text:
Population numbers in the presence of restricted resources
I wonder if the following simple system is considered in population dynamics, under which name, and in which textbooks.
Consider a population $X$ (also indicating its number of individuals) with a default birth rate $\beta_0$ and a default death rate $\delta_0$. Let the effective birth rate be given by
$$\beta = \beta_0\,\frac{\alpha}{\rho}$$
where $\alpha$ is the amount of resources available to each individual, and $\rho$ is the amount of resources needed by each indiv idual. We have $\beta > \beta_0$ when there are more resources available than needed, and $\beta < \beta_0$ when there are less resources available than needed.
For the sake of simplicity let's assume that the effective death rate is given by
$$\delta = \delta_0\,\frac{\rho}{\alpha},$$
i.e. the effective death rate decreases with increasing $\alpha/\rho$ and increases otherwise.
The equilibrium condition $\dot{X} = 0$ of the system $\dot{X} = \beta\,X - \delta\,X$ is given by
$$\frac{\beta_0}{\delta_0} = \frac{\rho^2}{\alpha^2}$$
With the final assumption of restricted but fully exploited resources, specified by
$$X\,\alpha = R = \text{const.}$$
we get the equilibrium condition
$$\frac{\beta_0}{\delta_0} = \frac{\rho^2}{R^2}X^2$$
Resolved with respect to $X$ we have the equilibrium population
\begin{equation}
X_0 = \frac{R}{\rho} \, \sqrt{\frac{\beta_0}{\delta_0}}
\end{equation}
The next step would be to consider systems of populations $X_i$ competing for the same resources $R$, especially with different values of $\alpha_i$ (indicating different fitnesses in the struggle for resources), but also with different values of $\rho_i$ (indicating different efficiencies in utilizing the resources). But I'd like to take the first step first. Is it a sensible approach?

Birth rate cannot increase exponentially with the number of avaliable resourses. Each birth requires some amount of resources, so it increases at best linearly. In reality, there is some limit on how much resources each specie can process, so the birth rate is limited.

There are still some aspects of this that are unclear to me. Is $\alpha$ meant to be a constant valuable rather than a dynamical variable? That wouldn't make sense because then we'd just have exponential growth (and your constraint wouldn't make sense). If $\alpha$ is meant to be a dynamic variable then we have $\alpha \propto 1/X$ and we get something of the form (I think) $\dot X = c_1 - c_2 X^2$, or $d(\log X)/dt = c_1/X - c_2 X$. As @user31264 points out, the per capita birth rate diverges at $X=0$, which is weird.

This is somewhat similar to a single-species version of ratio-dependent predator-prey dynamics (e.g. https://pubmed.ncbi.nlm.nih.gov/19083063/ ), which has been argued about a lot "Since the ratio-dependent model always has difficult dynamics in the vicinity of the origin ..."

@BenBolker: I consider the total amount of resources $R$ to be a constant, the amount of resources available to a single individual (of which there are $X(t)$ at time $t$) is $\alpha(t) = R/X(t)$.

If we express your equations in their simplest form (by substituting $R/X(t)$ for $\alpha(t)$) we get
$$
\dot X = (\beta_0 R/\rho) - (\delta_0 \rho/R) X^2
$$
or
$$
(\dot X)/X = \dot{(\log X)} = \frac{(\beta_0 R/\rho)}{X} - (\delta_0 \rho/R) X
$$
(assuming I didn't screw up the algebra — however, the important point here is the form of the dependence on $X$).
This means that the per capita reproductive rate diverges as $X \to 0$, which is weird/unbiological. That's not necessarily a deal-breaker — there are plenty of models that are pedagogically or practically useful (e.g. see Lehman et al 2020 for models where the population density diverges in finite time) — but it does ring an alarm bell.
An initially linear growth rate (i.e. constant absolute growth rate near 0) is more typical of abiotic resources that are being considered to be added to a system at a constant rate, as in a chemostat model.
This model reminds me of ratio-dependent predator-prey models, which have been extensively analyzed in the math-bio world (see this Google Scholar search), but much less used by ecologists. Abrams and Ginzburg (2000), whose co-authors are respectively a strong opponent and a strong proponent of ratio-dependent models, might be a good starting point in the ecological side of the literature.

Abrams, Peter A., and Lev R. Ginzburg. “The Nature of Predation: Prey Dependent, Ratio Dependent or Neither?” Trends in Ecology & Evolution 15, no. 8 (August 1, 2000): 337–41. https://doi.org/10.1016/S0169-5347(00)01908-X.
Lehman, Clarence, Shelby Loberg, Adam T. Clark, and Daniel Schmitter. “Unifying the Basic Models of Ecology to Be More Complete and Easier to Teach.” BioScience 70, no. 5 (May 1, 2020): 415–26. https://doi.org/10.1093/biosci/biaa013.


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Can RNA be extracted from tissue suspended in formalin?
There are two tumor samples floating in a 10% formaldehyde solution (i.e formalin). Is there a protocol for RNA extraction under these circumstances? I am concerned that using the protocol for Formalin Fixed Paraffin Embedded (FFPE) tissue will damage the RNA, since there is no paraffin for the xylene to remove.
If I were to use the FFPE protocol without xylene, should I homogenize the tissue before removing the formalin, or after?

Can you please link to or describe in detail this FFPE protocol that you're referring to?

@MattDMo It is the RNeasy FFPE Kit mentioned in WYSIWYG's answer.

Formaldehyde forms adducts with RNA and can also make it more susceptible to degradation. It can also cause crosslinks to form between RNA and proteins (or possibly other RNAs). For all these reasons extraction of high quality RNA from formaldehyde fixed samples is very difficult and the yields are low (Howat and Wilson, 2014).
Have a look at this article by Evers et al. (2011) which explores optimal conditions for removal of the formaldehyde adducts. However, this study does not involve actual RNA extraction from fixed tissues, which would be even more difficult.
RNeasy FFPE Kit from Qiagen claims to be specially designed for RNA extraction from formaldehyde fixed samples. The product description says that the lysis buffer contains substances that reverse the modifications formed because of formaldehyde. There is a similar kit from Thermo-Fisher. Russel et al. (2013), report that the RNA yield was similar between fixed (using Qiagen RNeasy FFPE kit) and unfixed samples (using Qiagen RNeasy Plus mini Total RNA extraction kit).

should I homogenize the tissue before removing the formalin, or after?

Homogenize after removing formalin. Since the tissues are already brittle because of formaldehyde fixation, you need not use harsh homogenization procedures. Pipette gently. You can use proteinase-K and DNAse to remove proteins and DNA respectively (RNeasy kit involves these steps).
For future experiments, you can store the tissues in RNAlater solution (Thermo-Fisher; or similar formulations from other vendors/lab). Store one part of tissue in formaldehyde for IHC/ISH and the other in RNAlater for RNA/DNA extraction.

If I recall correctly, the RNeasy FFPE kit is designed for extracting RNA from formalin-fixed, paraffin-embedded tissues; however, I've heard that it works fine for just formalin-fixed tissues, skipping the deparaffinization step.  I haven't tried it myself, though

source: Stack Exchange

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Questions regarding a particular paper
With respect to the following paper:
Automated identification of protein-ligand interaction features using Inductive Logic Programming: a hexose binding case study
I have a few questions:

in page 2, in the table, what does 501 mean in GLC-501(I searched for GLC-501 in PDB,couldnt find anything)
in page 3, in the table, the cavity center column has got two entries, what does that mean? does one entry belong to the protein and another entry to the ligand(left for protein and right for ligand)??

related http://biology.stackexchange.com/questions/31918/how-is-protein-cavity-centre-related-to-binding

501 denotes 501st residue in the corresponding PDB entry — 1BDG. See here
A single protein can have multiple cavities (see here) and the multiple entries denote centres of different cavities.

so why exactly two has been given? Has this paper calculated these centers or are these available somewhere?

and why is a number given to a residue? What does that imply?

@user3237995 I am not an expert in this but I think all ligand residues are numbered in the PDB file. Just a way of listing the number of entities I guess. From this page:  The ligand is assigned a unique residue number within chain to which it is bound. The residue that binds the ligand retains its standard name in both coordinate and SEQRES records.

and why only two numbers listed?

@user3237995 Regarding your first comment. Perhaps they are interested in checking all possible binding sites in the protein. And why 2 sites; perhaps there were not more. Note that some have three as well

@user3237995 They have possibly taken this data from Nassif et al. Their negative dataset consists of 80 PDB examples: 22 binding sites that bind hexose-like ligands (e.g. hexose or fructose derivatives, 6-carbon molecules, and molecules similar in shape to hexoses), 27 other-ligand binding sites and 31 non-binding sites. The non-binding sites are sur- face pockets that look like binding sites but are not known to bind any ligand. The negative dataset is presented in Table 2 (non-hexose binding sites) and Table 3 (non- binding sites)

one more question, is L-glutamate a ligand??

@user3237995 In some cases it is; for example, in glutamate receptors.

how is it different in different cases

@user3237995 L-glutamate can be a part of the polypeptide chain also. In some cases it acts as a ligand.

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


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What information does the KEGG Module statistics page show?
While browsing through the home page of KEGG Module, I clicked the button named Module statistics.
Can someone tell me what does these numbers signify? What are they the statistics of?

My understanding is that these statistics show the coverage for each KEGG Module in the particular phylogenetic group. For example, M00001, is found in 275 of the eukaryotic organisms in KEGG (which represents 90.5% of the eukaryotes in KEGG). The same logic applies for other groups.
An quick example demonstrating this hypothesis, done with the Protists group found in KEGG Organisms (since it is easier to count by eye). There are 43 protists, and in the statistics it says (as of 2015/7/9) that module M00001 is found in 33 of them, hence: $33/43=0.7674419$ which agrees with the 76.7% shown.


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Drinking water after eating banana
Why elders advice not to drink water after eating banana? Is there any science behind or is it a myth?
Found a website supporting this (so called?) myth.

Welcome to Bio. If this is a persistent and widely known myth please give a few sources.

@AliceD I found this on internet

That is some random comment on a random site. We run a scientific stack and discussions of rumors are off topic.

@AliceD disbelieve are accepted in stackexchange

here I have also heard elder people say we shouldn't drink water after eating melon or peach, but that is probably some myth that grew after someone got unwell after doing so

Added a link. Replace it if you find a better one.

Related: http://skeptics.stackexchange.com/questions/4134/drinking-after-eating-fruits-causing-belly-ache

Seems to be a cultural thing, like some religions not mixing meat & milk at a meal.  AFAIK the belief is unknown (or at least not common enough for it to have come to my attention) in the US or Europe.


text:
What kind of fish is this? I don't remember the full name but it started with Tiger
name starts with tiger, forgot the rest, please help

Where is it from? Do you know that?

I got it from a local pet store called Elliot's

In which country is it?

Please add some more information about it, like its size, habitat (where you live), etc.

You could just go to the pet store and ask.

It's probably a juvenile tiger loach, or tiger botia.

Adult Tiger Loach

Younger individual of another species
These fish are from the genus Syncrossus and the family Botiidae which include many common aquarium fishes. This genus comes from India, Myanmar, and Southern Asia.
These fish can grow up to 20-25cm (~10in).
Syncrossus species can be told appart using appropriate litterature. This specie sheet from seriously-fish is well documented and provide interesting links from further reading and a quick explanation of its taxonomy easily accessible for the average guy,


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Can anyone identify this bug/insect?
!Saw this bug/insect/spider? on a ranch in Santa Ynez, CA. Pretty fast moving-this was the only photo I could get. The creature is the thing in the photo that looks like two puff balls on a very black body. (The smaller puff is the front of the body.) Maybe a bumble bee? Did not appear to have wings.

Welcome to Biology.SE. Can you please indicate the approximate size and speed (as well as mode) of displacement. It might be hard to say anything with this picture.

You might want to edit the post to improve the grammar, start sentences with a capitalize letter and don't end sentences with things like ...!]

Perhaps it was a species of velvet ant (a type of wasp from the genus Dasymutilla). The females lack wings, and it appears like what you describe and vaguely see in your image.
Here are some photos:

Photo 1 Source
Photo 2/Information Source


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Is this a variety of banana slug (Ariolimax columbianus)? (California)
These very dark (dark grey to black) banana slugs are an anomaly. I live on the north coast of California and see many slugs every day. These particular slugs I find only on the west-facing headlands at the ocean. There is no cover from the sun since there are no plants taller than about a foot. Also these particular slugs are never longer than 2-1/2" to 3". Are they a sub species, a variety, or something else? Thanks for taking the time to answer.

Banana slugs are comprised of three species:

Ariolimax californicus
Ariolimax columbianus
Ariolimax dolichophallus

Ariolimax columbianus, or the Pacific banana slug is known to have black spots, sometimes so large as to cover their entire body (Source). This is certainly the genus of the slug you've shared.
At times, you could be seeing a Black slug which is well-established in Washington and Oregon. I only include this information as I have noticed this species occasionally in Southern British Columbia and wondered if it was the same species as the Banana slug. It isn't. The picture you've attached is not a Black slug (note the pronounced frills on the back of the Black slug specimen)


text:
What is the difference of function between palisade and spongy layers of leaf?
I was just wondering that, what are the differences between the spongy and palisade mesophyll cells?

Did you do any research at all before asking? Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Well I'm assuming that you already have a fair idea of the structure of a leaf (of course, why else would you ask this question), so I'll just come straight to the point.
The major difference between the two is that the palisade layer lies just above the spongy layer, and vice versa. That's understood.
So firstly, the palisade layer consists of closely packed cylindrical/rectangular cells, while the spongy layer has loosely packed cells with many air pockets.
Secondly, these cells mentioned above are cylindrical/rectangular in the case of palisade layer, and cells in the spongy layer are rounder in shape.
Thirdly, cells of the palisade layer contain more chloroplasts than the cells of the spongy mesophyll layer. A probable reason is that since the spongy layer is comparatively much further into the leaf, it doesn't get as much sunlight as the palisade, which is a lot closer to the surface.
Lastly, palisade layer helps in photosynthesis, (in fact palisade cells are the site of photosynthesis) while the air pockets in the spongy layer allow exchange of gases like CO2 required for photosynthesis. So there's a difference in function.
There are also other differences, since the spongy layer contains other components like  vascular bundles, but I believe these are the major ones.


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Is it possible to estimate the age of a wasp nest by its size?
Long story, but briefly I am debating knocking down a paper wasp nest. I don't want to kill the wasps, because (1) they're beneficial wasps, and (2) I would not have even known they were there, except I came face-to-face with the nest (~1 foot) and they didn't act remotely aggressive at all (karma).
My concern is that I've been out of town for a couple weeks, and I don't know if the nest has been under my deck all year and they were actually relatively sedate, or if the nest has developed recently. I mow regularly, and my big concern is that the noise of the mower and weed eater is going to agitate the wasps into stinging.
The wasp nest is under my deck, and my dog crosses the deck to get to the back yard frequently. I also have a toddler, but we generally play with him in the front yard, which is separated from the back yard by a fence.
So, tl;dr - A wasp nest is a little smaller than a baseball and covered in about 15 wasps. Has this nest been under my deck all year (and I can mow without worry as I have in the past), or has this nest sprung up since I stopped mowing (about 2 weeks) and I should remove it before I mow again?

It sounds like a small nest that can very well have developed recently. However, the size of the nest is also species dependant.

What season and climate is it where you are living? Most (or all?) colonies of social wasps in temperate climate only last one season. So it will go away in the autumn. (Also, nice to see someone caring about wasps!)

@picapica - I'm in Southwest Virginia. Being mid-September now I figured they were probably on their way out, but I mow every Saturday morning, except I've been out of country for two weeks. The nest is in an obscure location that I found on sheer coincidence after I got back (scouting for a DIY project). I thought I had read that they generally form the nests in Spring or early Summer, and if that's the case then I'd leave it, but I'm worried my mowing kept them away and when I stopped they built that nest, and if I mow again I'll get swarmed. I don't want to kill them if I don't have to.


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Organ of ingestion in lice
I want to know that what the name of the organ used by lice for ingestion is? (also please explain if possible). In my research, I got this wiki page that didn't help me out. Then I found this link which says that it sucks blood and pumps up that with a tube so, I want the specific name of that organ.

What louse are you interested in? Human head louse? Louse is a pretty big taxon/group.

human head lice @Tytoalba

Okay. Can you do some research specifically on it? A good set of keywords would be 'head louse feeding'. If you don't find your answer and share the things you found, your question is likely to be reopened for answering.

new edits up in the discription, you must check that out @Tytoalba


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Identification of an insect found near Shirdi, Maharashtra

I found the insect nside house near Shirdi, Maharashtra. I have captured the image

Please add some description about it, like its size.

It's a household centipede whose scientific name is Scutigera coleoptrata.
It's venom doesn't do much harm to humans.
Sources:
Picture 1 and   Picture 2

I agree completely with the genus, but I don't know enough to be able to say if the species ID is correct. How do you know it's coleoptrata rather than another Scutigera species?


text:
Can genetics be an answer to our human flaws?
Ok I have been thinking genetics is that part of biology wich has the ability to change the genes of an organism as such it changes their abilities as well if so why cant we use this technique to change the problems that we face for example:
The cells of plants contain chlorophylle as such they can create their own food thanks to sunlight+water+CO2 what if we take the gene responsible for this and transfer it to a human being like this he will not have any need to eat(but he still can if he wants for more energy like meat-eater plants) however a downside would be green skin but I think is worth another one would be the lizards wich have the ability to regenerate limbs and other body parts that were lost this can help those who suffer from absence of body parts. Wouldn't this be amazing like a human with different abilities to adapt and survive these that I mentioned are simply core of our problems these days there can still be more to it.  SO why isn't this technique used for a solution to our problems?

Making green humans wouldn't work, as a human doesn't have nearly enough surface area to collect the energy they need to survive - even if they lay on a sunny nude beach all day :-)  It takes roughly an acre (about 4000 m^2) to support a human.

It would be much easier to make a glow-in-the-dark human with some GFP as it has been done with cats already.

Related http://biology.stackexchange.com/q/17676/3340

Here are three elements you want to consider

we are not able to make genetic manipulation of all the cells in a grown-up individual. There exist a whole bunch of treatment making use of genetic engineering in adult humans but they are typically quite costly.
The phenotypic traits that you mention are extremely complex. There is no simple gene that will allow a lizard to regenerate a lost limb. You will have to learn more about cell specialization in order to understand why lizards have a power of regeneration that we don't. Similarly, you can't just transfer a few genes and expect a human to be able to photosynthetize. Photosynthesis is a very complex process which require the ability to perform a whole bunch of reaction, which require organelles we don't have for the reactions to take place, which requires the ability to gather and concentrate lots of $CO_2$, etc... It is really really not that easy. You should learn more about the specific traits you are mentioning to get a notion for why it is not that easy.
Genetic manipulation on human is vastly illegal for ethical reasons. But these ethical reasons are to be discussed on philosophy.SE.


text:
Are there more than Five kingdoms?
Is it true that scientists have disregarded their belief that there are five kingdoms and instead, they have theorized that there are multiple kingdoms?

What research have you done to find an answer?

Can you provide a source that led you to ask this question? If you do not provide more information and/or indication that you've researched this yourself, your question will likely be closed and not answered. Please take the time to improve your question. See How do I ask a good question? on our help page.

Taxonomic classification is a large area of controversial debate. See for example Cavalier-Smith's system of classification, they described eight kingdoms, then six, then 7 kingdoms in subsequent publications.
Other (older) theories describe 6 kingdoms, two prokaryotic (Eubacteria and Archeae) and four Eukaryotic (Protista, Plantae, Fungi, Animalia) See image on Wikipedia's "Kingdom" explanation
The three domains Eubacteria, Archeae, and Eukaryota are less disputed.

You shoudn't be answering this until the OP has shown some effort to answer his own question.

I agree in general, in this particular case, however, I shared kind of personal interest


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What is the difference between these two depictions of chromosome?

I understand that this is a single chromatid, but would this be considered a chromosome? Also before mitosis, the chromosomes appear as single chromatids but during interphase they replicate to form sister chromatids which are attached by a centromere and are also collectively known as a chromosome.
I do not understand the difference between the two of them. Are they both to be termed chromosomes?

Here is the thing, chromosome refers to a lot of different things ( however, all are coiled up DNA).
Let me explain step by step.
You have DNA, it has a diameter of 2nm, it is coiled with histone proteins and make 10-11nm fiber. This is what we refer to as the chromatin fiber(Beads on a string). At this point we are in interphase where too much coiling is not required because a lot of transcription, replication going on. At the S phase of the interphase, DNA replication takes place and sister chromatids are formed or do they? The answer is yes and no. The thing is even though DNA has replicated and coiled upto certain extent, we dont call the replicated dna as sister chromatids because we only consider them to be sister chromatids when we can clearly see them as separated threads connected at centromere during the M Phase.
So, to put it in simple words, you have the sister chromatids formed (during the S phase) long before you are actually calling them as sister chromatids, you just wait for them to condense further and when you can finally see them as distinguishable threads you call them as sister chromatids.
Now, your real question can be answered. You have posted two chromosomes, one green and the other is red, red has two chromatids connected at centromere. Lets start with the red chromosome. The red one is the metaphase chromosome. Try to remember cell cycle. You have your DNA replicated by the S phase of interphase, then comes G2 and then M Phase starts with prophase, at this point your chromatin fiber gradually starts getting condensed and by the end of prophase, your 10nm coiled DNA (Chromatin fiber) ends up coiled to 700nm fiber but remember, you have two 10nm fibers connected at centromere after the S phase but they were so thin that you could not distinguish the two threads separately, now you can because they coiled in a very organized manner and now you have two 700nm fibers attached at the centromere, this is the maximum condensation achieved and as this final condensed version is observed at the metaphase it is named metaphase chromosome.
So, the red one is definitely a chromosome. What about the green one? That too is a chromosome. the green one is formed at the next step of cell cycle that is anaphase. Here the two sister chromatids split at the centromere and move towards the opposite poles of the cell as  new chromosome. but wait, haven't I called them sister chromatids throughout the answer and suddenly calling them chromosomes? Yes, the previously called sister chromatids are called as  individual chromosomes the moment they are separated from each other at anaphase.
So in summary, the thread like structure that you see in interphase are coiled DNA(Not called chromosomes), chromosomes are also coiled dna but the difference is that these are way more coiled. The red one is metaphase chromosome (1400nm) with two sister chromatids(700+700=1400). The green one is also chromosome but these are actually sister chromatids that got separated at anaphase(only 700nm), you can call them as daughter chromosomes
I hope this helps

Before S-phase the nucleus has two copies of each chromosomal DNA, e.g. a pair of Chr-1 DNA molecule.
During S-phase each DNA molecule replicates and after condensation ends up forming a chromosome(dyad) with two chromatids (sister chromatids). At metaphase a cell has 46 dyads (considering mitosis/Meiosis-I).
This dyad then separates at the centromere in Anaphase and the two chromatids move towards two opposite poles. On reaching the poles they are called chromosomes.

The word for such chromosome is dyad, but it is relatively less in use I would say.


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Why are red blood cells preferred to study the structure of plasma membrane?
If we wanted to study the structure of a plasma membrane, why are red blood cells a more attractive cell type to work with than other cell types such as liver cells or kidney cells?

Did you try to find an explanation anywhere else before asking here? Why do you think that might be the best way to harvest cell membranes?

What is unsatisfactory about the explanation?

I would actually say they are all pretty terrible, unless you wanted something specific to look at in a cell type. The correct answer would be liposomes in a biophysical context, endosomes in a biological context, nanodiscs in a structural biology context (other answers of of course acceptable)! Whole cells are a nightmare unless you need some cell-specific information. Without knowing the explanation given, this question is unanswerable.

@James - I don't know if I could disagree with you more. The answer is really obvious.

@anongoodnurse Perhaps my comment was a little facetious, but I am trying to say that the question is missing a key point; some sort of testable hypothesis. The question remains unclear. If I want to study the PM structure relative to other bilayers structures, I don't need to work with specific cell types, rather many cell types (Sharpe et al 2010). If I want to compare the PM to other cell types, I need other cell types. If I wanted a crystal structure of how a particular protein sits in the PM, I need a nano-disc etc.

@anongoodnurse If I want to answer "If we wanted to study the structure of a plasma membrane, which of the following would be the best cell to do so?" My knee-jerk response is "It depends on what you want to know" regardless if there is an easy-to-handle option (and still, there are easier to handle options than RBCs).

@James - I understood that (believe it or not), and generally agree with your argument. However, the question was basic and non-specific; rbcs are basically just cell membranes surrounding an easily separable 'cytoplasm'. Lyse the cells, wash, and violà. Which cells would be easier? (I'm sincerely curious.)

@anongoodnurse I see your point and you've convinced me that the question has value. I've removed the homework-y-ness of the question and limited it to specifically whole cells making my comments redundant :P Until OP comes back with some research, the question still stands at risk of closure for lack of effort.

@James - Fair enough, and I've already VTC.

@AlwaysConfused Liposomes and endosomes are typically less messy when it comes to results analysis for many experiments, particularly for molecular biology. Whilst the RBCs are relatively simple cells, they still contain a lot of proteins that may interfere with your interpretation of the results. To reiterate, this depends on what you are wanting to know specifically, which the question is currently missing. After my edit, these options aren't viable since they're not complete cells, but rather bilayer models.

Thanks for the help everyone. No, there is no explanation. I'm a junior in high school and came across this question in a biology practice book. That's all it stated, which cell would be the best for studying the structure of a plasma membrane? Only thing we have in our course is the fluid mosaic model and lipid bilayer so I guess it refers to that. The solution said RBC but didn't give any explanation, so i asked it here as I am curious to know why.

@AlwaysConfused I've only been involved in the biophysics end of molecular biology so I'm quite narrow minded about methods. RBCs are simple to a cell biologist, but those same cells might be too complex for a molecular biologist!


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How do I improve expression using the GAL1 promoter in S. cerevisiae above the "leaky" level I'm currently seeing?
I am attempting to express GFP in S. cerevisiae using the GAL1 promoter.
I always grow an uninduced (in dextrose based SD medium) culture alongside my induced (in galactose based SD medium) culture. I see approximately the same very low level of fluoresence in both cultures, and also a band at 27kD on a PAGE gel. There is no overexpression of the GFP happening, the fluorescence is very weak by eye, and the cultures are not green in visible light, like E. coli cultures overexpressing GFP.
On the PAGE gel the amount of protein appears to be the same in both the uninduced and induced samples. I need to overexpress the protein, this leaky level of expression isn't acceptable. How do I go about fixing it? I am currently growing up a culture to do a plasmid prep to send for sequencing to make sure the promoter region of the plasmid is intact.

There are a couple of things that are strange here. First, you have low expression in the presence of galactose. The GAL1 promoter is really strong, so that strikes me as odd. Even if it was leaky, induced vs uninduced should be night and day. However, you should keep in mind you still may not be able to see it by eye. Second, it is weird that it would be leaky in the presence of glucose (or dextrose, in your case). The glucose should not only prevent the promoter from activating, but it should actually repress it.
A few potential fixes that come to mind:
1) Check your strain genotype. Some strains do not have gal4, the transcriptional activator of the GAL1 promoter, so if you don't have this, the system will not work in your strain. Likewise, you may not have an intact UAS, which would make the repression fail. Other issues may also arise which may make a strain unsuited for this system.
2) Sequence your promoter/gene. It is kind of a pain, but if you have a mutation in your Gal1 promoter, this could be the reason for all your problems. Also check the UAS, as this would create repression problems. Finally, check if the gene itself is inserted in the place you think it should be, if you got some recombination mishap this may be the problem. The appearance of an extra band at a low molecular weight makes me suspect this may be an issue.
3) On that note, try picking a different clone. Maybe you got unlucky and the colony you picked had a defect, and a different colony will be what you think it is.
4) If you haven't already, make fresh stocks of your galactose and glucose media. Maybe you got impurities or some other issue in your media, and therefore what you think you are giving the cells is not what you are giving the cells.
Anyway, that's all I got. Good luck!


text:
Which biological kingdom comprises the greatest biomass on Earth?
Which of the five biological kingdoms - animalia, protista, plantera, monera, or fungi - has the largest biomass?
To clarify, if the biomass of every species in each of these kingdoms was added up, which kingdom would have the greatest sum?

A really clear, well defined question with great biological significance. In a silly way, this number can help us quantify which is "winning"! Welcome to Bio.SE!

Please note that the 5 kingdoms you list are NOT monophyletic groups.

Probably Eukaryotes. Specifically, plants.
This is a very fundamental question of life that is often overlooked. It goes without saying that plants and animals are the strongest contenders. However bacteria may also rival them. Be aware though that this is a contentious claim given more thorough estimations that take into account fluctuations in bacterial presence. This EMBO Reports science and society article claims that plants account for 99% of Eukaryotic biomass.
For further reading the Wikipedia page on biomass doesn't seem too shabby for more details on tonnage and methods of calculation.

The most numerous organisms could possibly be viruses or bacteriophages depending on if you count viruses as "living".


text:
Effect of ethanol and detergent on cell membranes problem
I am currently writing my biology report for an experiment I did on how ethanol and detergent affect the cell membrane. For my ethanol experiment, all went as expected. However, for my detergent experiment, the results seemed quite strange. The absorbency rate was higher for the 20% and 40% detergent than it was for the 100%. It seemed as though the results were backwards. I'm really confused.
What might have happened? Was it just an experimental error or is there a reason behind this? Can you also please explain to me what detergent does to a cell membrane exactly?

See https://www.thermofisher.com/in/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/detergents-cell-lysis-protein-extraction.html (membrane disruption, protein binding & solubilization). It says only moderate concentration is useful, though I couldn't the reason.

Can you please describe what you actually did? Are we talking about whole cells in a photometer or just a membrane experiment such as black lipid membranes?

Detergent and membranes
Moderate concentrations of non-ionic detergents facilitate lysis of cells. This can be exploited for extracting soluble proteins, often in their native form (ThermoFisher). Detergents affect the membrane at concentrations lower even than those that cause an increase in membrane solubility (Ahyayauch et al., 2010). Two ways this manifests is an alteration of the flip-flop effect (the lipid action caused by flipases) and leakage.
Note that the relationship between detergents and membranes aren't mechanistically well understood, and there aren't yet good general mechanistic rules that explain the relationship between concentration and permeability.
Your experiment

The absorbency rate was higher for the 20% and 40% detergent than it was for the 100%. It seemed as though the results were backwards.

It depends on your specific experiment, but typically the higher concentrations will more readily lyse the cell/make them more permeable. It's hard to say exactly what went wrong here without more information. Unless you were using an exotic detergent, it is quite likely that there was an experimental error and the test should be repeated. Alternatively, the results have been misinterpreted and indeed at lower concentrations, there was no cell lysis, and at 100% there are no cells left intact or something along those lines.


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Can ants survive a plane ride?
I just came back home a few hours ago from the airport and my aunt had peaches in her car full of ants. This made me wonder if the ants had joined us from the plane?
This leads to the question can ants can survive at high altitude?

mind that your title question differs from the final question. Surviving at high altitudes is not the same as surviving a plane trip. Conditions are very different.

It depends on the altitude of the plane, species of ant, flight length, location in hold, and more, but generally yes, they should be able to survive. At such locations that a plane flies at, the temperatures range from 0 to -50 degrees Centigrade. At such extreme temperatures the ant's entire body system is brought to an almost complete stop, where their heart is barely beating, and nervous system barely functioning other than to tell the heart to beat, and other normal involuntary actions. This means they won't need to consume as much oxygen (because their slowed brain won't need as much) allowing them to survive with the minimal oxygen in the atmosphere.

But only jet planes fly in that altitude. Propeller planes fly low. Considering that the plane was transporting fruits, I don't think it would have allowed the temperature to drop to such low levels (that would have ruined the fruits). Regarding oxygen: I guess, since ants thrive in deep underground holes, they can tolerate low oxygen levels.

You have a point, but the same would apply on a smaller scale in a prop. plane, correct? @WYSIWYG

Isn't the pressure and temperature in the cabin controlled to some extent?

There are several problems with the question, which prevent a clear answer. For example, the ants were perhaps most likely colonizers from the vicinity of the car and not plane. Specifically, it's unlikely that you transported a whole colony in a single peach (even if you got a queen, it would be a fairly slow process). Next, it's unclear if you mean crevice/outside of the plane, or inside the cabin (see comments above). It would also be helpful to tell which flight locations and species (roughly) were involved, in the case of cabin transport.

Yes @Luigi But they were in the hold, not the cabin

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How do marine mammals and penguins maintain bone density?
After much searching on Google with no results, I decided to ask my question here.
If I'm not mistaken, swimmers' bone density is less than normal; at least for lifetime swimmers. Astronauts also lose bone mass from the lack of stress (from gravity) on their bones; it stands to reason that being in the water and thus being weightless, would lead to bone loss.
So my question is, how do marine mammals and penguins maintain their bone mass?

Wouldn't bones nearly completely wither away in a weightless environment, such as underwater?

Thanks for the input. Question though, why do lifetime human swimmers lose bone mass, shouldn't the muscular activity required for swimming keep the bones strong? What about the hormonal component?

See this article

Do you have a source for the bone loss in human swimmers? any vigorous activity puts stress on the bone, swimmers are not massless they still have to push hard against the water itself to swim. Also consider the alteration of an organism during its life is very different then evolutionary adaptation to an environment.

I wouldn't refer to it as "bone loss" but more as bone strength. Lifetime swimmers spend a lot of their time in the water. As in water yes they are almost "weightless" and their bone strength will decrease because it has gotten used to the "low" gravity. Now in the case of penguins and other Marine mammals, they have adapted to the force that the water applied to them.
Here is a link to a picture of penguin's flipper.

This answer gives two reasonable hypotheses for a putative answer, however it lacks reference. Could you please provide some evidence for your suggestions?

How do you define bone strength? What do you mean by "adapted" as in "in the case of penguins and other Marine mammals, they have adapted to the force that the water applied to them"? It says nothing about the bone strength, however it is defined, and its evolutionary adaptation. What does the picture say about bone strength of a penguin's flipper?


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What step of the cloning process requires an egg cell? Have alternatives been attempted?
In the famous Dolly the sheep an egg cell was required. Why was specifically an egg cell required compared to say sperm cells or any other cell types?
Given that egg cells are not trivially harvested and culturable, have clones from alternatives been attempted?

This question doesn't show a lot of effort or nuance, but I am a bit puzzled why someone voted to close it for not being clear without providing some sort of comment.

I think this question deserves a chance and could yield some interesting answers. I've edited it to clear up any uncertainty.

egg cells are not required for cloning, plants for instance can be cloned just fine without them. Oocytes are commonly used in animals becasue they already contain some of the chemical markers and enzymes to begin development in the mother's body and keep her immune system from attacking it. In more derived animals development is not solely controlled by the the embryo but also by the mother, so using an egg cell helps trigger those processes of the mother. If you used a standard stem cell likely the mother immune system would just destroy it as a foreign entity.

"some of the chemical markers and enzymes to begin development" is almost an understatement.While it is almost possible to make specific cell types out of stem cells, the processes needed for embryo development are even more complex than that and as of today noone would be able to make a stem cell into an viable egg cell or embryo

Actually they have in mice, http://www.the-scientist.com/?articles.view/articleNo/47256/title/From-Stem-Cell-to-Oocyte-In-a-Dish/

oh wow, I didn't know that (was already possible). Thanks for the link.


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Finding a reaction from a KEGG map
I have come across a map and a part of it looks like this:

Now I have not been able to locate the reaction that converts alpha D-Glucose to Glucono-1,5-lactone but was successfully able to locate the reaction that converts alpha D-glucose Glucose to Glucose-6P. Since an arrow exist from alpha D-Glucose to Glucono-1,5-lactone, i am assuming that such a reaction exist. But could not locate it. I clicked on the arrow marked in blue in the picture, but could not find the desired reaction.(alpha D glucose and beta D glucose are different compounds)  What is the reaction and how is it possible to find the reaction from the map?
NB: The arrows are clickable so are the circles that denote the compound.

It was a simple search. You could have easily searched for glucose oxidase in KEGG, and you would have got this reaction.
In fact if you had clicked the link for glucunolactone's compound page, you would have got a list of many different reactions that convert glucose to glucunolactone.
You can even click the arrow which opens the KEGG-ORTHOLOGY page. You can find a field called RN in the section called "Other DBs". The links corresponding to this field would give you the exact reactions, that the pathway uses.


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Do the antibodies in a patient suffering from Hashimoto's, attack the thyroid hormones or the thyroid gland (or both?)?
If oral thyroid hormone supplement is administered, is the attack stopped or does it just create an excess of thyroid hormones so that even after a lot of it is destroyed by the antibodies, there is still enough for normal bodily functions?

Welcome to Bio. Where did you hear that thyroid hormones are targets for antibodies? Could you add that source in the question?

Thank you. It was based on a misunderstanding.My endocrinologist just said that the antibodies attack the "thyroid". While he might have thought it's obvious that "thyroid" means the the "thyroid gland" ,for someone with very basic knowledge in biology like me, it either meant the "thyroid hormones" or the "thyroid gland".I had previously asked a question here on stack which was based on this misunderstanding and the responses that I got made me realize that something wasn't right.This question was intended to get things completely straight and to clarify a few things( as you can see ).

Hashimoto's Thyroiditis is an autoimmune disorder where autoreactive attack on the actual thyroid tissue results in hypothyroidism. Pyzik et al., 2015, provides a good review of what we know about HT. The prevailing theory is that nonspecific infection can induce HLA expression on thyroid cells through the action of interferon gamma.
HLA is an antigen-presenting complex in humans that in our case is the major histocompatibility complex II or MHC-II you will see in texts (to avoid confusing names). Processed segments of protein are loaded onto the MHC-II, and displayed to the extracellular space where T cells positive for CD4 can recognize them. CD4+ T cells, upon recognition of MHC-II, are stimulated into T-helper or Th cells that are specific for the protein antigen they found on the MHC-II. The problem with MHC-II expressed by thyrocytes and the like is they can load either foreign or self peptides, so if it loads a part of thyroglobulin (Tg) on there and that's what the T cell recognizes, it's going to produce an immune response specific for Tg in a complex series of downstream events.
Being said, supplementation of thyroid hormone is a good treatment for hypothyroidism but it won't stop the attack on the actual gland. Thyroid hormones aren't often attacked by autoimmunity because they aren't protein antigens, and different subsets of cells respond to non-peptide antigens.

Thank you so much! So,ultimately would the entire thyroid gland be destroyed bit by bit and will the patient have to completely rely on supplements ?

It can boil down to that. Cases/treatments vary and one of the things you have to watch out for during the course of HT are malignant B cell clones in the actual thyroid, in which case excision of the entire gland might be necessary. A medical doctor will know the best route of treatment for a given patient.

I've an appointment with an endocrinologist but it's not in another couple of weeks.I decided to get a head start here and I am glad I did. Just one last question though. Is there anything that can actually suppress the antigen attack like maybe a drug or leading a very healthy lifestyle ?


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Energy consumption of a resting synapse
What is the energy penalty of maintaining rarely used synapse?
I'm wondering if forgetting is cheaper than remembering unnecessary details.

Short answer is yes, of course. Maintaining a healthy synapse is very energy-consuming process.
Let me first note that forgetting as we know it is more complicated than just pruning of synapses. It might involve rearrangement of proteins in pre/post-synaptic membrane and near it, local de-regulation of local protein synthesis, decrease in synaptic mRNA content and epigenetic change of transcription.
Secondly, average energy spending on a synapse, if it is not being used too often, includes mainly maintaining of membrane potential at resting -80mV level. Cellular membrane is a leaky barrier, so that without ion pumps, such as $K^+/Na^+$-ATPase, potential will quickly go to zero. Maintaining and recycling neurotransmitter pool also require energy.
Action potentials itself are passive processes, its generating does not require energy. ATPase will have to maintain potential at rest and keep it from fluctuating.
You can read this review for more: Synaptic Energy Use and Supply (Neuron, 2012). It generally describes where energy comes from and how it is being used.

Let me first note that forgetting as we know it is more complicated than just pruning of synapses. Yes. You took the comment right out of my mouth.


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Can the "Cas9"(involved on the Crispr-cas9 mechanism) be considered as a restriction enzyme?
I have many questions about the Cas9 enzyme. When the Cas9-guideRNA (crRNA and transcrRNA) complex is attached to the DNA sequence, what is the type of bond that cuts the Cas9? Does the Cas9 degrade all the sequence of DNA complementary to the guide RNA?
If the question before is "Not", then how is the sequence that is going to be cut on the DNA complementary to the guide DNA, determined? What type of enzyme the Cas9 is?

Cas9 is an endo-deoxyribonuclease (UniProt-Q99ZW2). It also has a 3'-5' exonuclease activity by which it trims the DNA a little bit, from the cut site (but not too much).
Although, Cas9 is an endonuclease and is evolved as a mechanism of immunity against viruses (like restriction enzymes), they are not considered restriction enzymes. One of the most important differences is that the restriction enzymes do not need an RNA or a DNA as a tether to identify the target sites in the DNA; their DNA binding domains can recognize the restriction sites by themselves.
Cas9 cannot just cleave any DNA complementary to the guide RNA. It needs PAM (protospacer adjacent motifs) sequences adjacent to the target site to cleave that latter.
For details check out the wikipedia page on CRISPR or read a review.


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How does mad cow disease evade immune system?
The mad cow disease is caused by prions right?
So how do prions avoid white blood cells and antibodies?

where have you looked for answers on this question? there is a lot of information that is easily accessible on the net.

Your question is a bit broad. There are many review articles written on prion infection and transmission. You can have a look at those and narrow down your question a little.

Prions are proteins that we produced but that are misfolded and affect the folding of other proteins. As we produce these proteins, we don't recognize them as antigens. If we were to recognize our own proteins as antigens, then the immune system would constantly be fighting against ourselves. This is what is called a autoimmune disease.
While this was a simple explanation, the reality on how the immune system interact with prions might be a little more complicated. Bradford and Mabbot (2012) might be a good place to start for further learning

Oh wait, i didn't mean how it avoids antigens. i meant how it avoids antibodies :P lol srry

I did not even notice the typo. It is fine, just edit your post to fix it.

thx :) but does antibodies and white blood cells ignore them in the same way?

antibodies are created kinda randomly and are retained only if they fail to match molecules from the body. Given that prions are produced by the body, any antibody that recognize the prion as an antigen will not be retained. (note btw, I am not an immunologist)

If you think I answered your question, then you can click on the checkmark. You might eventually want to wait for more answers and more peer-reviewing though.


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Why electroporator need a cuvette?
I have never obtain an Electroporator for my home-lab. Because it's very expensive, I'm trying to create a diy cheap version for myself. In all commercial design, I see that we need to put the sample to a 0.1cm-0.2cm cuvette to doing an electroporation, can I just replace it with an eppendorf plastic tube and put my 0.1->0.2cm alumium electrode inside?

Generally I would advise against making a home-brew electroporator: the voltage needed for electroporation is so high, that even with professional equipment you can easily get arc lightning. In an self-built device that would pose a serious fire hazard.
However even theoretically there are problems with the design you propose:
1) It is important that ALL bacterial cells in the cuvette get exposed to electrical field induced by the high voltage spike. If you use simple electrodes you will only affect the few cells directly between them, which will drastically reduce efficiency of the electroporation. For your design to work properly you would need electrodes that exactly match the dimensions of an eppendorf tube to make sure all bacteria will be squeezed between them.
2) With your device you can only do one electroporation, then you have to thoroughly clean the electrodes. This has to be done for two reasons: first you don't want any carry over bacteria (or as Chris pointed out DNA) from one batch to another. Secondly the electrodes need to be clean of any salts (or other molecules that increase conduction in a solution) to prevent arc lightning between them.

Great! Thank you very much for point out. I will buy a cuvette and be very careful making this.

It's not only bacteria. It's even more important to not carry over DNA between transfections as this can lead to unexpected results. Washing the cuvette for a short time with diluted HCl helps here. Avoid prolonged incucation in the acid as this corrodes the electrodes, so washing it afterwards is important.

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Lambda red recombination without electroporation
All protocols that I found about Lambda red recombination are using Electroporation as a method to introduce (inject) the homologous DNA (usually a PCR products or a linear dsDNA) to the E.coli cell. Can I use chemical method (CalCl2 + PEG) and heat shock method instead ?

Rubidium chloride method and the Inoue's method of making chemical competent cells give higher efficiency than the CaCl₂ method.

@WYSIWYG thank you for this info. But "Rubidium" sounds very strange to me. if it not popular, as I might think it will expensive than CaCl2 .

It is certainly more expensive than calcium chloride. Rubidium an alkali metal and you can check out the protocol for RbCl competent cell preparation, here. It also uses other salts. These salts may be slightly more expensive than CaCl₂ (because these metals are rarer) but would still be cheaper than buying an electroporator and the cuvettes.

@WYSIWYG Thank you alot. But any evidence that RbCl will work with lambda red recombination? If electroporate is just firing a high voltage between 2 electrode, I'm planning to purchase a high voltage generator module on Ebay, edit it a bit and put it directly to a plastic tube. Will be much cheaper?

You can make a DIY electroporator but I don't think an Ebay product will work that well (you'll just end up wasting more time). You need to generate a pulse and you need to have proper electrodes. I have not worked with lambda red. This site says that recombination rate is less than 1:10000. You can get efficiency of ~10⁷/µg with RbCl method which means you should get ~10³ colonies. You can use a selectable marker to select the positive cells.

Since Lambda red recombination is a rare event you want to have to have a good transformation efficiency, thus electroporation would be your best choice. Also since the expression of the recombination system usually needs growing bacteria at 42º you will probably inhibit the expression of the recombination machinery with the chemical method.

Thank you for answer. Because electroporator is so expensive so I'm finding a more cheaper protocol.


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Mathematical model about the relationship between two animal species
I'd like to relate a mathematical model with  two animal species. This is the model:
$$
\begin{split}
\frac{dN}{dt} & =rN-\frac{rN(N+M)}{k} \\
\frac{dM}{dt} & =r'M-\frac{r'M(N+M)}{k'}
\end{split}
$$
The model means that there is competition within the population of the first species ($N$) and the population is also affected by the population of another animal species ($M$).
Something similar occurs with the population of species $M$.
My question is:

What kind of animals would fit this model?

I was thinking about white sharks as $N$ and whales as $M$. Clearly the first equation would be correct but the second equation would be saying that the population of whales is affected by sharks, which I think is not true. Is it?

Welcome to Biology.SE! I'm not sure if you're asking specifically whether populations of whales are affected by sharks (it would also have to apply vice versa) or more generally what kind of relationship has to exist for this model to apply. Can you clarify? (Personally I think Ben's answer covers the 2nd very well, and I also think that would be the more useful question to ask.)

@arboviral Thanks . At first I wanted to consider a model related with white sharks, but after reading Ben's answer I definitely should not consider the shark-whale example. Now I just need to find something that can be represented by the model. Do you know of any example so I can consider it?

Related question on logistic competition models (that I've answered before), that allows for asymmetrical competition: Stochastic parameters in population growth equations

The model you present here is a special case of the Lotka-Volterra competition equations, where the two species have the same effect on each other (i.e., symmetric competition). Some things to think about in interpreting this:

each species has a negative effect on the other (i.e., increasing the density of either species lowers the other's population growth rate), hence this is a "negative-negative" interaction; it makes more sense for two species that are competing with each other (for resources, space, enemy-free space, etc ...) than for a predator-prey system such as the shark-whale example you give.
In contrast, in predator-prey (or more broadly "enemy-victim") systems, one species (the predator) benefits from the association - its population growth rate increases when the density of the other species (the prey) increases - and the other species (the prey) suffers (its population growth rate goes down when the predator density increases)
the fact that the competition is symmetric (this happens because you are using the sum of the population, $M+N$, and not using a competitive asymmetry parameter, e.g. $M+\alpha_{MN} N$) means that this would be most suited to modeling the competition between species that were very similar to each other (e.g. the same size, resource-gathering ability, etc.)

Thank you for your answer Ben. After reading your answer I agree that the example shark-whale does not work. What could  be a good example ?

Any two similar species of plants or animals (as I said in my answer, "similar" would mean about the same size, living in the same habitat, eating similar diet, using similar resources ... Since this is tagged as homework, I'm not going to come right out and give an example ...

Ok. I think could be jaguars and panthers?

seems reasonable.


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Is it feasible to eradicate a virus without vaccines?
Although a vaccine for hepatitis C virus (HCV) remains elusive, new direct-acting antiviral (DAA) drugs can cure HCV effectively and conveniently. The latest DAA, Epclusa, can cure 95-99% of chronic hepatitis C regardless of genotype (e.g. see here). So if DAA drugs become universally available, will HCV be the first virus eradicated solely by drugs?

It is not the answer you are looking for, but for the fun of it: Yes, simplest situation being to eradicate all the vectors of the virus = eradication of the virus itself. :)

Is it feasible to eradicate a virus without vaccines?

It is possible? I would say yes. But feasible... I think not. Consider this, once vaccinated, a person is usually immune to the virus. And you only need the vaccine to take hold, for an individual to acquire life time immunity. However with drug treatment... even once the treatment succeeds, the person can be reinfected. And you will have come back with drug treatment again.
Given the difficult in vaccination campaigns (ie polio) to eradicate the last reserved of a virus... I think a similar drug based campaign would a lot more difficult. There is no herd immunity to prevent the virus from reinfecting the wider population when it leaves its strong holds.

You're right. Chronic hepatitis C doesn't confer any protective immunity, and those cured are still susceptible to reinfection.

Herd immunity is a good point. I haven't thought of it.

I would also add that outbreaks of measles when herd immunity breaks down show how easy it is for a virus to breakout.

To the question I would say certainly yes, since the only viruses that have been eradicated (to my knowledge) are smallpox and rinderpest, both via vaccine campaigns (as well as the usual tools of quarantine/isolation).
Note: I did not mean to suggest that "if drugs are widely available they will definitely eradicate HCV".  I interpreted the question as "if HCV is eradicated by DAA, will this be the first disease eradicated by drugs?"
Vaccines are typically used as prophylactic treatments, i.e. they are applied before an individual gets infected. Drugs can also be applied prophylactically (e.g. antiretroviral drugs against HIV), and vaccines can also be used post-infection, e.g. for rabies. In order for a cure (i.e., a treatment that is applied after an individual becomes infected) to eradicate disease, it must be applied soon after enough infection that it cuts down the infection period sufficiently to reduce the average number of secondary infections per infected person below 1. Analogously, when prophylactic treatments are given by age, as in the case of vaccines for childhood diseases, they must be administered to children young enough that most of them will not already have been naturally infected [and passed the virus on to others].

I think it is interesting to see how it goes. For HBV, we have vaccine but not cure, while for HCV we have cure but not vaccine. We can compare which is more efficient at shrinking the reservoir.

My guess is that vaccines are more efficient at eradicating acute diseases(smallpox, polio, measles) because you can hardly have those infected get treated before they can transmit the disease. While for persistent infections(HIV, HCV, HBV) a cure may be more efficient. Because it takes long time for infected people to die out.

Due to the long time people can be infected with no or almost no symptoms, I doubt that. A vaccination is much more reliable here.

One could certainly evaluate all of this using a simple model. To know the cure rate, you'd need to know (1) the untreated R0 of the disease; (2) how much of the force of infection is mitigated by the cure [i.e., we need to know the infectious period, how much of it is asymptomatic, and the rate of cure administration - expected time from appearance of symptoms to cure]


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Why doesn't HIV spread through vectors?
HIV spreads only through body fluids. If a mosquito bites an HIV infected individual and then an uninfected individual, will the virus spread  to the new individual?

This doesn't take much effort to answer!  Googling "HIV mosquito" brings us straight to this blog post, which gives three main reasons (along with more details, links to other resources, etc.):

Only saliva is injected into humans when a mosquito bites and thus HIV positive blood that a mosquito may have previously ingested is never transmitted to other humans.
Unlike mosquito borne diseases, HIV is unable to replicate within the mosquito's gut and therefore is broken down.
HIV circulates in human blood at a far lower level than would be necessary to create a new infection.


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Difference between IC50 and Michaelis-Menten constant
I am new to biology, and getting to know the term IC50, I found that there is a connection between IC50 and Michaelis-Menten constant by the Cheng-Prusoff equation
$K_{i}=\frac{\mathrm{IC}_{50}}{1+\frac{[S]}{K_{m}}}$
where $\mathrm{K}_{\mathrm{i}}$ is the binding affinity of the inhibitor, $\mathrm{IC}_{50}$ is the functional strength of the inhibitor, [S] is fixed substrate concentration and $\mathrm{K}_{\mathrm{M}}$ is the Michaelis constant in the MM equation:
$\textrm{rate} = \frac{V_{\text{max}} [S]}{K_M + [S]}$
where $V_{\text{max}}$ is the maximum rate of reaction.
Suppose IC50 of the drug is $x$. From my understanding that means- the concentration needed to decrease cells viability by $50 \%$. Since Michaelis-Menten constant means the substrate concentration such that the reaction rate is half of maximum, it seems quite the same. What is  wrong in my view? Both seems to cause $50 \%$ of effictiveness

I have added a ref to Cheng-Prusoff.  I hope you don't mind. I was tempted to modify your opening sentence to "... Michaelis-Menten constant by the Cheng-Prusoff equation for competitive inhibition", but I was afraid I might change your meaning. In pharmacology, especially when dealing with receptor-agonist relationships, it is often assumed that inhibition is competitive (see here, for example). But there is the rub with IC50 values: how do you know that the inhibition is competitive?


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Do the phage repressors CI and Mnt exhibit crosstalk?
I am interested in using the CI and Mnt proteins as well as their respective promoters (pR and Pmnt) within the same synthetic system, but am concerned as to their similarity and potential crosstalk. A quick search of the literature yielded no results and a Multalin did show some significant sequence homology (although Mnt forms a homodimer while CI does not).

Sequences: CI and pR, Mnt repressor and Mnt promoter
Has it ever been reported that the CI or Mnt repressor exhibit crosstalk on the pR and Pmnt promoters?

There are no reports for it yet. I don't think just because they show overall homology, they would exhibit crosstalk. Just see the alignment of the DNA binding domains of these proteins first ~70 residues from N-terminal. Moreover their DBDs belong to different PFAM families.
Similarly with the promoter sequences.
As reported in iGEM website:

Mnt promoter: tagatctcctatagtgagtcgtattaattt
cI promoter: gtgttgactattttacctctggcggtgata

They are quite different.
Moreover, if iGEM has a reported standard part such as a bistable system component: Mnt/cI promoter (BBa_K228003) then it would have been pretty much standardized. iGEM parts are usually reliable.


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Why cells have a membrane potential?
What is the function of the membrane potential? Cells invest huge amounts of ATP to drive ion pumps to sustain this potential. Therefore it must have a very important function.
I read somewhere that the membrane potential acts as a battery, which can be used to energize other processes. But probably most of these processes could be energized with ATP just as well, which could be used directly instead of wasting it into building a potential first.
In muscle cells and nerve cells changes in the membrane potential are used to transmit information, so that is one use for it. But what about all the other cells?


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Specific activity vs turnover number of enzymes in BRENDA
From my understanding, the specific activity (A, units: umol/min/mg protein) can be derived from the turnover number (k, units: 1/seg) and the molar mass of an enzyme (MW, units: g/mol):
A = k / MW / 60000
When I try to do this for several entries in the BRENDA database, I don't get an agreement, sometimes the equality is off by an order of magnitude.
However I understand that there can be experimental errors involved, or I might be using the wrong MW (sometimes it is not clear what specific protein the value refers to).
Am I doing something wrong in this calculation?


text:
Where can I find the metabolic network for the human erythrocyte?
Where can I find the metabolic network of the human erythrocyte (red blood cell), in SBML format? The red blood cell metabolic network is a model that's usually employed in the literature [see refs below] to demonstrate mathematical techniques of analysis of metabolic networks.
Despite this common use, I haven't been able to find a metabolic network of the human erythrocyte in SBML format, which is commonly employed for these networks (for example, in the BiGG database, http://bigg.ucsd.edu/) because it is easy to use with the COBRA package (http://opencobra.sourceforge.net/).
So, anyone can tell me where I can find an SBML model of the metabolic network of the human red blood cell?
References where the red blood cell metabolic network is used:

Wiback, S. J., Famili, I., Greenberg, H. J., & Palsson, B. Ø. (2004).
Monte Carlo sampling can be used to determine the size and shape of
the steady-state flux space. Journal of Theoretical Biology, 228,
437–447. doi:10.1016/j.jtbi.2004.02.006
Braunstein, A., Mulet, R., & Pagnani, A. (2008). Estimating the size
of the solution space of metabolic networks. BMC Bioinformatics, 9, 240. doi:10.1186/1471-2105-9-240
Jamshidi, N., Edwards, J. S., Fahland, T., Church, G. M., & Palsson,
B. Ø. (2001). Dynamic simulation of the human red blood cell
metabolic network. Bioinformatics, 17(3), 286–287.
Kauffman, K. J., Pajerowski, J. D., Jamshidi, N., Palsson, B. Ø., &
Edwards, J. S. (2002). Description and analysis of metabolic
connectivity and dynamics in the human red blood cell. Biophysical
Journal, 83(2), 646–662. doi:10.1016/S0006-3495(02)75198-9

The model used by Jamshidi et al. can be found in the BioModels database with acession no. MODEL1103210001  http://www.ebi.ac.uk/compneur-srv/biomodels-main/MODEL1103210001
A more recent model has also been described in Bordbar et al. iAB-RBC-283: A proteomically derived knowledge-base of erythrocyte metabolism that can be used to simulate its physiological and patho-physiological states. BMC Systems Biology 2011, 5:110 The model file in SBML format can be downloaded from the Additional Files section (http://www.biomedcentral.com/1752-0509/5/110/additional) or BioModels (http://www.ebi.ac.uk/compneur-srv/biomodels-main/MODEL1106080000).

What about the model used by Wiback et al? The paper has the stechiometric matrix, but in pdf format, which is useless.

Indeed, I couldn't find any model file for that. I wouldn't call it completely useless though. If you are using for example COBRA Toolbox or CobraPy, you can construct the model yourself from the matrix, then save it to SBML. I'd expect to use a couple of hours.


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What are the factors that contribute to genetically identical individuals behaving differently?
If you run the same task on a pair of identical computers, you will end up getting the same results, even with the same response time.
But let's say you line two different person, and ask them the exact same question. Each will answer totally different, even if they are twins, raised in the same family, went to the same school and shared the same roof, and probably had the same experience in life. One of them may love carrots, one may not.
The question is, what is generating such different behaviour and way of thinking? Aren't they sharing the same genes?
If yes, the question is still standing.
If no, then we'll have another question:
If we create 2 identical clones of a person, raise them in the same situation, will they think identical too? If not, why? And what's the reason of this?

This is a classic and in my opinion interesting debate; nature versus nurture. It has filled textbooks, journal articles, and popular books. This question isn't a good fit for the site because it's too broad, unclear (what constitutes "thinking identically", how do you want to measure that), and a matter of opinion. If you're interested in the topic, consider narrowing down your question to "what evidence suggests they would think similarly" and ask over at cogsci.SE. This still, however, may be too broad.

Thanks for your comment. I'm not expert in biology, my first question here. Please suggest / direct edit the question if you think it can be improved. I think you know what i'm after. As a computer programmer this question is bothering me for a long time, that why humans don't produce same results as computers.

Your example is flawed.  If you have two identical computers (that is, identical hardware), and install Windows on one and Linux on the other, they will behave quite differently.  Even two different versions of Windows or Linux will have differences, or two copies of the same version of Linux with different choices made during install.

@jamesqf Even the same program with identical command-line parameters may produce different results or execute faster/slower if you use a random number generator or multithreaded code, or just have other programs running at the same time (the OS itself included).

@jamesqf i mentioned to run the same task.

@Jack Johansson: Yes, I understand that, but I'm considering 'task' to be at a high level, similar to your example of two people being asked a question.  So if the task is for instance "display a web page", the Linux browser will do it somewhat differently than Windows/IE.

Your question has actually more to do with developmental biology and the origin of phenotypic variance in populations than with neuroscience.
Here is a list of factors which variance explain observed phenotypic variance in a population:

Genetics (incl. additive, dominance and epistatic variances)
Environment (incl. macro and micro environments)
Developmental noise (incl. cellular noise)
Epigenetic
All the covariances among above factors

Of course, when you consider a pair of monozygotic twin as your population, there is little to no genetic variance. They will also likely experience little epigenetic variance. Assuming they live together, practice the same sport, eat the same type of food, etc... then they will also experience little macro-environmental variance. Micro-envrionmental variance and developmental noise are probably the main factors causing these two hypothetical twins to differ.
You might want to read the post Why is a heritability coefficient not an index of how “genetic” something is? to better understand the current post.

Can you please expand on what remains unanswered?

If you create 2 clones from an individual person (assuming it's technically possible) and put them under same circumstances, will their brain function identically?

Yes as you will still observe micro-environmental variance, variance due to developmental noise and epigenetic variance (and their covariances). If it is unclear you might want to read the post that I linked at the end of my answer.


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Is sugar absorbed into the bloodstream through the walls of the mouth?
If you let a piece of candy melt in your mouth, but did not swallow it, would the sugar be absorbed through the walls of your mouth?

Welcome to SE kindly read tour page about how to ask question and modify yours accordingly. Your question would be downvoted or closEd  as it shows no effort to answer  and any kind of research.

@Chemist Answering questions that are not well-researched rather encourages people to post such questions anyways.

@BryanKrause Answering poorly researched questions isn't to me inherently wrong. The issue is that you cannot tell what the question is. Is this person asking about how digestion works? How sugar is tasted? If sugar can be absorbed directly as well as or instead of absorption in the gut? Is it asking about dissolving sugars? Is it asking about the composition of saliva? There is too much to unpack here to make an answer useful.

Possible duplicate of What nutrients can humans absorb in the mouth?

@James, the title of the question says: "Is sugar absorbed into the bloodstream through the walls of the mouth?" so this is clearly about absorption and the topic is very interesting in the context of treatment of hypoglycemia, as I answered.

@Jan That is a very nice answer! But it doesn't address the question in the context of candy ;). I suggest you edit the question; I think you see the value in this question and how it could be made into a good clear question.

@James, well, the "candy" in the question was just used as an example. OK, I'll edit it.

Simple sugars such as glucose, fructose and galactose will be absorbed.

They are most probably transported by a common carrier, which is why if you present both glucose and galactose, the presence of one will inhibit the absorption rate of the other.
Uptake rate also seems to partly depend on the concentration of sodium ions in the buccal cavity. This was identified and explored subsequently.
It seems that at the cellular level, absorption is not the quickest but there is a lot of vascularization which allows it to enter the bloodstream quickly, regardless.

Here's a back-of-the-envelope calculation: about 10mg is absorbed in 5 minutes when you hold a solution of 3.6g/l in your mouth. A normal gulp volume is around 10ml. That's 36mg of sugar in a mouthful. Result: you can absorb 10mg of sugar from a theoretical maximum of 36mg. In other words, within 5 minutes, you absorb ~30% of all available sugar. That's pretty good, given that a sugar solution is not a more concentrated, solid sugary food!
Worthy to note that most complex sugars will not be absorbed. Note that many complex sugars actually won't be uptaken even in rest of the GI tract, like cellulose.
See other posts already here on the topic.

@Jan Of interest.

Yes, there is sucrase in the mouth, but not human in origin! Bacteria that live in the mouth produce glucansucrase that can break down sucrose.

The absorption of sugar from the mouth is possible and it was successfully tested for treatment of hypoglycemia. In all mentioned studies, they used D-glucose (dextrose), which is a common natural or added sugar in foods and beverages.
1) Sublingual sugar administration as an alternative to intravenous dextrose administration to correct hypoglycemia among children in the tropics (Pediatrics, 2005):

Sixty-nine children with glucose concentrations of < 0.8 g/L were
  assigned randomly to 1 of 4 methods of administration, 1 with 3
  different doses of sugar, as follows: oral group (OG) (n = 15): 2.5 g
  of sugar; sublingual group (SG) (n = 27): 2.5 g of sugar under the
  tongue, with 3 treatment subgroups, ie, 0.1 g/kg, 0.15 g/kg, and 0.2
  g/kg; intravenous group (IG) (n = 8): 8 mL of 30% dextrose in a single
  bolus; water group (n = 11)...Bioavailabilities were 84% and 38% in
  the SG [sublingual group] and OG [oral group], respectively. The
  sublingual administration of sugar proved to be effective among
  moderately hypoglycemic children.

2) Impact of buccal glucose spray, liquid sugars and dextrose tablets on the evolution of plasma glucose concentration in healthy persons (ResearchGate, 2009):

Analysis of regression coefficients after 30 min compared to the
  control session, demonstrated an increase in PG [plasma glucose] with the sachet of
  liquid sugars (0.068 mmol/l/min, p = 0.001) which was greater than a
  single dextrose tablet (0.052 mmol/l/min, p = 0.002), but no
  significant PG increase was found after buccal glucose spray. Liquid
  sugars or dextrose tablets, but not the buccal glucose spray, are
  effective means to increase PG within 10 minutes after ingestion.

3) Dextrose gel for neonatal hypoglycaemia (the Sugar Babies Study): a randomised, double-blind, placebo-controlled trial (The Lancet, 2013):

Our findings show that treatment with 40% dextrose gel is more
  effective than feeding alone for reversal of neonatal hypoglycaemia in
  at-risk late preterm and term babies in the first 48 h after
  birth....Our study is the first report in babies showing that buccal
  dextrose gel is a safe effective treatment for management of
  hypoglycaemia.

4) Sublingual sugar for infant hypoglycaemia (The Lancet, 2014)

We showed that sublingual absorption was faster than the oral route.
  An increase of 2 mmol/L in blood glucose concentration was achieved in
  10 min, and 64% of children had a blood glucose concentration of more
  than 3·3 mmol/L after 20 min.

5) First aid glucose administration routes for symptomatic hypoglycaemia (Cochrane, 2019):

Providing sugar under the tongue (sublingual) resulted in a greater rise in blood glucose after 20 minutes than giving the sugar orally,
  but this was in a specific setting including children with
  hypoglycaemia and symptoms of concomitant malaria or respiratory tract
  infection. On the other hand, giving glucose by the buccal mucosa
  route resulted in a lower plasma glucose concentration than with the
  oral route. For dextrose gel (where uptake of the glucose occurs
  through a combination of oral swallowing and via the buccal mucosa),
  no clear benefit was shown compared to oral glucose administration
  (glucose tablets or glucose solutions).

Important: Currently, buccal glucose is not recommended to treat hypoglycemia, except in uncooperative children who refuse to swallow glucose (International Liaison Committee on Resuscitation, 2019) .