Your question "are all of these relevant" doesn't make much sense to me, but I am going to assume you are talking about it in terms of terminology and answer that way.

The "vertical" connections you describe are usually referred to in the context of cortical "columns" and are therefore referred to as "intracolumnar." Within a column, intralaminar connections by far dominate the total number of synapses, but connections between layers are also important (note that my answer Cortical projections from layers 2/3 back to 4? covers some of this as well, though that question is much more specific).

Horizontal connections refer to connections between cortical columns of the same cortical area (e.g., from V1 to V1 with a different orientation selectivity). These are often stronger between the same layers, but simply saying "horizontal" does not specify that you mean intralaminar horizontal connections.

"Intragyric" is not a word that is used - I think you made it up. Gyri aren't really specialized functional units, and although there may be some brain areas that are localized within a gyrus many span either several gyri or share a gyrus with other areas (for example, "Heschl's gyrus" isn't even just one gyrus). Therefore, you can't really generalize "gyric" connections as being in a particular class, you would have to refer to the specific areas that are connected to understand the nature of those projections.

Interhemispheric connections are fairly ubiquitous in neocortex, and they make up several white matter tracts that connect the hemispheres, most prominently the corpus callosum. As such, those connections are also often referred to as "callosal" projections.

Other terminologies that are used are "top-down" versus "bottom-up" according to the position of areas in the cortical hierarchy. "Lower" areas are considered to be those with primary sensory and motor functions, whereas higher areas are associative/executive areas. The canonical reference for these projections is Felleman, D. J., & Van Essen, D. C. (1991). Distributed hierarchical processing in the primate cerebral cortex. Cerebral cortex (New York, NY: 1991), 1(1), 1-47. The key feature of top-down versus bottom-up projections is a difference in the interlaminar pattern of connectivity between different cortical areas. It can be hard to really parse the precise hierarchical of some of the higher-order cortical areas, and the patterns of top-down and bottom-up are fairly mixed for areas at similar levels of the hierarchy, however.


Explaining a branch with visibly different leaves on Citrus japonica

What you are seeing here is an example of a winged petiole. The petiole is the leaf stalk and these can have wings called stipules.

According to this source kumquat leaves have narrow petioles. I can't explain why you are seeing variation on a single plant, but I recall seeing similar variation on garden citrus in California, so I suspect it isn't unusual.


Has the protein composition (with identification) in honey and other honeybee byproducts been studied?

First of all: Honey is not a byproduct of bees - it's their main and most important product which stores energy for the bee hive for the time when no flowers are available.

Honey itself consists (according to the USDA database) to about 99.5% of water and sugars (82.5% sugars, 17% water). The sugars are mostly fructose and glucose, but also some other mono- di and tri-saccherides in traces. See reference 1 for details. It also contains trace amounts of vitamins and minerals, see table from the Wikipedia on Honey:

The protein content varies between honey sample but is somewhere in the range between 0.2 and 0.5% (see also reference 1). The proteins come from flowers (pollen incorporated into the honey) as well as from the bees (see reference 2). Paper 1 lists a number of enzymes as most common bee proteins in the honey, but doesn't go into much more details here. These are invertase, diastase, glucose oxidase and catalase.

You could now go into the sequence databases (Apis mellifera has been complete sequenced) and look up the sequence information of the enzymes. Information can be found here and here.

References:

A review of the analytical methods to determine the geographical and
botanical origin of honey
Source of the honey protein responsible for apple juice
clarification


What is meant by 'genes overlapping inherited structural variants'?

If I understand correctly, what this paper is looking at is rare copy-number variation in ASD cases relative to controls. So in the context of the paper, the passage you quoted is basically saying we found genes that had copy-number variation between cases and controls, i.e. the cases had a pattern of more/fewer copies of a stretch of the genome that includes a gene than the controls. Then they look at the functions of the genes they found in a gene ontology database to see if they seem like they might relate to ASD.


Are there completely self-sufficient autotrophs?

It really depends on what you mean by "organic matter".  No cell is going to be able to grow and reproduce without an appropriate source of CHON atoms (plus lesser amounts of the other necessary elements).

So, if by organic matter you mean CHON+, then no, everything needs organic matter to grow and reproduce.

If by organic matter, however, you mean natural organic materials like soil or groundwater, then yes, there are lots of things that can live on chemical mixtures that can be produced by purely synthetic means.  A simple example is M9 media, which is a commonly used bacterial culture medium.


Which sources can I use to study botany and horticulture?

This book could be a good start: Botany by Mauseth. However if you don't have any knowledge about biology I suggest you to get starting with the basics of cellular biology. A good book could be "The cell" by Cooper, you can find it in electronic version.  There are many books about cellular biology but I recommended this because it is complete and detailed without being too long compared with others.


Why don't antibodies generally bind to food and drugs?

B cells containing receptors against food's or drug's molecular structures may exists. However if the naive B cell binds the molecule without a second signal coming simultaneously from CD4 Tfh cells (linked recognition) the B cells recognizing this antigen will become anergic or will die by apoptosis. This occurs with antigens to which we are chronically exposed, like food.

Reference: Janeway's Immunobiology, 8th edition. Chapter 8 (The development and survival of lymphocytes). In particular section 8-26, p320-321.


To a population with no immunity, why is smallpox or measles more deadly compared to COVID-19?

I think this is an interesting question, and I've been struggling to put together a good answer to it for a while. Unfortunately, everything I came up with just boils down to "some viruses are more deadly because they kill more cells faster" which is pretty circular. A detailed understanding at the subcellular level of what happens during virus infections doesn't exist.
It's instructive here to look at the evolutionary pressures on human-infecting viruses. SARS-1 was about 10x as deadly as SARS-2, but it was contained quickly, while SARS-2 is on track to infect a substantial portion of all humans on the planet. SARS-2 is more successful because of, not in spite of, its lower lethality. Because many infections are asymptomatic, the infection can't easily be contained. If we look at things this way, the asymptomatic infections are the ones that go "according to plan" for the virus, and the severe cases and deaths are unwanted collateral damage. Severe cases of COVID are associated with the presence of viral RNA in the blood. But SARS-2 primarily enters new hosts through droplets expelled from infected hosts' respiratory systems. Any viral activity outside of the respiratory system cannot produce these droplets, and is therefore "wasted effort". This is similar to polio, which causes no symptoms when it transmits successfully by replicating in intestinal cells, but causes paralysis when it gets stuck in the dead end of its host's nervous system.
So, if viruses are most successful when they cause no disease, shouldn't they all quickly evolve into harmless versions? They don't because the "sweet spot" of asymptomatic transmission is the unstable result of an immune response that is just effective enough. If a virus fights the immune system either too hard or not hard enough, the infection will end too fast to spread effectively; due to the death of the host or the virus, respectively. Similarly, if a virus is too "aggressive" in entering cells it will damage tissues that don't lead to transmission or new infections, but if it is not aggressive enough it will not be enter those tissues it needs to make, e.g. respiratory droplets carrying new virus in the case of SARS. Since a lethal disease still results in some transmission but complete suppression by the immune system doesn't, it's more evolutionarily favorable for viruses to err on the size of causing worse disease.
Edits for changes in the question:
I think the differences between covid-19 and smallpox are a bit misleading. The big differences between the two diseases is that, while the human populations most affected by smallpox were naive to the virus, the virus was not naive to them. Smallpox is believed to have been infecting humans since at least the 3rd century BCE. It had a lot of time to evolve tricks to defeat the human immune system. And as a dsDNA virus with a 186,000 base pair genome, it had plenty of space to store those tricks. For comparison, SARS-CoV-2 has a 30 kb RNA genome, and poliovirus has a 7.5 kb RNA genome. However, Herpesviruses have been infecting humans since before humans were human, have large genomes, but only cause disease when the immune system is suppressed or nonfunctional. In those cases, however, it is quite effective at spreading throughout the host and can kill. So we see that herpesviruses also rely on the immune system of the host to stay in their sweet spot, they just have a different strategy than smallpox. Since smallpox has been exterminated and herpesvirus is in nearly every human on earth, we can say the mild strategy is the unequivocal winner, at least for now.


Does suffocation pain involve nociceptors?

This is more of a hypothesis

I am not sure if suffocation per se would cause pain. Asphyxia, as RoryM indicated in their comments, can lead to anxiety and panic but not really pain. However, forceful breathing may lead to muscular fatigue which may result in pain. Pain induced by muscle fatigue is called myalgia. Myalgia is possibly triggered by low pH generated by lactic acid, via ASIC3 (Acid Sensing Ion Channel) receptor. Carbon dioxide has no role in this process either directly or as a synergist.

Reference:

Alan R. Light, Charles J. Vierck, and Kathleen C. Light. (2010) Translation from Mouse Sensory Neurons to Fibromyalgia and Chronic Fatigue Syndromes. Boca Raton, FL: CRC Press; Chapter 11 (Myalgia and Fatigue)


It is Pneustocerus gravelyi, a species of stilt bug that lives in India.

In both of these images, you can clearly see the the bright red coloration of the joint on each leg. The pronotum is also the exact same shape and color, and the bright red abdomen extends beyond the closed wings.

original unmodified image source


Did Plant Cells Evolve from Animal, Protist, or Fungal Cells?

Plants were almost always considered a separate group from fungi and animals.

As per the latest classification both animals and plants are included in the clade Opisthokonta: animals and related unicellular organisms (holozoa) form a sister clade with holomycota (contains fungi and Cristidiscoidea).

Plants (archaeplastida), aveolates and rhizaria are now grouped under Diaphoretickes (previously they were grouped under Bikonta).

To cut short the plant and animal lineages merge only at the level of the last eukaryotic common ancestor. This means that plants are as unrelated to fungi as they are to animals.

Protista is no longer considered a proper clade. It used to be a group where all unclassified unicellular eukaryotes were dumped. Now these organisms have been reclassified; some are closer to animals (for e.g. Amoeba), some are closer to plants (e.g. Plasmodium) whereas some are part of a group that is distantly related to both plants and animals (for e.g. Euglena).

Have a look at this WikiSpecies site for a detailed classification (latest and historical). It also cites proper references.


Yes.

  Research in cnidarians shows that even pre‐bilaterian animals can develop neoplasia (Domazet‐Lošo et al., 2014). Two different species of Hydra have presented with tumour‐bearing polyps. The cells in these tumours were invasive, which suggests that metastatic capacity has ancient roots. Additionally, the tumours had several orthologues to tumour‐related genes in mammals and displayed parallels to the hallmarks of cancer in vertebrates. The proposed mechanism for tumourigenesis in Hydra is the accumulation of stem cells if they are not appropriately removed by programmed cell death (Domazet‐Lošo et al., 2014). Scientists have also identified several cancer‐like lesions in corals (Aktipis et al., 2015).

--From humans to hydra: patterns of cancer across the tree of life


What moth is this and how do we get rid of them?

That is an Indian meal moth Plodia interpunctella. Family Pyralidae. They are very common household pests. https://www.doyourownpestcontrol.com/indian_meal_moth.htm
They breed in grains or cereals. You need to look through your pantry, and find out what they have been breeding in. Seal up your grains and cereals in plastic, or put them all in the fridge.


Public database of animal specifications

You might be interested in the PanTHERIA database for several thousand mammalian species.  It has up to 53 characteristics for each species (but many fields have no entry).  It is available as two plain text files, each with one line per species (plus header line) and fields separated by tabs.  The files and data descriptions are available at http://esapubs.org/archive/ecol/E090/184/


Are STOP codons impacted by base insertion or deletion mutation?

Yes. Mutations can affect STOP codons and they do relatively commonly. These are important because they can lead to significant changes in the resulting peptide and are likely to affect protein functions or phenotype.

For a point mutation (a single base substitution), there are several possible effects:

silent mutation is a synonymous base substitution which does not change the encoded amino acids (this is neutral variation).
missense mutation is a non-synonymous bass substitution which changes only one amino acid in the protein (these can affect protein functions but do not always).
nonsense mutation is a change in a coding codon to a STOP codon (this truncates the encoded amino acid sequence prematurely resulting in a shorter peptide).
nonstop mutation is a change from a STOP codon to a coding codon (this means the amino acid sequence will continue to the next STOP codon resulting in a longer peptide).

Insertions and Deletions in DNA sequence (InDels) are important because they change all codons that follow it (not just the base substituted):

frameshift mutation adds or removes a base which resulting in a change in the reading frame: all bases following will result in new codons, including STOP codons (this commonly results in entirely new protein domains and proteins of different lengths as STOP codons will also be changed. They are encoded in the reading frame like all other codons.

As you can see, mutations which affect STOP codons are very important as they drastically change the protein sequence. This usually disrupts the protein function and causes diseases or inviable embryos. Most of these are removed from populations long-term by natural selection. However, it can rarely lead to entirely new proteins beneficial to the organism and evolutionary changes. This is more likely with duplicated genes where one can change while the other retains the original function.

As such, mutations involving STOP codons are among the most biologically important.  Another important case is splice functions. Point mutations and frameshifts can also affect intron-exon boundaries, resulting in new splice variants, skipped exons, and reading further into introns (which may contain splice junctions or STOP codons).


Yes you are wrong I am afraid. Evolution is the process of change through time of species by inherited changes. Heritable differences mainly come about from random mutation in the genome. These genetic differences between individuals lead to fitness differences between individuals, ie one individual is better able to produce offspring, thus spreading more of its genes in to the following generation, than another individual. For example, environmental change causes selection for a dark body morph in moths, stabding genetic variation and new mutations affecting body colour is then more favored by selection, and those with the dark body genes survive and reproduce better.

There is no end or goal to evolution. It is often mistakenly said that humans have stopped evolving. This is wrong and to suggest we have is to suggest that evolution is directed and has an ultimate goal. As long as genetic fitness variation exists there will always be some level of evolution because there is a difference between individuals in selection coefficient. Selection is also very unstable, it can change drastically an rapidly, evolution could only then stop if selection was constant and favored one "ultimate genotype" over all others in which case all genetic variation would cease to exist.

If we found another planet which had the exact same conditions and time as earth we may find the same species, but it is not likely. It requires the same mutations and selection processes occurring. Analogous to this is the observation of "many solutions to one problem" where different species use different adaptations to deal with a common problem. For example, geting oxygen is difficult for water deelling species. Sea mammals like whales gather oxygen by going to the surface and breathing and then holding their breath. Fish have evolved gills, a different solution to the same problem, to harvest oxygen from the water. These solutions evolve from random changes with selection acting only on the results (those that could filter oxygen from the water or hold their breath the best survived and reproduce best).


How do neurons receive the ions needed for creating electrical pulses?

Short answer
The sodium-potassium pump in the epithelial cells lining the brain capillaries pumps Na+ and K+ into the brain.

Background
The blood-brain-barrier is formed by the endothelial cells lining the capillaries in the brain. Not many compounds can pass this lining, especially not when they are hydrophilic, such as charged metal ions. However, as you rightfully state, somehow these metal ions, and especially Na+ and K+ need to get access to the brain because they are crucial for membrane potentials and action potentials, and hence for neuronal survival and function. And indeed they can, albeit the exchange between blood plasma and brain is slow compared with other tissues.

Intravenously administered K+, for example, exchanges with muscle K+ in 1 hr, but K+ exchange in brain is only half completed in 24 to 36 hr. Na+ exchange is somewhat faster, with half-exchange into brain occurring in 3 to 8 hr. Despite its relatively slow entry into the brain, Na+ exchange across the blood—brain barrier appears to occur by mediated transport. This occurs, in part, through brain capillary Na+,K+-ATPase (the sodium-potassium pump). The Na+,K+-ATPase in the brain also may mediate removal of interstitial fluid K+ from the brain and thereby aid in brain K+ homeostasis.

Reference
- Laterra et al. In: Siegel et al. eds. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th ed. Philadelphia: Lippincott-Raven; 1999


Is there any relationship between DNA methylation as a level of
  stability to epigenetic states and genome size?

I would say yes, because methylation is used to disable genes in differentiated cells. Disabled genes in differentiated cells generally need to stay disabled to maintain normal behavior for the cell type. Larger genomes usually encode more different types of cells.

  it is claimed that DNA methylation is not required for epigenetic
  stability in Drosophila melanogaster and yeast, both genomes much
  smaller than mammalian or plant genomes.

According to my book (S377 molecular and cell biology, book 2, p140) Drosphila don't need methylation because they perform transcriptional regulation by persistent chromatin remodelling instead. Yeast being single celled would have less need for this type of control.

  Could it be that DNA methylation is needed to help activate/repress certain genomic regions on top of other epigenomic marks when the genome is so vast that there is a need for an extra level of marking?

It is used as a repressor because it inhibits  hydrogen bonding of transcription factors and the like. I have not heard of it functioning as an activator.

There are also other uses for methylation, for example  newly synthesized DNA is hemimethylated - where the parent strand is methylated and the child one not. From this it can be determined which is the parent strand during DNA repair.


What software is there available for quantitative structure–activity relationship (QSAR) pharmacological studies?

On the G6G Directory of OMICS and Intelligent software, I searched for "QSAR Analysis, and received two product abstracts:

1) SYBYL®-X Suite which contained:

3D QSAR: use the power of industry leading CoMFA in a new way to
generate novel ideas for R-groups - predict the level of biological
activity or potency based on structure-activity data, Not just yes/No
activity predictions;
Cheminformatics: produce highly focused queries that avoid false
positives using a rich set of 3D queries; on-the-fly conformational
searching means you only store a single conformation of your
molecules, keeping database size small and very transportable; and...

Link to this abstract:
http://g6g-softwaredirectory.com/bio/proteomics/structure-modeling/20710-Tripos-SYBYL-X-Suite.php

2) Fujitsu GhostMiner

GhostMiner can be employed in a number of business intelligence areas and the following areas:

Bioinformatics - genetics, proteomics, Quantitative Structure
Activity Relationship (QSAR) modeling...

Link to this abstract:
http://g6g-softwaredirectory.com/ai/neural-networks/20154-FQS-Poland-Fujitsu-GhostMiner.php

Perhaps the above will help.


Would it be correct to say that viruses are genotoxic?

From wiki

  In genetics, genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations

While some viruses tend to cause mutations, most don't have such a strong mutagenesis effect. As such, they are not really genotoxic. Also, even if a virus is genotoxic, one should definitely not reduce the activity of a virus to its genotoxicity. A virus has a life-cycle and is able to reproduce. It is clearly more than a simple genotoxic chemical agent such as metal chromium.

So, in short

Reducing viruses to their genotoxic effect would be a misrepretentation of what virsues are
Most viruses don't have a strong genotoxic effect and therefore you can not make the claim in the general sense.


Interpretation of graph from evolutionary biology

I assume that the figure comes from a section on genetic drift (since this seems likely), and it shows how the allele frequency will change over time under drift in a diploid population. So in short, each line represents the distribution of allele frequencies in different hypothetical populations, that all started with the allele frequencey p=0.5.

As for your specific questions, as the comment from @remi.b says, t is expressed as generation time since this is the relevant time scale for evolutionary changes. The reason why it is a function of population size, N, is that genetic drift acts more stongly in small populations, since it is essentially a sampling effect. You can see it as a repeated application of binomial sampling. So in small populations different populations will quicky drift away from the starting point of p=0.5, while this takes a longer time in larger populations. The effect of population size is clearly shown in this article from Nature education, where you can see the distribution of allele frequencies after one generation in populations of different sizes.

The change in allele frequencies over time under drift has been modelled by a diffussion approximation (see Kimura, 1955 for the original results). His results show that heterozygozity decreases at the rate of $1/(2N)$ per generation, and after 2N generations the distribution of allele frequencies is essentially flat (if you started at p=0.5). The degree of heterozygocity at time t is given by:

$$H_t = H_0*e^{-(\frac{1}{2N})t}$$

However, your graph does not show populations where fixation has occured (only heterozygous populations), and this proportion will increase over time in the absence of new mutations. So what is missing are bars at 0 and 1, and these will become higher as time goes by (more populations will have become fixed for one of the alleles). It should also be mentioned that these results deal with the effective population size, so $N$ is really equal to $N_e$.

As for the confusion of frequency/frequencies; the graph shows the frequency of one allele in different populations (so the allele frequency on the x-axis), but each line shows the distribution of allele frequencies in different populations. This is probably why you found this confusing.

However, your question is a bit unclear since you haven't described from where you got the graph and exactly what it is supposed to represent.


Disclaimer: the denaturation is the process of protein unfolding from their native state. Since vitamin C is not a protein, it cannot denaturate. I think that the word you're looking for is simply "degradation".

Vitamin C can exist either in its reduced form L-ascorbic acid (L-AA) or in the oxidised form dehydroascorbic acid (DHAA). The active (antioxidant) form of vitamin C is the former; however, there are enzymes in our body that can convert DHAA back into L-AA.

In this article, the authors seek to evaluate the thermal stability of both L-AA and DHAA in broccoli. Their results are the following.

  Thermal treatments (for 15 min) of crushed broccoli at 30 to 60 degrees C resulted in conversion of l-AA to DHAA whereas treatments at 70 to 90 degrees C retained vitamin C as l-AA.

So, cooking the vitamin C does not alter its structure and your body will still be able to use it. Another reason to eat broccoli, I guess.


Clarification of the procedures to amplify cDNA needed

Here is the rough procedure that I've used to prepare cDNA before

Extract RNA from desired tissue (select for mRNA using the polyA tail of mRNA)
Conduct reverse transcription. This requires a primer complementary to the polyA tail to get the reverse transcriptase started (Edit:You could also use random primers to prime reverse transcription. This eliminates the redundant polyT sequence from the cDNA. This is the method used in the Illumina TruSeq high throughput sequencing library prep kit). Now you have a collection hybrid RNA/DNA double strands
Digest the RNA strand specifically. This can be accomplished with RNAse H as you mention, or by introducing basic conditions, which degrade RNA much more rapidly than DNA due to the 2'OH of RNA. Now you have linear ssDNA complementary to the inital mRNA templates.
From this point your applications may differ. If you are doing microarrays, all you need is ssDNA, since you want to hybridize the cDNA to the array. If your downstream use of the cDNA requires dsDNA, then you need to synthesize a complementary strand to the cDNA (and potentially amplify the product). This can be accomplished through PCR random primers, or some more complicated PCR that will incorporate extra sequences on either side of your cDNA (e.g. bar-codes and adapters in RNA-Seq).

  How is [the cDNA] protected from the nucleolytic activity?

If you are digesting the product of reverse transcription with RNAse H, that enzyme digests RNA specifically, so your DNA is unharmed. If you are going with an alkaline conditions treatment, then the RNA will be degraded in those conditions much more quickly than the DNA due to the presence of the 2' OH group in RNA which can act as a nucleophile for a self-cleavage reaction.


What would happen if brain neurons did not reduce their sensitivity to neurotransmitters after prolonged exposure?

Short answer
As far as I am aware, neurotoxic effects of chronic excitatory stimulation are not prevented by receptor trafficking.

Background
I think the question assumes that 1) neural damage related to continuous activation (excitotoxicity) is preventable by 2) the dynamic regulation of receptor numbers on the neuronal membrane. As far as I can see, these two processes are unrelated.

Excitotoxicity is

  ...the ability of glutamate or related excitatory amino acids to mediate the death of central neurons [...] for example, after intense exposure. [...] Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload (Choi, 1992).

Hence, it is the influx of toxic amounts of Ca2+ that induce cell death. Not much Ca2+ is needed to accomplish this. For example, a status epilepticus (a sustained epileptic seizure) can lead to hippocampal damage, due to persistent excitation and glutamate release (Meldrum, 1991). Epileptic seizures lasting longer than 5 minutes are regarded as dangerous in this sense and after 30 minutes they are potentially fatal (often not directly related to excitotoxicity though) (Cherian & Thomas, 2009). In this short time span regulation of cell-surface receptor densities are unlikely to play a substantial role. For example, serotonin-specific reuptake inhibitors need 2 weeks to lower the amount of 5HT1A receptors (Tylee & Wolters, 2009).

Dynamic regulation of receptors. The regulation of the number of receptors is linked via feedback loops. A great example is the way glutamatergic AMPA receptors are regulated through endocytosis (Fig. 1).

Fig. 1. AMPA receptor trafficking. Source: Anggono Lab.

AMPA receptors are the principal receptors that mediate most of the fast excitatory synaptic transmission in the mammalian brain (Purves et al., 2001). The dynamic trafficking and proper synaptic targeting of AMPA receptors are crucial in determining the strength and plasticity of excitatory synaptic transmission. This dynamic regulation may also impact learning and memory processes. The process of receptor trafficking is, as far as I know, typically not associated with emergency rescue operations to prevent excitotoxicity. Nonetheless, these mechanisms, are essential to sustain an adaptable brain capable of learning, forgetting and restructuring itself.

References
- Cherian & Thomas, Ann Indian Acad Neurol (2009); 12(3): 140–53
- Choi, J Neurobiol (1992); 23(9):1261-76
- Meldrum, Epilepsy Res (1991); 10(1): 55-61
- Purves et al., Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001
- Tyllee & Wolters, BMJ (2007); 334(7600): 911–2


Genomic location-coordinate of RdRp of SARS-CoV2

A useful database and exploratory tool is the UCSC Genome Browser wuhCor1 assembly browser instance.

A synonym for nsp12 is Pol. Its position range in the wuhCor1 assembly is NC_045512v2:13,442-16,236.

There are several ways to extract sequence, but one programmatic way is to get the FASTA from UCSC Goldenpath for the assembly, and extract the characters of interest from the position range for the gene of interest using standard Unix tools:

$ wget -qO- ftp://hgdownload.soe.ucsc.edu/goldenPath/wuhCor1/chromosomes/NC_045512v2.fa.gz | gunzip -c | tail -n+2 | tr -d '\n' | cut -c 13442-16236 | awk '{print ">nsp12"; print $0}' > nsp12.fa
$ cat nsp12.fa
>nsp12
TCAGCTGATGCACAATCGTTTTTAAACGGGTTTGCGGTGTAAGTGCAGCCCGTCTTACACCGTGCGGCACAGGCACTAGTACTGATGTCGTATACAGGGCTTTTGACATCTACAATGATAAAGTAGCTGGTTTTGCTAAATTCCTAAAAACTAATTGTTGTCGCTTCCAAGAAAAGGACGAAGATGACAATTTAATTGATTCTTACTTTGTAGTTAAGAGACACACTTTCTCTAACTACCAACATGAAGAAACAATTTATAATTTACTTAAGGATTGTCCAGCTGTTGCTAAACATGACTTCTTTAAGTTTAGAATAGACGGTGACATGGTACCACATATATCACGTCAACGTCTTACTAAATACACAATGGCAGACCTCGTCTATGCTTTAAGGCATTTTGATGAAGGTAATTGTGACACATTAAAAGAAATACTTGTCACATACAATTGTTGTGATGATGATTATTTCAATAAAAAGGACTGGTATGATTTTGTAGAAAACCCAGATATATTACGCGTATACGCCAACTTAGGTGAACGTGTACGCCAAGCTTTGTTAAAAACAGTACAATTCTGTGATGCCATGCGAAATGCTGGTATTGTTGGTGTACTGACATTAGATAATCAAGATCTCAATGGTAACTGGTATGATTTCGGTGATTTCATACAAACCACGCCAGGTAGTGGAGTTCCTGTTGTAGATTCTTATTATTCATTGTTAATGCCTATATTAACCTTGACCAGGGCTTTAACTGCAGAGTCACATGTTGACACTGACTTAACAAAGCCTTACATTAAGTGGGATTTGTTAAAATATGACTTCACGGAAGAGAGGTTAAAACTCTTTGACCGTTATTTTAAATATTGGGATCAGACATACCACCCAAATTGTGTTAACTGTTTGGATGACAGATGCATTCTGCATTGTGCAAACTTTAATGTTTTATTCTCTACAGTGTTCCCACCTACAAGTTTTGGACCACTAGTGAGAAAAATATTTGTTGATGGTGTTCCATTTGTAGTTTCAACTGGATACCACTTCAGAGAGCTAGGTGTTGTACATAATCAGGATGTAAACTTACATAGCTCTAGACTTAGTTTTAAGGAATTACTTGTGTATGCTGCTGACCCTGCTATGCACGCTGCTTCTGGTAATCTATTACTAGATAAACGCACTACGTGCTTTTCAGTAGCTGCACTTACTAACAATGTTGCTTTTCAAACTGTCAAACCCGGTAATTTTAACAAAGACTTCTATGACTTTGCTGTGTCTAAGGGTTTCTTTAAGGAAGGAAGTTCTGTTGAATTAAAACACTTCTTCTTTGCTCAGGATGGTAATGCTGCTATCAGCGATTATGACTACTATCGTTATAATCTACCAACAATGTGTGATATCAGACAACTACTATTTGTAGTTGAAGTTGTTGATAAGTACTTTGATTGTTACGATGGTGGCTGTATTAATGCTAACCAAGTCATCGTCAACAACCTAGACAAATCAGCTGGTTTTCCATTTAATAAATGGGGTAAGGCTAGACTTTATTATGATTCAATGAGTTATGAGGATCAAGATGCACTTTTCGCATATACAAAACGTAATGTCATCCCTACTATAACTCAAATGAATCTTAAGTATGCCATTAGTGCAAAGAATAGAGCTCGCACCGTAGCTGGTGTCTCTATCTGTAGTACTATGACCAATAGACAGTTTCATCAAAAATTATTGAAATCAATAGCCGCCACTAGAGGAGCTACTGTAGTAATTGGAACAAGCAAATTCTATGGTGGTTGGCACAACATGTTAAAAACTGTTTATAGTGATGTAGAAAACCCTCACCTTATGGGTTGGGATTATCCTAAATGTGATAGAGCCATGCCTAACATGCTTAGAATTATGGCCTCACTTGTTCTTGCTCGCAAACATACAACGTGTTGTAGCTTGTCACACCGTTTCTATAGATTAGCTAATGAGTGTGCTCAAGTATTGAGTGAAATGGTCATGTGTGGCGGTTCACTATATGTTAAACCAGGTGGAACCTCATCAGGAGATGCCACAACTGCTTATGCTAATAGTGTTTTTAACATTTGTCAAGCTGTCACGGCCAATGTTAATGCACTTTTATCTACTGATGGTAACAAAATTGCCGATAAGTATGTCCGCAATTTACAACACAGACTTTATGAGTGTCTCTATAGAAATAGAGATGTTGACACAGACTTTGTGAATGAGTTTTACGCATATTTGCGTAAACATTTCTCAATGATGATACTCTCTGACGATGCTGTTGTGTGTTTCAATAGCACTTATGCATCTCAAGGTCTAGTGGCTAGCATAAAGAACTTTAAGTCAGTTCTTTATTATCAAAACAATGTTTTTATGTCTGAAGCAAAATGTTGGACTGAGACTGACCTTACTAAAGGACCTCATGAATTTTGCTCTCAACATACAATGCTAGTTAAACAGGGTGATGATTATGTGTACCTTCCTTACCCAGATCCATCAAGAATCCTAGGGGCCGGCTGTTTTGTAGATGATATCGTAAAAACAGATGGTACACTTATGATTGAACGGTTCGTGTCTTTAGCTATAGATGCTTACCCACTTACTAAACATCCTAATCAGGAGTATGCTGATGTCTTTCATTTGTACTTACAATACATAAGAAAGCTACATGATGAGTTAACAGGACACATGTTAGACATGTATTCTGTTATGCTTACTAATGATAACACTTCAAGGTATTGGGAACCTGAGTTTTATGAGGCTATGTACACACCGCATACAGTCTTACAG

Another option is to visit the Pol link again and look for the "View DNA for this feature (wuhCor1/SARS-CoV-2)" link, click on it, and click on "get DNA" to get a similar FASTA file. But if you're going to do bioinformatics, knowing how to string together Unix tools is a valuable skill.

To get the amino acid sequence, visit the Pol link, look for the Swiss-Prot record information, and do a search through UniProt for the record P0DTD1.

Via the "RNA-directed RNA polymerase" entry for P0DTD1, you can click on the "RNA-directed RNA polymerase" post-translation product to get to a record with the amino acid sequence: https://www.uniprot.org/blast/?about=P0DTD1[4393-5324]&key=Chain&id=PRO_0000449629


Is "computational biology" different from "bioinformatics"?

I found this post by Russ Altman quite good.  Below is his opinion about the two similar but distinct fields:

  Computational biology: the study of biology using computational
  techniques.  The goal is to learn new biology, knowledge about living
  sytems.  It is about science.

  Bioinformatics: the creation of tools (algorithms, databases) that
  solve problems.  The goal is to build useful tools that work on
  biological data.  It is about engineering.

Just as a note:

This is just one persons opinion and I have heard many other definitions for both of these terms.  For example, one person I know mentioned that he believes computational biology is concerned with very theoretical research such as NP-hardness (ie. articles published in the Journal of Computational Biology). Other people think that bioinformatics is an applied field that is essentially using already published tools.


pure randomness does not seem like something that can survive in a long evolutionary process.

I think this is because you don't quite understand (no offense) the interplay between mutations and natural selection. You should have a look at Understanding Evolution.

  The overall discussion of mutagenesis I can find focuses entirely on "damage"

This is because the vast majority of mutations are deleterious (=damaging). But obviously, not all mutations are deleterious, otherwise no adaptation would be possible (only purifying selection would occur).

  In a similar vein, I don't see not much of anything about evolution and [..]

I don't understand this paragraph.

  Basically all of evolution and natural selection seems about how to survive into fertility and select a partner [..]

No! There is much more to evolution than that. Note that the semantic of evolution and natural selection is wrong as they are used in your sentence. Again, check out an introductory course.

  I think that this kind of viewing the message in the DNA as isolated from its medium

No! The environment is a fundamental tenet in evolutionary biology. The association between genotypes to fitness is a function of the environment as well.

Are mutations random?

The mutation rate varies dramatically among species and along genomes (roughly speaking from $10^{-2}$ to $10^{-10}$). For example microsatellites (repeated sequences) are highly mutable. Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication). The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants typically). The environment affect the mutation rate and the environment can be chosen by some species (avoidance) or even constructed in some species (niche construction). In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. However I have never heard of any studies showing such behaviours in order to affect the mutation rate. Epigenetic changes (does not concern all species) can also the mutation rate and even into what new nucleotide the old nucleotide will be mutated into (with a given probability). Mutations are more likely to be transitions than transversions. If a specific region is under environment-depend selection, then a mutation that would allow to drastically increase the mutation rate at this nucleotide whenever the organism has a low fitness (or even whenever the trait of the organism is unfit for the specific environment) could reach fixation. This process (and maybe others I am not aware of) are I think encapsulated within a hypothesis called (and it is a horrible name as it can yield to confusion) adaptive mutation hypothesis. But really don't start studying any field of science by jumping into an advanced subject (or even worst, a controversial subject). You should start with an introduction.

However, the impact on fitness (and on phenotype) of a new mutation is essentially random. An organism has absolutely no way to know what protein will be caused by a given new mutation. Selection then select upon the variance created by the mutations, the variance decreases and adaptation occurs. The impact of new mutations seem to follow more or less two weighted gamma distributions (added to which a bump of probability density for lethal mutations).


What makes the neurons of the auditory nerve with such high-speed?

High Speed vs High Frequency
For starters, what you are describing is a high frequency signal, not necessarily a high speed signal.  High speed signals are caused by myelination (a sheath of fat deposits that encases neuron fibers), and by minimizing the number of actual dendrite/Axon junctions you need to pass through to get from point A to point B.  In this respect, the nerves responsible for muscle control tend to be very long and have similar myelination to the cells in your ear; so, muscle control neurons would if anything transfer a signal faster than the more densely packed neurons in your ear.
Now to Answer the actual question: Why the Higher Frequency?
No one nerve in your ear actually needs to transmit a signal at a higher frequency than those nerves used by muscles.   Instead you have a number of different nerves detecting for different audio frequencies, and your brain then receives a combination of signals that tell it that various Audio Frequencies are being detected 1.  Each of the hairs in your inner ear tapers from the base to the apex such that the apex begins being stimulated by low frequencies, but the base only begins being stimulated by higher frequencies 2.
Each auditory nerve fiber is actually a cluster of nerves that work together at different frequencies to create a more complex signal. This results in a number of parallel signals that is interpreted as a complex (high frequency) signal.
Here is a simple diagram showing how low frequency signals can merge to make a higher apparent frequency.


ChIP-exo does seem to be the "ChIP-seq killer." I've seen Dr. Pugh present it a few times, and the audience is pretty much always impressed.

One thing I'd do if I were of the "experimental bent" would be to add random degenerate barcodes in the library prep to control for potential PCR artifacts. I imagine that since the "peaks" in ChIP-exo seem to be quite a bit narrower than ChIP-seq, I reckon it'd harder to use some coverage-in-local-neighborhood to remove such biases (assuming you wanted to do so).

To give you an idea of what I'm thinking of -- it would be somehow similar to what is depicted here.


Why does walking mitigate the urge to urinate?

This is what we call a displacement behaviour (or displacement activity, the term used by Konrad Lorenz - see below). Funnily enough, that's exactly the same general mechanism involved in the behaviour described in my previous answer here at Bio SE.

In short, a displacement behaviour is a behaviour that occurs when the animal (human beings are animals, of course) faces itself in a situation of conflict: you want to urinate, but you are inside a train, or in a concert, or in the theatre during the best moment of that movie, or the bathroom line is simply too huge.

In that moment, you realize that you need to hold it a bit longer. That's when you start your displacement behaviour.

When people need to hold a very strong impulse to urinate, the most common movements/behaviours are:

stamping the feet
squirming
walking, as you said
humming

Therefore, walking is just one among several behaviours we show when we need to urinate but we can't: there is nothing special with walking in this situation.

Another common displacement behaviours that humans show in other situations are scratching the head, rubbing hands, drumming the fingers or biting the nails.

Konrad Lorenz explains displacement behaviours in his The foundations of Ethology:

  When two conflicting motor patterns are activated simultaneously, it can happen that the organism performs a third pattern which may belong to an altogether different system. This curious effect was first described in avocets, Recurvirostra avisetta, by G. F. Makkink, the Dutch ornithologist who called the movements thus elicited "sparkling-over" activities (Über-sprungbewegungen). The accepted English translation is "displacement activities". Although "displacement" means something entirely different in the psychoanalytical literature, this term will be used here.

Further down, giving examples of displacement behaviours in human beings, he says:

  Locomotion, too, is often disinhibited in conflict situations; some people tend to walk restlessly to and fro while delivering a speech, and so on.

Sources:

En.wikipedia.org. (2017). Displacement activity. [online] Available at: https://en.wikipedia.org/wiki/Displacement_activity [Accessed 1 Jul. 2017].
Lorenz, K. (1981). The foundations of ethology. New York: Springer-Verlag New York.


If the top epidermal layer is burned away, what is it replaced with?

The epidermis is a four- or five-layered epithelium. The top layers are squamous whereas the bottom ones are more columnar (http://en.wikipedia.org/wiki/Epidermis_(skin)). The lowest layer is separated from the dermis by the basal membrane (a.k.a. basal lamina, basement membrane).

The process of wound healing in skin is extremely complex and obviously depends on the individual wound and how many layers are destroyed. There is a lot of detail on Wikipedia: http://en.wikipedia.org/wiki/Wound_healing.

If the basement membrane is not disrupted, there are two main components as a rule of thumb: 1) outwards-inwards migration, i.e. cells surrounding a wound will migrate into the wound. 2) bottom-upwards differentiation, i.e. the bottom-most layer contains replicating cells which will differentiate and squamify to regenerate upper layers.

Something like this (picture modified from Wikipedia):

If the wound is bleeding, this means the basement membrane is disrupted and the dermis underneath is also wounded (the epidermis itself contains no blood vessels). In this case, the dermis needs to regenerate first, in a process which is probably similar as described above. Simultaneously, the bottom-most epidermal cell layer will proliferate to close the gap, and then deposit new basement membrane. Remember that the basement membrane is a mesh of proteins, not an actual cell layer.


Is this an Emperor Penguin or a King Penguin?

Found this image here. I've also seen references to the "closed orange ear patch" of the King Penguin, which fits with the image. So my vote is for the DK image being a King Penguin.


The image you gave is not clear because it does not show the fact that the divergence pattern of light from a close object is different from the divergence pattern of light from a distant object.

Light rays from a close object (first image) diverge, and therefore they are in focus for the myopic eye.

Light rays from a distant object (second image) is approximately parallel, and therefore they are not in focus for the myopic eye. The lens corrects for this inability to focus and allows the distant object to become in focus.

Also note that the myopic person is still capable of focusing on close objects despite the lens because the lenses are still capable of dynamic adjustment, but less so than a person with perfect eyesight. You can test this by focusing on a near object, then putting on your glasses. The object should be initially out of focus, and then become in focus as the eye lenses adjust to the distance.

Myopia/presbyopia is fundamentally an issue of the focal range of the eye becoming limited to a specific range. If the ability of the eye lenses to dynamically adjust is further weakened, it may require progressive lenses or bifocals to correct the issue.


Can acetylcholine leak away from the synapse and cause spasms?

The enzyme responsible for the breakdown of acetylcholine (Ach), i.e., acetylcholinesterase, rapidly degrades, and inactivates Ach in the synaptic cleft after release. This process is particularly fast, as the synapse has to be cleared of neurotransmitter for a next action potential to occur (Čolović et al., 2013). So no, Ach does not leak away under physiologiocal conditions (Fig. 1).

In fact, common cholinesterase inhibitors that lead to Ach buildup by inhibiting its degradation, do not cause involuntary muscle twitches (spasms) as side effect. However, they do evoke muscle cramps, but that is easily explained by the increased retention of Ach in the synaptic cleft, leading to prolonged muscle contraction.

Fig. 1. Cholinesterase is active in the synaptic cleft. source: Health & Fitness.

Reference
- Čolović et al., Curr Neuropharmacol (2013); 11(3): 315–35


What factors must be taken into account for the maintenance of the immunogenicity of ovalbumin antigen?

Ovalbumin is frequently used in immunology to induce an immune response (see some publications about mice and ovalbumin here.
You usually inject it together with an adjuvans to enhance the reaction. The factors that must be taken into account for its maintainance are the same as for the other antigens, so you should boost this "vaccination" from time to time.


How was the first ribosome theorized to have been made?

An interesting take on this question is addressed in Bokov and Steinberg's hypothesis.

They have proposed the ribosome has evolved from a short length (~110bp) of RNA that did not have the translational activity that we associate with ribosomes today.

Instead this short length of RNA carried out alternative functions on RNA in RNA based life. Then overtime the accumulation of mutations occurred, such as duplication events that allowed the RNA strands to fold around one another forming a larger unit. This larger unit may have been able to add building blocks together. Over time natural selection will have guided these strands to be more precise in their building actions.

The details of course aren't entirely filled in yet (it's difficult to do because how long ribosomes have been a staple of life), but it's important to take any seemingly complex structure in organisms, and break them down into potentially useful intermediate evolutionary steps.

Some more reading on this subject here -

An article giving a background of Bokov and Steinberg
Bokov and Steinberg's 2009 paper (believe it's paywalled)
Origin and Evolution of the Ribosome (paper)


Osmoregulatory Acclimatization in amphibians

It will depend on how quickly the salinity is raised and to what level.  Two studies (Karraker 2007, Karraker et al. 2008) looked at the effects of road salt (used to reduce icing on roads in winter) in the spotted salamander, the wood frog (a small frog), and the green frog (a big frog). Their studies showed that survival decreased, especially for larval individuals, as salt concentration increased. Deformities in embryos and larvae increased with salt concentrations$^1$.

Another study (Shpun et al. 1992) showed that a few species of frogs and toads that could tolerate high levels of blood plasma urea concentrations could also tolerate elevated levels of NaCl in their environment (but not all species that had high urea tolerance could tolerate high environmental salt concentrations.)

There would naturally be an upper limit of salt tolerance in amphibians, especially if they are not able to retain or regain water at a rate they are losing it to the high salinity environment.  The studies suggest that higher salinities do decrease survivorship and increase deformities. While they may acclimate to the short term, I would question long term adaptation unless the rate of salinity increase is very gradual.

Footnote

They made their salt solutions based on conductivity, measured as microsiemens. For lab experiments, they made salt solutions that varied from 5 µS (control) to 3000 µS. These translate to 1 mg/L to 945 mg/L Cl$^-$.  In the field, they measured salt concentrations that were more than 3000 µS.

Literature Cited

Karraker, N.E. 2007. Are embryonic and larval green frogs (Rana clamitans) insensitive to road deicing salt? Herpetological Conservation and Biology 2: 35-41.

Karraker, N.E. et al. (2008). Impacts of road deicing salt on the demography of vernal pool-breeding amphibians. Ecological Applications 18: 724-734.


Maximum loading volume for agarose gel with 10 well comb

How many samples have you got? You can tape neighbouring teeth of the comb together to create double- or triple-wide wells to load more sample.

I don't normally load more that about 20 µL.

You could also make the gel thicker potentially.


Epimysium is the specialized fascia located at the muscle.

  Epimysium is a layer of connective tissue, which ensheaths the entire muscle. It is composed of dense irregular connective tissue. It is continuous with fascia and other connective tissue wrappings of muscle including the endomysium, and perimysium [1].

The fascia that covers muscle is named deep fascia:

  The deep fasciae envelop all bone (periosteum and endosteum); cartilage (perichondrium), and blood vessels (tunica externa) and become specialized in muscles (epimysium, perimysium, and endomysium) and nerves (epineurium, perineurium, and endoneurium) [2].

References:

Wikipedia contributors, "Epimysium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Epimysium&oldid=540536396 (accessed June 27, 2014).
Wikipedia contributors, "Deep fascia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Deep_fascia&oldid=593605746 (accessed June 27, 2014).


Individual cells don't live forever because they are damaged by their environment, for example by chemicals, radiation and mechanical wear and tear, or by other organisms (see this review). In multicellular organisms, such "worn out" cells are typically dismantled by programmed cell death and new cells are generated to take their place.

The life span of animal cells varies widely depending on their location and function. For example, epithelial cells lining the skin and intestines are exposed to a harsh environment, and consequently live only a couple of days. At the other extreme, neurons, which are safely lodged in the protected brain tissue, can live as long as the individual (or even longer).

Note that the life span of a given cell is very different from replicative age, which refers to the number of divisions a cell lineage has undergone, measured from some progenitor cell. Most animal cells are allowed only a limited number of cell divisions (known as the Hayflick limit) and thus their lineage is "mortal", while that of microorganisms are not.


Is eating cooked food an evolved behavior or rather an intelligent one, passed down via culture?

Its almost certainly instinctual, humans along with other great apes (any many other animals) show a preference for cooked foods over raw in testing, the number that prefer it increases drastically if they are have sampled cooked foods before. So it is likely as built in as your desire for sweets and salt.
Just becasue something is instinctual does not mean you don't have to learn HOW to do it. Language is instinctual in humans, but what language you learn is up to your upbringing (the same is true in some birds), and denied another human to interact with until puberty you will not develop language. that does not make language itself cultural, just the particular language you learn.
No one would argue lions do not have an instinct to hunt, but they still have to learn how to be successful at it.
https://evolutionaryanthropology.duke.edu/sites/evolutionaryanthropology.duke.edu/files/site-images/Wobber%20et%20al_%202008_%20Great%20apes%20prefer%20cooked%20food%281%29.pdf


Can epigenetics have positive impact on the genes are development?

First, let me qualify the idea of "problematic" epigenetic modifications by saying that the impact of a modification on an organism is often dependent on the environment.  That is to say that outcome is dependent on the interaction of genetics (or epigenetics) and the environment in which the associated genes are expressed; e.g. a mutation or modification that confers an advantage in a nutrient-limiting environment may be detrimental when nutrients are plentiful.

Second, it is helpful to think of epigenetic modifications as reversible switches rather than entities that "degrade the genes".  In fact, the etymology of "epigenetic" implies that such changes work at a level above that of the gene sequence, i.e. gene expression.  Canonically, DNA methylation and histone modifications (acetylation and methylation) modify the expression of a gene by regulating the ability of RNA polymerase to access that gene, either by directly influencing transcription factor binding or modulating the associations of nucleosomes and DNA. Read up on facultative heterochromatin.

As for examples, I point you to a set of papers that show associations between human starvation, epigenetics, and disease / mortality outcomes across generations.

DNA methylation as a mediator of the association between prenatal adversity and risk factors for metabolic disease in adulthood

  [DNA methylation] at six CpGs, including at previously [serum triglyceride]-associated CpGs at TXNIP and ABCG1, mediated the association between famine exposure and [serum triglyceride]. [DNA methylation] at these CpGs was likewise associated with the expression of genes implicated in cell growth and energy metabolism.

Note that the authors present caveats to their analyses in the discussion. The New York Times also covered this publication.

Paternal grandfather’s access to food predicts all-cause and cancer mortality in grandsons

This publication is essentially a replication of the published works concerning transgenerational epigenetics in the Överkalix cohort.  They give a concise summary of how epigenetic changes caused by environmental stress may be heritable:

  An intriguing aspect of these studies is the conjecture that an epigenetic pathway, carrying information across generations, may open up just before puberty, during the so-called slow growth period (SGP). Pre-puberty may be one of several “windows” for germline reprogramming in response to nutritional signals. A number of mechanisms for transmission across generations have been suggested, usually involving DNA methylation, chromatin formation or small noncoding RNAs. After fertilization, in the preimplantation embryo, epigenetic modifications acquired early in life are then usually erased, but not fully. Imprinting on specific loci may resist the post fertilization wave of reprogramming, eventually causing changes in offspring phenotype that are not driven by changes of the DNA sequence.

If you're looking for more examples, research genomic imprinting.


How long can I store autoclaved disposables and reagents?

Not really an answer I know, but too long for the comments...

This is still too broad a question.  a well sealed, sterile plastic usually has a use by date, but can probably be used more than a year after you receive it.  But these cases are not usually the issue.

Its sterile medium and chemicals, each of which needs to have their own due date.  LB can be used months after autoclaving, but antibiotics break down chemically in weeks (ampicillin 1000x stocks lose their potency in a month).  Even in the refrigerator Agar plates show colonies after a couple of months and dry out quickly.

So more details would be necessary and the case by case policy is the rule.

added in response to comments

Its really a matter of how well they are sealed. An autoclaved bottle will stay sterile forever, until something gets into the bottle - it depends on how well you have sealed things up and the storage conditions.  For stuff sterilized in lab I would tend to use it within a couple of months. For eppendorfs we'd tend to sterilize a few hundred in a beaker and not worry about them...

Our experiments were working with purified protein were only medium sensitive to bio-contamination; they would be done in a few hours and then sterile filtered again.  If you were purifying RNA for instance you would be much more paranoid I'm sure.

If you start to see contamination I would lower the use date and or improve your protocol.

Plastics that come sterilized and sealed by the manufacturer in 3-5 mil plastic bags have really long use by dates and I've used them for up to a year after we received them.


Is there any danger in putting a magnet in your ear (next to your brain)

Every pair of earbuds/headphones have magnets in them, as of now there's no solid evidence that proves that they are harmful or harmless to humans. Keep in mind that, what may be harmful to lab rats may not be harmful to humans as we are more resilient to radiation, etc. (In reference to a study done on truly wireless earbuds.)


Why is carbon dioxide produced in alcohol fermentation but not in lactic acid fermentation?

Glycolysis needs a steady supply of NAD+ to happen - this is the driver for the anaerobic oxidation to lactate and ethanol, although this is energetically much less favorable than the complete oxidation. But without oxygen there is no other way to keep the glycolysis active for at least some energy supply.

The difference is located in the enzymes available for the conversion of the pyruvate. This is the Lactate dehydrogenase in humans (and other mammals) and the Pyruvate decarboxylase in yeast. The first catalyzes the reaction from Pyruvate to Lactate, the second from Pyruvate to Acetaldehyde and CO2, the Acetaldehyde is subsequently converted to Ethanol. Only the second step produces NAD+.

See the illustration (from here) for further understanding:

The CO2 produced in this reaction does not occur due to oxidation, but is released from the decarboxylation of the Pyruvate. See the illustration below (from here):

In the production of lactate no decarboxylation is happening which allows the backreaction from lactate to pyruvate once enough oxygen is present again.


An Introduction to Enzymes (pdf) can be found here.

  Excerpted from a very popular Worthington publication which was
  originally published in 1972 as the Manual of Clinical Enzyme Measurements. While some of the presentation may seem somewhat dated, the basic concepts are still helpful for researchers who must use enzymes but who have little background in enzymology.

Source: Worthington Biochemical Corporation.

The quantity or concentration of an enzyme can be expressed in terms of activity in enzyme units. See Wikipedia:

  Enzyme activity = moles of substrate converted per unit time = rate × reaction volume. Enzyme activity is a measure of the quantity of active enzyme present and is thus dependent on conditions, which should be specified. The SI unit is the katal, 1 katal = 1 mol s−1, but this is an excessively large unit. A more practical and commonly used value is enzyme unit (U) = 1 μmol min−1. 1 U corresponds to 16.67 nanokatals.

Here are some additional useful, simple videos explaining enzyme activity:

How Enzymes Work
Explain factors affecting enzyme activity


Can I use fluorophore conjugated antibody as neutralizing antibody?

In short, yes, most likely.  When an antibody binds to the antigen at a region (epitope) that is needed for the antigen's activity then the activity is reduced ("neutralized").  The (proper) labeling of an antibody will usually not affect which epitopes it binds to, and so it will work OK (but it may have lower titer than the unlabeled antibody).  As always, there may be some exceptions to this.


You're talking about long-wave UV, or UV-A radiation. In the 80s, experts claimed that this was a safe wavelength. Protection against UV-A was not part of sunscreen in the early days. Consequently, UV-A was (and still is) used in tanning beds due to its perceived safety over UV-B. However, a lot of research has been done since.

UV-A is well understood now to also be unsafe in unreasonable amounts. Currently, UV-A protection is a typical feature of sunscreen and tanning beds are still not a healthy alternative to moderate, healthy doses of sun. Here is a recent review covering some of the aspects comparing different UV range effects on skin. I really suggest you put a search engine to good use here; it makes little sense for us to expound on the literature when it is so clear and easily available.

In summary,

UVA certainly contributes to the development of skin cancer.
UVA penetrates deeper into the skin than UV-B (which is largely responsible for 'burning' of the topmost layer of skin, without directly affecting the deeper layers). For this reason, UV-B is associated primarily with burning and UV-A is primarily associated with aging and aging diseases like cancer.
It is important to note that 95% of UV light in every day life is UV-A, because it does not vary seasonally and can penetrate clouds and windows. Therefore, in spite of the fact that short wavelengths carry more energy per photon, the ratios of UV-A and UV-B exposure are far from equal.

These are only a few of the explanations as to why we observe an incidence of aging and skin damage and disease upon UV-A exposure.


The snails enlarge the shell by adding material at the lip.  The addition of material is sometimes noncontinuous and shows up as rings, sort of like tree rings.  You can see the growth rings in this photo.

I found the photo here http://ediblesouthflorida.ediblecommunities.com/things-do/snails-slugs-millipedes-oh-my

As the shell spirals outward the diameter of the added rings gets larger and larger.  It has to get larger if it is to spiral - addition of the same sized rings would make a donut-like torus.


Question about radiation and how it affects biological systems

The absorbed dose describes the amount of radiation absorbed by an object or person, i.e., the amount of energy that radioactive sources deposit in materials through which they pass. The units for absorbed dose are the radiation absorbed dose (rad), or better: the gray (Gy) unit.

One gray dose is equivalent to one joule radiation energy absorbed per kilogram of organ or tissue weight. Rad is the old and still used unit of absorbed dose. One gray is equivalent to 100 rads.

1 Gy = 100 rads

Equal doses of all types of ionizing radiation are not equally harmful. Alpha particles, for example, produce greater harm than do beta particles, gamma rays and X rays for a given absorbed dose. Alpha radiation is the most dangerous because it is easily absorbed by cells. Beta, gamma an X radiation are not as dangerous because they are less likely to be absorbed by a cell and will usually just pass right through it (source: BBC).

To account for this difference, radiation dose is expressed as equivalent dose in units of sievert (Sv). The dose in Sv is equal to absorbed dose" multiplied by a radiation weighting factor (WR - see Table 1 below). Prior to 1990, this weighting factor was referred to as Quality Factor (QF).

Note that the heaviness of the alpha particle makes its penetration rates very low. Hence, it will not easily penetrate through the outer layers of the skin.

Table 1. Recommended Radiation Weighting Factors. source: Canadian Centre for Occupational Health and Safety

Now to your question:
Ionizing radiation has more energy than non-ionizing radiation. Ionizing radiation can cause chemical changes by breaking chemical bonds and damage living tissues.

Shorter wavelength UV begins to have enough energy to break chemical bonds. X-ray and gamma ray radiation, which are at the upper end of the EM spectrum, have high frequencies (~100 billion billion hertz). Radiation in this range has high energy and it can strip electrons from an atom or even break up the nucleus of the atom.

The process in which an electron is given enough energy to break away from an atom is called ionization. It results in the formation of two ions: the molecule with a net positive charge, and the free electron with a negative charge. Each ionization releases a large amount of energy which is absorbed by the surrounding tissues.

There are three main kinds of ionizing radiation:

Alpha particles, which include two protons and two neutrons; beta particles, which are essentially electrons; and gamma rays and x-rays are photons. Alpha particles, beta particles and neurons are not part of the EM as they are energetic particles as opposed to pure energy bundles (photons) (source: ARPANSA Australia).

So in the EM realm, frequency is proportional to energy and hence to tissue damage (Fig. 2) and hence to rads.

Fig. 2. EM spectrum. source: ARPANSA


How does formaldehyde cause protein-DNA crosslinking?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866014/

In this work they find that formaldehyde crosslinking happens by formation of a methylol adduct (due to nucleophilic attack by N or S in case of proteins) in protein which then attacks the DNA or vice-versa.
The final crosslink is by a methylene bridge

Formaldehyde can react to amino groups in nucleotides and proteins and form a schiff's base, but i dont have a clue how this is involved in crosslinking


What's the relationship between oxygen consumption and ambient oxygen concentration for a lobster?

Increasing the ambient oxygen concentration increases diffusion of oxygen across the gills, thereby increasing the oxygen uptake by the lobster.
This can be proven by the fick's law of diffusion-

r=[-DA(P2-P1)/L]

L=thickness of diffusion membrane

D=diffusion coefficient

A=cross sectional area of diffusion membrane

P2-P1=pressure difference


We know that the hepatitis C virus can live on surfaces for at least six weeks. Maybe longer. The infectivity study ended after just six weeks; why?

They ran out of samples

Their test is destructive, they can't test the same sample twice. They planned out a number of samples to test for each time period and tested them. At the end of six weeks, they were done.

It doesn't really matter

The point of the paper is that HCV is infectious long-term on surfaces when not cleaned properly, indicating there is a risk of fomite transmission long after an infected patient leaves the area.

They also show that if surfaces are cleaned, the virus is killed effectively. The authors are not advocating to quarantine a hospital room until any residual HCV dies from air exposure, they are advocating being sure to appropriately clean hospital surfaces to prevent potential disease.

It isn't typical (in fact, it is impossible) for a single scientific study to answer all open questions in one shot. If someone wants to put an upper bound on the duration that HCV remains infectious in the world they can do a new study with longer time points.


In scuba diving, are nitrogen narcosis and high pressure nervous syndrome the same thing?

These are different things.

Nitrogen Narcosis or more commonly Gas Narcosis is the narcotic effect of gasses like Oxygen and Nitrogen under pressure. The effects are most prominent under 30m and commercial/technical dives doing dives to 40/50m on air tend to experience the effects most. (Narcosis is managed by adding an inert gas - in most gases Helium - to air to form a mixture referred to as Trimix (Helium/Oxygen/Nitrogen) this then produces an effect as if the diver is diving to a shallower depth and is referred to as Equivalent Narcotic Depth, in some cases Heliox (Helium & Oxygen) was also used)

High Pressure Nervous Syndrome is an interesting aspect of deep diving and used to be called Helium Jitters/Tremors as the accepted standard was that it was caused by breathing Helium mixtures under 150m. Some people hold this to be true and others claim that it has nothing to do with Helium but rather the pressure disrupting the flow of electric signals thru the nervous system.

What is interesting is that they found that if you used Trimix (Helium/Nitrogen/Oxygen) rather than Heliox (Helium/Oxygen) the onset happened later or not as severe. And the slower your descent is the slower the onset of the symptoms.

Some Docs to Read:

Narcosis - Relatively simple document on Narcosis

Narcosis - "Narcosis is not unique to nitrogen; however, it can occur with many of the so-called “noble” or inert gases, with the exception of helium. Add to this the fact that other inert gases each have their own brand of narcotic effects at depth, and you have a complicated picture for technical and commercial divers. One of these rare gases, argon, for example, has about twice the narcotic potency of nitrogen, but helium has very weak narcotic properties and is less soluble than nitrogen in body tissues."

HPNS - Relatively Simple doc on HPNS

HPNS - Very technical discussion on gasses, from a HPNS and Narcosis view point.

References:

Bennett, P.B. 1982b. The high pressure nervous syndrome in man. In: The Physiology and Medicine of Diving and Compressed Air Work. (P.B. Bennett and D.H. Elliot, eds), Balliere-Tindall, London. pp. 262-296.

Bennett, P.B. 1990. Inert gas narcosis and HPNS. In: Diving Medicine, Second Edition (A.A. Bove and J.C. Davis, eds.).W.B. Saunders Company, Philadelphia. pp. 69-81.

Bennett, P.B, R. Coggin, and J. Roby. 1981. Control of HPNS in humans during rapid compression with trimix to 650 m (2132 ft). Undersea Biomed. Res., 8(2): 85-100.


What evolutionary advantages does a longer muzzle have against a shorter muzzle and vice versa

Its mostly due to different forms of predation.

Longer jaws are deeper and can reach farther around a prey item, it also increases the chances of catching a moving target in the jaws becasue the area the jaw covers is larger, all things being equal it should always be favored but things are rarely equal, everything has a cost. It is common to see longer snouts in animals that hunt primarily with the jaws. There two ways to do this which depends on how big the pery to are after is, for predators going after relatively small prey they favor long thin snouts, is really noticable in aquatic predators like gharials, it makes for a very fast bite with a wide attack range. Alternatively if they are going after large prey they need to balance strength with speed so you see long, but not as long, more robust snouts. Think alligators, hyena, wolves. Whereas cats who attack with their forepaws can use a smaller head and jaw and favor a more precise bite, becasue they are moving with the prey becasue they have grabbed it, the arms are absorbing most of the stresses. Cats favor grabbing and strangulation for which a small short jaws works fine. Energy and material saved here can be used elsewhere. A longer snout would be weaker unless they add a lot more muscle to stabilize it. In terms of resources it is a lot of cost for little gain, whereas in wolves it is worth the cost becasue they need that strength anyway, becasue they jaw is where all the stress of the struggling prey is being transmitted.

You see the same thing in dinosaurs, predators that can attack with the claws have weaker bites/smaller heads. In the case of dinosaurs however snout length varies less because the small heads favor slashing bites, which favors a longer snout (thus a longer cutting row of teeth) there heads get narrower and weaker more than shorter.  Mammals can't use this strategy because they don't get replacement teeth, and they would quickly not have a tooth in their head, so instead you see strangulation favored instead.

Of course an animal can try to balance a range of strategies and there are all kinds of specialized forms like saber teeth, venoms, ect. Of course this is also simplified a lot of other things effect snout length as well, things like climate (long snouts cause less heat/water loss through breathing), sense of smell, or even vision.

https://www.cambridge.org/core/journals/paleobiology/article/dinosaurian-and-mammalian-predators-compared/BE3492DA7E0A103C6F6E77B9611D86A9

https://link.springer.com/chapter/10.1007/978-1-4615-0161-9_14

https://www.cambridge.org/core/journals/paleobiology/article/constraint-and-adaptation-in-the-evolution-of-carnivoran-skull-shape/77B1591461066F9D0E30F309F6C495C6

https://www.sciencedirect.com/science/article/pii/0034568770900757


Infection of urinary tract if the pH of urine is made alkaline

There is a huge misconception here.  Morphine overdose is treated with Narcan (naloxone).  Phenobarbiton overdose is treated with artificial respiration (in extreme cases), blood pressure medication, and management of low heart rate.  The concept of lowering the pH of the urine to increase a drug excretion is (to my knowledge) never used in emergency settings.  Dialysis, which filters the blood, would be used to 'clean' the blood of toxins.  Think about it.  Time is life, and changing the composition of your fluids would take a lifetime compared to the implemented measures in emergency rooms.  You body has an extremely sensitive acid-base balance.  You do not want to try to increase or decrease the pH of your bodily fluids.


As you will see in the Species section of the Wikipedia Xerocomellus genus page you linked, Xerocomellus chrysenteron has a basionym (original name) of Boletus chrysenteron.  The Xerocomellus genus was first described in 2008.  The Wikipedia page for the X. chrysenteron species similarly gives three synonyms for X. chrysenteron in the box at the top; among them is Boletus chrysenteron Bull. (1789).  Thus the two names are referring to the same mushroom species.

One should note that Wikipedia says about this species:

  Macroscopic observation of Xerocomellus chrysenteron is not sufficient
  to determine this species with certainty, as many intermediate forms
  occur between it and other taxa

It appears from this that correct identification of a mushroom as being X. chrysenteron is not a trivial task.


The more generally accepted theory for conjoined twins is fission, in which the fertilized egg splits partially. So I don't think that what you said is possible. Not seen this happening before... even the conjoined twins share same placenta indicating they originate from same fertilized egg.


While the most popular image of a fish for many is as you say, a more "vertical" than horizontal body shape, however there are many different adaptations to body shape depending upon the lifestyle of the fish. An ultimate example would be the flat fishes, such as flounder and halibut, which lay on one side essentially flat on the ocean floor or other similar surface. These fish however have adapted to have both eyes on one lateral side. There do exist other fish, such as some angler fish, especially in the family Lophiidae, which are more wide than tall, and they sit on the ocean floor and use a lure like appendage to attract prey so that they can ambush it, using their fins more to walk along the bottom surface. The feeding/hunting style is also highly related to the body shape of a fish, some shapes are more suited for moderate constant speeds, while others are suited for short quick bursts. Generally though, flat fish are not well suited for swimming at the middle of the water column, giving them a smaller habitat in which to live, while the more commonly found fish body shapes are used by much more species throughout the water column.

More information from MEER:

More information regarding Fish locomotion on Wikipedia.


Why proprioceptive fibres (of CN V) have their cell bodies in mesencephalic trigeminal nucleus?

The mesencephalic nucleus of trigeminal nerve is involved with reflex proprioception of the periodontium and of the muscles of mastication in the jaw that functions to prevent biting down hard enough to lose a tooth. To subserve this reflex protective function, mechanoreceptive nerves in the periodontal ligament sense tooth movement and project to the mesencephalic nucleus.

The functional significance of this anomaly is unclear, although there is a hint of special neural processing in the fact that, unlike DRGs and normal cranial nerve ganglia, MesV neurons receive synaptic input. Another hint is that while at spinal levels opposing extensor and flexor muscle blocks are roughly equal in size, in the orofacial motor system there is asymmetry. Jaw-closing muscles, the flexors, are massive and powerful with rich muscle spindle and Golgi tendon organ innervation. The jaw-opening muscles, the extensors, are small and delicate and lack muscle spindles and Golgi tendon organs

Reference

It is responsible for unconscious proprioception that stems from muscle spindles in the muscles of mastication and other muscles of the head and neck. It is thus essential in the process of receiving sensory information about tooth pain, helps prevent excessive biting that may break a tooth, receives information about stretch sensation from the muscles of mastication, and serves as the afferent limb of the jaw jerk reflex.
Reference


Frog identification - two different frogs seen in New Zealand

the first frog(the green one) resemble GREEN AND GOLDEN BELL FROG - Litoria Aurea

Description of the frog -

Have golden-bronze colored spots
Have a black line from the eye to the nostrils
Found in northern Island

And coming to the second frog it resembles Southern Bell Frog - Litoria Raniformis

**Description of the frog - **

Have a distinctive black line running through their back
Found almost everywhere in new Zealand
They have black-brown patches on their skin (can increase in blackness based on the surrounding environment)

Coming to your question , the golden bell frog seems to stay in small temporary water ponds even puddles

On the contrary the southern bell frog lives permanently in a pond so probably it lives somewhere nearby

That'll be it


How long do viruses, such as Zika, stay in the body?

According to the CDC the zika virus persists in the blood for around a week.

  Zika virus usually remains in the blood of an infected person for about a week but it can be found longer in some people. - CDC

I can't find much information on how long the Zika virus specifically can persist after recovery, it seems unknown just now. However, it is advised to be careful about sexual contact after infection, which suggests longer persistence is suspected in other fluids/tissues.

  British health authorities have suggested using condoms for at least 28 days. - NYTimes

Some viruses do persist for a while after recovery, including Ebola Virus Disease, which can be sexually transmitted for around three months after recovery:

  Some viruses, including Ebola, can linger for some time after recovery in parts of the body (for example, testes, eyes, spinal column fluid) not easily reached by the immune system. - CDC

These parts of the body have immune privilege. This means they can be infected by antigens without producing strong immune responses. This is thought to occur to protect vital tissues/areas which could be damaged by inflamation and the immune response, such as the brain, eyes, spinal column, testes, and fetuses.

Since I wrote this answer there have been several reported cases of sexually transmitted zika, highlighting the problems that can arise from immune privilege.


The "bump" on an earthworm (i.e., a worm species of the order Opisthopora) is a clitellum. Clitella are only visible on earthworms when they're sexually mature [Sources: 1, 2, 3]. So the absence of a clitellum does not preclude your specimen from being a member of this order.
The species in your photo is almost undoubtedly some species of earthworm. Without clearer images or more detail, I can't imagine someone taking the time to try to ID to species.
There are many species of earthworms present in Pennsylvania (though likely none of them are native to the US: see here). Keep an eye out for a recent invader, the "Asian Jumping Worm" [read more].


Can antibodies be formed against white blood cells after blood transfusion?

Antibodies and other immune responses do indeed occur against the donor's white blood cells. However, white blood cells are present in relatively tiny quantities (3-10 million WBCs per ml of blood vs 4-6 billion cells per ml).

Because the number of WBCs is so low, the immune reaction to them is also proportionally lower, with fever being a typical (and minor) complication of the reaction to WBCs. Some blood banks remove WBCs from blood to prevent these reactions.

For more information on the possible types of reactions to blood transfusions, see Wikipedia.

EDIT: Even in cases where the transfusion does not produce any symptoms, an immune reaction is most assuredly happening. In those cases, the immune system is simply killing off the foreign WBCs without any fuss.


What species of snake found in central Alabama, US?

Definitely looks like some species of rat snake (genus Pantherophis). Based on the size, location and coloration, I'd say it's a dark variant of a Gray rat snake (Pantherophis spiloides).

It might also be a cross between a black and grey rat snake (i.e., Pantherophis spiloides x obsoletus).

 Source: Todd Pierson

 Sources: Alan Brumbeloe | Bill Funderburk

Description: Adults usually 99-183 cm long; dark to light gray with darker gray or brown blotches

  Unlike other Pantherophis, whose conspicuous juvenile pattern fades into adulthood, gray ratsnakes do not undergo drastic ontogenetic changes in color or markings. These snakes retain the juvenile pattern of dark elongate dorsal blotches separated by four, or more, pale gray body scales, a light gray crown with dark striping that forms an anteriorly facing spearpoint, and a solid band which covers the eyes and extends rearward to the posterior upper labial scales. The venter is usually off-white or pale gray with darker irregular blotches, and a double row of black spots behind the divided anal plate of the vent. The dorsal scale rows around midbody are usually weakly keeled. Because the gray ratsnake shares its range with other members of its genus, hybrids of midlands x eastern ratsnakes are not uncommon. [Source].

Note, According to here one could have a difficult time IDing juveniles between species of rat snakes:

  The juveniles of all subspecies [of rat snakes] resemble the gray rat.

However, your specimen's size indicates it's likely an adult, and therefore its strong patterns preclude the black rat snake.

Distribution:  commonly found in the forests of eastern and central United States, including throughout Alabama:

 Source: Trey Dunn

Behavior: Gray ratsnakes are agile climbers and can be found in tree tops as well as barns/sheds/buildings close to forests

  The gray ratsnake will defend itself by raising its head and bluffing a strike. If handled, these snakes will musk a victim by releasing the foul-smelling contents of their cloaca, and will bite if necessary. [Source].


What does "delineate" mean in this context?

To delineate an experiment is to describe precisely the conditions and the states of all the parameters.

So in your sentence it probably means a scientist might struggle to keep track of all the confounding factors (changing salinity, composition, dissolved gases, particulates, pH, temp, etc.) which might affect an experiment in such a dynamic system as the ocean.


No, it doesn't seem to be common practice. A telomerase treatment would probably do more harm than good, and may be completely unnecessary in the first place.
Betts and coworkers published a study in which they examined telomere length in cloned cattle. They found that while telomere length in cloned embryos does start out somewhat shorter than in naturally produced embryos, by the time that the normal processes of embryonic development were in full swing telomere length in cloned and natural embryos was equivalent.
Betts' results make sense in light of the fact that telomerase activity (and the activity of many, many related proteins) is normally upregulated in embryonic cells.
As for Dolly, while it is true that her telomeres were shorter than those of an average age-matched sheep at the time of her death, it's far from clear that those short telomeres had anything to do with her decline. Also keep in mind that she didn't just keel over suddenly in the night, she was euthanized. A subsequent autopsy showed that she had a form of lung cancer caused by a retrovirus common in sheep.
Edit: why were Dolly's telomeres shortened?
This is a good question, as the findings of shortened telomeres in Dolly's case do contradict the findings in the Betts paper. Clearly we need more citations:
-"Analysis of telomere lengths in cloned sheep." Shiels et al, 1999
This is the original citation for the claim that Dolly's telomeres were shortened. There isn't too much extra information to be had as it's a very short paper (1 page letter). They did look at other cloned sheep created from types of cells other than skin cells (as Dolly was) and saw the same kind of telomere shortening relative to controls. They also make a point of mentioning that Dolly's telomere length may be within the normal variation for sheep.
-"Remarkable differences in telomere lengths among cloned cattle derived from different cell types." Miyashita et al, 2002
The investigators found that telomere length in cloned cattle was strongly dependent on the type of cell from which the clone was derived. For example, clones made from mammary cells tended to have shortened telomeres, whereas those derived from muscle cells had normal length telomeres.
-"The analysis of telomere length and telomerase activity in cloned pigs and cows.", Jeon, 2005
This group found that cloned cattle had normal length telomeres, whereas cloned pigs had elongated telomeres. By way of explaining these results, they found that telomerase activity was upregulated in cloned pigs relative to control pigs, whereas telomerase activity in cloned cattle matched that of control cattle.
How should we take all of this information? At the very least we can say that telomere length in clones is highly dependent on species and on source tissue, and that telomere length can increase, decrease, or stay the same in cloned animals relative to control animals. Clearly telomere length in cloned animals is a fiddly property. It is very likely that it also depends on the exact details of the cloning protocol as it was carried out (i.e. how much did the experimenter's hands shake when they inserted the needle to suck out the nucleus?, etc.).
So I would say not to read too much into Dolly's shortened telomeres. They may have been a result of her being a clone, or they may have been a result of natural variation. In either case the shortened telomeres were not linked to her ill-health, and it's likely that small tweaks to the cloning protocol would eliminate any telomere length discrepancies in future clones.


Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles?

There is no intention in evolution. Purging refer to the action of selection at removing deleterious alleles. This term is specifically used when a population goes through a demographic change under which purifying selection becomes more efficient (such as an increase in inbreeding coefficient).

  Do the individuals/couple with deleterious alleles that breed together, pass down the purged genes EACH AND EVERY TIME they produce offspring? Does it happen every time they mate or just some times?

Purging is a population-level process so your second question does not make much sense

Rephrasing the above a bit differently, purging refers to the reduction in frequency of deleterious alleles in the populations. Individuals will transmit whatever allele they can transmit.


Is there any clear relationship between physical characteristics and patterns in the genome?

This kind of question is what developmental genetics is all about. The answer turns out to be, in general, 'no'. There is no neat mapping between spatial dimensions of an organism and its genome. (There is one exception to this in some organisms called the Hox cluster, but they are kind of a freak case).

The reason for this is that in general you should think of the genome as being a recipe for a developmental process, rather than a description of the end product. You might have, say, a specific set of genes which is active in all limb buds, which are the structures that become limbs and fingers etc. These genes would be active at different levels, at different times and places, in your different fingers. E.g. length of time one gene is on could control how long the finger grows for and thus how long it gets.

There are some genes which are only active in specific parts of the body, but you don't necessarily need a particular set of genes for each distinct finger/limb etc. And these genes certainly don't need to be in the same place in the genome. Your left and right hand are going to have identical gene expression for instance.


Why do some cuts leave scars, while others do not?

This depends on a number of factors. Here are the first two that come to mind:

1) Is the cut deep enough to reach the dermis (this is the layer below the epidermis) where scar tissue will form?

2) What is your general state of health, and was there an infection at the site of the cut, which would have altered the normal healing process.

Basically, not all cuts are created equal, especially if some are deeper than others and become infected.

This article studied scratch depth
http://www.ncbi.nlm.nih.gov/pubmed/17440346


What is the symbiotic relationship between truffle fungi and their host trees?

A truffle is the fruiting body of a subterranean Ascomycete fungus, predominantly one of the many species of the genus Tuber. Truffles are ectomycorrhizal fungi and form symbiotic relationships with the roots of several tree species including beech, birch, hazel, hornbeam, oak, pine, and poplar.

Mycorrhizal symbiosis is a mutualistic association between a fungus and the roots of a plant (usually a tree) in which (typically) the fungus obtains energy in the form of carbohydrates from the plant, and the plant gains the benefits of the mycelium's higher absorptive capacity for water and mineral nutrients, partly because of the large surface area of fungal hyphae, which are much longer and finer than plant root hairs, and partly because some such fungi can mobilize soil minerals unavailable to the plants' roots. The effect is thus to improve the plant's mineral absorption capabilities.

Based on the quote below from the website of a truffle nursery in Australia (http://trufficulture.com.au/what_are_truffles.html), it sounds like truffle symbiosis is a completely standard mycorrhizal symbiotic relationship.

  The truffle coats the tips of the tree roots to form mycorrhiza which
  act as an extension of the tree's root system. The tree provides the
  truffle with a source of photosynthesised carbohydrates, and in return
  the fine, thread-like filaments (mycelia) of the truffle, extract and
  trade soil minerals and nutrients which would normally be unavailable
  to the tree. Thus the mycorrhiza is able to increase the effectiveness
  of the trees roots, enabling the tree to grow in soils which would
  normally be too nutrient deficient to support them.


Movement of stem cells from mother to fetus

Since the maternal cells can be found in a number of tissues including

  In second trimester fetuses the thymus, lung, heart, pancreas, liver, spleen, kidney, adrenal gland, ovary, testis and brain had maternal Mc (microchimerism)

it's clear that these are stem or stem like cells that are being incorporated into fetal tissue.

Since these cells arrive while the immune system is developing, they are considered as self and not foreign. But a breakdown of that immune tolerance is thought to be involved in a number of autoimmune diseases, especially systemic sclerosis which resembles a host vs graft disease where the patient's immune system attacks tissues holding the maternal cells.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3516290/


What does the evidence suggest about how Neanderthals became extinct?

This is one of those active areas of research where there isn't a lot of consensus among researchers. There isn't even consensus as to whether it was an extinction in the strictest sense, because we now have evidence from genomic research that Neanderthals interbred with modern humans. Research is still being done on a lot of different hypotheses.

This article by K. Harvati is a decent short summary of the current state of the field, and includes references to recent articles.


What are the application areas of Pattern formation studies specific to biology?

Ok, I'm not quite sure if we are at the repairing an organ phase, but here are a few interesting examples:
1. Philip Maini at Oxford has used pattern formation to give insight into jaguar patterning: Paper. He also has a book chapter Pattern formation and wound healing that could of of interest, although I'm not sure if this is a direct application as much as a heuristic understanding of how wound healing happens.

From the biomedical side, Michael Levin at Tufts is doing amazing work in regenerative medicine, and a lot of what he does is inspired by pattern formation as well, although I am not sure if it explicitly uses the theory - his papers.
This paper is one of my favorite from Ron Weiss - engineered pattern formation. Will most likely have important biomedical applications some day, although not currently.