlings are initially bright white nymphs and continue inflating themselves with air, becoming harder and darker within about four hours. Their transient white stage while hatching and later while molting has led to claims of albino cockroaches.[22]Development from eggs to adults takes three to four months. Cockroaches live up to a year, and the female may produce up to eight egg cases in a lifetime; in favorable conditions, she can produce 300 to 400 offspring. Other species of cockroaches, however, can produce far more eggs; in some cases a female needs to be impregnated only once to be able to lay eggs for the rest of her life.[22

You can find more about their control here
Cockroach oothecae

perhaps it's a fly chrysalis. If you had a mouse that died, that would do it. put them in a jar and wait. https://www.insectes-net.fr/pieride/images/pier159gf.JPG


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Is fructose really a poison like alcohol?
I came across this video claiming that fructose is like a poison with detailed explanation on how it is metabolized. With a search on internet I found an article which challenges the claim and sounds convincing. In the article I also learned that the original claim was made by Dr. Robert Lustig.
Dr Lustig is a scientist and the article is not a peer reviewed scientific article. I am not an expert in the field and I am not sure which side is right.
Could you tell me which side is right?

I'm voting to close this question as off-topic because this is definitely better of Skeptics.SE

Everything is a poison with the right dosage Here is a fun chart you can use to see what I mean. Even water is poisonous if you drink enough of it.
fructose in no more poisonous than glucose. No study has shown fructose to be dangerous when eaten in normal healthy diet. It is poisonous but only in the sense that water is poisonous if you drink to much of it.
And you should reread your own source the article concludes it is NOT more poisonous than glucose. It also concluded that the paper that claimed so was erroneous because it used animals with different metabolic pathways and the differences were not significant in any case. Nor is it possible to eat a diet high in fructose without it also being high in glucose (see above study) so it would not be an issue even IF Dr. Lustig was right about the lipid metabolism.
News media loves to focus on single isolated studies with odd conclusions which is basically the worst way to represent science, wrong or erroneous things get published all the time and get quickly found out but the media tend to latch on to the former and never report the latter.
Processed sugar is bad for you for completely different reasons, basically the same reasons donuts and bacon are bad for you, they are empty calories, it is just that Americans (and a few others) eat way way more refined sugar than the other two, absurd levels of it, for comparison it is as if you were eating large amounts of bacon for every meal levels of absurd. There is also the aspect of diabetes which has to do with how much and how often we eat sugar not an issue with the sugar itself. (if we instead ate half a pound of bacon grease every day that would be the thing causing problems.)

What makes processed sugar worse than the same sugar in a fruit? It is the dose what make the poison, as you say.

It is the fact you are getting a lot of sugar and nothing else, with fruit you are getting vitamins, fiber, even small amounts of nucleic acids, proteins, and lipids that both slow down how fast you absorb it(blood sugar rises slower) and help make you feel full so you eat less. for instance you would have to eat about 3 apples to get the same sugar as an average (~300cal)candy bar or one bottle of soda  but three apple would fill you up and take longer to digest. taking longer to digest gives our insulin levels a chance to compensate for the rise in sugar and helps us eat less.

But that doesn't maker sugar per se bad, but the way of nutrition.

sugar is an essential part of nutrition you need a certain amount of sugar, you need a certain amount of lipids as well,eating bacon is not inherently unhealthy, but eating a tub of bacon grease would be bad for you. It would be impossible to eat a tub worth of grease by eating bacon you would get full first, by separating the grease it becomes much much easier to eat to much. The same is happening with sugar by separating it from the fruit, we can easily eat to much of it. which is what american especially are doing, mostly by adding it to everything. It is even added to many meats.