What is the etymology for Pinus halepensis?

If you search for this plant (properly spelled Pinus Halepensis) in the International Plant Names Index (IPNI), you'll find this page providing publication reference for this species of pine:

Gardeners Dictionary, Edition 8. London

According to IPNI, this publication by Phillip Miller in 17681 was the first to officially name this species. You can find the first half of he publication online here and the portion of the publication with info regarding P. halepensis here [p. 477].
Miller 1768 provides the following:

Pinus (Halepenſis) foliis geminis tenuiſſimis, conis obtuſis , ramis patulis. Tab. 208, Pine-tree with two narrow leaves in each ſheath, obtuſe cones, and ſpreading branches. Pinus Halepenſis, foliis tenuibus lætè viridibus. Rand. Hort. Chelf. Cat. 158. aleppo Pine with very narrow dark green leaves.

* Note: a longer description about this tree also continues on the subsequent page in Miller's book -- you can find it in the middle of the right column of the following page.
However, this publication does not make clear why Miller chose this specific epithet.

Elwes & Henry (1906)2 likewise describe this species [see online here] and mention that the epithet had been used for more than 100 years. However, they, too, do not provide meaning behind its use.

Further sleuthing suggests the following:
From Antropocene.it:

The specific epithet halepensis derives from Aleppo, the current city of Haleb in northern Syria.

Note, however, that this specific epithet doesn't only apply to this species of Pine. Linnaeus assigned this epithet to a grass (Sorghum halepense) he called Holcus halepensis (Linnaeus Sp. Pl. (1753) 1047)3 more than a decade before Miller named the pine in question.
Using this connection, SEINet suggests the following etymologies for halepense:

Halepense means "from Aleppo, Syria."

This is the best I could do for you in a short amount of time. I, like you, could not find much explicit explanation for this word, and I admit I find its use a little strange given the relatively widespread range of the species mentioned (at least that both exist much wider than Aleppo).

 1. Miller, P. 1768. The Gardener's Dictionary, ed. 8. London. Pinus no. 8
 2. Elwes, H.J. and Henry, A., 1906-1913. The Trees of Great Britain and Ireland. Edinburgh: R & R Clark, 7.
 3. Linnaeus, C. 1753. Species plantarum. https://doi.org/10.5962/bhl.title.669. [more info here and on wikipedia]


Why don't primates have galactose-alpha-1,3-galactose (alpha-gal), but other mammals do?

The general idea is that infectious agents use certain cell-surface proteins to enter the cell, and presumably recognize them by their particular glycoproteins. There are examples (cited in the extract below) of changes in e.g. blood group antigens in populations that are thought to convey (at least temporarily) an advantage against particular pathogens.

In this context, let me cite the rest of the section of the article that you didn’t have access to:

  However, after the geographic separation of Africa and South America,
  Old World primates appear to have been subjected to a selective
  pressure for the suppression of autologous α-galactosyl epitope
  synthesis and for the subsequent production of anti-Gal. Possibly, an
  infectious agent endemic to the Old World, which was detrimental to
  primates, and which expressed α-galactosyl, or α-galactosyl like
  epitopes, exerted a selective pressure for the evolution of Old World
  primates able to suppress autologous α-galactosyl epitope expression.
  Thus, immune tolerance toward this epitope was lost and anti-Gal
  antibodies could be produced in these primates as a protective
  response to such putative pathogens.

  An alternative scenario for the
  evolutionary suppression of α-galactosyl epitope expression could
  have been one in which ancestral Old World primates suppressed
  expression of these epitopes on their cell surface glycoconjugates as
  a result of exposure to a pathogen which exerted its detrimental
  effect via α-galactosyl epitopes functioning as receptors. A current
  example for such a pathogen is Clostridium difficile. Enterotoxin A
  produced by this pathogen was found to bind to the cells it damages
  through interaction with α-galactosyl epitopes on cell surface
  glycoconjugates [12, 56]. A bacterial toxin with a similar ligand
  specificity and which was detrimental to ancestral Old World primates
  could exert a selective pressure for the evolution of primates which
  suppressed the expression of α-galactosyl epitopes and, thus, lost
  the immune tolerance toward this carbohydrate structure.

  [12] Clark GF, Krivan HC, Wilkins TD, Smith DF (1986) Toxin A from Clostridium difficile binds to rabbit erythrocyte glycolipids with terminal  Galα-3Galβ1-4GlcNAc sequences. Arch Biochem Biophys 257:217
  [56] Krivan HC, Clark GF, Smith DF, Wilkins DT (1986) Cell surface binding site for Clostridium difficile enterotoxin: evidence of a glycoconjugate containing the sequence Galα→3Galβ1→4GlcNAc. Infect Immun 53:573

Whatever the reason, the consequence of this was:

  This also resulted in the loss of immune tolerance to the α-galactosyl epitope and the production of anti-Gal.

I presume this explains the IgE problem referred to in a comment, and I would consider this as an unfortunate side-effect of the change, and not a reason for it.


How is hibernation/aestivation different from anesthesia?

I'm going to answer the question of whether aestivation/hibernation can be activated in humans or other apes, because it's more interesting.

Mammals, as a clade, have three major subgroups. Bats, shrew-likes, rodents, and then everything else including primates. One family of the shrew-likes hibernates, some rodents(but not all) and some bats can hibernate or enter a period of extended torpor. The only kind of primate that can hibernate is the dwarf lemur, which does so in a strange way(fully asleep for 6-8 months, little regulation of body temperature). Other hibernating animals regulate their temperature but keep it low, and wake to roll over or whatever every couple of days. Plus lemurs are on the edge of the mammal cladogram, so they're just pretty weird.

Phylogenetically, it's not likely(imho, but I'm not a mammalian phylogenetics expert) a primate ancestor of humans has ever had the ability to hibernate. It seems more likely that primates lost the ability if it was a capability of mammalian ancestors and dwarf lemurs re-evolved it. It's possible atavistic remnants of such a system might still exist, but extensive hormonal and possibly surgical treatments would be required to induce it. Not to mention you can wake animals from hibernation by poking them, so it probably would be a substandard anaesthesia method.


Which cells will pass cancer to offspring?

Red blood cell

Will probably not. You inherit blood type, but not actual erythrocytes (though the mother's erythrocytes do interact with a fetus).

T cell

Will probably not. However, while in the uterus and for the first few weeks outside the uterus the Mother's immune system is effectively the newborn's immune system. While the mother doesn't pass on any myeloid progenitor cells, a disease affecting a leukocyte might also be passed on to the child (HIV).

Skin (epithelial) cell

Will not. You inherit many traits to do with skin (melanocyte activity resulting in melanin concentrations, for instance), but no skin cells are involved in the creation of the fetus.

Neuron from the brain

Will not.  Neurons are the last time of cell I'd expect to vertically pass on a mutation, not only because their environment is usually tightly controlled (Schwann Cells, Blood-Brain Barrier, etc.), but also because the fetus will develop the beginnings of its nervous system very early on and I'm not aware of the mother's CNS or PNS interacting with the fetus in any significant way.

Sperm cell

Can certainly pass on a mutation as long as the mutation is part of the sperm's DNA. Though the particular gene the mutation exists on may be inactivated, it would still be passed on to the offspring and potential future generations.

Cell from lining of the uterus

I'm not positive on this one. The fertilized egg cell must implant itself in the lining of the uterus, and the landing location eventually becomes the umbilical cord. I suppose it's possible, particularly if the mutation occurs closer to the child's end - like the obliterated artery.

Placenta cell

Probably not, though like Cell from lining of the uterus I'm not super positive on this one. Given that the placenta is detached from both the mother and child soon after birth, a mutation in a placental cell that hasn't metasticized won't affect either. However, there may be interactions I'm not aware of.

Stem cell

"Stem cell" is a little vague. The body has many specific types of stem cells, and the fertilized egg itself basically turns into all of the stem cells the developing fetus will ever have. If it's referring to the daughter cells of a fertilized egg, then only the child will have the cancer, as the genetic inheritance is unidirectional (the mother's genome is not modified to resemble the child's in any way).

If someone has better knowledge on the interaction between the fetus and the uterus/mother or can come up with some references, listen to them. It's been a while since I've studied development.


I think that you are expecting for some complicated system while such things are not necessarily involved. You basically just need a protein that is light-sensitive and some cascade of signal transduction. A light-sensitive protein is just a protein which conformation is changed in the presence of photons of a given wavelength. This cascade of signal transduction can be very standard. It doesn't need to be anything extraordinary.

Consider a mutation that turns a given protein into a light-sensitive protein. Such mutant protein could easily still activate the same cascade (and eventually regulate the expression of the same gene) and may eventually be beneficial. A visual signal (presence/absence of photons of a given wavelength) directly affect the conformation of the protein which in result can activate a whole cascade. The cascade doesn't need to have evolved after the protein had acquired the ability to response to photons. You may want to dive into the details of how the structure and function of the opsin proteins.

This article describes how an ancestral non-light sensitive protein (coded in GPCR gene. The proteins are also called serpentine) evolved into a light-sensitive protein (opsin). The article also link to other articles that discuss this transition.

There are several types of light-senstive proteins in different kingdom, including plants and bacteria that don't have nerves.

You can learn more about the cascade of transduction on wikipedia (here or here for example). You may want to learn more about opsin proteins and learn more about light-sensitive proteins.

Wikipedia page: Evolution of eyes > Early Eyes will probably interest you as well. Depending on the definition you use for "eye" (note, "eyes" have evolved independently 50 to 100 times), Planarian might be a good example of a species that have a primitive eye.


Looking for protocol to produce a drosophila primary cell line

This is the original 1972 paper describing the isolation of the S2 cells from Drosophila. However it would be best if you specify what application you are planning to pursue with the cells, which would make it easier to suggest which ones to isolate. I have personally isolated garland cells, which are visible with the naked eye and highly suitable for endocytic assays. It takes a few minutes to isolate them and all you need are two grade 5 or grade 4 sharp tweezers and 2nd or 3rd instar  Drosophila larvae and a dish and some PBS to submerge the larvae in. You don't even need to pin them! If you are interested I can edit this response and write their isolation technique as I can't find a good technique online.

EDIT:

I have not personally isolated S2 cells although I have extensively worked with S2 and S2R+ cell lines (which are embryonic). Garland cells are excellent to work with for endocytic assays using Dextran (fluorescent dye used for bulk endocytosis assays) and Dynasore [dynamin inhibitor] (and infact they were used to characterise Drosophila dynamin homologue, shibire, here and here and its temperature sensitive behaviour in Shi[ts] mutants and shi role in endocytosis) as an example shown here in fig 6 using S2 cells. I have never cultured the garland primary cells so I do not know their PD and how they behave in Schneider+FBS (since I only isolated them and performed andocytic assays with them while they were in schneiders) and I don't think anyone has (but have a look) so it would be a great protocol to stablish and publish in a methods paper. I'm more than happy to share the isolation technique with you, tried looking on jove or youtube for a video but failed to find one, and let you know what to look for if you wish. Just as a cautionary note, garland cells are multi-nucleated (i have seen up to 4) so it might not divide very well or at all so just bear that in mind.


In DNA there are four nucleotides or "bases", each of which can be matched with a complementary base on the partner chain in the double helix. Thus:

Adenine (A) and Thymine (T) are complementary and Cytosine (C) and  Guanine (G) are complementary.

So, a nucleotide sequence is said to be a palindrome if it has an even number of base pairs and is equal to the reverse of its complementary sequence.

For example, in a single strand of DNA the sequence of bases CCATTAATGG is palindromic because the sequence of bases in the complementary strand is GGTAATTACC, its reverse.

A pseudopalindrome is a DNA sequence with an odd number of base pairs yielding a symmetrical complement except at the central base-pair. For example, the DNA sequence ACCTGGT is pseudopalindromic, because its complement on the other strand is TGGACCA, which is its reverse except for the central element.

[There may be some confusion in the literature. The example cited in the question, GATC, is a palindrome, having CTAG as its complement, not a pseudopalindrome.]


Why does a cell produce a lot of p53 protein only to later degrade it?

This answer is not reserved for the example you cite but for all proteins/RNAs which have high turnover. So your question generalizes to

What is the advantage of having high turnover? or in other words, What is the advantage of regulation via degradation?

Fast responsiveness. If your protein/RNA has a low turnover then it would take a lot of time for it to clear up from the cytoplasm even after the activating signal is gone. Enhancing the degradation will make the response fast. Cell cycle proteins such as p53 have to clear up as soon as the cell progresses to the next phase.
In certain cases an additional degradation control makes the regulation more efficient. If the "regulated" gene happens to be in turn an activator of many downstream genes, then efficient control actually helps in saving the cellular resources. I can't cite any literature for it but I have observed this in one of my unpublished research work using mathematical models.


Flow diversion for cerebral aneurysms or stabilizing the hemodynamics?

I don't quite understand the dichotomy you present between diverting flow and stabilizing hemodynamics. The former is a direct outcome and the latter is a secondary outcome: both are goals.

The overall goal is to isolate the blood in the aneurysm and allow it to clot and heal over time. Embolic coils are also used to assist the process, in which case the flow diverter helps to keep the coil in place and the resulting embolism out of the primary circulation.

One would not typically deploy a flow diverter over branches that one wishes to remain patent, although patency can be maintained in smaller vessels. In many neurovascular situations, collateral circulation can make it acceptable to occlude a branch, however.

You may be confusing plain stents with flow diverters; a plain stent has as few struts as possible while maintaining structural support (though high flow through the struts can cause turbulence and is something you want to avoid if possible), and creative stent placement techniques including deployment of multiple stents and use of balloons to break open strut configurations can be used. These do not block flow per se, but can help keep coils in place and maintain the desired structure of the vessels involved.

I've included several references that I quickly gathered; these may not be the most ideal references but should give you a look at some of the approaches used. I would strongly suggest you look through the rest of the literature using search terms from your question to get an idea of how interventionalists approach different situations.

I'll add that I am not a physician and am not up-to-date with the latest guidelines or standard of care, but in my experience with the literature a lot of these decisions are up to the experience of the physicians involved and based on a lot of case study; randomized trials aren't really possible to cover all the anatomical variety that is experienced.

Burkhardt, J. K., Riina, H. A., Tanweer, O., Shirani, P., Raz, E., Shapiro, M., & Nelson, P. K. (2018). Flow diversion and microvascular plug occlusion for the treatment of a complex unruptured basilar/superior cerebellar artery aneurysm: case report. Journal of neurosurgery, 1-6.

Chow, M. M., Woo, H. H., Masaryk, T. J., & Rasmussen, P. A. (2004). A novel endovascular treatment of a wide-necked basilar apex aneurysm by using a Y-configuration, double-stent technique. American Journal of Neuroradiology, 25(3), 509-512.

Miyachi, S., Matsubara, N., Izumi, T., Asai, T., Yamanouchi, T., Ota, K., ... & Wakabayashi, T. (2013). Stent/balloon combination assist technique for wide-necked basilar terminal aneurysms. Interventional Neuroradiology, 19(3), 299-305.

Puffer, R. C., Kallmes, D. F., Cloft, H. J., & Lanzino, G. (2012). Patency of the ophthalmic artery after flow diversion treatment of paraclinoid aneurysms. Journal of neurosurgery, 116(4), 892-896.

Siddiqui, M. A., Bhattacharya, J. J., Lindsay, K. W., & Jenkins, S. (2009). Horizontal stent-assisted coil embolisation of wide-necked intracranial aneurysms with the Enterprise stent—a case series with early angiographic follow-up. Neuroradiology, 51(6), 411-418.

Wong, G. K., Kwan, M. C., Ng, R. Y., Simon, C. H., & Poon, W. S. (2011). Flow diverters for treatment of intracranial aneurysms: current status and ongoing clinical trials. Journal of Clinical Neuroscience, 18(6), 737-740.


Unlike humans and most of mammals, which have a biconcave (or "doughnut shaped") RBC, camels have oval shaped (or elliptical) erythrocytes.

The very first result in Google shows this:

That feature (which protects them from dehydration) is not unique to camels, but occurs in other Camelidae as well. This is an image of Llama blood:

Those are reliable sources of images (optical microscopy) of real cells.

However, for your project, I believe a scanning electron micrograph can better show the shape.

This is an SEM of elliptical camel (a) and alpaca, another Camelidae (b and c), erythrocytes:

For comparison, this is the biconcave human erythrocyte:

PS: There is this misinformation that camels' erythrocytes are nucleate. You can read this in several web pages. I have no idea who made this up, or why people keep sharing this wrong information: camels, like any mammal, have anucleate erythrocytes. See the post Do camels have nucleated RBCs or enucleated RBCs? for more information.

EDIT: The way your question is worded it really seems that you're just asking about the reliability of those sources. However, according to your comment below, it seems that you are indeed looking for better images. It's hard finding better ones than those indexed by Google, but since your goal is modelling those cells, here are two papers (about a protozoan parasite of camelids) which has some SEM that may suit you. The images are not high-resolution, but the cells are shown in several angles:

https://www.omicsonline.org/open-access/babesia-cameli-as-a-new-species-infecting-camels-camelus-dromedariusat-assiut-locality-2155-6156-1000700.php?aid=79911
https://www.ecronicon.com/ecmi/microbiology-ECMI-02-000040.php

In both papers the SEMs are at the bottom (just skip the optical ones, they are not good).


Were there any marine/aquatic dinosaurs?

There are a couple of specimens of a dinosaur species named Liaoningosaurus paradoxus that have been found with fish in their stomachs and skeletal features suggesting it was at least semi-aquatic.  It is a member of the ankylosaurian dinosaurs from the early Cretaceous period of China.

From Fish Hunting Ankylosaurs( Dinosauria,Ornithischia) from the Cretaceous of China:

  With elongate and fork-like denticles of cheek tooth crowns,L.
  paradoxus has a dentition capable of penetrating into animals like
  small fishes. The carnivorous adaptation of the dinosaur is also
  supported by the ungual modification to a sharp claw in both the
  fore-and hind-limbs. The evolution of a shield-like ventral armor
  plate and the loose sacrum-pelvic connection suggest that L. paradoxus
  may have adopted an aquatic way of life,using the ventral armor plate
  to protect the body from underwater attacks; as such,the open suture
  between the neural arch and centrum of the vertebrae cannot be used to
  indicate the juvenile nature of the type specimen. L. paradoxus is the
  first carnivorous ornithischian dinosaur since dinosaur was first
  known in the 18th century and represents not only the first aquatic or
  semi aquatic example of armored dinosaurs but also the smallest
  species of ornithischian dinosaur so far known.

Image Source: [Paleontology • 2016] Liaoningosaurus paradoxus • Fish Hunting Ankylosaurs (Dinosauria, Ornithischia) from the Cretaceous of China


What Role Antagonists Play in the Study of Drugs?

An antagonist is a substance that blocks a particular pathway (a receptor). You can therefore test whether a particular drug acts through the opioid system by using an opioid antagonist. If your substance still works despite the presence of the antagonist (which should block the opoiod receptors), you can conclude that it is not working thorough the opioid system.

Conversely, if your drug is blocked by an opioid antagonist, that is good evidence that your drug works through the opioid system.


Is it possible to knock out a gene in adults?

Actually, Cas9 system might be a possible method to achieve your aim in the future, research teams are trying to utilize cas9 in vivo, which means maybe someday we can doing some genetic modification in body cell precisely. However, this is only a future direction and we still can not say its fit for a knockout.(Patrick D. Hsu, Eric S. Lander, and Feng Zhang, (2014) Development and Applications of CRISPR-Cas9 for Genome Engineering. Cell 14(6): 1262-1278)
And for editing some cell gene in a limited area, some research are on going for therapeutic purpose (Liqun Zhang et al.CFTR Delivery to 25% of Surface Epithelial Cells Restores Normal Rates of Mucus Transport to Human Cystic Fibrosis Airway Epithelium), but haven't seen research are trying to built KO cell in vivo.


Extremely rare occurence of Heart cancer?

This is a specific version of the great cancer question: "Why are some cancers more common than others?" The answer is either "Some have more common causes", and (or) "Some are cured spontaneously more often". So now all you are asking is "What causes cancer?" and "How do we cure it?"

Given that, I don't expect a general definitive answer will be forthcoming. A specific answer might be possible, but I doubt there will be any existing experiments that address this. With the obvious caveat that only experimental or statistical results can really answer your question, here are a couple of off-the-cuff hypothesis for consideration:

1 - Differences in stem cell populations.

Apparently, differentiation can actually be targeted as part of a treatment in some neuroblastoma cases - see the section on "Differentiation therapy" in this page from Sloan-Kettering. Cardiac stem cells seem to exist, but a difference in relative population and turnover rates between brain and heart might be related to the relative frequencies of these types of cancers. @WYSYWIG referred to neural progenitors in his comment above.

2 - A filtering effect due to a more extreme selection pressure in the uniformly stressful environment of the a beating heart.

Although there is a relation between elevated levels of oxidative stress and cancer causing mutations, it could be that this only matters in a punctuated stress environment, where cells have down time to recover. A sustained stress environment might actually helps prevent cancer. The path from normal to cancer cell requires multiple mutations, and I would not expect most pre-cancerous cells to be more fit than correctly wired ones. The extra stress of the cardiac environment might produce an elevated mutation rate, but also produce an even higher rate of apoptosis in early "sick" cells before they accumulate enough mistakes to become become cancerous, resulting in a net decrease in the rate of cancer.

Both of these ideas fit with heart cancer being less common and with metastasis from elsewhere being more common in heart than primary cancer, but unfortunately, a higher rate of clearing of sick cells would necessitate a higher rate of replacement from stem cells, so these two hypotheses partially cancel each other. Again, hypotheses without experiments are not really answers.


Keep in mind that the citrate utilizing strain appeared after over a decade. Also, Escherichia coli could always metabolize citrate, but the citrate transporter that brings it into the cell is only expressed under anaerobic conditions [1]. The strain that evolved to import citrate under aerobic conditions had a duplication of the transporter gene which put it under the control of a different promoter that drives expression under aerobic conditions [2]. Baker's yeast doesn't have amylase or debranching enzyme genes [3], so a similar evolutionary mechanism cannot occur. Developing such enzymes de novo doesn't seem trivial, but perhaps the enzymes involved in glycogen metabolism can be repurposed. The only way to know is to try.

References:

Blount et al., 2008
Blount et al., 2012
Ostergaard et al., 2000


What information do microarray image convey?

Each spot overlaps with an oligonucleotide probe, that is designed to identify a specific nucleic acid sequence. Gene expression arrays have probes which are complementary to sequences derived from the exons; therefore they will hybridize with these sequences.

Before hybridization the cDNA (in this case) is labeled with a fluorescent molecule such as Cy3 or Cy5 (two dyes can be used to differentiate treated and control). Note that each spot will have many probe molecules.
Fluorescent intensity is proportional to number of hybridized DNA strands, which in turn is proportional to its expression in the sample.

Extensive amount of texts are available on microarray data analysis which you can find quite easily.


Is there an advantage to having cellulite

There's no advantage or disadvantage (beyond personal perception of attractiveness).

It's a benign condition that can occur with hormone changes, weight changes, and especially genetic predisposition.

It occurs in most women (up to 90% will have it at some point) and some men, and physicians consider it 'normal.'

http://www.mayoclinic.com/health/cellulite/DS00891


The scientific answers are pretty clear: Gingkos are not closely related to the conifers, they are closer related to the cycads. See this phylogenetic tree based on the 18S RNA from paper 2:

It shows that conifers and Ginkgos are relative close related, but not on the same sub-branch of the tree. The last common ancestor between Ginkgos and Conifers is older than the one between Ginkgo and Cycadales. This classification has been made on the basis of genome comparisions and also based on an analysis of the chloroplasts.

References:

Chloroplast Phylogenomics Indicates that Ginkgo biloba Is Sister to
Cycads
Molecular Phylogeny of Ginkgo biloba: Close Relationship Between
Ginkgo biloba and Cycads
Advances in Ginkgo biloba research: Genomics and metabolomics pe
rspectives


How does the choice of blood draw site influence the possible specificity of a serological test?

This ref, https://academic.oup.com/ajcp/article/144/6/885/1761216
show that drops of finger prick blood vary more than venous blood.

The main reason for using venous blood is licensing. A test is licensed only for an exact procedure and materials. If you vary any conditions the license is invalid.

However, I would not expect a test for antibodies (present vs. absent) to show much variation except for detecting the lowest levels of antibodies. (Sorry I cannot find a ref for this).


Flow Cytometry to learn about Cell cycle

The basis of analysing flow cytometry data in regard to the cell cycle is the fact that DNA synthesis occurs in S-phase and therefore cells before S-Phase (G0/G1) have half the amount of DNA compared to cells after S-phase (G2). [M-phase lasts to short to be of any relevance for this kind of analysis]. Signals that have less DNA than the cells from G0/G1 phase are either artefacts or apoptotic cells with fractured DNA (these are labelled as sub G1).

In order to measure the amount of DNA per cell the dye PI (propidium iodide) is used, since its quantitatively binds to DNA. Therefore the distribution of the PI signal can taken as a distribution of the different stages of the cell cycle.

This wikipedia article also explains the analysis in more detail and provides further references.


How many times have the cells in a human body divided?

The supplemental material of the paper that Dirigible references in a comment to my question gives a rough estimate of these values. If I understand their simple model correctly, then we can estimate the average number of times that the stem cells in various types of tissues have divided over an 80-year lifespan from Table S.1 by finding the row corresponding to a cancer of that tissue, and then calculating $\log_2(s) + d$, where $s$ and $d$ are given in the table. (For specialized cells, I guess you'd add 1 more to capture the final cell division that produces the specialized cell?)

I haven't done the math out, but glancing over the table, it looks like the generation number varies widely between tissues, from a low of about 27 for some brain cells to a high of almost 6000 for cells in the colon and rectum.


I too had difficulty finding any textbooks or notes that focused solely on genetic engineering. However, after some rather intense looking, I did come across several textbooks that may be helpful. I wasn't sure how basic of a text you were looking for but I'm hoping college level is okay because that is all I have been able to find.

The first book was An Introduction to Genetic Engineering by Dr. Desmond S.T. Nicholl.

Another was Principals of Gene Manipulation and Genomics by Sandy B. Primrose.

If you need a more basic biology text for reference, I would recommend Miller & Levine Biology by Prentice Hall (Pearson Prentice Hall). Also, you could do a quick-study on genetics on Khan Academy - Crash Course: Biology and Ecology.

I hope this information was helpful for you!


DAM enzyme distances move along the genome

Dam methyltransferase methylates large DNA molecules in a processive manner, with an effective range of up to 7 kb on either side of an initial methylation reaction.

My answer is taken from this paper:

  Urig, S. et al. (2002) The Escherichia coli Dam DNA Methyltransferase Modifies DNA in a Highly Processive Reaction J Mol Biol 319 1085-1096

The authors report on a kinetic analysis of E. coli dam methylase. For anyone using this system as described by the OP, this paper is essential reading. Their conclusion is that the methylation process is highly processive, which is to say that a single dam-DNA interaction leads to multiple methylations before the enzyme dissociates from the DNA.

I'll restrict myself to describing just two of their experiments:

Figure 5
In this experiment they analysed the time course of methylation of an end-labelled 879-mer with 4 GATC sites, using DpnI digestion to detect methylation. In this experiment all DNA was found to be either fully methylated or unmethylated - no evidence for the presence of partially methylated DNA molecules was detected.

Figure 6
In this experiment they analysed the methylation of λ DNA (48.5 kb) and were able to detect partially methylated molecules. A kinetic analysis of the data results in the following conclusions (MTase; methyltransferase):

  From these simulations, we [determine] a processivity of nav=3000. This means that after binding to the λ-DNA and starting the one-dimensional diffusion process, one MTase on average meets 3000 dam sites before it dissociates from the DNA. Since the enzyme performs a random walk, it will hit many sites more often than only once and the effective range of processivity corresponds to the square root of nav. Therefore, the dam MTase is able to methylate approximately 55 GATC sites on λ-DNA in a processive reaction in vitro. In this simulation, 4.6 associations of an MTase molecule to the same molecule of λ-DNA are required to obtain fully methylated DNA.

In a random DNA sequence GATC should occur on average every 44 = 256 residues. This suggests an approximate range of (55/2)*256 = 7 kb on each side of an initial methylation reaction.


In SDS-PAGE, why are the sample buffer and running buffer different in concentration?

The reason why the sample buffer is more concentrated (typically 2x or 5x depending on your protein concentration) is its dilution when you mix it with the sample. You mix 4 parts of your sample and 1 part of 5x sample buffer, so that the final concentration of this buffer is 1x.

If you use 1x sample buffer together with the same amount of sample, the final concentration of the sample buffer would be 0.5x, if you do the same 4+1, it would only be 0.2x in the end.

This dilution is too strong and the buffer will not fulfill its purpose, the complete denaturation of all proteins in the sample, so that their distribution on the gel depends only on their molecular weight and not also on their tertiary/quarternary structure.

Using a 5x buffer allows you to add a lot of sample when diluting it to 1x without changing the concentration of the protein too much. It also allows to load larger amounts of sample compared to 2x buffer, interesting when the protein concentration is low.

The running buffer is not further diluted by adding sample, so that it has to be diluted to 1x in order to have the right ionic strength. Since these are often used in big quantities in the lab, it is more convenient to prepare concentrated buffers in smaller quantities and dilute them before usage than preparing big tanks of buffer.


Since there are different formulations for anti-aging creams, it would be helpful to focus on the specific compound or combination of compounds.

According to a comprehensive literature review done in 2007, certain compounds (Vitamin C, alpha-hydroxy acids, Vitamin A, Vitamin B derivatives, and botanicals) have had varied success in literature demonstrating anti-aging efficacy with Vitamin C and alpha-hydroxy acids being the better candidates.

Vitamin A/retinols have been shown to reduce wrinkles in some studies but no large studies have been conducted to show efficacy, Vitamin C has been shown to be the most effective (statistically significant improvement in texture, wrinkling, etc.) and alpha-hydroxy acids have been shown to increase collagen density, for example among other improvements.  A lot of these and other compounds have had positive or encouraging results replicated in literature, on mostly animal and human cell models so whether they actually have a significant effect on a large group of people needs to be looked at but to assess whether or not they actually "work" depends on what issues of skin damage as a result of aging one is targetting, the severity, the age at "treatment" and whether you're referring to over the counter or prescription-strength.

Huang, C. K. and T. A. Miller (2007). "The truth about over-the-counter topical anti-aging products: a comprehensive review." Aesthet Surg J 27(4): 402-412; quiz 413-405.


What color does the other cone in Tetrachromacy correspond to?

According to Deeb (2005), there are two relatively common types of causes for tetrachromacy in humans:

The common Ser180Ala polymorphism, which results in two spectrally different red pigments in the retina. This mutation also plays an important role in variation in normal color vision. This polymorphism most likely resulted from gene conversion by the green‐pigment gene.
Another common variation are several red/green pigment chimeras with different spectral properties. The red and green‐pigment genes are arranged in a head‐to‐tail tandem array on the X‐chromosome with one red‐pigment gene followed by one or more green‐pigment genes. The high homology between these genes has predisposed the locus to relatively common recombination events that give rise to red/green hybrids and deletions of green‐pigment genes. Such events constitute the most common cause of red‐green color vision defects. Only the first two pigment genes of the red/green array are expressed in the retina and therefore contribute to the color vision phenotype. The severity of red‐green color vision defects is inversely proportional to the difference between the wavelengths of maximal absorption of the photopigments encoded by the first two genes of the array. Women who are heterozygous for red and green pigment genes that encode three spectrally distinct photopigments have the potential for enhanced color vision.

Reference
Smeeb, Clin Gen (2005); 67:(5): 369-3

Further reading
- Color vision across species


Are neurons capable of buffering a signal to sync up with other data?

For this answer, I'll use a very broad definition of "buffer" as a mechanism to integrate information at different delays. I have no interest in getting into specific computer science definitions of what a buffer is and I don't think it makes any sense to use them in biology.

Parallel processing and predictive coding
The brain is a massively parallel system, so of course there are different "streams" of information flowing at all times. Certainly the brain as a whole does some level of buffering, though the mechanisms available to individual neurons are unlikely to do what you suggest. The "buffering" in individual neurons has a lot more to do with learning and memory, for example in spike-timing-dependent plasticity which incorporates a physical record of past inputs in a learning rule.
One model of cognitive function is predictive coding, in which the brain holds a model of the world at different hierarchical scales and updates this model with new information. This model is effectively a buffer against which new incoming information is compared to draw attention to discrepancies that require further attention (such as the sudden appearance of a predator).
Audiovisual integration
One simple example of buffering is in audiovisual integration: the brain's processing of visual information is much slower than auditory information, and yet the perception of, say, a human speaker's voice vs. lips or the sound and sight of a bouncing ball are perceived in synchrony (see for example Recanzone 2009; note this has absolutely nothing to do with speed of sound vs speed of light).
It's important to understand that the visual system doesn't process visual information anything like a computer. There are no frames in biological vision. That said, humans can deal with a lot of unnatural sensory input, and they also use a lot of other visual cues besides stereo vision, the so-called "monocular cues".
Motion parallax and wiggle stereoscopy
One of these monocular cues is motion parallax (binocular vision can also utilize parallax without motion). Wiggle stereoscopy simulates motion parallax, as if your head were oscillating back and forth, to create an illusion of 3D, and seems much like what you are proposing. It doesn't matter whether you view the image with one eye or two.

Recanzone, G. H. (2009). Interactions of auditory and visual stimuli in space and time. Hearing research, 258(1-2), 89-99.


Question about the consequences of non-random mating and allele frequencies

Out of context at least the small piece of text you cite is very poorly phrased and partially wrong.

First, you should have a look at Solving Hardy Weinberg problems. Take your time and read that post... Done? Good.

  More homozygote and less heterozygote individuals in the population

This is wrong as non-assortative mating might be disassortative mating where individuals are attracted to individuals of different genotypes.

However, it is true that population structure will cause excess of homozygotes. This is called the Allee effect. The loss of heterozygosity due to population structure is equal to twice the variance in mean allele frequency among those populations. These details sounds a bit too advance for your needs though so I won't go any further.

  Allele frequencies are constant (not in case of negative density dependence)
  Genotype frequencies change

Constant over what? Change over what? Not over time necessarily (at least not unless some other assumptions are being made).

I guess what is meant is that if in a given generation mating is not random (due to population structure for example), then you expect the same allele frequency as if it was random but not the same genotype frequency. If it is not clear why, you should probably reread the post "Solving Hardy-Weinberg problems"

Much further discussion in both english and french on @AlissaDeschamps misunderstanding can be found here.


Are oxygen and carbon dioxide simultaneously present in red blood cells during gas exchange?

For diffusion to occur there must be a "concentration gradient", that is one area where the substance that is diffusing from, to where it is diffusing to. Where the substance is diffusing from, the concentration is high and where it is going to, the concentration is low. Our bodies continually use up oxygen and produces carbon dioxide. Carbon dioxide is generally carried in the blood plasma, and oxygen is generally carried by the red blood cell (erythrocytes).
Whereas, it is true that in diffusion an equilibrium is usually achieved, in this case you mention there is no equilibrium. Our physiological processes (respiration) continually maintains that concentration gradient and so carbon dioxide always flows out and oxygen always comes in. Too much carbon dioxide in the blood will raise the pH and cause serious metabolic problems with enzymes and their efficient function.


Why would an Eadie-Hofstee Plot be non-linear?

The reason is that the inhibition models are inherently wrong.

Inhibitors bind to enzymes with the same mass action principles as substrates do so the term that should describe their binding should mirror the form of the MM equation i.e. ([S]/([S]+km)).  However all the traditional equations use (1+([I]/Ki)) rather than ([I]/([I]+ki)).

To compound this problem the (1+([I]/Ki)) term multiplies into the Km in competitive inhibition but divides into the Vmax in the noncompetitive equation.  It is therefore not affecting these terms in the same way in these separate equations and leads to the conclusion it is upside down in the competitive equation.

The plots above are deceiving as they allow the user to look at a linear plot and assume mechanism based on axis intercept pattern without analyzing the actual change in kinetic parameters produced by the inhibitor.  Kinetic models should be only fit using global data fitting to the proposed inhibition model.  This can be done quite easily using excel, for an example of how this can be done check out Kemmer and Keller 2010, or check youtube.

Kemmer G, Keller S. 2010. Nonlinear least-squares data fitting in Excel spreadsheets. Nature Protocols 5:267-281.

By realizing that the change in enzyme kinetic properties relates directly to inhibitor binding the logical hyperbolic shift in values exactly like the hyperbolic curve of the MM equation must be acknowledged and finite changes in the kinetic parameters must be accounted for.

i.e. Km = Km-((delta Km)*([I]/([I]+Ki)))

  Vmax = Vmax-((delta Vmax)*([I]/([I]+Ki)))

While I have been told this may be over fitting as the competitive, noncompetitive, mixed noncompetitive equations define inhibition with one or two inhibition constant (Ki alphaKi), these terms eliminate the need for all of these equations and the family of equations that they spawned as they proved ineffective over the years (such as uncompetitive, partial competitive, partial noncompetitive, partial mixed noncompetitive, I could go on but I think you get the point).

Additionally the competitive, noncompetitive and mixed noncompetitive equations define the effect of the inhibitor with the equilibrium binding constants and do not allow for the possibility that complete inhibition may not occur (no delta terms), leading to the family of equation to try to make up for this, i.e. partial competitive and partial noncompetitive.

Use empirical models and stop trying to force mechanistic models, the data will suggest the mechanism with good experimental design.


Why is there a seeming dichotomy between mobility and photosynthesis?

The difference in energy requirements of a motile species make photosynthesis an unsuitable form of primary energy generation for them.

Since plants are sessile, their energy consumption rates are lower. Plants have approximate respiration:photosynthesis rates of 0.35-0.9, as can be seen in this table (click to enlarge):

Once the energy consumption rates exceed 1, the organisms will, by definition, no longer be full autotrophs, as they will need to obtain their energy from alternative sources. Therefore, the relative low energy content of sunlight makes it impossible for motile animals, which have a larger energy requirement, to survive fully via photosynthesis.


What is the effect of flash pasteurisation on Maillard reactions or production of AGEs in milk?

This is only an partial answer, as I do not have the time now to look for other references.

In the chapter about milk, Harold McGee's beautiful book "On Food & Cooking" says (pg. 21 of the 2004 edition, bold is mine):

  Flavors from cooking
  Low-temperature pasteurization slightly modifies milk flavor by driving off some of the more delicate aromas, but stabilizes it by inactivating enzymes and bacteria, and adds slightly sulfury and green-leaf notes (dimethyl sulfide, hexanal). High-temperature pasteurization or brief cooking - heating milk above 170°F/76°C - generates traces of many flavorful substances, including those characteristic of vanilla, almonds and cultured butter, as well as hydrogen sulfide. Prolonged boiling encourages browning or Maillard reactions between lactose and milk proteins, and generates molecules that combine to give the flavor of butterscotch.

He continues by speaking about the different types of pasteurization, and says (pg.22-23)

  The third method of pasteurizing milk is the ultra-high temperature (UHT) method which involves heating milk at 265-300°F/130-150°C either instantaneously or for 1 to 3 seconds, and produces milk that, if packaged under strictly sterile conditions can be stored for months without refrigeration. The longer UHT treatment imparts a cooked flavor and slightly brown color to milk; cream contains less lactose and protein, so its color and flavor are less affected.
  Sterilized milk has been heated at 230-250°F/110-121°C for 8 to 30 minutes; it is even darker and stronger in flavor, and keeps indefinitely at room temperature.

So, it appears as if indeed there may be some Maillard reaction going on in UHT, although it is probably minor (otherwise the milk would be much darker in color, as it is the case for sterilized milk).

The book also speaks about homogenization, but it does not mention anything specific about Maillard reaction there (homogenization is not carried on at high temperatures, so it does makes sense not to have it).

To answer your question:

  Does this effect the nutritional value of the milk?

Well, according to this presentation (but, be warned, it does not cite any reference!) it seems that it does, although I don't think the Maillard reaction is specially involved.

http://www.slideshare.net/Aslal_saja/effect-of-uht-treatment

Specifically it says that the irreversible changes that occur are:

Whey protein denaturation (35 to 100% of denaturation of $\beta$-lactoglobulin)
Slight increase in the size of casein micelles
Whey protein-casein micelle interaction
Maillard reactions
Fat globule composition changes (although no changes in nutritional value of milk fat)
Vitamin content changes (20-30% loss in vitamin B1 and B12. Markedly reduced content in vitamin C and folic acid if high level of oxygen were present during the treatment, no changes in vitamins A, D, E and beta-carotene).

It also says that:

  Biological value and net protein utilization of UHT milk were lower for stored milk than directly used milk. Lysine loss during UHT is high but not significant to affect milk nutritional values.

I don't know whether the fact that you have problems when drinking UHT milk has anything to do with Maillard reaction or any of the other modifications brought by UHT treatment, and I will not venture in there, as I am not an MD and prefer not to give any sort of medical advice.


Why are most transcription factors enhancing the expression rather than repressing?

I can answer this question only based on guesses because I am not really sure about your claim that activators are higher in number than repressors. So consider this as an extended comment.

  While activators can interact directly or indirectly with the core
  machinery of transcription through enhancer binding, repressors
  predominantly recruit co-repressor complexes leading to
  transcriptional repression by chromatin condensation of enhancer
  regions

Not really true. A repressor can simply sit on the the promoter and prevent RNAP from binding the to the latter.

  Abstract

  Transcriptional repressors are usually viewed as proteins that bind to
  promoters in a way that impedes subsequent binding of RNA polymerase.
  Although this repression mechanism is found at several promoters,
  there is a growing list of repressors that inhibit transcription
  initiation in other ways. For example, several repressors allow the
  simultaneous binding of RNA polymerase to the promoter, but interfere
  with subsequent events of the initiation process, eventually
  inhibiting transcription initiation. The recent increase in the number
  of repressors for which the repression mechanism has been
  characterized in detail has shown an amazing variety of strategies to
  repress transcription initiation. It is not surprising to find that
  the repression mechanism used is usually exquisitely adapted to the
  characteristics of the promoter and of the repressor involved.

Some justification on why the number activators would be more:

A network perspective:

Lets assume an that gene-A somehow causes the repression of the gene-B. This repression can be either direct (A being a repressor of B) or indirect via some other genes. In the case of indirect regulation you just need one repressor in the network path A → B to result in repression of the latter.

So all repressive paths would minimally require only one repressor, all other steps in the path can be activation; whereas in an activating path you would need 'n' activators for 'n' steps.

Post-transcriptional Regulation:

Now if you include post-transcriptional regulation then you can find more number of repressors: miRNAs (2588 reported in humans: miRbase-21) and many proteins as well (For an e.g. see here). Most cases of events leading to translational activation are actually derepression. It is logical in a way because an mRNA is a temporary product; it should not by default require an additional signal to start producing proteins.


Are there any multicellular forms of life which exist without consuming other forms of life in some manner?

Yes, plants for example!

Autotrophs vs. heterotrophs

Plants are autotrophs while animals and fungi are heterotrophs. Have a look at the Wikipedia articles. In short, autotrophs organisms are organisms that synthesize their own compounds from inorganic compounds. Heterotrophs organisms are organisms that synthesize their own compounds from organic compounds.

Therefore, any multicellular plants are multicellular organisms that "exist without consuming other forms of life" (with the exceptions of carnivorous plants).

Consuming nonliving organic matter

Of course, many life forms feed on organic matter but only on non-living organic matter. Such life forms do not kill to feed. It is the case of all detritivores (such as earthworms) and decomposer such as fungi.

Competition vs predation

As @TechZen said, not consuming other organisms doesn't mean that the existence of an individual of this species is not causing the death of another individual (competition and parasitism that does not involve consuming the other individual).


What types of archaea have been found in animals?

Humans:

A pioneering study using 16S RNA primers found only Methanobrevibacter smithii in the human intestine.

  Eckburg PB et al. (2005) Diversity of the human intestinal microbial flora. Science 308 1635-1638

In a recent review there is a comprehensive Table of archaea found in humans (this includes non-intestinal flora):

  Dridi B et al. (2011) Archea as emerging organisms in complex human microbiomes. Anaerob2 17: 56-63

Much of the work that is catalogued by Dridi et al. is repeated identifications of Methanobacteriales (Methanobrevibacter smithii, Methanosphaera stadtmanae and Methanobrevibacter oralis), but there are others from the Thermoplasmateles, the Halobacteriales and the Sulfolobales, plus some that are thought to be members of unknown archaeal orders.


How does the mutualism of figs and wasps exactly work?

Ficus sp. (various sorts of figs); have a close relation with a sort of Wasp's reproduction.

Tiny flowers of Ficus are enclosed inside a hollow, pear-shaped concave  special-type of inflorescence, also called hypanthodium (term commonly used in flower-stage) or Syconus(term commonly used for fruit stage) when flower stage sometimes c ( from outside it looks like a single fruit but it is not).

There is a very narrow entry-hole or orifice at the apical portion of the inflorescence.

Inside the inflorescence, there are  3 types of flowers.
1. Male flowers, 2. Female-flowers, and 3. 'Gall-flowers' those are assigned as female flowers but their 'style' is much shorter.

Male flowers located towards the orifice, whereas female and gall-flowers locates in deeper regions.

Blastophaga, a genus of wasp, brings in required pollen,  also called gall-wasp, lay eggs inside figs.

To do that, they enter inside the fig inflorescence, lay eggs on these dwarf 'gall flowers' using ovipositor.

The eggs develop larvae, which fed on some ovules, and form pupa.  When the pupa-stage develop into mature wasps, the try to crawl-out from the orifice, they brush against the male flowers.

This pollen-laden insect when enter in another fresh fg, it also pollinate that-fig.

Image URL : https://media1.britannica.com/eb-media/17/24017-004-98EF07A1.jpg .

Image Page-Source: https://www.britannica.com/animal/fig-wasp

  Source: College Botany, Vol-1 / Gangulee, Das, Datta; New Central Book Agency.

P.S: I think my answer is NOT satisfactory enough

This question require more scientific details.

Widely known fact is, fig-wasps pollinate figs. But really there is a lack of detailed information like does the mother-insect die inside the fig and only the young insect go-out? or the mother insect come out from fig after laying eggs? if the larvae eat the ovules then isn't it harmful to the fig plant at any extent? How female-figs (in dimorphic members) are pollinated... does the wasp travels from one fig to another? When the young wasp come out from the fig it certainly take some months to reach maturation to lay eggs. Within that period does the pollens sticked in their body , and viable to germinate on stigma? There are many sorts of figs. Does all of them require wasps? Would figs survive without the wasps? --- What the question seeks, is, out of the popular children-book story; the Scientific-details behind figs and wasps. I assume the answer would not broader than reasonable; if someone knows their life-cycles and structures, I think it is possible to give very point-to-point answers within limited space.


Why does the insulin taken from pig when injected into humans causes allergy but not the insulin taken from bacteria?

Proteins and peptides vary across species, even if we give them the same name. Some are very homologous among even distantly related organisms, others differ even within a genus. Of course there are also variations across individuals of the same species.

Insulin from pigs and horses is pig or horse insulin. It differs slightly from human insulin because the genes that encode insulin in pigs and horses are slightly different than the genes that encode insulin in humans.

We inserted the genes responsible for producing insulin in humans into bacteria, so the insulin produced by recombinant bacteria is actually human insulin. That's why it doesn't produce an immune response.

There is also the issue of isolation and purification, and it is easier to produce very pure insulin free of other contaminants from recombinant sources than from animal sources.

That's the idea, anyways. Many humans tolerate porcine insulin just fine, and it isn't necessarily clear that human insulin is actually better (for example, this study).


How are amino acids neutral at physiological pH?

You are right, most of the amino acids have pI around 6, so they are slightly negative at pH 7.

Calculating approximate isoelectric points for amino acids and peptides

The isoelectric point depends on the amino and carboxylic-acid groups and the groups of the side chain. E.g. lysine has an amino group on the side chain, so it has a pI of 9.74.


What is this 2-3cm insect found in South-Eastern Brazil?

Maybe a cassadine beetle ?

You are correct! This insect does belong to the subfamily Cassidinae (common referred to as "tortoise beetles"), and is of the species Stolas aenea.


I believe this is the Hairy Flower Wasp, Scolia soror. I don't know what you mean when you refer to six wings, however. Like all other wasps, this species has four wings.


Question about *Cryptosporidium hominis*

This page seems to indicate that it adheres to the epithelium of different internal organs. They write:

The sporozoites are released and parasitize epithelial cells (b, c) of the gastrointestinal tract or other tissues such as the respiratory tract.

Here is the figure from that page:


I'm not a metallurgist, which you should probably ask... but there is this that I found:

Low Melting Fusible Alloys

Both Cadmium and Lead are toxic, but Bismuth, Indium, and Tin are not. An alloy of those might be what you're looking for. Indium raises the price-point considerably, as it's a few magnitudes more expensive than Bismuth and Tin.


How does sodium ion increase blood pressure?

Sodium acts on the juxtaglomerular cells of the kidney, which are then activated to produce and secrete renin. Renin hydrolyses angiotensinogen into angiotensin I. Next angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II.

Angiotensin II is the product that causes the increase in blood pressure, because it is a potent vasoconstrictor. With peripheral vasocontriction the heart has more resistance to pump blood against, thus higher blood pressure. Additionally, angiotensin II stimulates secretion of aldosterone from the adrenal glands, which acts on the distal tubules and collecting ducts in the kidney to retain sodium and water, thereby increasing blood volume and thus blood pressure.

Image: RVC 2008

This pathway is one reason why ACE-inhibitors, such as benazepril, enalapril, lisinopril, or perindopril, are used to treat hypertension (high blood pressure). With less activity of ACE, there is less angiotensin II, and blood pressure goes down. Hypertensive patients are told to consume a lower sodium diet because that will lead to less activation of the JG cells in the kidney, which will eventually result in less angiotensin II, and thus lower blood pressure.


It's actually not a seed pod, but rather a gall (see here or here for more info about galls). Specifically, it most likely is a gall belonging to the Oak Apple Gall Wasp (Amphibolips confluenta). You can read about this species and its gall here.


What is the criterion for genetic similarity among siblings and humans in general?

Your slight suspicion is close to correct. There are two different ways to discuss 'proportions of shared DNA' (identity by state, versus identity by descent). If two individuals share an allele that is identical by descent, it must by identical by state, but the reverse isn't true.
The 99% figure comes from comparing all of the base pairs and follows the concept of 'identity by state', where 'state' is A, T, C, or G. If individual 1 and individual 2 both have an A at position 39, they match. Average over all positions in the genome, and there's your 99% figure.
The second part of your suspicion is not quite correct, largely because of assortative mating and drift within local populations. The 50% figure comes from classical theory of Fisher, Haldane, and so on. They were trying to solve the mathematics starting from pedigrees and Punnett squares. They didn't have access to the high-throughput DNA sequence data that is common today, but you can follow a rare allele through a pedigree if it causes some observable outcome in its carriers. As a consequence, the classical theory is defined in terms of 'rare' alleles and follows the concept of 'identity by descent', and is tightly linked to the sorts of things you can observe in a pedigree. Having examined many pedigrees, you can generalise the patterns to derive classical population genetics theory. The key thing to remember here is that this branch of theory is expressed in terms of limit formulae: 'as variant A becomes rare, statement Y becomes closer to true'. In that context, the 50% figure is approximately the probability that your full-sibling has a rare allele, given that you have it.
That 50% is a direct consequence of the mechanics of meiosis: you have two copies of each allele. One copy of each allele was inherited from your mother, and the other from your father, at random. As a result, offspring have an exact 50% chance of inheriting any rare allele carried by one of their parents, and so are exactly 50% identical by descent to each of their parents. By the same reasoning, individuals are 50% identical by descent to their full-siblings, on average. In contrast, all humans are 99% identical by state, because a large portion of the genome is shared by all humans.


I usually find the treatment of Ethidium bromide in the lab widely exaggerates the true dangers of this chemical.
It is not really toxic (the LD50 is 1.5 g/kg bodyweight, as a comparision NaCl has a LD50 of 3 g/kg). It has also only been shown to exhibit mutagenic potential to bacteria after it had been treated with liver extracts. This means that some of the metabolized products of EtBr in the liver are mutagenic, but EtBr itself not. See reference 1 for details here. It is also not classified as a cancerogenic substance by the regulation bodies (for example see the National Toxicology Program of the US on Ethidium bromide).

As already mentioned, it is used to cure Trypanosoma infections in cattle (reference 2). Here up to 1 mg/kg bodyweight are given, with no signs of toxic or other adverse effects. The typical concentration used in the lab to prepare gels is 1 μg/ml. It works as a drug by interfering with the mitochondrial DNA (changing it to the Z-form, which is not available for replication). See reference 3 for details. Ethidium bromide also acts as a Topoisomerase I inhibitor as other chemotherapeutic drugs. See reference 4 for more details.

Additionally, EtBr is negatively charged and cannot enter cells or the nucleus, since cannot pass the membranes. I would wear gloves and also apply the usual safety rules when working with gloves (do not touch anything you don't need to touch, especially things like door knobs, keyboards or phones as you might spread contamination) dispose your gloves when not needed anymore and you should be fine.

References:

Detection of carcinogens as mutagens in the Salmonella/microsome
test: assay of 300 chemicals.
Comparison of isometamidium chloride and homidium bromide as
prophylactic drugs for trypanosomiasis in cattle at Nguruman, Kenya.
A low dose of ethidium bromide leads to an increase of total
mitochondrial DNA while higher concentrations induce the mtDNA 4997
deletion in a human neuronal cell line.
The geometry of DNA supercoils modulates the DNA cleavage activity
of human topoisomerase I


What are the side-effects of long-term liquid breathing?

Overview.

This is a very interesting question. The ideas behind this have been around for a while and the methods are covered in great detail elsewhere.

The overall answer to the hypothetical question is rather surprising. There may be actually potential benefits to perpetual liquid ventilation for people with certain diseases. Trials so far have not found side effects in fluorocarbon liquid breathing.

So lets talk about the history of liquid breathing and case studies, then we will move onto the hypothetical situation of liquid breathing indefinitely.

A great review (Shaffer et al, 1992) covers the field in great depth.

@MCM pointed out in the comments that my original answer did no emphasise that animal diaphragms are not powerful enough to move the liquid in and out of the lungs. I should mention now that the below cases all use ventilators to pump the fluid into and out of the lungs. The difficulty of breathing this without a ventilator is emphasised by David Blaine at 4:54 in this TED talk who said it was like trying to breathe with an elephant standing on your chest.

Case studies.

As early as the 1920s, poisonous gas research that lead to the infamous mustard gas found that lungs could tolerate large quantities of saline briefly without damage.

Animals.

Kylstra, the first pioneer introducing the idea of land animals breathing liquids (Kylstra et al., 1962), found mice could withstand 4 hours of 160 atmospheres of pressure.

Clark found that mice and rats could breathe oxygen bubbled silicone oils and survive for a few hours after emersion.

In 1965, he discovered that the fluorocarbon known as FC75 not only supported respiration during total immersion but the mice survived indefinitely in apparent good health.

The most recent study I can find is the partial use of fluorocarbon liquid ventilation in adult respiratory distress syndrome (ARDS) of rabbits. The same improvements in breathing were not observed in saline liquid breathing or conventional ventilators.

Humans.

In humans PFCs were first used successfully in 1989 for the ventilation of young infants near death.

  Marked improvement in lung compliance, without a compromise of cardiovascular status was noted in all three patients.

All three infants died of their severe preexisting respiratory complications, but the trial showed liquid breathing can support gas exchange in humans. However developing lungs of infants cannot rely on mechanical ventilators for prolonged periods as nearly a quarter of premature infants of those that do later developed chronic breathing problems.

Biomedical application.

There are a fair few researches and doctors who believe fluorocarbon liquid ventilation has some advantages over gas ventilation. It reduces stress at the area of interfacial surface tension in the distressed, surfactant-deficient lung. This would be ideal and appropriate for ARDS in human adults. A more sophisticated use would be using fluorocarbons as a drug delivery system straight to damaged lung tissue.

(All the above can be found in the 1992 review. There is also data on the different properties of suitable FCs)

Real world potential.

  Is perpetual liquid breathing possible? ...And healthy?

So this is where we stand with the case studies; mice can breath liquids indefinitely and stay in good health, rabbits with ARDS survive where breathable gas would not help, and there is a contingency in the biomedical community that it can be better than gas ventilation for medical treatment. To me it seems that there is nothing to suggest a fully grown adult would suffer from breathing liquids. The inertness of the fluorocarbons implies any toxicity would only reveal itself in a timescale of years, and everything else about the compounds pose no danger and may make gas transfer across the lungs easier.

This relatively modest success is perhaps no surprise. The exchange interface of our lungs relies on a mucous (liquid) so the gases can permeate the lung tissue. Expanding on that idea should certainly not rule out the possibility of liquid breathing.

The biggest drawback, besides the cost of a long term experiment and being dependent on a mechanical ventilator, is that these are very small case studies of success. Given the massive amounts of unknowns (particularly for long term studies), switching to  purely liquid ventilation in an adult human could have unforeseen risks and would be considered dangerous by any ethics board (or insurance company)!

On a lighter note, here is a YouTube video of what Maddie, a biology podcaster from the BBC, had to say on the matter of living in total submersion. Lots of skin problems, risk of infection after a few days etc.

Again, a very interesting, albeit understudied, topic!


Do nucleosomes ever completely unwrap during transcription?

Yes, nucleosomes are completely unwound. Histone chaperones such as FACT (for H2A/H2B) and ASF1, CAF-1, HIRA, Nucleophosmin etc (for H3/H4), associate with RNA Pol II and handle the displaced nucleosomes. As you surmised, the histone octamer complex is disassembled, into the H3/H4 tetramer and two H2A/H2B dimers. Right behind the elongating Pol II, the chaperones reassemble nucleosomes. During the process of reassembly, it has been shown that "new" H2A/H2B dimers (and possibly H3/H4 tetramers too) can get incorporated into an "old" histone octamer. Finally, nucleosome remodelling complexes such as SWI/SNF re-space the nucleosomes.

This is a decent review of the process (by one of the discoverers of the FACT complex, incidentally): "New chaps in the histone chaperone arena". Campos & Reinberg. Genes & Development (2010): 24: 1334-1338

This is a comprehensive review of histone chaperones and nucleosome dynamics during various DNA-dependent processes (such as transcription, replication and repair). There is an entire section on their role in gene transcription, which is the main thrust of this question: "Histone Chaperones: Assisting Histone Traffic and Nucleosome Dynamics". Gurard-Levin, Z.A., Quivy, J., and Almouzni, G. Annual Review of Biochemistry (2014): 83: 487-517

And finally, a good overview on histone dynamics and chromatin structure during transcription: "Histone exchange, chromatin structure and the regulation of transcription". Venkatesh & Workman. Nature Reviews Mol. Cell. Biol. (2015): 16:178–189

I should add that an inability to disassemble nucleosomes (or displace any other factor bound very tightly to DNA) can actually pause an elongating Pol II complex.


Can breathing in helium (from balloons for example) cause damage to the throat in the long term?

When we speak, our vocal cords vibrate to the air. Helium makes them vibrate a lot faster (that's what makes the funny sound of your voice after inhaling helium), because its atoms are a lot lighter than nitrogen and oxygen atoms. Obviously, lighter atoms, can travel faster. This faster vibrations are unusual to the cords and they can cause sore throat or even strong throat ache. After you stop inhaling the gas, things should get back to normal, especially if the inhalation really is infrequent.

Breathing helium balloons at parties is a very dangerous fun activity, because it replaces the oxygen and this could lead to hypoxia - a condition when tissues can't get enough oxygen one reason or another. In some cases, this could even be fatal.

Even though inhaling of pure helium is dangerous, in submarines, divers breathe a mixture of nitrogen, oxygen and helium as helium is better under higher pressures. At these depths the low density of helium is found to considerably reduce the effort of breathing. Divers often have problems with dry throat and constant thirst due to the need of more oxygen. At least, inhaling helium, when it's mixed with oxygen, is far less harmful than breathing it directly from a balloon.


Moth that resembles a leaf. What species is this?

It resembles Pelagodes antiquadraria, which belongs to the moth genus Pelagodes in the family Geometridae.

Image Source: FlickRiver


How to determine whether a newly discovered dinosaur is not a young one and not an entirely different species?

Diagnosing extinct species is even more difficult than extant taxa (see this question). Because systematists describing fossil species (usually) only have skeletons, they compare to other fossils. You are correct that diagnosing a species from only a skeleton can be tricky. What defines what you call a genus, a species, etc.? How morphologically dissimilar can two skeletons be before you call them different species? The running joke is that if you found fossils of a chihuahua skeleton and a great dane skeleton, you would certainly call them different species. But by modern biological species concepts, they are the same species. Then there are extant species that are essentially indistinguishable in terms of their skeletons, but do not interbreed, and so are probably different species.

Sometimes there is consensus, and sometimes there is not. This disagreement can lead to a description of a new species by one person being reclassified ("revised" is the term used) as another species. There are lots of examples of this among dinosaurs. Most famously, Brontosaurus was revised as actually being Apatosaurus. More recently, and relevant to your question, Nanotyrannus is thought by some to be a juvenile Tyrannosaurus rex.

So then how did Fiorillo and Tykowski, who described Nanuqsaurus hoglundi, decide that it was (1) not just a juvenile T. rex and (2) that it was a new species? Their rationale is laid out really well in their paper, primarily in the sections "Diagnosis" and "Description". You rightly picked out the two questions that paleontologists reading this paper would want to know.

Nanuqsaurus is not a juvenile:

  The dorsomedial edge of the maxilla is marked by deep pockets separated by pronounced transverse ridges. These together formed a strong peg-in-socket articulation between the dorsal margin of the maxilla and the ventrolateral edge of the nasal. The same kind of deeply interlocking naso-maxillary contact is a well-documented character that is also present only in developmentally mature individuals of the derived tyrannosaurines Daspletosaurus torosus, Tarbosaurus bataar, and Tyrannosaurus rex 2, [6], [20], [21], [22]. The nasal-maxilla contact is either smoothly grooved or bears only weak scalloping in immature individuals and more basal tyrannosauroids 2, [6]. The presence of this feature in DMNH 21461 is evidence that the material also represents a developmentally mature individual.

What they are saying here is that maxilla (part of the front of the upper jaw) in Nanuqsaurus has a very characteristic relationship to the nasal bone in which they form a peg-and-socket joint. This relationship is found in tyrannosaurine dinosaurs like Tyrannosaurus, Daspletosaurus, and Tarbosaurus. But more importantly, it is only found in adult tyrannosaurines. So they conclude that Nanuqsaurus is an adult.

Nanuqsaurus is a distinct species from Tyrannosaurus and other tyrannosaurines

  In all three hypotheses of phylogeny, Nanuqsaurus hoglundi was found to be a derived tyrannosaurine, the sister taxon to the Tarbosaurus + Tyrannosaurus clade (Figure 6). This node was supported by a single unambiguous character, the presence of a dorsoventrally tall, paired sagittal crest on the frontal. The age of Nanuqsaurus hoglundi (70-69Ma) is consistent with its place in the recovered hypothesis of tyrannosauroid phylogeny, positioned in time between the more basal Daspletosaurus torosus (Middle to Late Campanian) and the more derived Tyrannosaurus rex (latest Maastrichtian) among other North American tyrannosaurines.

The authors ran a phylogenetic analysis of characters coded for Nanuqsaurus and about 20 other taxa. Nanuqsaurus has enough shared characteristics to put to solidly among tyrannosaurine (near Tyrannosaurus, Daspletosaurus, and Tarbosaurus). But, importantly, it has a characteristic that none of these others have: "the presence of a dorsoventrally tall, paired sagittal crest on the frontal."

Based on its being an adult and having a character that is not found anywhere else among tyrannosaurines, Fiorillo and Tykowski name a new species. I'm simplifying what they did, but that's the general idea. To their credit, they acknowledge that there is not a lot distinguishing the new species and discuss in much more detail their rationale and the implications of their results.


What are the blood groups for human beings?

As far as I am aware it is the RhD and ABO blood groups that matter with blood donation - though you may wish to contact a blood donation organisation for more specific information on how they handle & categorise the blood.

But using just RhD and ABO gives 8 combinations, positive and negative of A, B, AB, and O. You can find out more about the blood groups, blood donation, and the characteristics of blood groups here.

The subgroups you allude to are due to differences in the number of the antigens on the surface of the blood cell, for example the A1 group have ~1,000,000 A antigens per cell whereas A2 variants have ~250,000. The A group has ~20 subgroups, the vast majority of people are A1 (~80%) or A2 (~20%), and the other groups make up less than 1% of the population.

  These two subgroups are interchangeable as far as transfusion is concerned, but complications can sometimes arise in rare cases when typing the blood.


What concentration of hydrogen peroxide kills mold?

The CDC Guideline for Disinfection and Sterilization in Healthcare Facilities provides a good overview of various disinfectants and their effectiveness against different kinds of pathogens, along with citations if you're interested in more detail.
This document doesn't evaluate the effectiveness of Hydrogen Peroxide against Stachybotrys (black mold) specifically (the CDC specifically recommends Chlorine Bleach for this purpose), but it does describe it's effectiveness as a fungicide. Note that the level of disinfection needed to control pathogenic fungus in a healthcare setting is likely much higher than needed to control black mold in a house, but it can give you a sense of how effective Hydrogen Peroxide is overall:

A 0.5% accelerated hydrogen peroxide demonstrated bactericidal and
virucidal activity in 1 minute and mycobactericidal and fungicidal
activity in 5 minutes [656]
...
A 7% stabilized hydrogen peroxide proved to be sporicidal (6 hours of
exposure), mycobactericidal (20 minutes), fungicidal (5 minutes) at
full strength ... [655]
...
The 7% solution of hydrogen peroxide, tested after 14 days of stress
(in the form of germ-loaded carriers and respiratory therapy
equipment), was ... fungicidal (>5 log10 reduction in 20
minutes),[663]
...
A new, rapid-acting 13.4% hydrogen peroxide formulation (that is not
yet FDA-cleared) has demonstrated sporicidal, mycobactericidal,
fungicidal, and virucidal efficacy. Manufacturer data demonstrate that
this solution sterilizes in 30 minutes and provides high-level
...
Commercially available 3% hydrogen peroxide is a stable and effective disinfectant when used on inanimate surfaces
disinfection in 5 minutes [669]

From this, it seems like you'd want to use accelerated Hydrogen Peroxide, or 7% stabilize Hydrogen Peroxide to ensure fungicidal disinfection. 3% Hydrogen Peroxide is effective against bacteria, but the studies cited didn't test it against fungi.


Questions about Cohesin - what does the ATPase domain do, and any suggested PDBs to look at?

This article :
Prakash Arumugam, Stephan Gruber, Koichi Tanaka, Christian H. Haering, Karl Mechtler, Kim Nasmyth,
"ATP Hydrolysis Is Required for Cohesin's Association with Chromosomes",
Current Biology,
Volume 13, Issue 22,
2003,
at
https://www.sciencedirect.com/science/article/pii/S0960982203008042
Their conclusion is:
"Conclusions: Cohesin complexes whose heads have been connected by Scc1 must hydrolyze ATP in order to associate stably with chromosomes. If chromosomal association is mediated by the topological entrapment of DNA inside cohesin's ring, then ATP hydrolysis may be responsible for creating a gate through which DNA can enter. We suggest that ATP hydrolysis drives the temporary disconnection of Scc1 from Smc heads that are needed for DNA entrapment and that this process is promoted by Scc2/4."


Human Anatomy and Physiology - The Muscoskeletal System

For bone grafts, they usually use parts of the bones, so their removal should not result in problems with the "body weight maintenance" or "posture."

Parts of the fibula (calf bone) can be used, for example, as a graft to repair avascular necrosis of the femoral neck or congenital pseudoarthrosis of the tibia (shinbone) (International Orthopaedics).

For spinal fusion (joining the vertebra in the spine), they typically use the bone from the iliac crest (the top part of the pelvis) (OrthoInfo).

Other bones that can be used as grafts:

Parts of the ribs and certain skull bones for reconstruction of the facial bones
Parts of the mandible for tooth implants
Upper part of the tibia for various purposes
Distal part of the ulna for correction of the wrist in rheumatoid arthritis


Yes and no.

According to this paper, great apes and our ancestors had a life expectancy at birth of about 13 years (chimpanzees). Over a few million years of evolution, human life expectancy rose to >30 years in the 18th century. Industrialization and improved nutrition, hygiene and medicine resulted in a jump to >60 and now around 80 years in developed countries in just 200 years. The paper compares data from Sweden, but if you look at the data from gapminder.org, you see that this trend holds true for all nations (especially developing countries like India and China, who doubled their life expectancy in just 50 years).

So, while humans have evolved to live longer (as you asked in the title), due to a lower mortality and resulting increase in the age of maturity as well as the likely benefit of "grandmothers" (older, infertile females helping to feed their grandchildren) (discussed in this source), the recent increase in life expectancy in just a few generations is unlikely due to evolution.

While humans are still evolving, we have reduced the selective pressure. There is no benefit to the survival of the offspring when we live past 80-100 years. And comparing countries with lower standards in hygiene and medicine (I totally recommend playing with the gapminder tools), their life expectancy was still pretty low in recent years, only increasing with access to clean water, food and medicine. Comments on extending the lifespan usually refer to medical interventions to cope with the effects of aging.


Are there any strictly chloroplast/mitochondrion-residing ribozymes?

You've already mentioned rRNA. An interesting review (Tanner, 2006), outlines some more:

Group I Introns - self-splicing; "They are abundant in fungal and plant mitochondria..."
Group II Introns - some have been shown to self-splice; "...they are found in fungal and plant mitochondria, in chloroplasts of plants ... and especially in the chloroplasts of the protist Euglena gracilis."
RNase P - involved in tRNA processing, found in mitochondria

None of these are strictly found in mitochondria or chloroplasts. However, the paper goes on to describe VS RNA ribozyme:

The mitochondria of certain strains of Neurospora contain the Varkud plasmid (a retroplasmid), which encodes a reverse transcriptase, and a small, unrelated, RNA (VS RNA). The VS RNA is transcribed from circular or multimeric VS plasmid DNA by a mitochondrial RNA polymerase, and the resulting transcripts are subsequently site-specifically cleaved and ligated to form circular, 881 nucleotides long, RNA monomers. These monomers are then reverse transcribed and made double stranded to form the mature VS plasmid.
In vitro transcribed VS RNA precursors are cleaved and ligated by the RNA itself and this is presumed to occur in vivo as well. Of all the self-cleaving RNAs, the catalytic properties of VS RNA are the most poorly understood.

References

Tanner NK. 2006. Ribozymes: the characteristics and properties of catalytic RNAs. FEMS Microbiol Rev. 23(3):257-275.


How do the flowers of Diphylleia grayi become transparent after rain?

I have to hypthesise here:

the white colour you perceive is most likely near-to-full diffusion (or possibly better phrased: reflection with effectively undirected refraction due to multiple reflections) of light by structures on the surface of the petals and/or air space encapsulated in the petals. (This is true for most white flowers, by the way.)

Water fills the structures and/or the air space, which changes the refractive index of the petal surface.

In other words: the flower becomes like water, because the air is driven out.

Edit: seems I was right. SE asked me to add links to my answer, so I asked GoogleScholar about D. grayi and found this: "The inner part of the petal comprises numerous lacunae and intercellular spaces that are filled with air."
(source: Yong et al. (2015). Bioinspired transparent underwater superoleophobic and anti-oil surfaces. Journal of Materials Chemistry A, 3(18), 9379-9384.)


Why is Capsaicin injection not used instead of nerve surgeries for pain?

There is a simple answer to your question: it might cause a massive inflammation-like response and it might also hurt really, really badly.

Capsaicin activates heat receptors which are not only involved in heat reception (that would cause the pain as TRPV1, the receptor, is strongly activated at temperatures higher than 43 degree Celsius - accordingly, it will feel like burning from inside) but also in sensing inflammations within the body. That means that your body will think it has to take strong and immediate action if capsaicin enters tissues directly, flush out a bunch of neuropeptides and actually might start destroying the affected tissues.


Which part of the genome are the developmental sequences of embryogenesis located?

This is a very general question. The "developmental sequences" are just genes like any other. Like all genes they are semi-randomly distributed through the genome. While there are gene-rich and gene-poor areas in the genome, with some exceptions --notably the homeobox genes--, genes are not grouped by function.

As to how they are accessed sequentially, that is a huge question but it is not specific to embryogenesis. Genes will always need to be turned on/off at specific times and in response to specific stimuli. This is particularly obvious during development but is not exclusive to it.

The basic way this happens is through feedback and control loops. Gene A activates the transcription of gene B which activates gene C which then deactivates A. If you manage to turn on A, the rest will follow. One of the ways this can happen in developing embryos is through maternal mRNA. These are mRNA molecules that are present in the fertilized egg and which begin to be translated. This gives us a starting point to activate gene A, which then turns on B etc.

This answer is a huge simplification but a full answer could take up a couple (or 40) of PhD projects.


Do endosymbiotic organelles have Latin classification?

As any other organelle, endosymbiotic organelles do not have a systematic name. However, their descendant prokaryotic organisms do have a genus name.


Difference between micro RNA and short-interfering RNA and CRISPR Cas 9 system?

The CRISPR Cas 9 system is used to introduce insertion or deletion in a genomic sequence not mRNA.

https://www.addgene.org/CRISPR/guide/


Is mucus significantly affected by the presence of ions?

Yes.  Mucus is hydrated by the movement of ions.

Cells cannot move water.  Cells can only move ions, and water follows the osmotic gradient.  When hydrating mucus, cells move ions into the mucus and water follows.  A failure of this system is seen in cystic fibrosis.

Targeting ion channels in cystic fibrosis

  CFTR, the protein that is defective in cystic fibrosis (CF), directly
  mediates the transport of chloride and other anions through the apical
  membrane of several types of epithelial cells [1], [2]. Therefore,
  mutations impairing CFTR function cause a severe imbalance in ion and
  water transport that leads to a variety of negative effects in various
  organs. In the lungs, impaired secretion of chloride and bicarbonate
  appears to have multiple consequences. First, reduced secretion of
  electrolytes, and consequently of water, causes dehydration of airway
  surfaces with impairment of mucociliary clearance [3]...

People with cystic fibrosis have a defective chloride channel, and it cannot move chloride into mucus.  They therefore have thick mucus with abnormally low water content, and much of the trouble they have with their lungs is because this thick mucus does not perform its functions well.


Parallel nucleic acid double strand is possible but it is not as stable as the antiparallel form (Szabat and Kierzek, 2017). This is because the nucleobases are not aligned in a way that is conducive for the Watson-Crick (WC) type base pairing. In parallel conformation, the bases can form Hoogsteen (HS) and reverse Watson-Crick (RWC) type base pairing (see below).

You can see that these base pairs are not as strong as that in WC base pairing:

No triple bond between G and C in RWC base pairing
GC pair occurs in HS base pairing only when C is protonated at low pH

Formation of parallel helices, therefore depends on the sequence.

  In general, the formation of duplexes with parallel strand orientation
  is determined mostly by the sequence context and pH conditions.
  Fragments of RNA or DNA capable of forming a parallel duplex are often
  rich in A and C, which is related to their ability to become
  protonated, in middle acidic conditions.

However, it is not as simple as RNA/DNA base pairing with its complement. Parallel helices would not follow the WC base pairing rules and therefore predicting whether they will form is not that straightforward. However, parallel helices can form in vivo (see references 23–25 of Szabat and Kierzek, 2017).

You can also check out this article by Leontis et al. (2002) for hydrogen bond patterns in parallel and antiparallel helices.


What is the correct nomenclature for expressing a genotype where a recombination event may occur?

I would suggest "genotype".
A Punnett square is a visualization technique to help us think, it doesn't change the terminology.
If what you mean is the 1N genotypes represented in the rows/columns that combine to make the 2N genotypes, you might consider "haplotype" (haploid genotype). The haploid cells with those genotypes might be called gametes, but that refers to the cell and not to the genotype.
If you are specifically interested in those genotypes/haplotypes in which a recombination event has occurred (or not), you could call them recombinants or non-recombinants. In some cases you can encounter specialized terminology, for example in yeast tetrad analysis you encounter terms such as "tetratype", "nonparental ditype", "parental ditype". But those are not generally used outside the yeast field, I believe.


Why isolated, recombinant plasmid DNA without any restriction is often detected in agarose gel electrophoresis as three DNA bands?

These are the three forms of the plasmid: supercoiled (smallest 3D-structure, runs fastest), linear (runs in the middle) and relaxed, nicked plasmid (runs highest). You can have another fourth band, which is the circular single stranded plasmid (runs faster than the supercoiled version). See the following figure (from this article, which I recommend reading):


Do antisense transcripts have different names than their sense strand transcripts?

If the anti-sense transcript is correctly annotated and in the databases (a very very big if), then it will have a different name. For example, the mouse Msx1 anti-sense transcript has the RefSeq accession NR_027920 while the sense transcript of the same gene is NM_010835.

In general, each transcript that is transcribed from a given locus has a different accession. The same is true for alternatively spliced transcripts. If a given gene has 4 AS transcripts, each of these transcripts will have a different, unique accession. The human insulin receptor gene, for example, has two protein coding transcripts, each with its own accession: NM_000208 and NM_001079817.

You may be interested in a recent analysis of cis-NATs in 10 species[1] and also in NATsDB: Natural Antisense Transcripts DataBase[2].

Osato N, Suzuki Y, Ikeo K, Gojobori T. 2007. Transcriptional Interferences in cis Natural Antisense Transcripts of Humans and Mice. Genetics, 176(2): 1299-1306, doi:10.1534/genetics.106.069484.
Li JT, Zhang Y, Kong L, Liu QR, Wei L. 2008. Trans-natural antisense transcripts including noncoding RNAs in 10 species: implications for expression regulation. Nucleic Acids Research, 36(15):4833-44, doi:10.1093/nar/gkn470.


Name of this kind of stain on fruits and how do they form

You never visited the avocado blemish identification fanpage? do you use google? it's quite good.

http://ipm.ucanr.edu/PMG/C008/m008fpfrtdmg.html
Causes of avocado Damage

Avocado thrips

Anthracnose

Caterpillars

Branch canker and dieback

Fruit and stem-end rots

Genetic mutations

Greenhouse thrips

Latania scale
Mechanical injury

Nutritional disorders

Off-season fruiting

Persea mite

Phytophthora fruit rot

Sooty mold

Sunblotch

Sunburn

Vertebrates

Weather extremes

Wildland fire

mosty they are insects, funghi, viruses, mechanical forces, and sometimes, like the woody avocado, the cause is unknown:

referenced.


Identifying whether ELISA kits are authentic or fake

You are getting this Elisa Kit spam from China, too? The only way I see, would be to use a known reference standard so you can titrate both the specificity and the sensitivity of the kit. Ideally you would compare it with a known and proven kit. If you have the reference available in the lab and the cheap kit is not too expensive you can give it a try. I would do it, since work time and reagents also cost money.


How are the boundaries of a gene determined?

I know of only one naive approach to determining the boundaries of a gene : RACE-PCR. There are two kinds, 3' and 5' RACE, which allow to find the respective extremities.

The rationale is the following :

You perform a reverse transcription of the transcript of interest using a specific primer. At this step you have a specific single stranded cDNA.
Then you add a stretch of identical nucleotides called the homopolymeric tail in 5' of the cDNA.
Finally you perform a PCR using one specific primer and one universal primer that recognizes the homopolymeric tail. You can sequence your amplified cDNA and find where it is located in the genome with a 1 bp resolution.

For the 3'RACE, the concept is the same but the poly-A tail is used instead of generating it yourself with the terminal transferase.

See this paper for a detailed protocol :

 Sambrook J, Russell DW. 2006. Rapid Amplification of 5’ cDNA Ends (5'-RACE). CSH protocols 2006.

Also, the corresponding wikipedia article gives you more details about what is happening at each step, but beware, there is an error : it is said that for the 5'RACE, the terminal transferase appends the homopolymeric tail in 3' while it appends it in 5'


Biological implementation of convolutional neural networks

The eye might provide alone an example of a convolution neural network (as made popular for image classification tasks).

The cell types and synaptic connections in the retina are even organized in layers (laminae) to make the parallel clearer, as seen here:

source: http://webvision.med.utah.edu/book/part-vi-development-of-cell-types-and-synaptic-connections-in-the-retina/development-of-cell-types-and-synaptic-connections-in-the-retina/

The topology of the network is in a sense self-structured but a relatively slow process as the blueprint is a product of Evolution and the practical implementation (actual cells and connections) takes place during the development of the organ. "Weight tying" can then be seen as a result of having different cells types in the network.


What are the mechanistics of stinging nettles?

The stinging hairs (trichomes) of the common North American nettle (Urtica dioica) are sharp, pointed cells. These nucleated cells are embedded in a base of smaller epidermal cells. The shaft of the trichome is composed of silica. Upon touch, the tip breaks off, leaving a sharp tip similar to a hypodermic needle. The hollow trichome penetrates the skin, and toxin from the base is injected into the skin tissue. The stinging toxin includes a mixture of histamine, acetylcholine and 5-hydroxytryptamine (Online Textbook of Natural History).

Left: schematic of a stinging cell, or trichome of a nettle. Right: trichomes on the stem of Hesperocnide tenella. Source: Online Textbook of Natural History

I couldn't find any info on trichome pressure. It may be that the toxins are released passively. Otherwise, high concentrations of dissolved matter may attract water in the base, increasing the pressure (much like turgor present in many plant cells).