How long does it take for dopamine to reach normal levels after a significant drop?

I can see a couple of problems in the question:

First problem, you assume that anergia (not sure that's how you call being tired) after sex is caused by dopamine depletion, I'm not sure this is the case or that lack of dopamine has been related to anergia at all. We know from Parkinson patients that Dopamine is related with action initiation (http://www.nature.com/nature/journal/v466/n7305/abs/nature09263.html) not necessarily with lack of energy or motivation.

Second problem, depletion (the term you originally used) means no more dopamine is system, either because you block it somehow (antagonist), you block its receptors (receptor antagonist) or you block one of the precusors involved in synthesizing it eventually depleting your reserves. "Significant drop" needs to be quantified.

Dopamine (DA) synthesis is an ongoing process, and DA is an essential neurotransmitter / neuromodulator in the brain just like Serotonin (more on that later). This means that it probably has different roles. One phasic referring to its neurotransmitter properties and one tonic referring to its global levels in the brain and how it modulates ongoing synaptic activity.

Normal activity does not deplete DA, and yes, no matter how crazy you think you are, sex is considered normal activity. You can obviously have variations of basal levels of DA depending on your activity but they are way removed from the depletion criteria.

Furthermore, the brain is very parsimonious in its synthesis efforts, it has specialized molecules that recover neurotransmitters that where unused from the synaptic cleft, these molecules are appropriately called reuptakers.

Now to attempt to answer your question considering the problems:

I don't know about DA but I do have some experience with serotonin depletion.
Serotonin (5-hydroxytryptamine, 5-HT) is synthesized from tryptophan that you cannot produce endogenously. Lucky for us that tryptophan is in almost every food we eat which means that there is no lack of it.

You can, in experimental conditions, ask people to drink a glass of a very disgusting liquid that will bind to your tryptophan preventing it from being used in new 5-HT synthesis. It takes approximately 4-6 hours for it to work (e.g. http://web.stanford.edu/~knutson/ans/bjork99.pdf methods section), which means that in 5 hours you used up all your reserves of 5-HT. This meansthat your "refilling" process would be about the same time  in order to get to pre-depletion levels (you might be able to be in a functional regime before that if you ignore the reserves part).

So from this 5-HT example I would say that unless something is very different in the case of DA to recover from depletion it would have to be in the hours time frame.

Another way of looking at it can be looking at the half-life of the molecule which gives you an idea of how much time it lives. This can be used to calculate how much production there has to be to maintain a level of X. The turnover is the amount of time that it takes to, well, turn over, so replace DA in the system that should be in the same order of magnitude as coming back from a depletion experiment.


Genetic Imprinting and Cell differentiation

What if imprinted regions are immune to being wiped? Also, you may be confusing DNA methylation, and histone methylation (?). Classical biochemistry posits that DNA methylation states can be transmitted from a dividing mother cell to both daughter cells because after DNA replication the two daughter chromosomes will each be hemi-methylated, and a DNA methylase that finds a hemi-methylated site will methylate the other strand (like a corrective editing mechanism).
The third thing to consider in your question is that parental imprinting is established in the germ line. In terms of wiping other epigenetic marks during early embryogenesis, the only ones present would be the ones involved in gametogenesis.  In other words, as far as we know, genes activated in muscle development are never expressed after fertilization in the zygotic cells that will give rise to the primordial germ cells, so those muscle-specific epigenetic marks don't need to be wiped off in the embryo. Neither the sperm nor the egg ever expressed muscle myosin, etc.


If some humans inherited 3% of Neanderthal DNA, why are we 99.9% same genome?

3% and 99.9% are from different calculation method.

20% (a rough estimation, might be wrong) of neanderthal DNA survived in the modern human genome, but it is 'diluted' by the human population,  which lead to 2 percent of neanderthal DNA in each human genome. This is the number 3%.

But how can we know it's neanderthal DNA?

If DNA fragment contains several neanderthal special SNP (single-nucleotide polymorphism), we will treat it as neanderthal DNA. (Based on linkage disequilibrium, the inference is reasonable.) The fragment might of tens of thousands nucleotides, but the difference are just one or two base.

But when we compare two human, we calculate the difference at nucleotides level, rather than DNA fragment. This is the number 99.9% come from.

If we have the complete genome of neanderthal and human, by comparing them at base level, the similarity might be great than 99%, I suppose.


Ischaemia is lack of sufficient perfusion to a tissue.  Reduced perfusion could therefore mean decreased blood supply to organs and tissues and could also mean a complete cessation of blood flow to an area - therefore both can be correct as they are on a continuum.  Infarction is tissue death due to hypoxia which can result from ischaemia that is not swiftly resolved.


TCT AAC TGA TTA GC

T CTA ACT GAT TAG C

TC TAA CTG ATT AGC

AGA TTG ACT AAT CG <<< this is the ORF

A GAT TGA CTA ATC G

AG ATT GAC TAA TCG

If the sequence comes from the middle of a gene we assume it should encode an open reading frame.
For this sequence only 1/6 frames does not include a stop codon (shown above in italics). So in standard format, with promoter to the left we can write the ds sequence as:

5'-AGATTGACTAATCG

3'-TCTAACTGATTAGC

Since this is homework I'll leave the rest to you.


Is NADH found in all type of cell in human body?

As NAD+/NADH is involved in both glycolysis and in the tricarboxylic acid cycle it is difficult to imagine any cell capable of generating energy not having some NADH. (Are there any cells that are not capable of this? Calcified cells such as bone?)

A quick internet search for ‘microglia’ and ‘metabolism’ indicates that microglia have energy metabolism and so I would expect them to have NADH. How much (compared to NAD+) would depend on their metabolic state.


What is the difference between tissue engineering and 3D bioprinting?

Tissue engineering is research into ways of organizing cells and cell droplet/matrix structures into a useful form, usually for medical applications. In the near future, tissue engineering could refer to rewriting or genetically modifying cells for a new purpose or to enhance their existing function. Even more into the future and tissue engineering could mean custom-building multi-cell structures from scratch on a computer.

3D bioprinting is the practical or laboratory deployment of the first technology mentioned above - a subset of tissue engineering.

In a nutshell:

Tissue engineering = "Come up with a creative way to arrange these cells and cell structures into something useful".

3D bioprinting = "Use the above-mentioned technology to build part of a synthetic organ".


One may think that Argon, being an inert noble gas, causes no harm at all and can perfectly replace N2 in a mix with oxygen. After all, you've been breathing Argon your whole life, since approximately 1% of the air is Argon:

However, we are talking about a raise from 1% to 78%... and there are possible consequences here:

Argon is way denser than N2: Argon has a density of 1.784 g/L, while N2 has a density of 1.251 g/L (O2 has a density of 1.428 g/l). So, Argon is 40% denser than N2 (and also denser than O2 and denser than air). Without taking into account ventilation and other forces, there is a risk of argon not mixing properly with the incoming "air" in your lungs.
Argon is a narcotic: This may sound strange, but there are evidences that Argon has sedative properties. According to Nowrangi, Tang and Zhang (2014):

  Argon gas is considered a small noble gas element that has been applied in a number of fields. It has been generally classified as a
  nonreactive or inert gas providing a view that it does not contain
  any biologically active characteristics. In fact, argon has
  demonstrated characteristics such as narcosis [...] The mechanism in which argon displays its anesthetic ability has been suggested to be from the stimulation of γ-aminobutyric acid type-A receptors. (emphases mine)

As an additional information, there is an Argon-Oxygen mix, called Argox, which is used for decompression research only, not as a scuba-diving breathing mix.

Also, this question from WorldBuilding has some interesting information (and some wrong information as well).

In conclusion: this Argon-Oxygen mix is not harmless.

Source: Nowrangi, D., Tang, J. and Zhang, J. (2014). Argon gas: a potential neuroprotectant and promising medical therapy. Medical Gas Research, 4(1), p.3.


What are some useful (starter) metrics to use on phylogenetic trees?

Here are a few metrics you can calculate to get you started. You can use R to perform these calculations.

Net Diversification Rate (r)

Net diversification rate is (rate of speciation - rate of extinction). You can calculate it using the bd.ms or bd.km functions in the geiger package for R.

r = 1:

r = 2:

Tree Imbalance: Colless index (I)

Colless's index measures how imbalanced the tree is. It sums the differences in the number of clades in each pair of taxa. You can calculate it using the colless function in the apTreeshape package for R.

I = 0

I = 21

Branching Times (gamma)

The gamma statistic measures how much later or earlier branching times happen than what you would expect from a normal birth-death process. A negative value means branching times occur earlier, positive means branching times occur later. You can measure gamma (and generate a lineage through time (ltt) plot, as shown below) using the ltt function in the R package phytools

(From this Nature article)

These are just a few of many parameters you could calculate for a phylogenetic tree. It should be enough to get you started.


Do macrophages get nutritional value from the pathogens that they eat?

In this article it is described that starved macrophages 'consume' heat inactivated bacteria through phagocytosis with enhanced ability. Starving can also induce (macro)autophagy and the pathways are connected with phagocytosis,in the macrophages under investigation it was shown that autophagy did not play role in the enhanced ability of phagocytosis. The paper however does not mention anything about macrophages utilizing the resources obtained by the digestion of the bacteria. although it would seem logical. I'll keep looking.

Edit:

I found a text book that says:

  in general cells of the macrophage series have two major functions. On f their functions ,as their name ("large eater") implies, is to engulf and, with the aid of all the degradative enzymes in their lysosomal granules, break down trapped materials int ismple amino acids, sugars and other substances, for excretion and reutilization.

Source : IMMUNOLOGY A Short course 3rd edition by Eli Benjamini, Geoffrey Sunshine and Sidney Leskowitz 1996 pages 23-24. ISBN 0-471-59791-0. I only have printed copy, but I'll try to find online version.
The other function is antigen presenting.

Thus I can say that yes macrophages and other cells do utilize resources from digested pathogens.


Why are neutral [sterile] female flowers present in inflorescences when they are reproductively incompatible?

Sterile flowers enrich pollination quality by promoting pollen export and import, while limiting the mating costs of geitonogamy associated with large fertile displays.

You are actually looking for this paper: Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523656/

Sterile flowers increase pollinator attraction and promote female success in the Mediterranean herb Leopoldia comosa

  Key Results

  The presence of sterile flowers almost tripled pollinator attraction,
  supplementing the positive effect of the number of fertile flowers on
  the number of bees approaching inflorescences. Although attracted bees
  visited more flowers on larger inflorescences, the number visited did
  not additionally depend on the presence of sterile flowers. The
  presence of sterile flowers improved all aspects of plant performance,
  the magnitude of plant benefit being context dependent. During weather
  favourable to pollinators, the presence of sterile flowers increased
  pollen deposition on stigmas of young flowers, but this difference was
  not evident in older flowers, probably because of autonomous
  self-pollination in poorly visited flowers. Total pollen receipt per
  stigma decreased with increasing fertile display size. In the
  population with more pollinators, the presence of sterile flowers
  increased fruit number but not seed set or mass, whereas in the other
  population sterile flowers enhanced seeds per fruit, but not fruit
  production. These contrasts are consistent with dissimilar
  cross-pollination and autonomous self-pollination, coupled with the
  strong predispersal inbreeding depression exhibited by L. comosa
  populations.


What would be a single elegant-sounding word denoting controlled increase or decrease?

There's a reason why you encounter these words so frequently - they are widely understood, concise descriptions that almost any biologist will understand immediately. Almost any other terms you use in their place will only serve to obfuscate the actual biological phenomenon you're talking about.
That said, I've seen the words overexpressed and underexpressed to describe genes that are upregulated or downregulated, but they're not any less cumbersome words, nor are they used any more frequently outside the domain of biology. There are also may be some connotations about the cause of the effect, so there may be subtle differences between upregulation and overexpression depending on who you ask. I don't think there's any better terms than upregulation and downregulation for describing an effect of increased/decreased gene expression.


Draw simplified phylogenetic tree for kids

As per your requirements I will suggest:

http://www.onezoom.org/


How to produce correct epithet of a species named in the honor of a person?

You should check the article 60 of ICN: http://www.iapt-taxon.org/nomen/main.php?page=art60

See in particular Recommendation 60C about specific epithet, and in the specific case, the rule 60C.1 (specific epithet derived from a person name).

You can use the genitive case (as Plant of Vodyanitskiy) as in rule (a), which is independent of generic name, so  if the professor is male: X. vodyanitskiyi, and she is female: X. vodyanitskiyae.
or as adjective (so inflected according the genera), in rule (c): X. vodyanitskiyana, X. vodyanitskiyanus, X. vodyanitskiyanum

Note: there are other rules to have a valid published name, and it is recommended to explain why you choose such name. In additional to the ICN code, there is the companion book: The code decoded. A user's guide to the International Code of Nomenclature for algae, fungi, and plants(Regnum Vegetabile 155), by Nicolas Turland


Does the creation of memory involve mRNAs crossing the synaptic gap?

I have never heard of this pathway. Memory is usually assoiciated with synaptic plasticity by ‘Long-term potentiation’ (LTP), which has glutamate as a neurotransmitter. Neuroscience Exploring the brain (Bear, et al,. 2007), has a pretty good explanation of this process, if you're interrested. Motor patterns have more mechanisms than LTP, and are not as well understood.


Are there mechanisms that limit the amounts of time conjugation and F-plasmid transfer can happen? If yes, what are they?

Yes there are many such mechanisms.

One of the simplest, but perhaps most easily overlooked, is metabolism.  Conjugation requires ATP.  In environments with low levels of nutrients, heterotrophs might not have enough "extra" ATP to fuel the conjugation process.  Note that both donor and recipient need to expend ATP in conjugation.  The donor needs to make the nicking enzyme, the pilus, and extrude the DNA into the recipient, and the recipient needs to synthesize DNA from the single-strand DNA that it has received.


You can do with a single gRNA. All that CRISPR-Cas, ZFN or TALEN systems do is to introduce a double strand break at a specific site. The DNA gets repaired via two mechanisms — non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is error prone and it may introduce indels that can compromise with gene function (frameshifts etc). While HR can be used to integrate a transgene or repair a mutation, NHEJ can be used to create mutations.

I haven't really knocked out a gene using CRISPR-Cas but it is good to target the initial part of the ORF. There will be many other factors too that will determine what site should be chosen for targeting and an important factor would be the uniqueness of the target sequence. See this site for guidelines on selecting a good target sequence.

You would have to do rigorous screening nonetheless; the advantage of insertional knock out is that screening can much be easier (for e.g. by inserting GFP or puromycin-resistance gene).

You can have a look at this paper and the supplemental information; they have targeted 18080 genes with a CRISPR-Cas library.


can a point mutation cause a frameshift?

I saw the OP edited it's question quite a lot.. This answer answers the questions before the edit, I will not delete this because it will maybe help other people
I'm not sure if you fully understand the terms you used so I will start with clarifying these.
Missense mutation

  a point mutation in which a single nucleotide change results in a
  codon that codes for a different amino acid (wiki)

Example

    DNA: 5' - AAC AGC CTG CGT ACG GCT CTC - 3'
         3' - TTG TCG GAC GCA TGC CGA GAG - 5'
   mRNA: 5' - AAC AGC CUG CGU ACG GCU CUC - 3'
Protein:      Asn Ser Leu Arg Thr Ala Leu

-------------------------↓↓↓↓↓↓↓--------------------------
    DNA: 5' - AAC AGC CTG CTT ACG GCT CTC - 3'
         3' - TTG TCG GAC GAA TGC CGA GAG - 5'
   mRNA: 5' - AAC AGC CUG CUU ACG GCU CUC - 3'
Protein:      Asn Ser Leu Leu Thr Ala Leu

The 4th codon which was CGT (and GCA on the other strand) is changed because of a subtitution of the G for a T. Because of this change the codon will not code for Arg anymore but instead it will code for Leu. So a missense mutation causes the sequence to be in the same frame as before however a codon is changed and subsequently an other amino acid is added to the polypeptide chain during translation (this is not always the case see wobble)

Frameshift mutation

  A frameshift mutation (also called a framing error or a reading frame
  shift) is a genetic mutation caused by indels (insertions or
  deletions) of a number of nucleotides in a DNA sequence that is not
  divisible by three. (wiki)
  Example

    DNA: 5' - AAC AGC CTG CGT ACG GCT CTC - 3'
         3' - TTG TCG GAC GCA TGC CGA GAG - 5'
   mRNA: 5' - AAC AGC CUG CGU ACG GCU CUC - 3'
Protein:      Asn Ser Leu Arg Thr Ala Leu

-------------------------↓↓↓↓↓↓↓--------------------------
    DNA: 5' - AAC AGC CTG CTT ACG CT C    TC - 3'
         3' - TTG TCG GAC GAA TGC GA G    AG - 5'
   mRNA: 5' - AAC AGC CUG CUU ACG CU C    UC - 3'
Protein:      Asn Ser Leu Leu Thr Leu ..........

In this case the nucleotide T is removed and thus causing a framehift because we need tree bases to form a codon. by removing a nucleotide we just read further till we find a third base and this will be our "new" codon. This new codon does not code for Ala anymore but will code for Leu. (I added the dots because of the fact that the stop codon will/can be shifted and the transcript can be either shorter or longer (the previous stop codon will no longer exist).

  Could a missense mutation cause a frameshift

In the case of a missense mutation the DNA sequence will be in the same frame (no nucleotide is added or removed) and in the case of a frameshift a nucleotide needs to be added or removed and therefore a missense can't cause a frameshift.

  such that a mutation results in the sequence AUG?

Both a missense and a frameshift could result in a start codon.
Example (frameshift)

mRNA 5'     AAC AUU GAC 3'
Protein:    Asp Ile Asp
    -------------------------↓↓↓↓↓↓↓--------------------------
mRNA 5'     AAC AU G  AC.... 3'
Protein:    Asp Met   ........

Example (missense)

mRNA 5'     AAC AUU GAC 3'
Protein:    Asp Ile Asp
    -------------------------↓↓↓↓↓↓↓--------------------------
mRNA 5'     AAC AUG  GAC 3'
Protein:    Asp Met  Asp

So both a frameshift mutation and a missense mutation can introduce a Met --> a start codon.

  a mutation results in the sequence AUG to be present in the transcript
  but upstream the start codon?

A gene is only transcribed if this gene is preceeded by the appropriate sequences:

The start codon will be present in the first exon so the only way to put a start codon before the "old" start codon while remaining all other sequences(UTR,promtor, enhancers etc.) in tact is to "create" one just behind the 5' UTR and before the "old"  start codon in the first exon. This can be done by just inserting AUG in there, HOWEVER we are talking about point mutations:

  A point mutation, or single base modification, is a type of mutation
  that causes a single nucleotide base substitution, insertion, or
  deletion of the genetic material, DNA or RNA

The start codon we are talking about is positioned AFTER the 5' UTR (as said above):

By inspecting the "general" 5'UTR sequence we can see that there are already "start codons" (not really start codons because they are not translated") present before the start codon. We could probably add one using a frameshift or a missense mutation as described above and in your edited question:

  If the new ATG is close enough to the original one (so that it is
  within the processed transcript and downstream of a ribosome-binding
  site) and in frame, it will be used to initiate translation, adding
  amino acids to the amino terminus of the original protein

As far as I can reason is the only way to create a start codon BEFORE the old one is to change the UTR. As stated in your queation this can only "work" if the UTR parts which have an important function are not affected. Further to get this working the 5'UTR should contain a (not "important" )sequence which can be mutated tot form an AUG (see my explanation above)


SolarLunix posted an excellent answer detailing the criteria for being classified as "alive", and showed that by those criteria, mitochondria could be considered as "dead".

However, I would argue that the narrator's statement in your video does not make any sense. The currently-accepted theory of the evolution of mitochondria (and possibly other organelles) from free-living prokaryotes is called symbiogenesis and postulates that the mitochondrial progenitors began living symbiotically with the precursors to eukaryotes some 1.5 billion years ago. Life originated on Earth about 3.5 billion years ago, so eukaryotic cells (carrying mitochondria) have been around for a little less than half of that time.

In that incredibly large span of time (if you counted 1 number per second, you'd reach 1.5 billion in about 47.5 years), what used to be an independent organism (we assume) has become an organelle - an integral part of the eukaryotic cell. It absolutely could not survive outside the cell on its own, and relies on signals from the cell (mainly, the cell's energy needs as detected by "sensor" proteins to key molecules like glucose and ATP) to reproduce.

Therefore, it is most appropriate to think of mitochondria simply as another organelle, just like the endoplasmic reticulum, lysosomes, or the nucleus. It doesn't make sense to think of those other structures as "alive" or "dead", just as it doesn't make sense to think of mitochondria in the same way. Yes, they used to be independent, but are no longer; instead they are a well-integrated part of the whole cell.


How similar are Circulating Tumor Cells and Cancer Stem Cells?

There are several competing models of metastasis, and this question does go right to the differences between them.

The primary thing to remember about CSCs is that all evidence suggests that they are a tiny, tiny subset of tumor cells.

CTCs, meanwhile, consist of whichever cells manage to acquire the right combination of motility, invasiveness, and resistance to anoikis (apoptosis caused by lack of attachment to neighboring cells or extracellular matrix).

So, one possible explanation is that CTCs are drawn from the whole population of tumor cells, and that CSCs therefore make up a very small, nigh-undetectable subset of CTCs-- but that this is the subset that ends up founding the distant metastases while the rest of the CTCs get cleaned up by the immune system or lie dormant in the target tissue. You could call this the stochastic model: CSCs form some small, randomly determined fraction of the CTCs, but they preferentially survive and found secondary tumors.

Another model posits that the cells undergo substantial changes in phenotype driven by responses to their microenvironment. CSCs, like normal stem cells, presumably require a pretty specific niche to maintain their stemness. CTCs, meanwhile, acquire their invasiveness and anoikis-resistance in response to conditions in the tumor, such as hypoxia. So, another possiblity is that, in response to stimulus from the microenvironment, a cell with the potential to be a CSC undergoes some phenotypic changes and becomes a CTC. It circulates for a while, finds a target tissue, extravasates, invades the target microenvironment, then starts re-setting up the microenvironmental niche to re-establish its stem-like properties. Call this the dynamic hypothesis: it's a single potential CSC the whole time, but it looks like a CTC while it's circulating and like a CSC only in its niche.


This is a blue button jellyfish! they eat zooplankton and are usually found drifting along on currents
they aren't true jellyfish and just like a jellyfish have no blood, brain or nervous system. they aren't usually toxic enough to hurt but can cause irritation to the skin.
they live in warm waters off of Europe and in the golf of Mexico and the Mediterranean.
they are hermaphrodites and have both male and female reproductive parts. they lay eggs which turn into polyps
here is a website I found all about them as I'm not extremely knowledgeable on this species.
https://www.thoughtco.com/blue-button-jelly-porpita-porpita-2291819


Could we use viruses that only affect bacteria to act as antibiotics?

Yes. The specific class you're referring to is called a "bacteriophage".

There's quite a bit of research going on surrounding phage therapy as a stand-in or replacement for traditional antibiotics. Here's a Nature Biotechnology article from 2004 that discusses your very topic.

It is practical, carries some risks (mutations being a known and accepted risk), and I wouldn't be surprised to see phages in practice now or sometime soon.


It doesn't seem like a homogenization problem. Nonetheless you can try this:

Suspend the heads in trizol
Homogenize by passing through 30/31G needles (insulin syringe) up to 10-15 times.
Heating a little might help but I think it is unnecessary for these tissues.

Insulin syringe is much better than the hand held homogenizer. Freeze-thaw 1-2 times if you want (helps in homogenization).

During extraction you can add 5M LiCl (100µl) + Ethanol (1ml) to 400µl aqueous phase (instead of isopropanol), keep at -20⁰C for 1-2h before centrifuging. Alternatively you can add a little RNAse free glycogen to Isopropanol during precipitation.

PS: the liquid Nitrogen trick that rg255 mentioned is for quickly getting heads and avoiding the pain of dissecting each head.


Can a hairpin (stem loop) within a transcript stall a eukaryotic ribosome?

It seems that could happen.
C9orf72 translation is one of the examples. In this gene, GGGGCC repeats exist in 5' UTR of the mRNA (upstream of the first ATG). The repeats expand in subsets of neurodegenerative disorder such as ALS. The repeats can form a stem loop structure and stem loops of expanded repeats are more stable.

mRNAs having expanded repeats seems producing poly-GlyAla, poly-GlyPro, and poly-GlyArg peptides which codons are GGG-GCC, GGG-CCG, and GGC-CGG from different frames from GGGCC repeat.

This means the translation starts somewhere in or upstream of the repeat without ATG. To explain this, there is speculation that ribosomes stall because of the tight structure of the stem loop by expanded GGGGCC repeats, mistakenly take tRNAs and start translation. It is called "Repeat-associated non-ATG translation".

You might want to refer to:
Repeat-associated non-AUG translation and its impact in neurodegenerative disease.
https://sites.tufts.edu/als/the-answer/c9orf72/
RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders


Light and Dark Reaction of photosynthesis?

I can see your frustration if you meet errors such as NADPH2 but that is the price you pay for approaching as complex a subject as photosynthesis without a good biochemistry textbook. Even the on-line versions (e.g. Berg et al.) are unsatisfactory because of their layout. You will have to sit down and spend a couple of hours on the topic — all you can expect from a site like this is clarification of key points.

That said I'll offer some clarification. The first thing I'll say is that focusing on chemical equations is not the way to understand photosynthesis. It will demonstrate that the law of conservation of matter applies, but otherwise is a bit like doing a chemical analysis of a cell to try to understand how it works. This is because:

There are two quite separate reactions in photosynthesis. As the products of one are (more strictly can be) used in the second, overall equations cancel them out, and so ignore key features of the process.
Photosynthesis is concerned with the transformation of energy as much as molecular structure. Chemical equations do not really address this.
The generation of energy involves the establishment of a gradient of hydrogen ions across a biological membrane — something your chemical equation does not encompass.

So what are the key ideas to bring to the text book you are going to purchase?

The overall objective is to make sugar from carbon dioxide

This poses a problem, not particularly because of the chemical reactions, but because these reactions require energy of two kinds:

To join the carbons from the carbon dioxide into C-C bonds. This requires ATP, the free energy change of its hydrolysis to ADP being coupled to ‘drive’ the formation of a C-C bond.
To reduce the oxygen atoms of carbon dioxide to OH groups. The biochemical molecule that is used for this reduction is NADPH, so ‘energy’ is needed to reduce its oxidized form, NADP+. (I won’t go into why this can be thought of as energy — if interested you need to read about the free energy equivalents of redox couples.)

The sun provides the energy

The energy for creating the reducing NADPH and the ATP comes from the sun in a complex series of reactions (these do not involve carbon dioxide). Light of a particular wavelength is harvested and used to break a water bond so as to separate charge in a reaction that I will deliberately not balance:

(1) H2O + sunlight → O2 + H

A complex series of reactions transfer the H (more strictly an electron) between different molecules, eventually reducing NADP+ to NADPH. At the same time an equally complex process builds up a H+ concentration difference across a membrane which provides the energy to convert ADP to ATP (see also Where do the H+ ions come from in light reactions?).

This is what is called the light reaction of photosynthesis because it requires light. It occurs in the thylakoids of the chloroplast, particularly at the membrane, although the products are in the stroma.

After energy has been harvested from the sun chemical synthesis can proceed

Having harvested the energy of the sun the plant has the wherewithal to make sugar from carbon dioxide. This is referred to as the ‘dark reaction’ because it does not require light. But its name can be misleading to the neophyte as the process does not have to take place in the dark. The overall unbalanced equation is:

(2) CO2 + NADPH + ATP → C6H12O6 + NADP+ + ADP

This is actually a complex series of enzyme-catalysed reactions (known as the Calvin Cycle) and a triose is the initial product. It occurs in the stroma of the chloroplast.


What is the biology behind a skin "mole"?

A mole is simply a benign tumour, i.e. a proliferated cell growth that hasn’t become cancerous. So moles are not dead cells, they are very much alive. The colour is caused by a high concentration of the melanin, which is also responsible for normal darker skin.

Since moles are tumours, they can – but in most cases don’t – give rise to melanomas, malignant skin tumours, when they lose susceptibility to cell growth regulation and start invading surrounding tissue.

Scar tissue is entirely unrelated and due to regular regrowth of epithelial cells after injury forming a linear collagen structure (as opposed to the skin’s normal collagen structure, which resembles a “weaved“ structure).


Can spider silk be synthesized to be used for 3D printing?

The "...in large enough amounts to enable 3D printing?" part of your question is, I think, still unknown, but spider silk has been being synthesized in transgenic goat milk for quite a long time already, and I suspect that it's now just a matter of time before the answer to your question is an unqualified "yes."

See Macromolecules, 2011, 44 (5), pp 1166–1176, doi:10.1021/ma102291m


How to use swiss-mod to predict the secondary structure and 3D structure of a protein?

3D structure.
Use the PDB to identify structures that are similar to the one you have found (you can use BLAST to search the PDB). A 30% match or above is usually acceptable, and multiple alignments are of course useful at lower match scores. If structures exist that are similar enough, you can use homology modelling to generate a 3D structure (this is what the SWISS-MODEL server does, and I think it automates the BLAST alignments from PDB). If there are no similar structures, you can resort to ab initio modelling if you have a reasonably straight forward globular domain, otherwise you might need to draw in additional expertise.
There are so many specific factors that need to be taken into account for a project like this. Depending on what the model will be used for, different questions are relevant.
Secondary structure.
You will need a few different secondary structure predictors to make it convincing and then you will need to check that your secondary consensus matches your 3D structure. If they don't match you need to think about "why not?"
If there is a difference it usually indicates that some 3D interaction is involved in the folding, so your 3D model usually trumps the sequence structure predictions, but do check your 3D structure against the secondary structure predictions.
Secondary structure prediction is more useful when a 3D structure is not available and modelling one is not an option.


What happens to our umbilical cord internally as we age?

The umbilical cord, which contains the umbilical arteries and vein so important for nutrient, oxygen and waste transport before birth, becomes useless pretty much the moment the lungs start working (the kidneys already started before birth). As the baby breathes, the two arteries constrict to stop flow from the newborn to the placenta. The Wharton's Jelly, a structural element in the cord, causes collapse of the vein on cooling to outside temperature. Within a matter of a few minutes, the whole system is shut down.

Within the infant, the umbilical vein and ductus venosus (which carried blood to the liver and the inferior vena cava) close up and degenerate into fibrous remnants known as the round ligament of the liver and the ligamentum venosum respectively. The round ligament basically just divides the left part of the liver into medial and lateral sections. The ligamentum venosum does basically the same thing on the posterior surface of the liver. Both ligaments maintain their attachment to the umbilicus. (The small paraumbilical veins are unimportant except in the case of severe portal hypertension, where they act as a portacaval anastomosis.)

The parts of the arteries closest to the navel degenerate into what are known as the medial umbilical ligaments (which basically serve no purpose whatsoever and are buried in the abdominal wall), while the more internal remaining sections are retained as part of the circulatory system as the umbilical artery.

The umbilical artery in adults is a branch of the anterior division of the internal iliac artery. The umbilical artery is found in the pelvis, and gives rise to the superior vesical arteries (supplying the superior part of the bladder, and parts of the ureters. In males, it also gives rise to the the deferential artery which supplies the ductus deferens.


I can't Identify this "bug" that seems attached to fresh cut wood

I think I may have it.  gOOgle terms "giant cricket wood tiger stripes" yielded very similar critters:  So-called "Camel, Cave, or Cellar Cricket."

Order Orthoptera (Ensifera), Family Rhaphidophoridae.

Genus and Species will be next to impossible unless I can capture one, but obviously one of the North American varieties that like to hang out in damp decaying wood.

From the interwebs:


Is there an adhesive that could used for larval fish?

You could try methyl cellulose, which my lab and others use. It's not exactly an adhesive, but it is quite viscous. It's common enough that it's in the Zebrafish Book: https://wiki.zfin.org/display/prot/Methyl+Cellulose+Mounting . Obviously, be sure whatever you do is approved by your animal care and use committee.


Would it be more genetically efficient to have shorter lifespans?

Extremely briefly, we do not evolve shorter lifespans because natural selection does not act for the good of the species.

As an interesting historical aside, August Weismann proposed essentially the idea you are suggesting in 1889, in his Essays upon heredity and kindred biological problems. Within a few years, however, he backed away from this hypothesis.


What is this bird - sound attached - (Atlanta Georgia)?

It sounds like a Chuck-will's-widow; click the "sound" icon in that link for the song. They're native to Georgia and sing interminably at night, so the story checks out.


Do hornets return to the same nest after winter each year?

If fail to get rid of the hornets this fall, will they return to the same nest next year (or overwinter and continue to live there)?

No. The nest, likely made of wood pulp (and maybe mud), will/should degenerate to unusable over the winter, though the bulk could remain for a couple of years. All wasps die, except for the new queens (fertile, mated females) who overwinter in sheltered crevices somewhere.

In spring, it is a single wasp that starts a hive: the new queen. She builds a new, small hive in which to lay eggs, which is added to initially by the queen and then by workers who have hatched.

While she will not return to an old hive, the conditions which appeared advantageous to one queen (shelter from rain, intense sunlight, winds, etc.) will also seem advantageous to other queens, which is why nests appear in the same places year after year.

Edited to add: It appears most likely that the queens that overwinter are "new queens", that is, mated female offspring of the queen. H/T @Brian Krause.


What controls leaf senescence in deciduous tree species, and how can I predict it?

One can sometimes notice street lights delaying the annual shedding of leaves in some species (a well-lit branch will be mostly green while the rest of the tree is turning). So at least part of it would be day/night length in at least some species.

I would expect, however, that the answer varies based on species, genus, and/or family, and that there are probably multiple causes at work (one obvious alternate cause being temperature). Just going from memory of my personal observations, years when autumn weather patterns start earlier do tend to have trees turn and lose leaves earlier, so it's not all day/night length.

Drought is also a factor. I live in a seasonal-rainfall part of the world (US Pacific Northwest), and if summer is drier than normal (and normal is pretty dry), by mid-August many of the native deciduous trees will be starting to drop leaves. (Not all of them, but some of them, definitely more than just a few, will be turning and dropping.)


A gene being dominant does not necessarily imply the gene is also common.

An easy counterexample is Huntington's disease. The gene is dominant, and only one mutant allele of huntingtin would result in development of the disease. However, the allele prevalence of the mutant is low in the general population.

In the absence of a selective advantage of green eyes over blue eyes, the two alleles of the gey gene should remain in genetic equilibrium, and therefore the number of people with green eyes will not increase. In fact, a similar misunderstanding applies to the disappearance of blondes/redheads. In both cases, the allele frequencies will remain unchanged in the absence of selection pressure.

The initial imbalance in the allele frequency could be due to many reasons. Population bottlenecks, genetic drift, and historical selection pressure could all be valid answers.


Shouldn't recording electrode have as low resistance as possible?

For accurate measurement of the membrane potential, it is crucial to have as little current flow through the measurement device as possible. Otherwise, the equilibrium of leak channels that generates the resting potential would be disturbed. See diagram and text from Axon Guide 3rd edition below:


Programmatic way to differentiate homodimers from heterodimers?

I'd just compare the amino acid sequences of the individual protein chains. With some leeway for residues not observed in the density, ie only require 90 or 95% sequence identity, or ignore gaps.

This will not tell you anything about whether the dimer (if you observe several molecules in the asymmetric unit) is actually real. For that, you'd need to do an experiment, literature research or see whether software like the PISA-server could give you a clue.


Difference between imputing and typing in GWAS studies?

'Typing' is an SNV-typing. It is an explicit SNV detection using Affymetrix GeneChip arrays, Illumina BeadArray.

'Imputing' is an imputation. It is a statistical inferring from existing genotype data using haplotype estimation. It is useful because different genotyping arrays genotype a slightly different set of SNVs and they can't detect all variants as whole genome sequencing is still pricey.


Yes, bones too bleed if they get damaged (break or bruise). This is because bones are highly vascularised organs and breaking of bones will indeed rupture the blood vessels causing bleeding. Main artery which supplies blood to bone is nutrient artery , others are epiphyseal, metaphyseal and periosteal arteries. Skeletal system receives about 15.6% of cardiac output.
Since bones contain very low percentage of water ( about 31% ) comapred to others like skin(64%),brain and heart (73%) and lungs ( 83%). So the saying "as dry as bone " stills holds well.

Sources:

1-https://www.mananatomy.com/basic-anatomy/blood-supply-bones

2-https://water.usgs.gov/edu/propertyyou.html


What happens to the human brain when unconscious?

We don't know. Disruption of cortex, thalamus, or brainstem structures (someone mentioned ascending reticular activation system) all can cause loss of consciousness. Different drugs have different mechanisms of action and some might cause different "types" of loss of consciousness - for example, ketamine and propofol seem very different, and trauma is a completely different issue.

The reason this is such a hard problem is that these structures are all interconnected, and there are likely proximate and distal causes of loss of consciousness. For an analogy, imagine you starve to death. You could make a convincing case that lack of food did it - so conclude food keeps you alive. But you weren't declared dead when you stopped eating; you were probably declared dead when your heart stopped. So conclude your heart keeps you alive. But in the middle somewhere, you had changes in ion concentrations in your blood, loss of glucose. So salts and sugars keep you alive. I can prove these are all true - take out your heart, you die. Stop feeding you, you die. Fill your arteries with KCl, you die.


If Evolution Is In Progress, Why Fight Extinction?

First, a shorthand definition of Evolution is heritable change and not 'progress' (which is a rather loaded word). Also, evolution is not 'supposed' to do anything, and can lead to both an increase or a decrease in diversity, since (local) diversity is simply the net result of speciation rate and extinction rate (if we exclude colonization of new species from other areas). Therefore, I think the question is framed in the wrong way.

Second, there are many reasons why biologists might want to halt species extinctions, as hinted in the other comments and answers. Most obviously, conservation biologists want to prevent man-made extinctions which are due to how we have influenced/modified/destroyed the natural environments. I don't think conservation biologists in general are determined to halt all 'natural' extinction. However, most of the time it is really hard to pinpoint what would be a 'natural' extinction. Either way, the current rates of extinction, which have been estimated to lie 100-1000 times (IUCN, 2007) above background rates (some say it's closer to 10000 times higher), indicate that most extinctions are man-made.

The rationales people use for preserving biodiversity can however differ. Three distinct categories are:

1) For human survival and/or economy, e.g. through ecosystem services or resources we rely on.

2) For human welfare, e.g. recreation or esthetical reasons.

3) Ethical considerations, e.g. inherent value of species or to preserve the unique evolutionary history of the system.

Another way to structure these is to label 1) & 2) as instrumental values and 3) as inherent values. The instrumental values can then be subcategorized as services, goods/resources, information (e.g. genetic to be used in medical research), and esthetical/spiritual values.

Since the direct value of individual species are often (usually) uncertain (irrespectivly of the direct rationales used) the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. However, other aspects of biodiversity are functional diversity, which focus on preserving functional groups of species, or phylogenetic diversity, focusing on taxonomic coverage and uniqueness (evolutionary history), instead of 'overall' biodiversity (see e.g. Flynn et al, 2011 for a discussion of these concepts). Under these perspectives less focus is placed on individual species.


What triggers programmed cell death in humans (from outside the cell)?

The answer is, in part, it depends. Let's think of the PI3K/AKT pathway. Akt actively phosphorylates BAD which abrogates the Bax/Bak apoptosis pathway. RTK's at the plasma membrane activate this pathway when bound with survival factors. In the absence of survival factors, Akt would become dephosphorylated and you'd have a net movement toward apoptosis. In a particular form of cell death called anoikis, this could be as simple as detaching from the extracellular matrix. So anything that halts the binding of survival factors could play a role.

In the case of immune response, activated Tc cells can induce apoptosis by secreting pore-forming enzymes as well as enzymes that directly activate caspases. The Tc cells also express Fas on their membrance which is involved in the extrinsic apoptosis pathway. TNF (tumor necrosis factor) may also bind cell surface receptors as sort of a death factor, and push towards apoptosis.

These are just examples, some generic searches about apoptosis, necroptosis, entosis, and a myriad of other programmed death mechanisms will yield a very comprehensive overview.


Why would growth hormone (somatotropin) cause both lipid AND glucose release?

Great question... and an important point about glucose and lipid utilization! The body can't turn fat into sugar, but it can turn sugar into fat. The more technical way to say this is that the body can't convert acetyl-CoA into glucose, but it can convert glucose into acetyl-CoA.

The enzyme that converts glucose to acetyl-CoA, pyruvate dehydrogenase, catalyzes an irreversible chemical reaction. Pyruvate dehydrogenase converts pyruvate into acetyl-CoA, which can be used in the Krebs Cycle, fatty acid synthesis, etc. Once acetyl-CoA is produced it cannot be converted back into glucose (carbohydrate) within the body. This is important because certain cells/tissues can use only glucose for energy production, while other cells/tissues like the liver can use both glucose and lipid for energy production.

This is where your question becomes very important, because the liver is the predominate organ that maintains glucose homeostasis (i.e. maintains blood glucose concentration) in-between meals or during periods of fasting. In periods of fasting, the liver uses free fatty acids released by adipose tissue for energy/ATP production in order to produce glucose through gluconeogenesis, an anabolic process that requires energy.

So, growth hormone increases fatty acid release from adipose tissue stores for uptake by the liver. The liver takes up the fatty acids from the plasma and uses them to produce glucose for release into the circulation for glucose-dependent tissues to use. During this time of fasting, tissues that can use fatty acids and glucose tend to switch to fatty acids as their energy source, while tissues that only can use glucose will continue to rely on glucose production from the liver for their energy source.

Here is a nice summary (open source) from National Library of Medicine explaining in more depth the basis for why fatty acids are oxidized to provide ATP for gluconeogenesis - "Energy Metabolism in the Liver".

Also, George Cahill, a famous physician-scientist at Harvard University who studied metabolism and starvation has an excellent review of fuel flux under fasting and starvation conditions that demonstrates the above mentioned principles as well "Fuel Metabolism in Starvation" - namely that free fatty acids released from adipose tissue are oxidized in the liver and used for anabolic processes in the liver, such as gluconeogenesis that maintains blood glucose concentrations.


What is the appropriate blender speed to maximize nutrition and digestion of fruits and vegetables?

I'm guessing that what they mean by 'maximize nutrition' for digestion is that they are assuming that the cells are broken open.  This would make the co-factors we call vitamins, protein and sugars freely available to the digestive system and more easily absorbed.

I think it is a marketing literature claim, though the blender may have some valid advantages... details below.

Stainless steel waring blenders used to be typical pieces of lab equipment which could be used to homogenize tissue to extract proteins or DNA from tissue.  These blenders would typically run from 10k-30k rpm.  The web search for 'cell lysis blender' gives lots of examples of prepping DNA from plants at these speeds, but they don't complain for speeds towards the lower end of the range.  A reputable looking example in my short search: This paper for tomato fruit cell wall preparations doesn't even give a speed the blender might have run at.

Cell lysis in the literature is not precise - the cell toughness, the strength of the tissue around it and other such factors all come into play.  Putting woody stems into your blender and those cells won't really get opened up at all.  Also in the cell literature cell lysis buffers may have detergents or other chemicals (the reference above is done in 50% ethanol) to weaken the cell walls.  Not exactly what you'd want to use if you were making a health drink.

In experiments they have to contend with oxidation that happens when the cells are broken open with all the air whipping through the mixture.  This is one reason you don't see blenders in labs to much anymore - hydraulic presses, sonicators, and bead beaters have taken their place - they have less aeration in the mixture and also deliver more power so that they can break open yeast and bacteria, which blenders really can't.

So there will be some vegetables where the cell walls won't break open and all the nutrients won't be so easily accessible.  It must help to be running at the top end of the range, but there will always be some vegetables which won't be broken open.  For most things like bananas and apples it sounds like you'll get similar benefit with other blenders too.  Just have to think about how much more are you paying for that extra 10k of rpm I guess.

Is there a benefit to breaking open the cells and letting all the nutrients (as well as cell waste) break out into solution?  It might give you a quick pulse of nutrition when you drink, but I'm pretty sure all the cells of a piece of fruit or vegetable will be pretty much broken down and extracted by the end.  On the other hand, it sounds like it will save the digestive system some work...  So there's that question too.


It is indeed the Nerium oleander.. For more info refer to this link and also this


Name (and meaning of the absence) of the white semicircle at the base of the fingernail?

The lighter crescent-shaped part at the base of the nail is called the lunula. It is a normal part of the nail matrix, and indicates nail growth. The faster your fingernails grow, the more obvious the lunula.

Absence of the lunula without any other abnormalities of the nail is not uncommon, and while it can indicate anemia or malnutrition, it is often found normally, and with aging. In this case, careful inspection of all the nails will usually reveal a lunula on the thumbs and the fingers closest to the thumb, but a very small or absent lunula on the other fingers.

In your picture, there is clearly a lunula on the middle finger, and, I suspect, a larger one on the index finger, and a relatively normal one on the thumb. This is not a finding of great concern in the absence of other pathology.

  The lunula: The small, whitish, half-moon shape that you sometime see at the bottom of your nails is called the lunula(pronounced loon-yoo-la). It's actually part of the matrix. You might be able to see it only on your thumbs, or maybe not at all. Don't worry if you can't see a lunula on any of your fingers. It's no big deal. It's there, just under your skin.

Examining the Fingernails When Evaluating Presenting Symptoms in Elderly Patients
Examining the Fingernails
Nails


Are there any open plant databases (database/library/collection), containing species information and pictures?

Large online floras have the advantage of not only having details and often photographs and illustrations, but also being (more or less) definitive, that is, botanists will refer to them.

See my answer here for links to examples, and also for some of the problems with using floras (e.g. not easily downloadable).


The tree is dying.  From what you say, it has no leaves wduring a time it should, it has saprophitic growth along the trunk; it looks like there's a crack in the bark on the right, and there are shoots coming up from the base of the trunk, the last hurrah from the tree to try to regenerate.

Trees send up suckers as a reaction to stress (like slowly dying). If you cut the trunk in such a way as to discourage rot, it will likely be replaced by this shrubby growth if the roots are sound. Some loggers use this as a way to quick-start new lumber trees.


Population genetics and the fitness probability distribution. Why is the arithmetic mean all we need?

It's simplest to think about a haploid population with size $N$. Say there are two alleles, $A$ and $a$, with $A$ having frequency $p$ in this generation. Each $A$ individual will have some realized fitness (i.e., number of offspring) in this generation; let's call this number $w_A^{(i)}$ for the $i^\text{th}$ individual. The total number of $A$ individuals in the next generation is then $\sum_{i=1}^{Np}w_A^{(i)}=Npw_A$, where $w_A$ is the arithmetic mean of the fitness distribution, $w_A\equiv\sum_{i=1}^{Np}w_A^{(i)}/(Np)$. So regardless of how weird the distribution of the $w_A^{(i)}$ was, all that matters (in the large-$N$ limit) is the arithmetic mean.


Is it true that oral sex exists in non-human animals?

Yes, it is true. Have a look at this post:9 Animals Who Are Into Oral Sex:

  A recent study of fruit bats found cunnilingus to be a major part of their repertoire. While following a colony of 420 bats roosting in a fig tree over the course of 13 months, researchers witnessed 57 incidences of sex — both oral and intercourse. The female bats who received oral sex before intercourse were found to last longer during copulation.

The paper they cite is this one.


Can someone identify this tree in Playa Del Carmen, Quintana Roo, Mexico?

The photos are blurred. We need a pic of the bark and of the fruit, sliced. Does it have pips or a nut? Perhaps a Palaquium variety, i.e.  Palaquium Gutta, which is for producing latex/rubber, because it's in a garden and its a useful commodity plant previously grown in south america. Perhaps slice and study the fruit for a better ID.
Latex plants attract bats.
You can check the bark for latex.
https://youtu.be/6DJHD91VKKY


Influence of artificial sunlight on the human body

Yes. Natural sunlight doesn't have a good substituent.

Melatonin levels and circardian rhythms are directly affected by natural sunlight.

As far as LEDs goes, a french study concluded that blue light may have photochemical risks and affect our retina.

Source

http://www.ledinside.com/knowledge/2014/4/effect_of_artificual_and_natural_light_on_the_human_body


SPINAL CORD: Do the axons from white matter synapse with the cell bodies in grey matter?

Here is a great diagram (from here) that outlines all of the different white matter tracts running up (blue) and down (red) the cord.

The portion in the center, as you have found in your research, is the gray matter.  In there are the different interneurons (cells that exist in the network to integrate information from descending controls and do further processing on it) and all of the different motor neurons.  The corticospinal tract descends to the appropriate level (for example, a neuron in charge of moving your arm, to keep it simple, will have a cell body in the brain, and descend to the thoracic level), enters into the gray matter and either synapse on an interneuron or directly onto a motor neuron).
The sensory neurons are a slightly different animal.  Some (pseudo-unipolar cells) have what are basically two "legs", one that runs out into the periphery, which will take the signal from something like a Pacinian corpuscle in the skin, propagates a signal to the cell body, which is outside of the spinal cord in the dorsal root (see below), and the other "leg" runs all the way up the dorsal column into the medulla of the brainstem.

from here
So that should give you some idea of the two major tracts.  To see some of the finer detail, you can look into the different layers (laminae) that the gray matter is composed of, so that you can trace the connections all the way in.


Clarification in the name "white cheeked barbet"

It seems as though it is named for feathers below the beak that have a barblike appearance, rather than actual barbs. It may be clearer from these images:

India Nature Watch

Or in this photo: SivamDesign - Flickr


Did dinosaurs have more than one brain? If so, why?

It would appear that at one time it was thought that a "gap" in the skeleton of a Stegosaurus was a space for another brain. This is now thought to be a storage space for extra food.
Googling your question brings up a number of answers along these lines:

https://en.wikipedia.org/wiki/Stegosaurus#%22Second_brain%22
https://dinosaurs.about.com/od/dinosaurdiscovery/tp/dinoblunders.htm
https://wiki.answers.com/Q/Did_a_dinosaur_have_two_brains


In short, it's because your brain processes external and self-produced stimuli differently.

If someone tickles you, you feel that ticklish feeling, but when trying to tickle yourself, there is a reduction in the sensation. When you are tickled by someone, a part of your brain activates causing you to laugh, etc., but it seems that when you trying tickling yourself, your brain doesn't react the same way and that section of the brain does not activate as if someone were tickling you.

Blakemore, S.J., D.M. Wolpert, and C.D. Frith. 1998. Central cancellation of self-produced tickle sensation. Nature Neuroscience 1(7): 635–640. doi:10.1038/2870


What is the perisomatic region of a neuron?

In cortical GABAergic cells with local axonal projections, the perisomatic region is defined as that part of the plasma membrane including the proximal dendrites, the cell body and the axon initial segment (Zabó et al., 2010).

Reference
- Zabó et al., Eur J Neurosci (2010); 31(12): 2234–46


Can you eat enough to make your stomach explode?

Here's a simple cross-section of the stomach (from here):

The stomach accomplishes much of its function by mechanically breaking down the swallowed food particles and mixing them with acid and enzymes into a sort of slurry. To do this, there are three major layers of muscle surround the stomach - from the outside, the longitudinal layer, the circular layer, and the oblique layer. The stomach also has two holes in it - the gastroesophageal opening, coming from the esophagus with the swallowed food/saliva mix, and the pylorus, where the food/acid/enzyme slurry exits into the duodenum, which is the beginning of the small intestine.

Due to the three layers of (rather strong) muscle, the stomach doesn't have a lot of expansion capability once it is filled completely to capacity. Fortunately, this almost never occurs (despite how we may feel after a large meal) because material is always leaving the stomach on its way to enzymatic digestion in the intestines. Additionally, once the stomach is filled to a certain extent, hormones such as leptin are secreted that give you the feeling of being sated, or full, triggering the brain to make you stop eating.

Of course, as we can see with the current epidemic of obesity around the world, the stomach can change its size over time. However, this is a rather slow process (weeks to months to years) of adapting to continuously consuming large meals.

But what would happen if you completely ignored these internal warnings, or were being force-fed, or whatever? Instead of rupturing (the biological equivalent of "exploding"), food would most likely be expelled either into the small intestine or back into the esophagus and back up the way it came down, i.e. causing vomiting.

For this answer to be complete, however, I should point out that stomach or gastric rupture is technically possible, although it is an extremely rare occurrence. Cases have been described in the literature (1, 2, 3, etc.), but they are rarely correlated with overeating or eating disorders like bulemia. In cases that are, other pre-existing conditions such as gastric ulcer have been found on autopsy that likely weakened the stomach wall in the first place. The bottom line - if you're an otherwise healthy person, a single instance of massive binge eating is very unlikely to end in stomach rupture, as vomiting will most likely begin well before you are in significant physical danger.


Could deutrium oxide be used to make organic compounds with Deutrium instead of hydrogen?

Yes, this is possible and inter alia used to clarify biosynthetic pathways.

For example in this study. Rats were given deuterated water and the average number of D atoms incorporated in cholesterol and fatty acids was determined. Also deuterium was found in plasma glucose and liver lactate and pyruvate.


Why is glycerol supplied/used as 87% solution?

Typically, a glycerol stock will have a final concentration of 10-20% of glycerol. Glycerol is highly viscous. Pipetting higher concentrations of glycerol is difficult (especially for smaller volumes). Therefore a lower concentration such as a 50% solution (works for me) is convenient: add 300µl to 700µl of bacterial culture.

Regarding 87%: some vendors provide 87% glycerol along with anhydrous (>99%) glycerol. The reason is probably the same: it is easier to pipette 87%.

From a vendor's website:

  Glycerol is a component of several buffers, media or reagents in
  biological research. It is supplied as glycerol anhydrous or 87 %, the
  latter containing 13 % water. Both glycerols are from the same
  quality, the 87 % glycerol has the advantage of a lower viscosity.
  Anhydrous glycerol can be pipetted with difficulty only, especially at
  low temperatures.

But the question is why 87% and not 90 or 80? See Michal et al. (2017)  for a relationship between viscosity and concentration of glycerol-water mixtures.

Another graph plotted from the data given in the document mentioned by iayork in the comments. Different coloured lines denote data at different temperatures (in °C). Original data from: The properties of ordinary water substance. Compiled by N. E. Dorsey, New York (Reinhold), 1940.

So I am guessing that 87% must have been optimal beyond which the viscosity just shoots up rapidly with a small increase in concentration. I wish to reiterate that this is just my guess. I could not find a authoritative (in fact any) reasoning on why precisely 87% glycerol is (or was historically) supplied.


Is APB an antagonist of the mGluR6 receptor?

APB (2-Amino-4-phosphonobutyric acid) is a metabotropic glutamate receptor agonist, not an antagonist, and in many publications it is indeed referred to as an agonist, so I think your question is somewhat ill-posed. For example:

Yamashita, M., & Wassle, H. (1991). Responses of rod bipolar cells isolated from the rat retina to the glutamate agonist 2-amino-4-phosphonobutyric acid (APB). Journal of Neuroscience, 11(8), 2372-2382.

You can find many many more by searching "2-Amino-4-phosphonobutyric acid glutamate" on Google Scholar.

The reason that APB suppresses ON bipolar cells is because metabotropic glutamate receptors are often inhibitory rather than excitatory. Glutamate is typically thought of as excitatory because ionotropic glutamate receptors such as AMPA and NMDA receptors are non-specific cation channels that depolarize and therefore excite cells. Metabotropic glutamate receptors operate through g-protein second messenger cascades. In ON bipolar cells in particular, there are cation channels that are closed by mGluR6 activation, which therefore inhibits them.

Here's a review article that describes this as well as other basic information about bipolar cell function:

Euler, T., Haverkamp, S., Schubert, T., & Baden, T. (2014). Retinal bipolar cells: elementary building blocks of vision. Nature Reviews Neuroscience, 15(8), 507-519.


It seems that, by and large, most animal and plant cells have primary cilia. To quote from this open access paper:

  ".[..] organisms that form cilia have a basal body or centriole-like structure as their microtubule-organizing center, whereas those that do not [e.g., yeast, higher plants] use morphologically distinct structures for organization of their microtubule cytoskeleton."

Other cases where cells lack primary cilia are when they possess motile cilia (e.g., sperm are mono-ciliated, respiratory epithelia are multi-cilliated).

Fry AM, Leaper MJ, Bayliss R. The primary cilium: Guardian of organ development and homeostasis. Organogenesis. 2014 Jan 1;10(1):62-68. Epub 2014 Apr 17.


What is the scientific opinion on plus lens therapy?

Plus lens therapy can indeed reverse myopia, but it does take time. Your eyes did not develop myopia in a few days.

The eye represents its environment. Fitting chicks, monkeys etc. with minus lenses always INCREASED the amount of myopia, while plus lenses always reduced myopia and resulted in hyperopia (lens compensation).

Putting monkeys in a confined environment showed a myopic shift. Monkeys in an open
environment showed a refractive state about +1.00 diopters.

IMPORTANT: As I have said: Unfortunately, it does take time! Do not expect results after 1 week of plus lens therapy. That is why so many people give up and think that myopia is irreversible. You also do not build muscles after 1 week.

Kind regards.

EDIT:

Optical defocus and effects in HUMANS: http://www.ncbi.nlm.nih.gov/pubmed/20592235
Defocus on chicks: http://www.iovs.org/content/44/7/2818.full
Monkeys in a confined environment: http://www.iovs.org/content/2/6/571.short


How do absorbance readings indicate diauxic growth of bacteria?

How is growth rate an indicator of carbohydrate use?

Carbohydrates are the carbon and energy source available for the microbes, and their assimilation is correlated to biomass production. The relationship between microbial growth rates in an aqueous environment and the concentration of a limiting nutrient or carbon source is given by the Monod equation 1 :
$$
\mu = \mu_{max} \frac{[S]}{K_M + [S]}
$$
This relation is linear when the substrate concentration is lower than the constant $K_M$, this is when it is not saturating.
Now, when the culture is in the log phase of growth biomass ($X$) can be described with the simple growth equation:
$$
\frac{dX}{dt} = \mu X
$$
where $\mu$ is the growth rate of the culture, and it can be interpreted as the biomass production speed. So the fastest carbohydrate use is, the highest the growth rate will be.

How do absorbance readings from a spectrophotometer show growth of bacteria if the absorbance readings are taken several times over the course of a day [and plotted on a graph]?

This is explained by the Beer-Lambert law. Simply put: the absorbance ($A$) of an entity is proportional to its concentration ($c$) - all else being equal.
$$
A = \varepsilon \ell c
$$
where $\varepsilon$ is the molar attenuation coefficient or absorptivity of the attenuating species, $\ell$ is the optical path length in cm, and $c$ is the concentration of the attenuating species.
So, the changes in the concentration of your bacterial population (its growth) are reflected in an increase in its absorbance.
If you find a lower absorbance value at time $t+1$ in comparison to time $t$, yes it could mean that the bacterial cell number at time $t+1$ is lower than at time $t$. However, we know neither the protocol you have been following, nor the values you have been obtaining, so there could be other explanations, such as error of measurement.

Do the presence of substrates affect the absorbance reading in other words do carbohydrates have any turbidity?

Yes, molecules in the medium can impact your Optical Density (OD) values. However, that would only be true if these molecules absorb light at the wavelength you are using to measure the absorbance (eg $600$ nm). This is why you should always blank with some filtered medium (or at least with some fresh medium).


What will happen when humans are injected with plant growth hormones

I will only give an outline based only on auxins otherwise the question may be deemed too long.I hope this helps a bit.

The first auxin was isolated from the urine of pellagra patients.

Most natural auxins are indole derivatives which are the intermediates or final products of tryptophan metabolism.Both vitamin B3 and auxins are consequences of tryptophan metabolism. [source]

POSSIBLITY 1-

Thus, auxin injected may be eliminated through urine.

We already understand that substances that are excreted via urine are either toxic to the body or above threshold.Perhaps this idea was harnessed by researchers to construct researches which proved that auxins have anti-cancer properties.

  given that the chemical structure of plant and human auxin is identical and that cytokinin IPA is found in human cells bound to tRNA assisting protein expression, presumably supplied by the consumption of vegetables in the diet, and that we observe a positive effect of plant hormones on pluripotency and key anticancer gene expression levels in mammalian cells [1],[2]

POSSIBILITY 2-

In proper dosage may be utilised for its anticancer properties.

Cytochrome and a series of enzyme system in liver cells are known to detoxify indole

Protein putrefaction in the large intestine results in formation of indole.This indole is carried by the portal system to the liver where it is detoxified to indican  with the help of the cytochrome P450 isoenzyme system and consequently eliminated via urine.

POSSIBILITY 3-

Thus auxins (being indole derivatives and moderately hydrophilic) may be detoxified in the liver and then excreted.
REFERENCE:[1],[2],[3]


Problem on Probabilty of a restriction enzyme cutting a random DNA sequence

EcoRI recognizes, binds to, and cleaves the hexamer 5'-GAATTC-3'. In a completely randomized DNA sequence, with 25 % A's, 25 % C's, 25 % G's, and 25 % T's we would expect to randomly discover the sequence GAATTC, once every 4,096 base pairs, on average. The actual distribution of EcoRI fragments (a fragment where each end contains a cleaved EcoRI site) in our random genome will vary and yield a normal distribution, or curve, with some fragments longer and some shorter. The mean value should be 4,096.

The expectation of 1 site per 4,096 bp is indeed (1/4)^6.

1/4 = 25 %

6 = the number of contiguous base pairs in the recognition site.

In a model like this it is important to keep in mind that the probability of one base occurring in the sequence is completely independent of the sequences before that base, and the sequences after that base. In other words, for each and every position the probability of getting a base that will contribute to an EcoRI site is 25 %, or 1 out of 4 = 1/4.

75% of the time, the next base will not contribute to an EcoRI site (and a quarter of the time it will).

Let's start with your 10 kb fragment, and go through from one end to the other, and mark every time a 'G' occurs. Theoretically those could all be the beginning of EcoRI sites, right? There will be approximately 2500 such 'G's. Now to match our pattern, we need an 'A' in the second position, so let's mark all those sites that contain the dinucleotide 'GA', there will be about 2500 x 0.25 = 625 of them. The next match we need is position 3, another 'A', so in a similar fashion, let's go through the positions of all those GA dinucleotides, and just mark the ones that have an 'A' at the next position. So that will be about 625 x 0.25, or approximately 156 'GAA's distrubuted randomly along the 10 kb fragment.

If we continue, essentially filtering out more and more of those 'G' sites in our initial list then we will find, on average, that there are

39 sites with GAAT

10 sites with GAATT

2 sites with GAATTC

If you don't believe me just pick a sequence and try it yourself.

10,000/4,096 ~ 2.5


ADCs: by what mechanism are antibodies internalised

What we're basically looking at with ADC internalization

Courtesy of Bayer

So the way an ADC works: The antibody-drug conugate binds to a target antigen like a transmembrane receptor, the cell in response engulfs the entire complex and send it to an endosome. What the cell can do with the endosome depends on the cargo. Digressing, the ADC internalization mechanism is often attributed to receptor-mediated endocytosis, where the most prominent mechanism of receptor internalization is the clathrin-mediated pathway. We're going to be referring here most of the time.

  Clathrin-mediated endocytosis commences with the recruitment of adaptor proteins, accessory proteins and a clathrin polymeric lattice to phosphatidylinositol-4,5-bisphosphate-enriched plasma membrane regions

A common adaptor protein here is AP2 that's capable of binding to motifs present on the cytoplasmic tails of membrane receptors. What it's doing is selecting which receptors are the cargo. Then the clathrin mobilizes to the now-enriched membrane regions, and the polymerization of clathrin causes the membrane to displace and curve. Dynamins, large helical GTPase proteins capable of stretching the invagination in the membrane to a vesicle, bind the phosphatidylinositol-4,5-bisphosphates in the membrane, and may work in concert with BAR domain-containing proteins and actin tension to stretch the membrane into a vesicle and cut it away (Doherty & McMahon, 2009).

Obviously there's some missing information, as we don't fully understand it. I think reading the first reference, published in mAbs in 2013, is a really good place to start however!


Summary:

The idea that primary sexual determination defaults to female was proposed several decades ago and is primarily based on the observation that, in the absence of Sry, ovarian development takes hold. However, more recent models suggest that both ovary and testis development require complex genetic regulation and neither can really be said to occur by default. Furthermore, maintenance of sexual determination is apparently a life-long process.

Quote from a Review (Yao 2005):

  We have just begun to glimpse into the mechanisms underlying ovarian development. Convincing evidence challenges us to reconsider the existing paradigm that describes ovarian development as a default system. The default concept was first proposed in the early 1950s when Jost performed the groundbreaking experiments to demonstrate mechanisms of sex differentiation of reproductive tracts (Jost, 1947, 1953, 1970). The term “default” was not originally intended to describe the developmental status of the ovary. Instead, it is referred to the female reproductive tract or the Mullerian duct based on the fact that the female reproductive tract forms in both XX and XY individuals in the absence of gonads. Indeed, now it has become evident that early ovarian development is an active process involving intrinsic cell fate decisions and complex crosstalks between germ cells and somatic cells. Most intriguingly, the appearance of testicular structures in XX individuals where Sry and its downstream components are absent further raises the improbable question: Could the testicular development be default after all?

Some Details:

Sex determination in mammals involves the development of a bipotential gonad into either a testis or ovary. Sertoli cell differentiation and thus testis formation is under the control of the regulatory gene Sry (Koopman et al. 1991). The Sry gene product was later shown to upregulate the expression of Sox9, which is key in testis development (Sekido and Lovell-Badge 2008). On the other hand, ovarian development is centered on β-catenin stabilisation by WNT4 signalling, which is thought to inhibit Sox9 expression (Bernard et al. 2012). Because Wnt4 is expressed basally in the genital ridge and testis development apparently depends on Sry expression, the ovarian pathway has often been described as default; in other words, the pathway that the gonad would take in the absence of Sry.

However, ovarian development is in fact an active process requiring the correct balance of many factors, including a transcription factor called forkhead box protein L2 (FOXL2) (Yao 2005). Studies in mice showed that Foxl2 is expressed in the ovary, both during development and in adulthood. Knockout of the gene prevented granulosa cell differentiation during development, leading to ovarian failure (Schmidt et al. 2004) and increased expression of markers for the testis development pathway (Ottolenghi et al. 2005). Furthermore, mutations of this gene are responsible for XX sex reversal in goats (polled intersex syndrome, PIS) (Pailhoux et al. 2001). Taken together, these experiments indicate that Foxl2 is required for ovarian development and that its absence can favour testis formation.

Many developmental process are dependent on correct timing of gene expression. Sry, particularly, must be expressed within a specific time interval or ovarian development will take hold (Bullejos and Koopman 2005; Hiramatsu et al. 2009). Research by Uhlenhaut et al. (2009), however, shows that this is not necessarily the case for Foxl2 mediated ovarian development, maturation and maintenance. A homozygous floxed Foxl2 mouse strain that expresses Cre under tamoxifen induction allowed conditional knockout of Foxl2. Three weeks after induction, cells of the ovary had transdifferentiated, adopting a morphology and gene expression pattern consistent with Sertoli and Leydig cells (which are normally found in testes). Notably, Sox9 expression increased drastically. Immunostaining showed that, while Foxl2 expression expectedly decreased after Cre induction, the increase in Sox9 was not observed until a day later, indicating that the expression of both is mutually exclusive and that FOXL2 may directly regulate Sox9.

This research presented a novel model for the maintenance of female ovary differentiation. During primary sex determination in females, activation of WNT4 signalling stabilises β-catenin allowing expression of female specific genes and the inhibition of Sox9 (Bernard et al. 2012). In adulthood, FOXL2 actively represses Sox9 expression in gonad cells, maintaining the granulosa phenotype. A similar model of maintenance has been proposed in males due to evidence that the loss of the transcription factor Dmrt1, which normally represses (and is also repressed by) Foxl2 expression, induces transdifferentiation of male mouse Sertoli cells to granulosa cells (Matson et al. 2011). In the case of both males and females, primary sex determination is not just a process that occurs during development but rather requires active regulation for the duration of adult life. This involves collective antagonism between various female and male sex determining factors, including Foxl2 and Dmrt1, and may dispel the notion that ovarian development occurs by default.

Further Reading:

The Genetics of Sex Determination: Rethinking Concepts and Theories

Genetics of sexual development: a new paradigm (Blecher and Erickson 2007)

References:

Bernard P, Ryan J, Sim H, Czech DP, Sinclair AH, Koopman P, Harley VR. 2012. Wnt signaling in ovarian development inhibits Sf1 activation of Sox9 via the Tesco enhancer. Endocrinology 153:901–912.

Blecher SR, Erickson RP. 2007. Genetics of sexual development: a new paradigm. Am J Med Genet A 143A:3054-68.

Bullejos M, Koopman P. 2005. Delayed Sry and Sox9 expression in developing mouse gonads underlies B6-YDOM sex reversal. Dev. Biol. 278:473–481.

Hiramatsu R, Matoba S, Kanai-Azuma M, Tsunekawa N, Katoh-Fukui Y, Kurohmaru M, Morohashi K-I, Wilhelm D, Koopman P, Kanai Y. 2009. A critical time window of Sry action in gonadal sex determination in mice. Development 136:129–138.

Koopman P, Gubbay J, Vivian N, Goodfellow P, Lovell-Badge R. 1991. Male development of chromosomally female mice transgenic for Sry. Nature 351:117–121.

Matson CK, Murphy MW, Sarver AL, Griswold MD, Bardwell VJ, Zarkower D. 2011. DMRT1 prevents female reprogramming in the postnatal mammalian testis. Nature 476:101–104.

Ottolenghi C, Omari S, Garcia-Ortiz JE, Uda M, Crisponi L, Forabosco A, Pilia G, Schlessinger D. 2005. Foxl2 is required for commitment to ovary differentiation. Hum. Mol. Genet. 14:2053– 2062.

Pailhoux E, Vigier B, Chaffaux S, Servel N, Taourit S, Furet JP, Fellous M, Grosclaude F, Cribiu EP, Cotinot C, et al. 2001. A 11.7-kb deletion triggers intersexuality and polledness in goats. Nat. Genet. 29:453–458.

Schmidt D, Ovitt CE, Anlag K, Fehsenfeld S, Gredsted L, Treier A-C, Treier M. 2004. The murine winged-helix transcription factor Foxl2 is required for granulosa cell differentiation and ovary maintenance. Development 131:933–942.

Sekido R, Lovell-Badge R. 2008. Sex determination involves synergistic action of SRY and SF1 on a specific Sox9 enhancer. Nature 453:930–934.

Uhlenhaut NH, Jakob S, Anlag K, Eisenberger T, Sekido R, Kress J, Treier AC, Klugmann C, Klasen C, Holter NI, et al. 2009. Somatic Sex Reprogramming of Adult Ovaries to Testes by FOXL2 Ablation. Cell 139:1130–1142.

Yao HH-C. 2005. The pathway to femaleness: current knowledge on embryonic development of the ovary. Mol. Cell. Endocrinol. 230:87–93.


I have no experience on mammalian expression analysis but I have seen these asymmetric plots quite a few times when cells were highly stressed. During one treatment they shut down protein biosynthesis and photosynthesis so downregulated genes vastly outnumbered the few genes which were involved in the adaptation response. I don't know if something similar could be happening in your samples?


Great picture and great find.  But unfortunately I don't think that is a new species of bird...or even a bird at all!

It looks like a hummingbird hawk-moth, Macroglossum stellatarum.

Here you can really see the 'little trunk' (as you described it) known as a proboscis, which it uses to feed on flowers.

Fun fact: It's believed not to be a mimic of the hummingbird, but rather an example of convergent evolution.


First a clarification: the mobile units are no so "mobile". Due to (1) the high protein:lipid ratio of the thylakoid membrane and (2) the packing of protein complexes, the rapid diffusion of components along the membrane is hindered.

It has been proposed the existence of small local PQ diffusion microdomains, based upon the percolation theory:

  From the percolation theory, above a critical density, immobile or slowly moving transmembrane proteins are, indeed, expected to form flexible 2D networks of closed compartments preventing long range movement of small molecules. (Kirchhoff, H et al. (2000) Biochim. Biophys. Acta 1459, 148–168)

For this reason the PQ are confined, on a short time scale, within these domains, preventing their "dispersion".

In addition of the low diffusion of mobile carriers, the geometry of the granal stacks mantains the contact area between the PSII of the appressed grana and the PSI in the margin annulus domains relatively large, enabling effective linear electron transport in microdomains.

Figure 2b of the paper cited below shows the geometrical organization of the stacked grana and its description says:

  The circular border between the appressed domain and the margin annulus (ring) allows a large contact area between the PSII and the PSI domains and efficient linear electron transport from PSII via plastoquinone (PQ), plastocyanin and cytochrome b6f to PSI at a short distance of ~30–60 nm in local domain.

Further informations can be found in Albertsson, P-Å. (2001) Trends Plant Sci. 6, 349–354.


Which immunosuppression caused by long-term usage of these antibiotics in untreated celiac disease?

One possibility is that these antibiotics could disrupt your normal gut bacteria. Given that your gut has the surface area of a tennis court and is typically coated with symbiotic microbes, antimicrobial therapies could dramatically change the population dynamics of your gut ecosystem. One might imagine that the immune system of the gut is in homeostasis with these gut microbes, and if they all die off all at once because you're taking some sort of 'cillin, your immune system might suffer for lack of stimulation. Fewer immune cytokines released by your intestinal immune cells into your blood => systemic reduction in immune function.

Other possibilities could include: the drug just randomly fits into a bad spot on some important immune protein; the drug targets bacterial-related genes in the mitochondrial genome and disrupts the metabolism of the immune cells; the drug disrupts your ability to absorb nutrients required for immune function...the list of potential mechanisms is undoubtedly long.


What does the MAF/MinorAlleleCount mean?

[W]hat is the Major allele [frequency]?

If the Minor Allele Frequency is $p$, then, for a bi-allelic locus, the major allele frequency is obviously $1-p$.

  [W]hy reporting the second most frequent allele is helpful?

Most polymorphic loci of interest are bi-allelic. Hence, the MAF is an indication of genetic diversity. One could similarly report the expected heterozygosity instead ($2p(1-p)$).

It is common to consider only loci with a MAF greater than a certain value. There may be different reasons for that. Here are possible two reasons.

Sequencing errors

When sequencing your sample, errors are being made. Sure, error rate is pretty good (see this table from Molecular Ecology) but error still do exist. A polymorphic locus with a minor allele count of less than, says, 3 alleles might well just be caused by sequencing errors.

To avoid considering as polymorphic loci that are in reality not polymorphic, we often just disregard any data with MAF is below a given threshold.

$F_{ST}$

$F_{ST}$ is a measure of genetic differentiation among population. When computed on loci with low MAF, the statistic is biased (Beaumont and Nichols, 1996). Hence, it is usual to only consider loci with a MAF greater than an arbitrary threshold before computing $F_{ST}$


use of adjuvants and peptides in modern vaccines?

In many vaccines, there are two components: One immunogenic substance, these can be parts or complete (inactivated) pathogens (for example the small pox vaccination), peptides or proteins (like the tetanus vaccination) or polysacceride components from the capsule of bacteria (for example against MenC). Against these components the actual immune response is directed. See references 1 to 3 for some more details.

Then they can (depending on the vaccine) contain adjuvants, which enhance the immunologic reaction of the body. This is done either to enhance the reaction and to get a proper immune reaction but also to be able to reduce the amount of injected antigen. So the adjuvant simply causes a general inflammatory reaction. Classically Alum (aluminium hydroxide is used here), newer adjuvants are squalen based oil-in water preparations or CpG olinucleotides (see references 4 and 5 for numerous examples on adjuvants and literature).

So what you basically do is to identify (more or less) a part of the pathogen which can serve as a vaccine and use this part for the vaccine.

Making Vaccines: How Are Vaccines Made
Designing Tomorrow's Vaccines
Strategies for designing and optimizing new generation vaccines
Dose Optimization Strategies for Vaccines: The Role of Adjuvants and
New Technologies
Vaccine Adjuvants Review


From this video demonstration in caltech, you can clearly see that Drosophila can fly forwards as well as backwards using high fps video image capture and it even does unexpected behaviours in times of perceived danger/threat.


Does the use of RNA as a primer affect the accuracy of DNA replication in E.coli?

E.coli use DNA polymerase for DNA replication too. Primase creates a short oligonucleotid (primer) in the start of string and DNA polymerase continues in work. RNA polymerase is using in synthesis of RNA molecules.


Where do I get an annotation file for yeast genome with ENSEMBL ids?

With a further search for the answer, I realised that unconventionally, ENSEMBL ids for yeast start with Y. That is strange. I guess this is because the yeast annotations are primarily maintained by SGD (yeast genome database) and ENSEMBL just hosts a copy of that.

Also these ids are called Stable Gene IDs.


Questions concerning synaptic input and dendritic processing

Started writing a comment and realized it was an answer...

These guys are basically saying "take a uniform spherical neuron" the same way you would say in physics "take a uniform spherical cow." There isn't a dendrite mentioned in the whole paper.

By "the membrane time constant" they mean exactly that: one membrane time constant, effectively the somatic time constant. They aren't talking about dendritic trees: they are essentially saying assume a uniform spherical neuron that gets inputs on its soma.

Membrane time constant is associated with the rate of change of the membrane voltage; synaptic time constant is associated with the rate of change of the synaptic current (this is what they refer to when they talk about exponentially decaying synaptic currents). Real biological synaptic currents have a time course governed my neurotransmitter concentrations and the gating properties of postsynaptic receptors. Real biological postsynaptic potentials (voltages) are governed by both the time course of the synaptic current and the capacitive properties of the membrane (i.e., the membrane time constant).

Instead of considering synaptic time constants, you could simplify a synaptic event as an instantaneous current impulse: essentially the entire current all in one instant rather than over time. The presence of the membrane time constant helps with making this assumption somewhat reasonable, because the membrane time constant ends up filtering input currents anyways, whether they are impulses or have a synaptic time constant.

In a simulated environment, you can make computations simpler by just adding a little time to the membrane time constant to roughly simulate the effect of the membrane time constant + synaptic time constant. Again, this is for computational efficiency, like when you assume a cow is spherical, not for perfect biological accuracy.


Hi again TheLast Cipher,
Enzymes in a cell are usually semi-quantified by the: Western Blot technique.
But there are lesser known techniques.
E.g. For a Western Blot the unit of measurement is the color intensity of the enzyme band on the blot membrane.
If I were you I would look for journal articles covering your pathway of interest.
E.g. https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1002/biof.5520320129
Covers the electron transport chain (Co-enzyme Q10)
If you can get through the pay-wall & read their results and you will find:

"Western blot analysis of membrane protein isolated from keratinocytes derived from one young and old donor. A representative picture out of five experiments is displayed."

Also they used and I quote:

"Arbitrary Units"

Maybe you could comment on which pathway and I can find some assisting material.


Melatonin production, sleep, and "cyan light"; how might this finding be possible?

Melatonin production is in response to photoreceptors in the eye, in part, the same photoreceptors in rods and cones that process and transmit information about the wavelength of light (eventually) to the visual cortex for vision. However, @uhoh was right to wonder whether there might be a separate receptor input for melatonin production.

There is an additional opsin (photosensitive protein), found in the ganglion cells rather than the rods and cones, that is sufficient for responding to light and causing the production of melatonin by the pineal gland (mediated by the suprachiasmatic nucleus of the hypothalamus). Processing of light signals by the circadian system is quite separate from processing by the visual system. This is discussed briefly in Chapter 47 of Kandel's Principles of Neural Science, but you can read more about it in this review.

The pathways involved in receiving and processing light as an input to the circadian system were discovered relatively recently. Consider that the optic tract was discovered in the 3rd or 4th century BC, and the retinohypothalamictract was discovered in 1971.


What makes teeth feel sticky after drinking Coca-Cola?

Glucose and other ingested sugars have a natural affinity to bind to surface proteins on teeth (as well as many other proteins in tissues). This process is called glycosylation, and is expedited both by acidic environments (such as provided by the acidic soft drinks as indicated by The Last Word) or metabolism of adherent bacteria on the tooth surface (see one example). A discussion of oral cavity lubrication and how this influences tooth surfance glycosylation and biofilm formation has also been reported. The fuzzy feeling is a result of plaque formation. Plaques form as a byproduct of metabolism of bacteria on the tooth surfaces, that ingest and break down dietary sugars, and also secrete acids as a byproduct of this metabolism. The result, if left long enough, is plaque formation and eventually tooth decay. You can also notice this fuzzy feeling after a day or so of not brushing your teeth, as the bacteria have had a long time to metabolize the sugars ingested over that period to produce a plaque.


Can memory be improved with mental training?

You are not alone.
I think most people do not use the memory capacity of the brain optimally.
Some people use it more optimally than others though.

The researchers who wrote the book "Make it Stick" researched exactly this problem.

Of their many excellent findings, I think the most important was that most people did not convert the knowledge that they accumulated in working memory into long term memory because they did not do spaced repetition of recall practice.

When we learn something new those synaptic connections are weak unless we strengthen them.
The brain seems to let go of information that it deems to be less important in this fashion.

Everybody forgets a little.
But if you practice recalling what you've learned at spaced intervals, that seems to greatly improve the ability to convert working memory to long term memory.

Its important that recall involve actually struggling to recall the information.
Its the struggling that seems to strengthen the synaptic connections.
Just rereading some material wont work.

I put everything that I learn into Q&A documents that I use for recall practice.
This seems to have significantly improved my ability to commit new knowledge to long term memory.