As the comments pointed out, this is not a hard question to answer with some research, but I'll add a few more details.

Dextrocardia is congenital. The human heart normally actually isn't so much on the left side - it's more pointed towards the left. In dextrocardia it points more towards the right side. This develops within the first few weeks of embryonic development, as the heart is one of the first organs to develop.

Source

It occurs in about 0.7 percent of live births and 2.7 percent of stillbirths, indicating that there are health problems in the fetus associated with it. After birth, it's possible that the heart functions perfectly fine, but often there are other heart defects associated with dextrocardia.

Dextrocardia with situs inversus is a condition in which the heart and visceral  organs are reversed. As for the cause, it's genetic and follows a recessive inheritance pattern, meaning both parents need to be carriers, but don't necessarily have the condition.


What is the best way to analyze non-quantitative mass spec hits from an immunoprecipitation pull down?

If they are available, talk to the people who analysed your data. Using their knowledge is intelligent.

I will assume two critical steps are completed. First that your results have been searched correctly. I will also assume that the peptide and protein identifications have been filtered to provide a false discovery rate of 1:100 at each level.

You can remove all the proteins that were identified in your affinity purification control. Another option is to use the Contaminant Repository for Affinity Purification (the CRAPome) which provides a formal framework for removing contaminant proteins. It is a nice resource if your data are compatible.

The remaining proteins are what you have to work with, this is the

  list of potential proteins that [your protein] interacts with.

Prioritise these proteins based on the biology of your experimental system. If the list is small work through the function of each protein and assess how it fits with the biology you are researching.

To assess the potential functional links between the proteins you can create an in silico network. Markov clustering can highlight the presence of functionally distinct groups of proteins within a network. String, linked above, can do this. Centrality measures can indicate the presence of proteins with the potential to influence the behaviour of the network.

For larger lists you can also assess the function of the proteins in the list by performing a functional annotation enrichment analysis. There are many other things you could do but the primary goal is to keep biology at the forefront of your efforts.

Finally you mention that repeats are necessary. Analysing the data is time consuming. If this was a test run verify that the test was successful and then run the replicates. Time spent analysing incomplete data can be spent completing the data set or ensuring the right data is collected. Quantitative data can be very useful and with care shotgun proteomics approaches can provide quantitative data but the people who run the machine need to be consulted when quantitative data is required.


Visual Quality Indicators for Soil and Plants

There are numerous visual indicators for various type of plants that determine plant health. For example the rigidity of the leaves can help you determine that enough water is supplied to the plant (1). Now you can also determine the leaf shape and detect for presence of disease (2), pests (3), and plant health in general (4). This research however mentions no correlation between lamina shape and area so you would need wiser methods for your corrlelation methodology(5). Moreover, you can look at the fruit shape/sizes to determine if plants have been supplied enough nutrients(6). Another study which is worth mentioning is using chlorophyl to determine plant fitness but this cant be done insitu and you would need lab analysis (7)
All these are visual indicators for the plants itself. As far as soil is concerned is it more challenging because you can make soil and compost using various materials and methods so there is no general approach that can be used to determine the quality. So if soils is your primary concern then as @PolypipeWrangler mentioned looking at the plant fitness can help you determine soil quality.


How does the dopamine spike from drugs compare quantitatively to pleasurable non-drug activities?

This review article [1] gives dopamine responses for rats (similar to the BBC article above) and includes references to the underlying studies:

Sex/Food:  150% - 300%
Alcohol/Ethanol:  190%  (1g/kg) *
Morphine: 200% (1mg/kg) *
Nicotine:  220%   (0.6mg/kg) *
Cocaine:  350%  (5mg/kg)
Methamphetamine:  1000%  (1mg/kg)

These are percentages of the baseline dopamine level (not percentage increases), so 100% would be no effect.  They correspond to dopamine levels in the Nucleus Accumbens, which is a brain region involved in processing reward.

Also, the drug effects are dose dependent, so the above values show the dosage with the largest effect among the dosages tested in this study [2], which was referenced from the review article.  The values marked with asterisks were estimated visually from the graphs.

[1] Allerton M, Blake W. The "Party Drug" Crystal Methamphetamine: Risk Factor for the Acquisition of HIV. Perm J. 2008;12(1):56–58.
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3042341/

[2] Di Chiara G, Imperato A. Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci U S A. 1988;85(14):5274–5278.
 https://www.ncbi.nlm.nih.gov/pubmed/2899326


Can one talk about deacetylation of a promoter rather than associated histone?

The authors obviously meant to write that the histones associated with the promoter become deacetylated. They cannot mean the promoter itself as that is DNA.

What they wrote is not shorthand or acceptable alternative usage, but just a mistake — published papers often contain typos and mistakes of this sort. Probably the authors meant to write the technically correct form of words but lost a phrase. Or perhaps they had exceeded the limit to the number of words allowed in the summary, and so they went through trimming, but trimmed too much.

Why didn’t the referees pick this up? Of course they should have, but they were probably more concerned with the contents of the paper and whether the experiments described by the authors justified their conclusions. They are busy scientists and probably doing the job voluntarily.

In conclusion, scientists are human, scientific writing is difficult, and everyone makes mistakes. But we should still try to convey our ideas as clearly as possible, and certainly not copy something that is technically incorrect or ambiguous, just because it has made it into print.


It looks like male Great Argus (Argusianus argus) displaying to a female. The circular markings on the male pheasant's secondaries are pretty distinct. The specific epithet argus refers to a hundred-eyed giant from Greek mythology.


Evolutionary origin and exogenous cues of ~28 day infradian rhythm?

A double-blind, prospective study during the fall of 1979 investigated
  the association between the menstrual cycles of 305 Brooklyn College
  undergraduates and their associates and the lunar cycles.

  .... Approximately 1/3 of the subjects had lunar period cycles, i.e.
  a mean cycle length of 29.5 ± 1 day. Almost 2/3 of the subjects
  started their October cycle in the light 1/2 of the lunar cycle,
  significantly more than would be expected by random distribution. The
  author concludes that there is a lunar influence on ovulation.

(Menstrual and Lunar Cycles, Friedmann E., American Journal of Obstetrics and Gynecology, 1981)

Another source supports this conclusion, finding that "a large proportion of menstruations occurred around the new moon."

Somewhat related, this study found that light exposure shortened menstruation cycles.

In summary, there seems to be a good amount of data suggesting that lunar cycles do in fact calibrate the length of human menstrual cycles to some degree.


Why is full cell/high antigen dose pertussis vaccine dangerous for adults?

It seems it is not about pertussis.

I have found information in the Infanrix-DTPa characteristic that it is not recommended for adults due to high dose of diphteria toxoid.

Both Infanrix-DTPa and whole-cell DTP vaccines contain over 30 international units (whatever it is) of diphteria toxoid while Boostrix contains "not less than 2 i.u.".


You are correct - they are all bases. However there are two types of bases. Purines and pyrimidine bases. Purines have two ring systems, while pyrimidines have only one. With this hint, I think you will be able to find the answer to your first question.

As for your second question. Can you give me a definition for what a mutation is? I think if you are able to define this word you will know why that answer is incorrect.

Also, bacteria are incapable of performing one of the four processes that you have listed - and that particular process, is therefore the correct answer to your second question.


Is the covid-19 vaccine-induced copy of the protein spike also damaging cells?

The spike proteins expressed by cells that take up mRNA or ChAdOx vaccines are modified so they cannot induce membrane fusion. However, the research article you refer to indicates that circulating spike protein damages endothelial cells simply by binding ACE2, which suggests vaccine derived spike protein could still cause this kind of damage if it enters the bloodstream somehow:

we show that S protein alone can damage vascular endothelial cells (ECs) by downregulating ACE2 and consequently inhibiting mitochondrial function.

Spike protein is necessarily attached to a membrane, so for it to damage cells by binding ACE2, bits of membrane containing the spike would need to be exported from the cells. The SARS-CoV-2 genes that allow it to do this in a real infection are not present in the vaccines, of course. The only other route I know of by which S protein could theoretically enter the blood is in exosomes. This article analyzed circulating exosomes from COVID patients and did not detect any viral proteins:

We did not identify viral proteins via the purification of exosomes; thus, we can conclude that viral particles were not purified together with exosomes

Research creating hybrid S-protein that can make spike-coated exosomes indicates the natural spike protein does not get into exosomes:

the S protein could not be detected in the sample from pSwt-transfected cells. In contrast, the SGTM protein could be detected in the pelleted supernatant of pSGTM-transfected cells.

I was not able to find any studies looking for spike protein in exosomes of vaccinated people, but it should be less likely than for the actual virus.


What coronaviruses have been identified in racoon dogs?

Here's an abstract for a paper from 2006: https://www.ncbi.nlm.nih.gov/pubmed/16450706

  An RT-nPCR assay was used for testing fecal samples of dogs, foxes, raccoon dogs and minks for the presence of canine coronavirus (CCV). The animals were raised in homes, dog schools or farms... Among 24 raccoon dogs samples, 22 were CCV type II-positive, and from those 16 were additionally type I positive.

Here's another paper from 2003: https://www.ncbi.nlm.nih.gov/pubmed/12958366

  A novel coronavirus (SCoV) is the etiological agent of severe acute respiratory syndrome (SARS)... Evidence of virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the same market.

So at least a couple types of canine coronavirus and other strains closely related (but not identical) to the coronavirus that causes SARS.


According to a paper by Walker et al. (2013) (found by googling "silverfish + silk", so not very hard to come by), silverfish can indeed produce silk. The paper also mentions that silverfish (Thysanura) and bristletails (Archaeognatha) use silk to transfer their sperm, and they also use it for "...tactile cue during courtship (Sturm, 1956)". This webpage (from NY State University) explains that male silverfish will deposit a spermatophore on a silk thread that is vertically suspended, and the spermatophore is later picked up by a female.

  Abstract:
  Silks are semi-crystalline solids in which protein chains are associated by intermolecular hydrogen bonding within ordered crystallites, and by entanglement within unordered regions. By varying the type of protein secondary structure within crystallites and the overall degree of molecular order within fibers, arthropods produce fibers with a variety of physical properties suited to many purposes. We characterized silk produced as a tactile stimulus during mating by the grey silverfish (Ctenolepisma longicaudata) using Fourier transform infrared spectroscopy, polarized Raman spectroscopy, gel electrophoresis and amino acid analysis. Fibers were proteinaceous-the main component being a 220 kDa protein-and were rich in Gln/Glu, Leu, and Lys. The protein structure present was predominantly random coil, with a lesser amount of beta-structure. Silk fibers could readily be solubilized in aqueous solutions of a mild chaotrope, sodium dodecyl sulfate, indicating protein chains were not cross-linked by disulfide or other covalent bonds. We conclude that entanglement is the major mechanism by which these silk proteins cohere into a solid material. We propose silks used as short-term tactile cues are subject to less stringent requirements for molecular order relative to other silks, allowing the random coil structure to be favored as an adaptation promoting maximal entanglement and adhesion.

The linked paper contains several references that should be useful if you want to look deeper into how silverfish use silk.

From what I've seen, they don't use silk for climbing. Silverfish can usually climb rough surfaces, but not smooth surfaces, which is why they are often found trapped in sinks, bathtubs etc.


How does pressure measured by sphygmomanometer translate directly to blood pressure?

Korotkoff sounds!

The blood pressure measurement process is fairly cool, and goes like this.

Inflate the cuff to well over plausible blood pressures (250mmHg or so).
Slowly deflate the cuff while listening to the artery.
When you start to hear sounds, that's when the systolic blood pressure is higher than the cuff pressure and the heart can squeeze a little blood through the cuff, which makes a little squirty noise.
As cuff pressure continues to drop it stays between the systolic and diastolic blood pressures and therefore bloodflow stops and starts and creates audible turbulence.
When the artery stops making noise, the cuff pressure is below the diastolic blood pressure and the cuff has no effect on the artery, so it goes back to laminar flow that doesn't make noise.

Measuring the pressure of the cuff is just part of controlling the pressure of the cuff. You could conceivably measure blood pressure by submerging their arm in water(mercury would not require a conversion, but vats of mercury are unpopular in doctor's offices) and listening for Korotkoff sounds and measuring the depths where they start and stop.

Edit: The actual question here is how does cuff pressure physically change the arterial surroundings, not how do we link the two clinically.

The body is mostly water, and water is incompressible. For small strains(amount of deformation) flesh isn't that springy and mostly "flows" like water. When you pressurize the cuff around the arm, the flesh of the arm equilibrates to the cuff pressure the way balloons equilibrate to the air pressure, only less dramatically because water is mostly incompressible. For small pressures and large cuffs, therefore, the cuff pressure is the pressure on the artery wall, and by listening for Korotkoff sounds while varying the cuff pressure the blood pressure can be roughly established.

The reason why you don't lose all blood flow to your extremities while diving underwater is because the systemic pressure on all of your body raises your internal blood pressure, making the net external pressure on any part of your body zero. (The cuff works by exerting a relative pressure difference on part of your body.) At high altitude the sphygmanometer is still accurate-ish because the cuff pressure relative to the atmosphere is still the same as the blood pressure, relative to the atmosphere. If you had air for blood(or any compressible fluid) your veins would collapse underwater. This is why your ears hurt while diving deeply if you don't equalize them: your ear is full of compressible air, and at depth the air attempts to shrink more than the flesh around it, pulling things out of place painfully.


Human Bones classification and anatomy quiz

@KMM's comment above appears to be on the right rack.

"plane" = "flat"
"mixed" = "irregular"
"even" & "odd" = "paired" & "unpaired"

That being said:

A = FALSE because jaw bones are not paired
B = FALSE because sternum is not a long bone (it's a flat bone)
C = FALSE because ribs are not irregular bones (they're flat bones)
D = TRUE because both are flat bones and protect organs
E = FALSE but ONLY under the assumption of the persistence of a metopic suture (frontal suture) causing the frontal bone to be split (and therefore "paired").


On the contrary it's not neutrophils that initially recognize a threat, but rather distressed epithelium, and immune cells like DCs or macrophages that are already distributed in the tissue that recognize pathogen- or damage-associated molecular patterns (see PAMPs and DAMPs). The primary response to these patterns is the secretion of cytokines.

Among the many cytokines secreted include a subset known as chemokines, from the Greek work for movement. The combination of chemokines and cytokines induce chemotaxis of immune cells circulating in the blood, such as neutrophils, by telling these cells that the nearby tissue is inflamed. IL-1ß, IL-6 and CXCL2 are examples of neutrophil attractants secreted by macrophages and monocytes. Complement fragments like C5a are also known to induce an inflammatory response, inducing the secretion of these molecules.


Is it possible to graft plants from different families?

No. Exceptions are always possible, but it would be a noteworthy.
I just find this notes in: https://courses.cit.cornell.edu/hort494/mg/specific.grafting/compatibility.html

Interfamilial
Although there are a few reports of short-term graft union formation between distantly related (interfamilial) herbaceous species, there are no confirmed reports of interfamilial grafts between woody perennials.
One extremely curious report of natural interfamilial graft compatibility which must be considered unconfirmed, and even unlikely, was the observation of La Rue (1934) [...]


Do mosquito repellent sprays work on all insects?

The most common active ingredient in insect repellents is N,N-diethyl-3-methylbenzamide (other name: N,N-diethyl-m-toluamide; abbreviated DEET). It provides protection against mosquitoes and many other insects. After various interesting hypotheses, it is currently assumed that mosquitoes simply smell DEET directly and avoid it.[1]


Is there any evidence telling us what the oxidation state of early earth's atmosphere was?

There are wikipedia pages on Geological history of oxygenation and on Great Oxygenation Event

I don't know much about geology and someone else might be able to give an exhaustive list of evidence (and method of measuring) concerning the oxygen concentration on earth but that would be a very long answer I guess! Rather than a full answer, I give you a list of wikipedia pages below that will interest you and should help answering your own question.

Banded Iron Formation
Evolution_of_dietary antioxidants
Huronian Glaciation
Ice core


Do all living humans literally descend from one ape?

Just 6 million years ago, a single female ape had two daughters. One became the ancestor of all chimpanzees, the other is our own grandmother.

Short answer
Whether or not the claim is true actually depends upon the specific DNA sequence you are considering. The claim is true for sequences without recombination (such as mtDNA and most of the Y chromosome). The claim does not hold true for most of the genome and it is therefore misleading.
Long answer
Basic knowledge required
First, if you don't know the concepts of

allele
haplotype
ploidy
selection
genetic drift
segregation
recombination and crossover

, then you might want to have a look at a short introduction of evolutionary biology such as Evo101 for example. The below answer will make more sense to you with some a priori knowledge.
Coalescence
Imagine there is today a population of $N$ individuals. We are going to look at this population backward in time (which is a little bit unintuitive). For simplicity, we will assume asexual reproduction, no recombination, absence of selection (only drift) and constant population size of $N$ individuals. The assumption of no recombination is key here. The other assumptions are details just to make my job at explaining coalescent theory easier.
We start at time t=0 and are going backward in time. If two individuals are siblings at $t=0$, then, it means that in the previous generation, they share the same parent. Therefore, if we connect individual from generation $t=0$ to their respective parents at generation $t=-1$, we see that some group of individuals (the siblings) "coalesce" to fewer individuals (their parents). Individuals at generation $t=-1$ that are not connected to individuals at generation $t=0$ are those who did not reproduce (or who did not leave offspring that have survived until adulthood).
You can keep iterating over generation $-2$, $-3$, $-4$, etc... At each generation, the number of individuals that are connected (that our ancestors) to present day individuals is diminishing as more and more coalescence happen. After a sufficient number of generations, eventually, only one parent will remain. This single individual will be the ancestor of all present individuals.
If you enjoy math, then note that such process is actually a simple a branching process for which it is relatively easy to calculate the expected time (and the whole PDF) to the next coalescent event and the expected time (and the whole PDF) until all individuals in the population coalesce.
So, assuming no recombination, if you consider individuals in a modern population, then you can be sure that all individuals share a common ancestor who is a single individual, at some point in the past.
Incomplete lineage sorting
The process of all individuals coalescing into a single ancestor takes a little bit of time. For recently diverged species (say species A and species B), it is possible that this common ancestor is older than the time of divergence between species. If this is the case, it is then incorrect to think of a mother who gave birth to two individuals, one becoming the ancestor of all individuals of species A and one becoming the ancestor of all individuals of species B. In such a case, we talk about incomplete lineage sorting.
Note that when we talk about 'incomplete lineage sorting', we are generally talking about specific genes as not all genes coalesce the same way when there is recombination and segregation (see below)
Recombination
Now the trick is that in the presence of recombination, different sequences coalesce differentially. It also means that when you look at two sister species, some sequences can show incomplete lineage sorting while others don't.
The presence of recombination therefore makes the claim false!
Do we recombine?
Yes, all of our genome recombines to the exception of two sequences

mitochondrial DNA (mtDNA)
Y chromosome not including the Pseudo-Autosomal Region (PAR)

mtDNA is maternally inherited (without crossover) and transmitted to all offsprings, while the Y chromosome is paternally inherited (without crossover) and transmitted to sons only.
So, is the claim true?
mtDNA
It is true that there was an ape who had two daughters. One daughter's mtDNA became the ancestor of all mtDNA we have in humans today, the other daughter's mtDNA became the ancestor of all mtDNA that exist in chimps populations today.
Of course, this daughter is the common ancestor of all modern mtDNA but is not necessarily the Most Recent Common Ancestor (MRCA). In humans, the MRCA to all modern mtDNA is called Mitochondrial Eve (mt-Eve or mt-MRCA).
Y Chromosome
The same claim is true for the Y chromosome (although I am not sure there was really not a single recombination event happening on the Y chromosome since). The MRCA to today's all Y chromosome is sometimes called Y-chromosomal Adam (Y-MRCA).
The names 'mt-Eve' and 'Y-chromosomal Adam' have of course been chosen in reference to the creation myth of Abrahamic religions.
Rest of the genome
The Y chromosome and mtDNA together represent less than 0.2% of our genome. The rest of our genome does recombine.
The claim does not necessarily hold true for 99.8% of the genome. I would therefore tend to think that the claim is misleading at best, wrong at worst.
Adam and Eve
We can call Adam the MRCA of all Y chromosomes today. Only Y chromosomes, not the rest of the genome. We can call Eve the MRCA of all mtDNA today. Only mtDNA, not the rest of the genome.
Of course, Adam and Eve did not live in the same time period and did not live at the same place. Adam and Eve never met. And of course, there were plenty of other humans around. They are in no way the first two humans.
Other popular source of knowledge
PBS Eons - The Two People We're All Related To


Lifetime of secondary messengers such as Calcium or IP3

The lifetime of Calcium can be considered infinite in biological time scales, it is not a real biomolecule. The half-life time of other biomolecules like IP3, PIP2, receptors, hormones, etc. is species-dependent and within the species strongly depending on the cell and its metabolic state.

Short answer: There is no overview for lifetimes of biomolecules. It is easier to search for a specific molecule in a specific cell. Perhaps you are lucky and somebody measured it.

Update to the comments:
All known second messengers, like Ca2+, IP3, PIP2, change their concentration in response to a stimulus, e.g. activation of muscarinic receptors causes activation of phospholipase C which cleaves PIP2 in DAG and IP3. IP3 causes release of Ca2+. Ca2+ never gets degraded or synthesized but the intracellular concentration changes. PIP2 gets degraded, i.e. its concentration becomes lower, while the concentration of its cleavage products, IP3 and DAG, increases. Those changes are temporary, after removal of the stimulus the 2nd messengers get degraded as well or e.g. Ca2+ is taken up into intracellular compartments.

A general overview about second messengers.


Here are the assumptions to the standard Hardy-Weinberg rule (HWr) formulation
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$
See Solving Hardy Weinberg problems for more info about this formulation.
Assumptions
The locus of interest is bi-allelic
This is an obvious assumptions, however it is very easy to extrapole HWr to any number of loci.
Organisms are diploid
This is another obvious assumption that is very easy overcome. This also means that HWr does not hold for loci present on sexual chromosomes as those chromosomes do not display a simple diploid behaviour.
Only sexual reproduction occurs
If some individuals are able to undergo non-sexual reproduction, then the rule does not hold anymore. See also Panmixia as these two assumptions are related.
Panmixia
Panmixia is often called "random mating". Panmixia is the state where each individual is equally to mate with any other individual in the population (including itself). There is therefore no population structure and no mate choice.
Let $N$ be the number of individuals in the population, in absence of selection (see If selection, it must be on fecundity alone), the probability to mate with any given individual (including itself) is $\frac{1}{N}$. You will note that it requires that individuals are able to self (but not clone as reproduction must still be sexual).
If selection, it must be on fecundity alone
If selection occurs, then it must on fecundity (right before reproduction). If selection occurs on survival during the lifetime, then the selected genotypes will be in excess in comparison to Hardy-Weinberg expectations.
If migration, it must be right before reproduction only
For the same reason as above, if there is migration, then it must be right before fecundity. If migration occur during the lifetime, then it will have a very similar effect than selection. Selection would increase the frequency of selected genotypes above HR expectations. Migration would increase the frequency of incoming genotypes above HR expectations.
Non-overlapping generations
This means that everyone reproduce in the exact same time and die right afterward. Very few species would qualify for such assumptions.
Population of infinite size
If previous assumptions already seemed hard to meet in the real world, the assumption of infinite population is absolutely impossible to meet.
Deviation from this assumption will cause deviations from expectations. Such deviations are often tested via a Chi squared goodness-of-fit test.
Note by the way that if the population is of infini size, there is no mutation, no migration and no selection, then there is no evolution.
Other assumptions
Biology is a science of complex systems. There are always other assumption one might want to consider. For example I did not talk about sex-specific selection or sex-specific mutation rate. But I am hoping that with the above I went over the most important assumptions.
So what's the point of HWr?
All models are wrong but some are useful. There exist no real life example of a population that perfectly fit into HWr assumptions but it does not mean the model isn't useful. Actually most population approximate HW expectations quite well. You will note also that it is by understanding how a scenario lead to a specific observation that we can interpret how derivation from the expectations can be achieved.
So yes, HWr is one of the most basic and most important rule in population genetics. It is so basic, that I would hardly name it in any fancy way as it is just the simple application of basic probability theory. See Solving Hardy Weinberg problems for more info.


How does an isotonic environment affect fish?

Some fish are isotonic to their environment (I read that in some book and they had examples but Google is failing me. Here is a paper instead talking about fish doing well in an isotonic environment). It isn't an issue for getting oxygen; I assume you think that because you think fish get oxygen via osmotic pressure, but "isotonic" (and "hypotonic" and "hypertonic") refer to the transfer of water via osmosis. A fish that's isotonic with its environment doesn't need to take special measures to avoid its cells swelling or shrinking as water floods in or out of them; it doesn't say anything about which specific solutes are in that water to make it isotonic.

As far as oxygen goes, oxygen is constantly being consumed by the fish's tissues so the diffusion is always going to go in the right direction (unless the water doesn't contain enough oxygen in the first place, in which case fish won't survive). In addition I imagine fish blood contains many molecules that preferentially bind to oxygen in ways that make this process even more efficient.


How to study the effect on tau protein isoforms on microtubule based transport?

You can do a microscopy based assay to quantify the transport rate (both retrograde and anterograde). Mitochondria can be labeled with fluorescent proteins such as mito-dsRed, and its movement along the axon can be tracked by live cell imaging. You can check this paper; they have done this experiment. (Others have also done it but I remember this paper because someone told me about it recently).

How do you plan to see the effect of different isoforms? It may not be that easy. You will have to replace the common isoform with the others. It is not very easy to control splicing. So you may have to make lines that express only one variant (exon deletion). Though this study reports that alternative splicing can be controlled by using antisense oligonucleotides, the technology is not standardized yet; you can try it nonetheless, because making knockouts is difficult (you would have to make KO mice and then culture neurons from it).


What are names of the colon delimited fields in this FASTA header?

According to ensembl's website (albeit somewhat buried in a page about downloading data via FTP) it says:

"The header line in an FASTA dump files containing DNA sequence consists of the following attributes : coord_system:version:name:start:end:strand This coordinate-system string is used in the Ensembl API to retrieve slices with the SliceAdaptor."

A brief rundown of these attributes as I understand them:

coord_system- Is simply the coordinate system used to locate a particular feature within an assembly: "chromosome" and "BAC clone" are common examples as described here.
version- This is the current version of the assembly reference. And refers to an Ensembl archive as detailed here. (Yours appears to be from the human GRch38 assembly).
name- This seems pretty self explanatory. In this case we are looking at chromosome 21.
start- Again, self explanatory. Any complete chromosome or contiguous sequence is going to start at "1".
end- End of the fasta sequence. [start] - [end] + 1 = total length
strand- This refers to orientation (i.e. forward or reverse strand) 1 is forward (-1 is reverse)

Here is a link to a pdf containing this information and more about using Ensembl (see page 23)...

Unfortunately, to answer your final question, there is no easy way to come across this information and there are as many ways of labeling fasta files as there are sequence databases. Sequence repositories have come a long way in the last 10 years but there is still a lot of work to do toward standardizing data formats and making databases more user friendly.


Is it possible to have raw ngs data to practice

At least PacBio do provide some example datasets on their DevNet resource. You should be able to get a lot of different Illumina data from the public data in BaseSpace. I am not sure where to look for official samples from Roche 454, but I wouldn't bother too much as it is discontinued anyway. Rather go for MinIon or IonTorrent data, if you want more.


What does the term "recruitment of T-cell" mean?

If I'm interpreting it properly, it's the adaptive response that's recruiting the T cell, evidenced by the last line in their abstract:

"Therefore, the contribution of a T cell clone to the immune response is mostly determined by the time of its entry into the immune repertoire, i.e., the time of first cell division after antigen encounter."

It's strange because when i think of recruiting a T cell it's always to the tissue or site of infection or what have you.


Why doesn't patients with chronic acne's body lower sebum production itself?

Short answer there is no feedback mechanism to tell the body it is overproducing, inflammation can have a huge number of causes, many of which could actually be worsened by decreased sebum production.

Also "overproduction" is a misleading term; it is overproduction compared to the norm for the population and may be perfectly normal for that individual. It is like asking why redheads don't start growing black hair when surrounded by surrounded by people with black hair.


To answer your last question first: as long as a restriction enzyme recognises a specific sequence then goes on to cut the DNA it really doesn't matter where the cut takes place, as long as the invading DNA is destroyed.

The WP page on restriction enzymes provides a useful summary of the various classes of restriction enzyme, and led me to a review about Type I enzymes here.

Unlike the familiar Type II enzymes, Type I enzymes require ATP, which they use to power their movement along the DNA, once they have been activated by binding their recognition sequence. The HsdR subunit of the enzyme (R, M and S subunits) contains sequence motifs which mark it out as being related to DNA helicases, which, of course, are able to translocate along a duplex and unwind the duplex.

One particularly striking demonstration of the DNA translocation ability of EcoK1 (a Type I enzyme) is described in

  Davies et al. (1999) The DNA translocation and ATPase activities of restriction-deficient mutants of EcoKI. J. Molec. Biol. 292: 787-796 doi:10.1006/jmbi.1999.3081

The experiments are based upon the mechanism by which phage T7 injects DNA into E. coli cells.  The phage ejects about 850 bp of the 40 kb genome into the host; the entry of the bulk of the DNA is coupled to transcription, first by host  RNA polymerase, and subsequently by the phage-specific RNA polymerase, once the corresponding gene has entered the cell. If the drug rifampin is used to block transcription then the whole process stalls. This block is overcome if the initial leader of 850 bp is engineered to contain a recognition sequence for EcoK1 whereupon the restriction enzyme is able to translocate the entire genome into the cell at 100 - 200 bp per second. Mutations in the helicase motifs of the HsdR subunit abolish this activity.


Why is wombat scat (feces) shaped like cubes?

I'm almost certain that your question is based on the press that Patricia J Yang's research is receiving (e.g., here and here).
Yang and her co-authors examined the structure and mechanics of some dead wombats to investigate this question further. They found that varying degrees of pressure in the latter portion of the wombat's intestines (in conjunction with a dehydrating of the fecal matter) led to the characteristic cube shape:
From their abstract:

In the final 8 percent of the intestine, feces changed from a liquid-like state into a solid state composed of separated cubes of length 2 cm. This shape change was due to the azimuthally varying elastic properties of the intestinal wall. By emptying the intestine and inflating it with a long balloon, we found that the local strain varies from 20 percent at the cube's corners to 75 percent at its edges. Thus, the intestine stretches preferentially at the walls to facilitate cube formation.

Why do this?
There seems to be two major reasons:

Mark territory
Attract mates

For example, see Wells 19891:

The rubbing of posts, logs and overhanging branches with their backs and rumps and deposition of faeces along trails may be a means of olfactory communication used in the maintenance of territories

One hypothesis is that by being square, the droppings don't roll as easily and therefore stay in the place that the wombat intended to mark.
I've also seen hypotheses about wombats stacking their square feces as some sort of signaling, but I couldn't find any reputable literature sources that make this suggestion.

1: Wells, R.T., 1989. Vombatidae. Fauna of Australia, 1, pp.755-768.


Carbohydrates- D-Glucose & L-glucose , alpha and beta

They are not the same. Because they are enantiomers, they do not have the same shape. Because they do not have the same shape, enzymes in metabolism that have evolved to use D-glucose cannot work on L-glucose.

L-glucose is not synthesized by organisms because life on earth shares a lineage using the R-enantiomer, so organisms don't encounter it, so there is effectively zero selective pressure to evolve the ability to metabolize L-glucose.

For alpha and beta glucose, see this question on Chemistry.SE; those terms refer to anomer forms of glucose that can interconvert in solution. Given enough time, glucose and similar molecules in solution will form an uneven but consistent ratio of alpha and beta forms.


Why isn't suppression of immune system for organ transplant not as dangerous as AIDS?

Patients receiving immunosuppressive drugs do fall into the same category as patients with HIV-related acquired immunodeficiency - that is, they are all immunocompromised and face similar risks of infection, cancer, etc. The difference emerges over time: when the immunosuppression is controlled and monitored, a patient can retain some immune function, and a physician can help a patient adjust and rapidly respond to opportunistic infections. Drugs can be given in calculated doses; viral infections which disable the body's ability to stop viral infections typically only get worse. To elaborate:

HIV causes immunodeficiency by killing T cells. Firstly, it preferentially infects CD4+ T cells. This process can trigger an inflammatory response and (1) kill the infected T cell, as well as (2) bystander cells. Once the virus has successfully infected a CD4+ T cell, it can happily produce more viruses without killing the cell, which is how the infection can spread - or it can (3) rupture the cell membrane and kill the T cell. Finally, CD8+ T cells can notice that CD4+ T cells are getting infected by a virus and start (4) killing CD4+ T cells.

Immunosuppression after organ transplant can be more specific. It is typically achieved via a combination of drugs which can (1) reduce immune cell activation, (2) slow down immune cell proliferation, or (3) block the activating receptors on T or B cells. The amount and type of suppressants depend on the phase of treatment: induction of immunosuppression, maintenance, or treatment of transplant rejection.1 These drugs are also often administered alongside preventative antimicrobial drugs.

The immunosuppressants which are administered during the maintenance phase - i.e. for the rest of the patient's life - are often the drugs which dampen immune activation instead of eradicating all T cells, and are given at much lower doses. For example, calcineurin inhibitors block the [calcineurin-NFAT pathway];2 when this pathway is blocked, production of immune activators like IL-2 is reduced, and reduces T cell function.

TL;DR: "induced AIDS" is milder and more controlled than actual AIDS, and doctors work very hard to keep patients within a safe range of immune function/suppression.

PS: Good question! Made me think :) I've written some papers on organ transplantation before so am happy to do some digging to add sources.


Water snake with a yellow criss-cross on a black background?

The useful relevant facts are:
Present in freshwater
Active in daytime
Yellow patterning
(photos from wikipedia)
I used the site
www.snakesoftaiwan.com/
This gives most likely candidates of:
Rhabdophis tigrinis subspecies formosanus, the Tiger Keelback.
Grows to 0.6 to 1.0 metres long.

more photos (cannot embed due to copyright) at http://m.blog.sina.com.tw/d100vs/article.php?pbgid=30839&entryid=404413
and
Fowlea piscator  the Checkered Keelback or Asiatic Water Snake. growing 1-2 metres long.

more photos at http://m.blog.sina.com.tw/d100vs/article.php?pbgid=30839&entryid=342476


What is the kind of this wasp killing spider from UK?

Hanging upside-down in a web suggests one of several groups, but in a building structure, and in what appears to be a messy, tangled web, I think we can safely put this one down as a member of the 'cobweb spiders' - the Theridiidae.  This group includes the infamous Black Widows, and some are known to successfully take relatively large and dangerous prey.
So, your particular spider has an obvious clue - the somewhat flattened dark abdomen with a large, light-colored patch in the middle of it.  The shape suggests Steatoda, and there is only one spider that this could be:  Steatoda nobilis, one of several spiders that frequently get called "False Widows".
Here are two links and a representative photo:
https://www.naturespot.org.uk/species/steatoda-nobilis
https://www.cabi.org/isc/datasheet/119917

Oh, I should add that despite the breathless hype the tabloids like to get up to, these spiders are known to be pretty harmless to people.  On rare occasions, a bite (which is not easy to get from these shy spiders) may produce symptoms like a mild Widow bite, but the discomfort seems to pass within a day or so.


Why is there debate about thymus being an endocrine gland?

In my mind as an immunologist, there is no debate. In order to be part of the endocrine system, a body structure needs to be a gland that secretes one or more hormones to induce signaling at distal targets. These hormones can have multiple chemical forms. However, the thymus does not do that. It was proposed beginning back in the 1960s that the thymus contained and produced something called thymosin, which was eventually separated in 40 separate substances, none of which acts as a hormone, and most of which are now known to be present in many other tissues. T cell production and maturation occur as a result of signaling induced by cell-cell interactions (ligands and cognate receptors on the cell surface) as well as the action of many cytokines and chemokines. These compounds are not classified as hormones, though.

It is possible that some hormones might be expressed in the thymus in very small quantities; however they are not secreted. This is due to a part of T cell development and maturation known as negative selection, where the thymus can ectopically express proteins typically only found in other tissues, such as the nervous system, pancreas, or lung, for example. This process allows for the removal of potentially auto-reactive T cells, which recognize self antigen.

Basically, knowing what we do about the function of the thymus in human and mouse, and how it does what it does, I honestly don't see how someone today could classify it as part of the endocrine system, even though histologically it may appear similar to glandular structures, and small traces of one hormone or another may be found in thymic extracts.


Can somebody identify this species of spider?

The white cross on the body makes me think it could well be an Araneus diadematus. It is quite common and not dangerous for humans. It paralyzes its preys using some venom, though.


We are carbon-based because carbon is the only molecule that is able to form the long, long chains of hundreds of molecules that are required to from proteins, DNA, etc. Absolutely no other molecule will do it. (Whatever you may have heard on Star Trek about Silicon-based life, Silicon doesn't form chains anywhere near as long.) Plus it's very handy in that its oxide is carbon dioxide, which is a gas, so using it and oxygen (another gas) as the end-points of respiration is very handy, you can get rid of a lot of gas very quickly. Silicon's oxide is, well, glass.

If you want to know why only carbon forms long chains, it's because of its size (not too large like silicon), its medium electronegativity (it's in a middle column of the periodic table, so it forms what are called "covalent bonds" very easily, especially with hydrogen, the #1 element in the universe by far; covalent bonds are easy to form and easy to break) and its valence (again, because of its position on the periodic table -- it forms four bonds, the maximum for a smallish molecule, giving it the geometry to form long chains).

For life to be based on anything but carbon, it would have to be made only of smaller molecules, which to our knowledge isn't very likely. Our DNA molecule is made up of billions of atoms; it's difficult to conceive how heredity could work on a small scale.


Are there any pre-Holocene venomous animals?

Squamates

Extant venomous snakes do have venomous ancestors. Fry et al. (2006) reported on finding venom toxins more broadly within Reptilia, beyond the well-known venomous snakes and the helodermatid lizards. They show that varanid and iguanid lizards also have venom toxins.

The same group of authors (Fry et al., 2009) then reported on the use of venom in the extant varanid lizard, Varanus komodoensis (Komodo monitor). This is a different hypothesis than the usual "toxic bacteria" hypothesis for predation in these animals. They then reinterpret the skull of the giant (~5.5 m) varanid Varanus (Megalania) priscus. They conclude, based on anatomical similarity and the close phylogenetic relationship between it and V. komodoensis, that V. priscus' predatory mode was more similar to other varanid lizards, likely involving venom delivery.

Archosaurs

Discovery of a venomous clade within squamates, including snakes and several clades of lizards, does not imply venom more broadly within Reptilia. Specifically, it would not parsimoniously reconstruct the presence of venom in Archosauria, the clade that includes dinosaurs. However, Gong et al. (2009) interpret the teeth of the dromaeosaurid theropod dinosaur, Sinornithosaurus as having venom grooves. These grooves are similar to grooves in the teeth of Uatchitodon, a Triassic squamate from Arizona.

There is currently no solid evidence that archosaurs could spit, nor is there ever likely to be.

Mammals

Venomous extant mammals include the platypus (Ornithorhynchus), Solenodon, and some species of shrews. The venom gland in the platypus is a modified sweat gland on the hind limb, which includes an ossified spur. A similar structure has also been found in the basal mammalian taxa Gobiconodon and Zhangheotherium (Hurum et al., 2006). Hurum et al. (2006) described a similar structure in the multituberculates. As the most basal clade of Mammalia, the authors conclude that an ossified spur is apomorphic for Mammalia and that the ancestral mammal may have used it for venom delivery. This structure would have been retained more-or-less unmodified in platypus and lost in other mammalian lineages. The authors' conclusions are supported by the presences of a non-venomous spur in the other clade of monotremes, the echidnas.

Fox and Scott (2005) report that the Palaeocene (~60 Ma) pantolestid Bisonalveus browni also possessed teeth with venom delivery grooves.

Non-gnathostomes

Szaniawski, 2009 used similar logic based on grooved "tooth" elements to conclude that some extinct jawless chordate conodonts may also have been venomous.


Is there any advantage to one blood type over another?

I've been doing a little more digging myself and have found a couple of other advantages:

Risk of Venous-thromboembolism (deep vein thrombosis/pulmonary embolism (1)).  Blood group O individuals are at lower risk of the above conditions due to reduced levels of von Willebrand factor(2) and factor VIII clotting factors.

Cholera Infection Susceptibility & Severity.  Individuals with blood group O are less susceptible to some strains of cholera (O1) but are more likely to suffer severe effects from the disease if infected (3).

E. coli Infection Susceptibility & Severity. A study in Scotland indicated that those with the O blood group showed higher than expected infection rates with E. coli O157 and significantly higher fatality rates (78.5% of fatalities had blood group O).(4)

Peptic Ulcers caused by Heliobacter pylori which can also lead to gastric cancer.  Group O are again more susceptible to strains of H. pylori (5).

Whether blood group antigens are displayed on other body cells or not has been linked to increased or decreased susceptibility to many diseases, notably norrovirus and HIV.  This is fully explained in the article that I was above summarising - "The relationship between blood group and disease" in addition to extended descriptions of the other two answers.


The triangular pattern and the lightly colored underside resemble typical patterns of Bothrops (lancehead viper). Without the head it is quite difficult to tell which species this is. Given the location, the most common lancehead viper would be Bothrops jajaraca, simply called Jararaca by the locals.

Images can be found here


I'm unsure about the use of the word "contagious" here. If you would describe it as an organism "catching something" from another only once, this answer applies (vaguely perhaps).

One example of "contagious" sperm: sea urchins spray their sperm (called milt) into the surrounding water, so that it can hopefully fertilize roe, which are fish eggs. The eggs are also expulsed for some species, but for others they stay on the surface of the female sea urchin, as this Wikipedia article explains.

  The gonads are lined with muscles underneath the peritoneum, and these allow the animal to squeeze its gametes through the duct and into the surrounding sea water where fertilization takes place.
  ...

  In most cases, the eggs float freely in the sea, but some species hold onto them with their spines, affording them a greater degree of protection.

Thus, it's entirely possible for a female sea urchin to be bombarded by free-floating sperm, to ultimately fertilize the eggs on its surface. I don't know if one would strictly consider this a contagion, but it's what I initially thought of after reading the question.

When referring to sexually transmitted disease however, sperm in itself is not contagious, as it would require the pathogen to "tag along with it" in whichever environment (whether it be airborne or aquatic). Also, if considering impregnation as "contagious", physical contact would certainly be required.

In short: For humans, no. For sea urchins (and likely other aquatic animals), sort of.


What evolutionary reason is there for having the urinary duct and reproductive organs so close together?

The reason lies within our wormy chordate ancestors - an orifice used to eliminate waste can also function as an orifice to eject eggs. My vertebrate zoology is a little bit rusty so I would suggest picking up any first-course book on the subject, most of them cover the evolution of urinary/reproductive organs extensively.


What is the role of glycine in the running buffer for SDS-polyacrylamide gel electrophoresis

The pH of stacking and resolving gel are set in such a way that one is above and one is below the pI of gly (5.97).Therefore, Gly has two different charges in stacking and resolving gel. That is in stacking gel gly has no charge (which will allow the protein to stack according to size in this part of the gel rather than separating because of presence of gly in between the protein molecules, constraint in separation of proteins) but in resolving gel charge is negative since the pH is higher (constraint in movement of proteins no longer present so separation of protein based on size possible).

Hope this was helpful..


How do cells age and die if they are dividing into new cells?

Human chromosomes contain certain DNA regions called telomeres. These regions are shortened on each cell division and once they are gone, the cell cannot divide. Therefore an average cell in our body can divide only about 50 times.

There are indications that longer telomeres may increase lifespan, however this remains controversial. Telomeres are believed to be a method of higher organisms to prevent uncontrolled cell division and cancer, therefore artificially increasing telomere length may not lengthen but shorten lifespan because of increased cancer risks.

Also, ageing is not (only) caused by individual cells growing old. Often it is the organization between the cells that breaks down. Scarring is a good example for this. The wound is closed but the tissue inside the wound was not able to organize into functional skin tissue again but rather "patched up" the wound with comparatively unorganized tissue.

The brain is another extreme example of ageing by disorganization. It has been shown that even adult brains contain neuron progenitor cells (albeit fewer than other tissues) so even adults can regrow neurons in the brain. However, while the cell body of the neuron can be replaced, all its (sometimes thousands) of connections to other neurons are lost. Therefore, brain tissue can be regenerated in principle, but the information it contained cannot.


This strange looking thing was on the leaf, can you identify what this is?

That is a butterfly chrysalis. Since it is clear, and you can see the wings, it is about to emerge. A chrysalis is the naked pupal stage of a butterfly, as opposed to a "cocoon", which is covered in silk.


Are there any DNA sequences shared by all/most Viruses?

No, virus are polyphyletic and there are no genes that are common to all viruses. There may be similarities in capsid structure due to convergent evolution, but these are not universal. See Moreira and López-García (2009) for further detail.


What is this insect? 6 legs and black spots

(Note: I'm going to be using the British English "ladybird" instead of the US English "ladybug" in this answer.)

This is a clearly a species of ladybird. Going by the number of spots, their size and not-perfectly-round shape, the positioning of the four central spots relative to the others, and the fact that its background colour isn't bright yellow... I'm pretty sure it's Harmonia axyridis, the species that us Brits refer to as a "Harlequin ladybird". I think Americans refer to it as an "Asian ladybug" or "Asian ladybeetle".

The spot patterns for this particular species vary a lot, as to some extent do the colours, so I've googled for images to support this answer. The below picture was posted to:

https://en.wikipedia.org/wiki/File:Harmonia_axyridis01.jpg

and is the IP of a user or organisation called Entomart. On the Wikipedia page and on their homepage, Entomart grant permission for the use of the image as long as they are given proper attribution, so I'm able to include it in this answer:

For more pictures of the Harlequin (again, showing how much the spot pattern and colouration vary), see:

https://scx2.b-cdn.net/gfx/news/hires/2018/amechanismof.jpg

For pictures of other ladybird species to compare the Harlequin with - as also one more of the Harlequin:

https://www.naturespot.org.uk/taxonomy/term/19357

Thanks for posting this question! I didn't expect to see a ladybird on Christmas Day :-)


It is a black-collared starling (Gracupica nigricollis).

According to the title of this other video, which is the same footage uploaded by another user and could be the original one, it has been recorded in Thailand, where the black-collared starling is common.

Also, from the same Wikipedia page:

  In Thailand the collared starling is sometimes kept in captivity and taught to speak.


base on a article they do the test of nano-Pt, kind of SOD, and they do the experiment in several steps, first choose C. elegans strains and growth conditions, meanwhile prepare the nano-pt. then, do the lifespan assay. thired is Oxidative stress resistance. the last step is Fluorescence microscopy. in the mictoscopy they do several steps, include Measurement of lipofuscin accumulation, Detection of ROS, Measurement of SOD/catalase activit, Thermotolerance and Effects of dietary restriction


Difference between PCR for linear template and a plasmid?

There's not much difference between them. The same enzyme and condition can be used whether the template is circular or linear.

You can amplify plasmids, but PCR intrinsically generates linear DNA fragments even if you use circular DNAs.


What happens to the food you accidentally aspire?

People can drown because of aspired food. If they don't then it can cause diseases, for example pneumonia. In extreme cases a tree can grow in the lungs. There are other aspiration/inhalation related diseases like silicosis or asbestos lung cancer. So it depends on the composition of the object (or liquid or powder) and other factors whether it causes a disease or not. I did not find anything about what exactly happens with these objects in the lungs. Probably the lung tries to get rid of them mechanically, if there is no success in that, then they cause a local inflammation, which can lead to diseases if it becomes chronic and/or the object contains pathogens.

  Common presenting symptoms (information available in 36 cases)
  included dyspnea (14), fever (9), and cough (6). A history of
  recurrent pneumonia was present in 9.

2007 - Pulmonary Disease due to Aspiration of Food and Other Particulate Matter: A Clinicopathologic Study of 59 Cases Diagnosed on Biopsy or Resection Specimens

  The annual overall inpatient cost associated with pediatric bronchial
  foreign-body aspiration is approximately $12.8 million. Combined, the
  rate of death or anoxic brain injury associated with pediatric foreign
  body is approximately 4%.

2014 - The national cost burden of bronchial foreign body aspiration in children

  Gastric aspiration is a high-risk condition for lung injury.
  Consequences range from subclinical pneumonitis to respiratory
  failure, with fibrosis development in some patients. Little is known
  about how the lung repairs aspiration-induced injury.

2015 -Resolution of Lung Injury after a Single Event of Aspiration : A Model of Bilateral Instillation of Whole Gastric Fluid

  Aspiration is a common but underrecognized clinicopathologic entity,
  with varied radiographic manifestations. Aspiration represents a
  spectrum of diseases, including diffuse aspiration bronchiolitis,
  aspiration pneumonitis, airway obstruction by foreign body, exogenous
  lipoid pneumonia, interstitial fibrosis, and aspiration pneumonia with
  or without lung abscess formation. Many patients who aspirate do not
  present with disease, suggesting that pathophysiology is related to a
  variety of factors, including decreased levels of consciousness,
  dysphagia, impaired mucociliary clearance, composition of aspirate,
  and impaired host defenses.

2014 - Aspiration-Related Lung Diseases
2012 - Aspiration and Infection in the Elderly
2015 - Pediatric foreign body aspiration: A nidus for Aspergillus colonization
2012 - All that wheezes is not asthma: a 6-year-old with foreign body aspiration and no suggestive history


Why do death cap mushrooms not warn of their poison?

Most of this type of evolutionary question are generally worthless, IMHO. You can rationalize anything post hoc and then go away with the misapprehension that you have been involved in science.

To add a few of those possible post hoc explanations (which took longer to type  out than think up):

1) The poison is only accidentally a poison.  It serves some other function in the mushroom's metabolism.  There are numerous possible examples of this.  For instance, the stalks of rhubarb are edible, while the leaves are poison; potatos are edible unless they've turned green from exposure to sunlight...

2) The poison might not be directed at humans.  The mushroom might have some warning that would be obvious to other species, for instance a smell or markings visible in UV (such as many flowers have).  We have lots of examples of poisonous plants that we grow because they're attractive to us: datura, lily of the valley, foxglove, oleander, delphinium...

3) If I'm not mistaken, mushroom poisoning takes rather a long time to kill, which argues against it being a defense.  The poison might have evolved as an aid to reproduction.  Mushrooms are the fruiting body of the fungus.  If an animal eats it, it consumes the spores.  If it dies hours or days later, it has transported those spores to a distant location, and the corpse provides nutrition for the new fungi.

However…

Doesn’t the all-white toadstool look distinctive and memorable to you? It doesn’t look remotely like the field mushrooms or other edible mushrooms I would collect. What edible fungus would you confuse it with?


What is this species of angiosperm from Morocco?

Look into the Symphytum genus, or related genera within Boraginaceae (the forget-me-not family). It is loosely similar to Symphytum officinale, but clearly not that species. The overall layout, size, leaves and hairyness of the stalks is similar to species in Symphytum.

Here is Symphytum officinale, as an example of the overall appearance:

Also similar from the Anchusa genus in the same family (Anchusa azurea):


In the vacuum of space would death be instantaneous?

Nope, you wouldn't die instantly. While explosive decompression has never been tested on humans (for obvious reasons), the dangers of a vacuum have mostly to do with the pressure differential between your body and the now pressure-less void around you. The most fragile parts of the biological system would be the lungs and ears, and the instantaneous transportation would cause a severe case of the Bends if you were rescued quickly enough. You would pass out within a few seconds stated by NASA when an experiment went awry, and death might be from lack of oxygen to the brain, although after a few minutes everything bad starts to happen so nobody really knows what you would die of:

  At NASA's Manned Spacecraft Center (now renamed Johnson Space Center) we had a test subject accidentally exposed to a near vacuum (less than 1 psi) in an incident involving a leaking space suit in a vacuum chamber back in '65. He remained conscious for about 14 seconds, which is about the time it takes for O2 deprived blood to go from the lungs to the brain. The suit probably did not reach a hard vacuum, and we began repressurizing the chamber within 15 seconds. The subject regained consciousness at around 15,000 feet equivalent altitude. The subject later reported that he could feel and hear the air leaking out, and his last conscious memory was of the water on his tongue beginning to boil.


How did the orchids evolve to support pseudocopulation when they do not have any organ for vision to see how insects look like?

Evolution does not work based on an organism (or designer) "seeing" a problem and seeking a solution. Evolution via natural selection works when members of a population that have a certain heritable trait are better at reproducing than other members of that population. Because they are better at reproducing, subsequent generations of the population have a greater percentage of individuals that have that heritable trait, and the process continues, sometimes to the extent that all the individuals of that species have that trait (this is called "fixation").

The way something like this would evolve is that some predecessor to modern orchids has some morphology or chemical secretion that was particularly attractive to insects. This increased the ability of that predecessor to reproduce. Over generations, any other random mutations that further promoted attraction of insects also were selected for, until they accumulated all of the adaptations we see in a modern orchid.

Today, we can study that process and realize post facto that "Oh, these adaptations worked because they tricked the insects into thinking they were copulating, when really they were just dispersing pollen."

However, the flower never needed any knowledge of insect copulation, it just happened that flowers that had those traits did better at propagating their genes to the next generation.

These types of questions are more easily understood with a broad understanding of evolution. One great resource is Understanding Evolution from Berkeley.


How is NAD+ used in lactic acid fermentation after it is oxidized from NADH?

Anaerobic Glycolysis

As this question refers to glycolysis in the context of lactic acid fermentation it clearly relates to anaerobic glycolysis, which is why I added that to the question.

I believe it is correct to regard the primary purpose of anaerobic glycolysis as being to generate ATP for the anaerobic organism or tissue.

To understand the roles of NAD and lactate in this process you need to consider the chemistry. The conversion of glucose to pyruvate is an oxidative process, with the oxidizing agent being NAD+, which itself is reduced to NADH. For glycolysis to continue the NADH must be reoxidized to regenerate NAD+. This is the primary purpose of the reduction of pyruvate to lactate and is summarized in my own diagram, below.

So, the answers to your (paraphrased) questions “what are NAD and lactic acid needed for?” and “are they waste products?” are:

NADH isn’t needed for anything — it’s the consequence of the oxidative function of NAD+. No, it is not a waste product — it has to be reoxidized otherwise glycolysis would stop for lack of oxidising power.
Lactate also is not needed for anything, as evidenced by the fact that other reduced products of pyruvate are produced in different organisms, most notably ethanol in yeasts. Ethanol can certainly be regarded as a waste product, although the carbon skeleton of lactate is salvaged in multicellular oxygen-breathing organisms.

The so-called cycle of Cori & Cori

In my opinion it is best to approach glycolysis as I have done above, without reference to the tissue or organism, so as to understand the essential features of the process.

In the specific case of mammals, some tissues perform glycolysis anaerobically, e.g. the red blood cell (which lacks mitochondria) or rapidly excercising muscle (where the blood supply and number of mitochondria are not sufficient to generate ATP for muscle contraction. The liver, in contrast, has a plentiful supply of oxygen and hence NAD+, and so can reoxidize lactate to pyruvate if the former is transported in the blood from the anaerobic tissue to the liver, salvaging the carbon skeleton.

Under conditions of low blood sugar (e.g. starvation) it is important that the pyruvate be reconverted into glucose in the liver by gluconeogenesis, rather than be converted to other products, and the glucose is released into the blood. In this case one goes full circle, this process is generally referred to as the Cori Cycle. I always avoided this term myself in teaching students as I found it caused confusion with cycles such as the tricarboxylic acid cycle and the urea cycle, where all the chemical interconversions take place in the same tissue.

Footnote: Glycolysis under aerobic conditions

Under aerobic conditions (e.g. in the liver after a carbohydrate meal) the purpose of glycolysis is not primarily to generate energy but to utilize the glucose, storing it as fat (after glycogen capacity is reached) or using it to synthesize intermediates. There are different fates for the pyruvate (acetyl-CoA is shown), but lactate is not one of them as the NADH can be reoxidized far more efficiently in the mitochondria, with molecular oxygen being the ultimate oxidizing agent.

Text References

Berg et al. Section. 16.1 covers glycolysis in great detail under aerobic conditions. The lactic dehydrogenase reaction is given little emphasis, but can be found in section 16.1.9.


It would be better to say that they go into an inactive, low metabolic state. This low metabolic state is often driven by the temperature in the air itself; ectothermic butterflies require outside heat-energy to become active. Basically they use this time to digest their food and produce sperm/eggs. (reference). At night, or during inclement weather, most butterflies perch on the underside of a leaf (this provides them with a bit of shelter from the rain and makes them less noticeable to prey), crawl deep between blades of grass or into a crevice in rocks, or find some other shelter to rest (reference).  In short, I would not call it sleeping but just a state of rest. Butterflies cant even close their eyes from the lack of eyelids (reference).


properties of lamps for indoor plant growth

I am not a biologist, but I have read up on this a little bit. I recommend that you do a bit of research online at your library or online because it can get somewhat technical. There are several variables to consider. You are correct that the bulbs emit different colors of light. Plants species may have different needs for different colors during their growth stage & their flowering /fruiting stage. You should investigate what your plant needs. The amount of the light emitted by the bulb is measured in a unit called lumens- this is usually on the package. More lumens= brighter light. For indoor hydroponic, there are expensive lighting systems using a variety of bulbs & lamps, like fluorescent, halide & sodium, each with specific uses & (dis)advantages. One recent development are LED grow lamps. The LED's advantage is that instead of having 1 large heavy & hot light bulb like with a halide or sodium lamp, you have many little LED light that can come in different colors, allowing flexibility in different life stages. The LED lamps also consume much less electricity & don't create a lot of heat- but they are more expensive. OK, good luck with your project. Also, if you like hydroponics, learn about aquaponics, an offshoot of hydroponics that incorporates an aquarium into the system. The water flowing through the plant's roots circulates down into the aquarium and back up again, so that the fish poop helps to nourish the plants and the plants' roots act as a filter for the aquarium water, creating a type of symbiotic ecosystem between the plants & fish.


See papers by D Bianchi for reports of miR levels in blood of pregnant humans, both of maternal and fetal origin.

A review by Steer and Subramanian offers a number of examples pertaining to your question.

Lastly, Vickers, Palmisano, et al. (2011) show that some miRs are present in the HDL-cholesterol particle and that those levels differ between normal and familial hypercholesterolemia human subjects.


Techniques to show a protein heterodimer-DNA interaction

How will you check that fra1 is expressed or not in these cells.

RT-PCR is a quick and an easy method to check for expression. However, it only tells you about the RNA level expression and you would have to work with the assumption that RNA concentration is directly proportional to protein concentration.

Considering that you do not have an antibody for fra1, you can go for mass-spectrometric protein quantification. It is good for a high throughput analysis and is generally wasteful when you just want to study one protein. However, people do carry out targeted proteomics to study a few proteins.

Alternatively, with some effort you can actually develop an antibody for fra1.

  How will you check that the heterodimer bound to the given DNA
  contains fra-1 along with c-jun.

Showing ternary complexes (fra-jun-DNA) are a bit difficult. It is relatively simple to show pairs. You can show that two proteins form a complex in vivo by doing a co-immunoprecipitation followed by detection by either western blot or mass-spectrometry.

You can also show interaction by biophysical techniques involving FRET and SPR but these cannot be performed in vivo (at least SPR. FRET can be done but there are limitations).

You can show the DNA-protein interaction by ChIP-seq as you mentioned in your question.

Showing all the three together is a bit tricky.

You can do it using in vitro assays that employ fluorescently labelled (one GFP and other RFP; or FRET pairs)/custom epitope tagged (for e.g. one FLAG and the other HA -tagged) proteins and a known DNA sequence generated by PCR/DNA synthesis. You can use EMSA along with antibody/fluorescence based detection to show the ternary complex.

You can indirectly infer the presence of the ternary complex when the ChIP-seq using antibodies for both the proteins shows up the same DNA sequence in the reads. You can also express a FLAG-tagged (or any other tag) protein, if in case you do not have an antibody for the proteins.


What is the basis for the determining sex from position of adult pelvis?

"Position of the pelvis" is pretty vague, but there are very clear differences in pelvic morphology between females and males. This sexual dimorphism looks like:

Female pelves are wider and flatter, which I think you could tell from surface anatomy. Of course if you could palpate, then you could tell for sure.


How many protons are pumped out per pair of electrons from NADH in oxidative phosphorylation?

It seems like the mistake is in complex III. Look at this image from here:

It clearly shows the number of protons reduced in (and taken from) matrix and number of protons pumped into inter-membrane space. So the data becomes:

Complex I:

matrix: 2H+ reduced (from NADH + H+) + 2H+ pumped out

IMS: 4H+ pumped in

Complex II:

matrix: 2H+ reduced (from succinate)

IMS: 0H+ pumped in

Complex III:

matrix: 2H+ pumped out (when not considering complex II, you'd count 4H+ here)

IMS: 4H+ pumped in (2 from complex II)

Complex IV:

matrix: 2H+ reduced (to H2O, we won't consider it as you said) + 2H+ pumped out

IMS: 2H+ pumped in

TOTAL:

matrix: 10H+ subtracted/pumped out (with 2H+ to water, total 12H+)

IMS: 10H+ pumped in

This satisfies your statement that "10 protons are supposed to get pumped out during the electron cycle". I Hope this helps ;)

IMS = inter-membrane space


In population genetics, with a simple one-locus two-allele model, we consider the frequency of the two alleles to be $p$ and $q$ where $p + q = 1$ (and thus $1-p=q$ and $1-q=p$). When an allele is recessive it is only expressed at the phenotypic level when the individual carries two copies of the allele.

Following from your example, gene $A$ might be responsible for hair colour, with alleles $A_1$ and $A_2$ where $A_2$ is a recessive allele responsible for purple hair. I will denote the frequency of $A_1$ with $p$ and frequency $A_2$ with $q$. This means that the frequency of individuals with purple  hair ($f_{A_2A_2}$) is $q^2$ and the frequency of people with not-purple hair is $p^2 + 2pq$ (assuming an idealised population). As such, a population of 500 diploid individuals* where there is 100 copies of the $A_2$ allele would have the following genotypic (& phenotypic) frequencies:

$$f_{A_1 A_1} = p^2 = 0.9^2 = 0.81$$
$$f_{A_1 A_2} = 2pq = 2 \times 0.9 \times 0.1 = 0.18$$
$$f_{A_2 A_2} = q^2 = 0.1^2 = 0.01$$

So the allele for purple hair would be present in 19% of the population, but the trait would only manifest in 1% (only ~5.3%, $\frac{1}{19}$, of the people that carry the purple hair allele exhibit the trait). Therefore selection would be quite inefficient at removing this allele from the population, even if you could prevent all purple-haired individuals from reproducing. To find the frequency of $q$ required to give a genotypic/phenotypic frequency where 1 in $x$ individuals have purple hair just take the square root of $1/x$. E.g. to get 1 in 1000 individuals expressing purple hair

$$q = \sqrt{q^2} = \sqrt{(1/1000)}$$

What does this mean for evolution? Alleles that are recessive deleterious are very hard to remove from the population because, at low frequencies, they rarely produce the detrimental effect. Assuming complete dominance ($A_1 A_2$ = exactly like $A_1 A_1$), denoted by $h = 0$, selection only acts on $A_2 A_2$ homozygotes. The frequency of the $A_1$ allele increases at the rate $1/(1-sq)$ where $s$ is the relative fitness advantage. Mutation can also introduce more copies of the $A_2$ allele to the population such that there will be an equilibrium, balanced by the rate of loss due to selection, and rate of gain by mutation. Furthermore, to further build on your analogy, a neighbouring population, where purple-hair is not selected against, may bring copies of the allele in by migration.

Suggested further reading on evolution here and reading on eugenics would likely be of interest to you.

* 500 diploid individuals = 1000 gene copies. Thus $q = 100/(500 \times 2) = 0.1$


Yes, that is a pillbug, or "roly-poly", Subphylum, Crustacea, class Malacostraca, family Armadillidiidae.  https://en.wikipedia.org/wiki/Armadillidiidae


How is the carrying capacity of a logistic growth model calculated?

@Remi.b is correct that you haven't given us very much information, but I think we can reconstruct what's going on. Suppose the population growth rate is written out as

$$
\frac{dN}{dt} = N ( b - \delta - \gamma N)
$$

then the equilibrium (carrying capacity) occurs when $N>0$ and $dN/dt=0$, i.e. $b - \delta - \gamma K = 0$.  Solving this for $K$ gives $(b-\delta)/\gamma$ (as you stated).

So what is $\gamma$?  It is the decrease in the per capita growth rate per unit of increase in population density, or more biologically speaking it's the decrease in the birth rate or the increase in the death rate per unit of increase in population density. This could be due to increased competition for resources, or decreased environmental quality, or attraction of predators, or ...

Another, vaguer way to say this would be to call it the "effect of density-dependence".

Given the equations you list in the comments, with a $-\gamma N$ term included in the per capita growth rate for each compartment ($S$, $E$, $I$), we can say more specifically that $\gamma$ determines the rate of density-dependent increase in the ("natural" or disease-independent) death rate per unit population density. This parameter would not typically be broken down into lower-level processes.


Could biofilms float and survive in the sulfuric acid clouds of Venus?

I have pondered life on Venus.  I think the biggest problem would be lack of free water.  The atmosphere is thick and under high pressure, and polar CO2 and H2SO4 like to bind with water.  There is no water there.  Mass action would pull water out of any concentration of water (like a Nostoc blob) and into the waterless density of the adjacent atmosphere.  It would be like putting a Nostoc in a tub of salt grains.

Dessication would be the biggest problem.  The other problem related to lack of water is its requirement for photosynthesis.  If you had a photosynthetic organism there would be CO2 in abundance, but green algae type  photosynthesis also requires water as a raw material:  CO2+H2O+ light -> O2 + CHO (carbohydrate).  If you have only the water you brought with to Venus, with no prospects of replenishing it, you will run out quick.

You would need an organism that is not only durable, but had the metabolic chops to either pry H2O off of H2SO4 or use sulfur as its reducing agent instead of water.  Purple sulfur bacteria can do sulfur chemistry like this but they like starting with reduced sulfur, not H2SO4.  Purple sulfur bacteria need water as a solvent inside the cells just like we do.  But maybe something that can handle H2SO4 can make water out of it also?


Why severely increased Ligand (eg Hormones) concentration downregulates the Receptor?

Gonadotropins are hormones synthesized and released by the anterior pituitary gland, which act on the testes and ovaries to increase the production of sex hormones and stimulate production of either sperm or ova.
The hypothalamus contains Gonadotropin-releasing hormone (GnRH). Intermittent released of GnRH is responsible for the biosynthesis and secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland.
LH stimulates interstitial cells to release testosterone, which triggers spermatogenesis. The rising level of testosterone exerts negative feedback control on the hypothalamus and pituitary glands.
GnRH has been shown here in a negative feedback loop
This feedback loop has great interplay with the number receptor levels as you suggest.
(From a quick search) I found one paper (behind a paywall) that states the following information when studying rats:

We observed an acute reduction of both GnRH and GnRH-R mRNAs 24 h after the injection [of GnRH agonist (triptorelin)] (about 38% of control).

Transcription does not equal translation, but it seems that acute increased levels of GnRH cause a reduction and mRNA of GnRH and GnRH-R and therefore potential reduction (down-regulation) of protein levels of GnRH-R.


Okay, theoretically possible, but only in theory.  Practically, it's totally impossible.  Let's start by defining why it would theoretically be possible.
Theoretically, there are only so many possible arrangements of proteins in the face, which would represent a limited number of possible facial appearances.  However, as you probably guessed, there are zillions of proteins being expressed in each body organ, such as an eye.  So just from the perspective of the number of different possibilities, it would be impossible.
One might think that since the facial features are controlled by genetic variation, eventually these features will begin to repeat themselves, but such is not the case, for two reasons:

There are way to many genes - and alleles - that control facial features.  We're talking thousands if not millions.  When you raise that number of alleles to each others' powers, you start to see the impossibility of repeating the exact same combination, especially since every new generation is introducing new alleles from a new blood line.

Genetic code is not the only thing that changes how you look.  A whole branch of genetics, epigenetics, is devoted to the changes of gene expression unrelated to DNA sequence.  The expression can be changed by environmental factors, even as early as when the embryo is forming the placenta.  This is why identical twins (who have identical DNA) do not actually look exactly the same, or even have identical fingerprints.

Bottom line, totally impossible.

Sources:

Face shape is in the genes, PLOS, 2016
Epigenetics, Wikapedia, 2017
Why do identical twins have physical differences?, Anonymous, 2005
Introduction to epigenetics, University of Leicester, 2013
How many Proteins exist in human body?, Innovateus, 2013


Does chromosomal crossover result in a mutation?

There are many different ways a DNA sequence can change. Labeling a change as a mutation implies that there was a biological process in which DNA was damaged then not properly repaired.

Crossing over during the formation of gametes does not result in a mutation.
Crossing over during repair of a double stranded DNA break does result in a mutation.


How to find sequencing data of a specific drosophila strain

As described in File S1 of Gutzwiller et al (2015) the relationship between the sub-strain of the ISO1 reference strain used by BDGP for the original Drosophila genome proejct, and the sub-strain in the Bloomington Drosophila Stock Center is complicated:

  "We investigated the cause of the discrepancy of Wolbachia sequences in the Berkeley Drosophila Genome Project (BDGP) and Bloomington Drosophila Stock Center (BDSC) ISO1 genomic data by first establishing the provenance of these lineages. As documented in the BDSC database, the BDSC ISO1 sub-strain was donated directly to the stock center by Jim Kenni- son in 1994. The ISO1 sub-strain used by the BDGP was obtained from Gerry Rubin’s lab in the late 1990’s (Roger Hoskins, personal communication). The Rubin lab ISO1 sub-strain was obtained in the mid-1990s from Jim Kennison via at least one intermediate lab (Todd Laverty, personal communication). Thus, in contrast to naive assumptions, the ISO1 sub-strain at the Bloomington Drosophila Stock Center is neither a direct descendant nor progenitor of the ISO1 sub-strain used in the D. melanogaster genome project, and these two sub-strains have had independent trajectories since at least 1994."

The PacBio dataset you refer to was generated using the BDGP sub-strain. The Illumina data you refer to was generated using the BDSC sub-strain and is available here: https://www.ncbi.nlm.nih.gov/sra/ERX645969[accn]


What are these two insects (or at least one of them)?

I the first insect is a cricket, female Fall Field Cricket,Gryllus pennsylvanicus.

It is widespread across much of North America.They are  often found around areas of human habitation.
The the coloration ranges from dark black to dark brown, although some specimens show a slight reddish tint. The black antennae tend to be longer than the body span of the species.

It is a female because it has a long blackish brown ovipositor.

References:

Wikipedia

pbase.com

bugguide


Why can bacteria resist topical antibiotics, but not compounds like Benzoyl Peroxide?

Antibiotics ARE compounds, and they kill or inhibit the growth of bacteria by specific mechanisms. Each class of antibiotics has specific mechanism of actions. Given enough exposure to these antibiotics compounds, bacteria can develop specific molecular mechanism to nullify their effect, and hence antibiotics resistance. Antibiotics resistance will eventually develop with enough exposure to drive the organism's evolution . Whereas there are combination therapy, there are multi-drug resistance; whereas there are wonder drug, there are super bug.

General disinfectant compounds such as benzoyl peroxide or sodium dodecyl sulfate (in soap and detergent) have no specific molecular target that would differentiate host and intruders and hence can harm bacteria as much as the host cells. They are safe to use only because you have skin to prevent their intake. Since there is no molecular target to mutate to develop resistance, the resistance to general disinfectant will simply take a very long time.

That is to say, who could ensure bacteria cannot develop resistance to benzoyl peroxide? Resistance to phenyl derivative has long been reported [1], and bacterial catalase can easily break down the damaging effect of peroxide.

[1] Heinz Berger and Orville Wyss. J of Bacteriology (1953) vol. 65 p.103


Number of autoregulation and FFL motifs in a network

The average number of auto-regulatory motifs (self-edges), is equal to the number of edges E times the probability that an edge is a self-edge which is $p_{self}=1/N$, with N being the total number of nodes. Therefore, $<N_{self}>_{rand} \approx E/N$
& 3. According to U.Alon's book ("Introduction to Systems Biology"), the mean number of times that a subgraph G occurs in a random network is given by the following formula: $<N_G>\approx a^{-1}N^n p^g$.

Explaining what each term of the formula means:

α: is a number that includes combinatorial factors related to the structure and symmetry of each subgraph, equal to 1 for feed-forward loop (FFL) and equal to 3 for feed-back loop (FBL)
$N^n$: is the number of ways of choosing a set of n nodes out of N. Because there are N ways of choosing the first one, times N-1$\approx$N ways of choosing the second one, and so on..(this approximation is true for large networks)
$p^g$ : is the probability to get the g edges in the appropriate places (each with probability p)


Parakeets are social animals that live in large groups (flocks). Under ideal environmental conditions, they can form flocks composed of thousands of birds. http://www.softschools.com/facts/animals/parakeet_facts/1274/

The fact that this tree is without leaves is irrelevant to the Parakeets. They may or may not have caused it. They chose the tree as a place to relax. It could have been any other convenient place though. If you search google images for "parakeet flock" you will see them perching on various other surfaces in a similar manner


Determining potential protease sites within a recombinant protein

LC-MS is certainly quantitative and will give you a definitive answer, but it is costly and requires access to such a machine.

I presume you're analyzing your protein based on western blotting.

The first thing you should always do is verify your DNA sequence is coding for the protein product you want. Once you're sure of this, the western blot will give you an indication as to where your protein is (approximately) being cleaved. Say you protein has a predicted size of 40 kDa and you see a band at 20 kDa, then your cleavage is somewhere in the middle of your sequence. There are a TON of proteases that could be potentially cleaving your peptide and you need to have a hypothesis as to what that could be. Your peptide could be cleaved by an endopeptidase (cutting within), or a carboxypeptidase (C-terminal cleavage) or an aminopeptidase (N-termainal cleavage). To go back to the 20/40 kDa example, it could be your peptide was cleaved N-terminally o C-terminally down to a size of 20 kDa, or that it was literally cleaved in the middle by an endopeptidase.

Something you may consider is the use of a general protease inhibitor cocktail (Roche makes a really good tablet product called Complete and Complete mini tab). These mixes have a bunch of general protease inhibitors which will stop most cleavage events. If you still see cleavage after using an inhibitor cocktail, you can reasonably expect that you are not inhibiting the protease with the tablet (thus narrowing down your search) and then you can better comb through Expasy's PepCutter data. You should also do a literature search to see what has been reported about your peptide or motif.


Do Angiotensin II Receptor Blockers (ARBs) or other factors control the level of ACE2 expression? [coronavirus receptor]

I should follow up with some things I've found.  As a starting point, the normal expression pattern is available at https://onlinelibrary.wiley.com/doi/pdf/10.1002/path.1570 - note the staining of simple squamous epithelium in the alveoli and the endothelia of blood vessels.  Another paper details a sharp decrease in expression with age in rats, but I don't know if that extends to humans.

For regulation of expression, I was surprised to see that Google Scholar actually provides a very good assortment of search results, easier to work with than PubMed, which were topped by the MI regulation I described in the question.  Additionally https://onlinelibrary.wiley.com/doi/abs/10.1002/path.1670 (yes, that IS a different link) describes ACE2 expression in renal disease but not in normal kidney.  ACE2 expression correlated with proteinuria, but negatively with GFR. https://link.springer.com/article/10.1007/s00125-008-0988-x  There are discordant notes in some other situations: for example, subtotal nephrectomy decreased ACE2 expression in a way that was partially prevented by ramipril. https://portlandpress.com/clinsci/article/118/4/269/68827/Reduction-in-renal-ACE2-expression-in-subtotal

The mRNA and protein are both described in atherosclerotic lesions: https://onlinelibrary.wiley.com/doi/abs/10.1002/path.2357

In the lungs https://jvi.asm.org/content/79/23/14614.short describes a positive correlation with differentiation state in airway epithelium.  The regulation by HIF-1 alpha in hypoxia seems of special importance: https://journals.physiology.org/doi/full/10.1152/ajplung.90415.2008 but it is complicated (both positive and negative).

ACE2 is also expressed at high levels in placenta during pregnancy - at least in rats. https://journals.physiology.org/doi/full/10.1152/ajpregu.90592.2008

Last but not least, pharmacologic data is reviewed at https://link.springer.com/content/pdf/10.1007/s11906-008-0076-0.pdf which describes up-regulation of ACE2 by angiotensin II receptor blockers, ACE blockers, and mineralocorticoid receptor blockers.  This includes the common drugs lisinopril and losartan.  (see also https://onlinelibrary.wiley.com/doi/full/10.1111/jcmm.12573 ) Unfortunately the paper did not report substances inhibiting ACE2 expression.  But https://journals.physiology.org/doi/full/10.1152/ajpheart.00239.2008 reported that high glucose (!) or PKC inhibitors could reduce ACE2 expression.  (but the high glucose was causing kidney injury, which as described above could mean more ACE2...)  The anti-diabetes drug liraglutide increased ACE2: https://academic.oup.com/endo/article/156/10/3559/2422879  To top it all off?  SARS itself decreases ACE2 expression, and this might be part of the process injuring the lungs: https://www.nature.com/articles/nm1267

This is by no means a complete survey, and there is much I don't understand.  The relationship between ACE2 biology and the emerging COVID-19 risk groups seems apparent - as is the urgent need for research to determine which manipulations to ACE2 expression have positive versus negative effects on the prognosis of that disease.

Update: a NEJM podcast today described this biology as 'complicated' link.  It is clearly of interest, but still under investigation.  For example, losartan is presently the subject of two clinical studies news, presumably these ClinicalTrials


What are the differences between carnitine forms?

Carnitine tartrate is a salt between carnitine (cation) and tartrate (the conjugate base of tartaric acid, anion). So in this case, tartaric acid is not covalently bound to carnitine.

The salt formulation is a little tricky, because carnitine is itself a zwitterion at physiological pH (it has both a positive and negative charge) and so is overall uncharged in pure form. I think the tartrate salt is formed because tartaric acid is more acidic (first pKa = 2.89) than the carboxyl group of carnitine (pKa = 4.09), which leads carnitine to become protonated and therefore +1 charged in a concentrated mixture. The formulation sold by Lonza (which seems to be a major provider) appears to be a ratio of 2 cartinine (68%) to 1 tartrate (32%), which would indicate that tartrate acts as a -2 anion in this mixture (this is a bit surprising as the second pKa of tartaric acid has pKa = 4.40, but maybe I'm missing something).

You can recognize that this is a salt from the naming: the form tartrate indicate a conjugate base of an acid (as in lactate, acetate), and when used in a two-component name like carnitine tartrate (or, sodium acetate) refers to a salt. On the other hand, a carboxylic acid covalently bound to another group is given the suffix -yl, so tartryl carnitine would indicate tartaric acid bound to carnitine, as in fatty acid oxidation.


What is the meaning of Sequestered germline?

"The germ line cells are sequestered" means "the germ line cells are separated from the non-germ line (somatic) cells."


ERBB2 appears to be a (tyrosine kinase) receptor; that is, it lives in the cell membrane; with a part that sticks outside of the cell, and part that sits inside.  When the right molecule attaches to the outside part, the inside part changes shape, which alters its function, causing it to start phosphorylating other proteins, which alters their functions.

So the ERBB2 pathway is the set of genes/proteins whose behavior is affected by ERBB2.

Google "ERBB2 pathway" and "tyrosine kinase receptor" for more info.


What determines the sex of hybrid offspring?

I am detecting a bit of confusion in you wording of Haldane's rule.
Haldane's rule makes predictions on the fertility of offspring from an inter-specific cross, not the sex-ratio of the offspring from the cross.

"if inter-specific hybrid offspring are sterile, then the sterile offspring will be of the heterogametic sex."

In inter-specific crosses there is not an effect on sex-ratio of the resulting offspring, but a effect on the ability of the F1 offspring to reproduce.
For the offspring, those of the heterogametic sex, males in mammals (XY) and females in birds (ZW) will be sterile while the homogametic offspring will not be affected by hybrid sterility.