Does modern theory of evolution include modification of physical environment?

Yes, such processes are considered but there is still a lot of work to be done in this field.

Because the question is open-ended I will just define two concepts of interest and let you go through papers if you want to understand how such processes are modelled.

Niche Construction

Niche construction is the process in which an organism alters its own environment. Sometimes, niche construction takes a broad definition and it then refers more globally to any environment change that is induced by an organism regardless of whether the individual/lineage experiencing the environment is the same one than the one causing the modification. Under this broad definition, niche construction has the meaning as ecological engineering to my understanding.

Some obvious examples are bird nests, beaver's dam and humans's houses. The process of niche construction gets really interesting when the niche is inherited by future generations.

Ecosystem engineering

Ecosystem engineering is the process in which an organism alters the its environment and the environment of other lineages/species. Ecological facilitation is one class of examples.

Ecosystem engineering vs Niche Construction

To my understanding, the term niche construction is more often used in the evolutionary ecology literature, while the term ecosystem engineering is more often used in the ecology literature. Note again that (in my understanding) niche construction in its broad sense takes the same definition as ecosystem engineering but not in its narrow sense.

Models of niche construction in evolutionary biology

There are a number of models of niche construction in evolutionary biology. I am not expert in this field and am not able to make a good summary (would take a while even for an expert anyway). Here are a few papers (that I haven't fully read) that you may want to consider

Niche construction - Odling-Smee et al. 1996
The evolutionary consequences of niche construction: a theoretical investigation using two-locus theory - Laland et al. 1996
Evolutionary consequences of niche construction and their implications for ecology - Laland et al. 1998
Macroevolution of ecosystem engineering, niche construction and diversity - Erwin 2008

Note that depending on your level of understanding of evolutionary biology, these papers may be a bit complicated to fully understand.


Directed evolution: Point mutation vs Insertion-Deletion vs Shuffling

In general, point mutations are introduced in the proteins of interest during directed evolution. These can be specific mutations in the active site of an enzyme if you would like to change its specificity towards a new substrate, for example. The point mutations can be introduced with primers when you amplify your gene of interest. However, if you don't know specifically what changes to make, then yes, a way to generate mutations is by error prone PCR or by Quick change PCR. If you'd like to see if a certain amino acid change abolishes activity/stability/etc, you would do Alanine scanning (https://en.wikipedia.org/wiki/Alanine_scanning).

I haven't heard much about introducing deletions or insertions for directed evolution. First of all, they have to be in-frame, so that the overall coding sequence does not change. People are usually introducing epitope tags on the N- or C-terminus for two reasons: 1) to purify the proteins; 2) to increase its solubility. But in general, the introduction of deletion will lead to unpredictable changes to the 3D structure of the protein of interest.

The DNA shuffling is very often used for directed evolution. Here is a figure from a Nature paper [1] describing DNA shuffling. The way it is usually performed is by using sequence homologs of the protein of interest. The different fragments can be obtained by PCR-amplification and introducing short overlaps with the neighboring fragments. The fragments can be then assembled by various methods, including Gibson assembly and homologous yeast recombination.  The advantage of DNA shuffling over introducing single mutations is that you have to screen fewer mutants and the activity/stability of the protein could be improved several hundred fold more.

DNA shuffling figure from [1]

Interestingly, a DNA shuffling using a method called SCHEMA [2] was developed in Chris Voigt lab. Shortly, SHEMA is a computational algorithm used to identify the fragments of proteins, or schemas, that can be recombined without disturbing the integrity of the three dimensional structure. It is based on the 3D structure (of one of the parents) and an alignment of the parental sequences. It calculates the interactions between residues and determines the number of interactions that are disrupted in the creation of a hybrid protein. A window of residues w is defined and the number of internal interactions within this window is counted. The window is slid and the schema profile is created. For example. in the figure below, the number of interactions that are broken in the possible chimeras are 0 on the right chimera and 3 on the left chimera. The right chimera will be used in the screening.

SHEMA method from [2]


Not that I'm aware of. There isn't any blood flow to either tendons or cartilage as an adult, so the pathway for migration doesn't exist.

Tendons and cartilage are tissues composed of dead cells after their formation (the cartilage growth plates cease to exist in your teen and completely ossify, tendons I'm not sure on). Damage to tendons and cartilage is permanent, and can cause arthritis (when the cartilage is completely worn away and bone-on-bone contact occurs at joints).

Unlike living tissue, because tendon cells are dead, they are much, much easier to transplant - they do not produce any signaling molecules or have any surface proteins which would trigger an immune reaction for the vast majority of people. Shoulder surgeries often utilize this to the benefit of the patient, especially acromio-clavicular injuries.

If living cells are brought to the dead tissue, some repair is initiated, as I do recall a technique where surgeons tapped into the marrow of a patient's femur to stimulate cartilage reconstruction, but I also remember reading that the new cartilage formed wasn't the same hyaline cartilage produced by chondrocytes of the growth plate, so the repairs were temporary.

Artificially produced tendons do exist, and many are braided in order to foster interaction with host tissues (when you suffer from tendonitis, the tendon itself isn't repaired - the tissue around the tendon is repaired and strengthened). I'm not aware of any successful attempts to regrow tendons.

Attempts to grow cartilage in vitro have been successful, but re-introducing it into the body to produce a surface to articulate against has presented significant difficulties. Because we cannot (currently) reproduce biological articular surfaces, joint replacement often uses composites or surgical grade metals (both of which present problems of their own, but arthritis is not one as there's no living tissue to feel pain).


That is a flower beetle in the family Scarabaeidae, subfamily Cetoniinae.
Derby's flower beetle (Dicronorrhina derbyana)
https://en.wikipedia.org/wiki/Dicronorrhina_derbyana


What they're doing is called two-step PCR. In step one, some gene-specific primers with tags amplify genomic DNA, but the product has adapter regions now added to each end. In the second step, you add primers that complement the tag/adapter region and have T7 promoter sequences at the ends. Your second product will have the adapter region, and the T7 promoters on the outside. The paper you provided shows they just modified the process: the first product is the gene of interest flanked by part of the T7 promoter, and the second product is the gene of interest, the T7 promoters, and restriction sites for cloning.

Design and implementation of high-throughput RNAi screens in cultured Drosophila cells

It looks like from what they know, adding the partial T7 in the first step is just optimization for their procedure. You want to add those restriction sites to wherever you can imagine you want your insert cut by the endonuclease. In a ligation step for inserting the gene fragment, you'll have cut your plasmid open with the same restriction enzyme you use to cut the insert, so that it ligates in nicely.

The HT115 strain has some nice properties you can read about here like a lack of RNase III that would degrade dsRNA, so it's suitable to produce the actual dsRNA inside of, and for the feeding experiment this is fine. For microinjection, they're using in vitro transcription kits to get dsRNA from the PCR product, which should be a gene of interest flanked by T7 promoters and restriction sites. T7 polymerase will simply transcribe everything downstream of it's promoter, so we don't have to worry about the restriction sites except for the feeding experiment.

MEGAscript® T7 Kit

The above kit comes with a T7 enzyme mix, NTPs, DNase, reaction buffer, a stop solution, precipitation solution, etc. You should be able to follow the manufacturer's direction and get 100 µg RNA per reaction, according to the webpage. Then you purify the dsRNA. It's literally just T7 polymerases transcribing whatever is between the two promoters into dsRNA -and for that kit, linear DNA does work- and then you degrade any DNA, leaving you with the dsRNA.


I think the statement above is slightly misleading. There are many many types of cell signalling, anything from RTK (at the cell surface or when its endocytosed), to steroid receptors, which operate on different time scales and produce different results depending on the type of signalling. Also it depends on what you are measuring/defining as a signal/response in lets say "cell signalling" because you could define cell signalling response as protein phosphorylation at any point in a signalling cascade or it could be the transcriptional activation itself (consider the MAPK pathway in Drosophila, at which point do you consider a response is produced? when Raf is activated? or when transcription factors such as pointed bind to their ETS binding site and start to transcribe as measured by luciferase? as you can tell the time difference between the two is quite large, well as far as I know after RTK activation in Drosophila it takes ERK 20 minutes just to translocate to the nucleus). A cell signalling response could also constitute changes in the rate of cell migration, cell shape etc, which can either be slow or fast depending on the signal in question. so I think the above question needs major rethinking and redefining.

Now getting back to your questions about key search terms, in my experience, over time you just end up developing a knack for what you consider to be key words after you carefully define the question and think bout its different aspects. A rule of thumb that I use is typing at name of proteins (e.g. JNK or RAS etc) or processes (transcription, phosphorylation etc) and use a word like rate, time-scale, half-life, turn-over or something like that if its measuring changes in time you are interested in. Just play around with words.

Also as a general advice you don't have to reference every snippet of every fact like "water is liquid at RT in standard atmospheric pressure" etc. References are meant to be there to acknowledge the work of others like "how DNA was discovered" so that people can't just lift paragraphs or pages out os someones research without acknowledging them and passing it as their own work.

Hope this helps.


Does recombination slow mutation accumulation in sexual populations? Is there any evidence?

It's a good question and one without a wholly satisfactory answer.  Here's a nice review from 2012 outlining the theoretical questions regarding Mueller's ratchet and recombination.

There also is "unequivocal evidence that deleterious mutations accumulate in low recombining regions of the genome, due to the reduced efficacy of purifying selection. " So if you accept this correlation between recombination and removal of deleterious mutations, then studies such as these are compelling evidence of what's happening in real populations .

One other thing to keep in mind that in terms of experimental evidence, it is non-trivial to translate theoretical measures of fitness (e.g. "selection coefficients") to something that we can directly measure in real populations.  So even determining if there is an increase/decrease in deleterious alleles is going to dependent on having useful data in the first place. The assignment of "true" measures of selection on individual genotypes is the mainstay of experimental evolution (nice review here) and is very labor intensive. Moreover, the vast majority of this work has been carried out in bacteria (due to their short generation times) so effects of recombination are not addressed. Nevertheless there are some cool comparative studies in yeast showing how recombination can make selection more efficient.


Why isn't meiosis II called mitosis (as the chromosome number doesn't half)?

Well, in my opinion, the entirety of the meiosis is a process (reproduction of sex cell) in which two levels of division occur, it's all kind of one process. Though meiosis II may seem to have many similarities with mitosis, meiosis II can only occur with sex cells, to my understanding that is the main factor which differentiates meiosis I and II from mitosis. Furthermore, regardless of the similarities, to call meiosis II the same as 'mitosis' (whilst meiosis II is still in the entirety of the meiosis process) is not only confusing but impractical. I'm sure, though, that somewhere along the line there are several detailed differences between the technicality behind the cellular division in mitosis as in meiosis II. But, don't listen solely to my answer, that's just my opinion since your question is subjective to my personal opinion...


Has interest in haplotype blocks waned over the decade?
No.
You can set a time range on Google Scholar, which the screenshot shows was not done. I did that and:

A search for ‘haplotype block’ from 2000 to 2009 gives 22,000 hits.

A search for ‘haplotype block’ from 2000 to 2009 gives 25,700 hits.

(The term haploblock is now often used as an abbreviation, but it turns out that haplotype block is still much more frequent.)
So I have to conclude there must have been something wrong with the approach adopted by the poster. It is worth mentioning, however, that a Google Books ngram analysis of haplotype block shows first usage in 2000, a peak at 2007 dropping to a approx. 30% of the maximum in 2019. This may just reflect an rush to publish books on a new topic that has subsided, although the rate of publication in journals has been more constant.
What are haplotype blocks, why are they interesting, and how do they differ from haplotypes?
This is illustrated by an interesting paper in a recent (2020) issue of Nature that comes from the work of a large consortium addressing the  question of the adaptation of sunflowers to different ecological niches. This involves the evolution of so-called ecotypes, differing in properties such as flowering time and ability to grow on sand dunes.
The problem is that these adaptations involve many different genes (and hence alleles) which means they involve different haplotypes, according to the definition in Wikipedia:

A haplotype (haploid genotype) is a group of alleles in an organism
that are inherited together from a single parent.

However these different sunflower ecotypes are not physically separated from others, so that one would expect hybridization between them to occur, resulting in the loss of the haplotype and the adaptation. As the paper points out, this problem is actually a reformulation of criticisms of Darwin’s theories by his contemporaries:
Romanes, G. J. “Physiological selection; an additional suggestion on the origin of species.” Zool. J. Linn. Soc. 19, 337–411 (1886).
(although I must admit not to have read the original.)
The fact that this does not happen is because the alleles constituting the haplotype exist in non-recombing blocks — haplotype blocks.

A haplotype block is a region of an organism’s genome in which there
is little evidence of a history of genetic recombination, and which
contain only a small number of distinct haplotypes.

What prevents the recombination of such blocks? It appears that the most come explanation is that rearrangement of the regions containing the haplotype blocks occurs, preventing recombination. One of the easiest rearrangement to understand is simple inversion, two large blocks of which were found on chromosome 5.
The studies in the paper started with two haplotype blocks which had been shown to be involved in the ecotypes shown, and which were found to contain genes previously implicated in these processes, such as FLOWERING LOCUS T and HEAT-INTOLERANT 1. By genome-wide association studies they identified a total of 37 haplotype blocks on the basis of linkage disequilibrium. A diagram of some of these blocks in different sunflower species may wet the reader’s appetite:

So, in answer to the poster’s specific query: The concept of haplotype blocks is very much alive!


What nutrients can humans absorb in the mouth?

Quite a bit can be absorbed through the mouth. Most commonly, starches are broken down to maltose (two glucose molecules formed by a condensation reaction) and are easily absorbed by the bloodstream.

A lot of other factors balance into this, ie pH, lipid solubility, and molecular weight. Generally, if a substance is easily dissolved in saliva, it can be administered buccally or sublingually because the only remaining step is the diffusion into the subepithelial capillaries. In regards to speed, anything properly absorbed via buccal or sublingual administration goes to work much faster than a standard oral medication, and with a higher availability in the bloodstream. You are taking first pass metabolism and enzyme breakdown in the stomach out of the equation by diffusing the drug directly into the bloodstream.

There is quite a laundry list of medications that can be administered transbucally or sublingually, just a few of these:
Nitroglycerin
Acetylsalicylic acid (aspirin)
Glucose gel (as you mentioned)
Fentanyl (a narcotic painkiller)
buprenorphine (for opioid dependency)
Benzodiazepines (alprazolam, clonazepam)


The best way is to choose a distance that represents what you want it to rather than necessarily relying on the Hamming distance.

If you simply want base-by-base difference then calculate that (this may help) but you may also want a difference that depends on the likelyhood of mutating between different bases in which case you want to define a function that translates the mutation into a score for each transfer, i.e. you might want to score a deamination from 5-methylcytosine to thymine as the most likely occurrence. Expressing the relative likelyhoods of different mutations is not an easy problem but there are a number of widely used options.

The important thing is to ensure you represent the underlying biology not ensure that you have the fastest implementation. Decide on this first, then on the algorithm that gives you the best speed (also, deciding on that algorithm is on-topic for Stack Overflow not this Stack Exchange).


In plant species' description, does the leaf length include the lamina and petiole, or only the lamina?

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001) [my emphases added]:

A leaf is "an expanded, usually photosynthetic organ of a plant"

A lamina is the "expanded portion" of a leaf

A petiole is a "leaf stalk" and a stalk is "the supporting structure of an organ, usually narrower in diameter than the organ."

I know you know the definitions here, but I'm using this as evidence that the petiole is often considered separate from the leaf itself.
I do not know of a flora, key, or guide that uses the petiole as part of the measurement.
Since Kew's Plants of the World Online lists this species as having 30 cm long leaves (and assuming they do not include the petiole as is common practice), I would assume your source likewise is not including the petiole.
Disclaimer: I have never seen Ramosmania rodriguesii, so I can't comment from personal experience/knowledge of this specific species. However, if typical measurement practices have been employed, I assume the petiole is excluded in leaf length measurements.


Spatial resolutions in optical microscopy

The theoretical resolution for an optical microscope depends on the wavelength used, but is close to 0.22 um (220 nm). Confocal microscopy does not greatly improve axial resolution; it dramatically improves the in-plane resolution (x and y directions, by excluding extraneous light). Theres not a lot to do to "cope" with that using those techniques. If you need more resolution, you can use the super-resolution techniques you mention, or the good old TEM.

There is some more information on the Nikon website: http://www.microscopyu.com/articles/formulas/formulasresolution.html

and on Olympus website: http://www.olympusconfocal.com/theory/resolutionintro.html


Why is hyper pigmentation the common aftermath of skin lesions and abrasions?

The upper layer of the skin (or the epidermis) is formed mostly by keratinocytes and some melanocytes (about 30-40 times more keratinocytes) and also fibroblasts (although they are not shown here). The melanocytes are found in the basal cell layer at the border between epidermis and dermis as shown in the figure below (from here):

The melanocytes spread out their dendrites between the keratinocytes and transport the melanosomes (pigment containing vacuoles) to them to pigment these cells. This is a highly regulated process and depends strongly on the interaction between keratinocytes and melanocytes.

In the so-called paracrine pathway the keratinocytes secret substances which regulate the production of melanin. These are for example alpha-MSH or ACTH, which stimulate the melanocytes to produces more melanin.

This regulation is the key to the hyperpigmentation. During the proliferation or the inflammation chemokines and hormones are produced (and secreted) in the skin which stimulate keratinocytes and fibroblasts. These are for example the keratinocyte growth factor (KGF), as well as the chemokines IL1-alpha and TNF-alpha. This stimulation leads to the production of ACTH (and derived peptides) by the keratinocytes and the secretion of stem cell factor (SCF) and hepatocyte growth factor (HGF) by the fibroblasts which all induce pigmentation. The chemokine secretion is also enhanced from the keratinocytes by KGF. If you are interested in a deeper view at this topic, have a look at reference 1 (and the references in the paper). Reference 2 goes deeper into the regulation of the paracrine signalling.

In an injury (especially in larger areas of the skin) a lot of cells are damaged and need to be replaced. This functions via cell division but also via the migration of cells into the affected area. This is described by the paper you link - here melanocytes and melanoblasts (melanocyte stem cells which can divide and then differentiate into melanocytes) migrate into the injured region to replace the destroyed melanocytes.

References:

Mechanisms underlying post- inflammatory hyperpigmentation: lessons
from solar lentigo
Hepatocyte Growth Factor Establishes Autocrine and Paracrine
Feedback Loops for the Protection of Skin Cells after UV Irradiation


Does a higher body temperature slow the corona virus down?

SARS-CoV-2 is believed to have spilled over into humans from a Rhinopholus (horseshoe bat) reservoir. During flight, bats' body temperature is maintained at levels associated with fever in other mammals. Rhinolophus bats are reported to reach skin temperatures of 41 C during flight. (From this review which describes why bats might be special sources for zoonotic viruses)
So, this virus is likely adapted to survive higher temperatures than a human host.


What is the use of shampoo; is it for the hair or for the scalp?

We shampoo our hair because of sebum. In humans, sebaceous glands are most numerous on the face and scalp, with (on the scalp at least) several glands plus a hair follicle making up a pilosebaceous unit.
Each gland secretes sebum, initially a colorless and odorless fatty substance (plus dead cells) that spreads from the scalp outward over the hair, but that breaks down by bacteria producing strong odors.
Look at a person who has not washed their hair in a week and it will be easy to understand why we wash the "dead" stuff on our heads. It looks oily and it eventually smells bad as well.


This will be a hypothetical answer for the moment, so take it with a grain of salt until I can find sources or someone else does:

My best (educated) guess would be that the smell is there all the time, and when you sneeze you reset what's currently being "ignored" (in that you are not aware of it, though it is being sensed) by your brain momentarily. The source of the smell may be up in the air - it could be cologne/perfume, fabric softener residue on your clothes, what you ate for breakfast and are currently digesting, the bar of soap in the kitchen, etc. - but I haven't heard of "scent illusions" before.

One very quirky way of possibly testing that out is to remove yourself from your regular environment, sniff some ground coffee beans for half a minute, and then re-enter your home or smell your clothes to see if any of the scents match up with what you do smell when you sneeze.

My apologies that this isn't a thoroughly-sourced answer, but hopefully it acts as a good starting point.


Is there a data base, tool or method I can use to find out which of my genes code for cytokine receptors?

I'm sure there are many ways to go about this (including literature research via PubMed), but for a start, I searched the GO term data base which, for the search term "cytokine receptor activity" returned this, which includes a number of genes which I can download as an excel file and match them with my gene set using R.


Bioinformatics tool for "pairwise alignment" of complementary sequences?

I'm not sure this is what you need since the sequences you posted are not actually complementary as far as I can tell. However, exonerate is one of the most powerful tools out there and can do this as well. Using these sequences as examples:

  >query
  TAGCTTATTGATGGGAGGAGAGTCCGTGCACATGACAGACCTTGGCTGTCCCAGACTGCAGGAAGCCCAGG
  >target
  CCTGGGCTTCCTGCAGTCTGGGACAGCCAAGTCTGTTATGTGCACGTACTCTCCTCCCCTCAATAAGCTA

And this command (should be run on a *nix system):

exonerate -m coding2coding -q qq.fa -t test.fa -s 0

I get this output:

C4 Alignment:
------------
         Query: query [revcomp]
        Target: target
         Model: genome2genome
     Raw score: 312
   Query range: 71 -> 0
  Target range: 0 -> 70

 71 :                                                          CCA       :  6
      CCTGGGCTTCCTGCAGTCTGGGACAGCCAAGGTCTGTCATGTGCACGGACTCTCCTCProTCAATA
      |||||||||||||||||||||||||||||| |||||| ||||||||| |||||||||||+||||||
      CCTGGGCTTCCTGCAGTCTGGGACAGCCAA-GTCTGTTATGTGCACGTACTCTCCTCProTCAATA
  1 :                                                          CCC       : 65

  5 : AGCTA :  1
      |||||
 66 : AGCTA : 70

vulgar: query 71 0 - target 0 70 + 312 M 30 30 G 1 0 M 26 26 C 3 3 M 11 11

C4 Alignment:
------------
         Query: query
        Target: target [revcomp]
         Model: genome2genome
     Raw score: 309
   Query range: 0 -> 71
  Target range: 70 -> 0

  1 :                      GTC                                           : 66
      TAGCTTATTGATGGGAGGAGAValCGTGCACATGACAGACCTTGGCTGTCCCAGACTGCAGGAAGC
      ||||||||||| |||||||||||+||||||||| ||||| ||||||||||||||||||||||||||
      TAGCTTATTGAGGGGAGGAGAValCGTGCACATAACAGA-CTTGGCTGTCCCAGACTGCAGGAAGC
 70 :                      GTA                                           :  6

 67 : CCAGG : 71
      |||||
  5 : CCAGG :  1

vulgar: query 0 71 + target 70 0 - 309 M 21 21 C 3 3 M 15 15 G 1 0 M 31 31

Basically it gives you two alignments, one reading the target 3->5 and the query 5->3 and one the other way around.

Alternatively, you could do a translated blast search, tBLASTx which will translate both target and query sequence and so, should find complementary regions.


What does basipetal succession (of flowers/leaves) mean?

The definition you quote is a bit misleading — what matters is where the lateral flowers are connected to the inflorescence axis, not where they are physically in space.

Thus, due to the way these cymes develop (starts with a terminal flower and then a lateral bud grows out to form anther terminal flower, etc.) they must be basipetal because the first flower to develop is the terminal flower.  In other words, for cymes the lateral buds tend to overgrow so it looks like they are above, but what really counts is where they are placed on the inflorescence axis (which is below).

You may find this explanation clearer than the one in your textbook.


Do voltage-gated channels in a neuron use ATP

No, they change conformation in response to voltage. Wikipedia has some general discussion of the gating process, as would any basic neuroscience textbook.
The primary energy (ATP) cost of neurotransmission is in establishing ion concentration gradients, via the sodium/potassium ATPase. You can think of this as a special case of secondary active transport, where the energy costs are in establishing a gradient that is then used for a later process which does not cost any direct energy.


Identifying the origin of replication of an unannotated *E. coli* plasmid

Plasmapper Is quite good a recognizing common origins of replication. You will have to look up compatibility yourself. It is what I usually use when confronted with unnannotated plasmids.


What's the difference between shotgun sequencing and clone based sequencing?

The v short answer is that in shotgun sequencing, the sequencer is fed a set of random sequences from the target.  This can be done for instance by mechanically shearing DNA and then building a set of shotgun sequencing jobs which are then compiled back together by a genome assembler (i.e. in whole genome sequencing projects) into a full sequence.

In clone based sequencing, the DNA to be sequenced is specifically sectioned off into sequence copied into of plasmids (BACs - bacterial artificial chromosome) to divide the sequencing job into sections- a divide and conquer strategy.  BACs can be 150 kb long just to give you an idea.

These are not mutually exclusive terms; clone-based sequencing projects usually use the large clone libraries to section the project into a set of shotgun sequencing projects.


Where to find gene manipulation video (or photos)

From the comment section:

We don't have to see the actual changes. It's like chemists who will mix compounds together and obtain a new molecule. They dont see the chemical reaction per se but can test the new molecule to make sure what they predicted would happen had happened. Finally we often use fluorescent proteins to track some of the modification performed (which could involve a microscope). For the how, well that's a bit broad and involves too many notions to make a summary here.


Molecular genetics textbook (free?) suggestion for first time

I can’t comment otherwise this would be a comment, not an answer, sorry...

If you can’t lay your hands on a cheap (legal) text book that is of quality and in digital format then  maybe check out course material from MIT open courseware or something similar. As a further alternative, you should be able to find decent pop science books which are applicable and may be more useful than you think. The Epigenetics Revolution, for example, provided me with a really solid grounding when first trying get to grips with the subject.


I assume you are referring to the "typical 5’—3’ order of appearance".
The correct way to pronounce these is with the word "prime", that is, "Five prime to three prime". These are not units but refer to the directionality of RNA/DNA and the numbers five and three refer to specific carbon atoms arranged in the sugar molecules that make up the RNA/DNA backbone.
RNA/DNA are typically "read" (and always written) from the 5' to the 3' end of the molecule by molecular machinery in the cell, so that's usually the order we read the sequences as well. "5' to 3'" in molecular biology effectively means "beginning to end".


How can a good SD / Kozak sequence enhance translation efficiency?

I would strongly recommend looking in more detail into available resources for SD and Kozak sequences, wikipedia basically answers these questions and has plenty of further reading if you desire to explore these questions.
At the same time, remember that these are statistical processes involving thousands of molecules, rather than deterministic processes happening at a single molecule. Thus, what changes with different sequences is a rate at which some step occurs (e.g. rate of ribosome assembly, rate of translation initiation, rate of start recognition); none of these steps will occur with 100% probability on every mRNA molecule.
What this means is that you can write down equations for kinetic models of translation, allowing us to apply principles of mass action and rates of reaction from elementary chemistry. Having a higher rate of ribosome affinity for a sequence is therefore similar in effect to just having more mRNA, in the sense that in both cases you will do more translation and make more protein.
Thus, it might be easier to use the terminology of "strong" and "weak" SD/Kozak sequences. A strong sequence has a high rate of reaction and a weak sequence has a low rate of reaction. Here, the "reaction" in question is ribosome binding, or translation initiation, or whatever process we're currently studying.
Now, as to the specific questions:

Sequences alter the rate at which downstream processes occur. So, e.g. a weak Kozak sequence will often simply not initiate translation, and the ribosome will fall off without translating anything. This will almost never happen with a strong Kozak sequence, so a strong Kozak is more "efficient" in the sense of more reliably leading to translation. A strong Shine-Dalgarno sequence increases the rate at which ribosome binding occurs.

Both ribosome binding and translation initiation are necessary for protein production, so if you increase the rate at which these processes occur, you increase translational efficiency in each case.

There is no "foreseeing". Think about this mechanistically. The ribosome scans 3' along the mRNA, starting at the point of attachment. Also, each ribosome attachment to an mRNA can only start one translation event. Once a ribosome stops scanning and starts translating, it does not recognize subsequent Kozaks.

Thus, if there is a strong Kozak sequence, then translation will almost always start at the strong sequence, and will never have the opportunity to start at a sequence further 3'. It is mostly only when a 5' Kozak is weak that further Kozaks get recognized at all ("leaky scanning"):

The first start codon closest to the 5′ end of the strand is not always recognized if it is not contained in a Kozak-like sequence. Lmx1b is an example of a gene with a weak Kozak consensus sequence.[22] For initiation of translation from such a site, other features are required in the mRNA sequence in order for the ribosome to recognize the initiation codon. Exceptions to the first AUG rule may occur if it is not contained in a Kozak-like sequence. This is called leaky scanning and could be a potential way to control translation through initiation.[23] For initiation of translation from such a site, other features are required in the mRNA sequence in order for the ribosome to recognize the initiation codon. (Wikipedia)

So it's not that Kozaks are required, necessarily. You just need some set of circumstances which increase the probability that the ribosome starts translating next to a start codon. The Kozak simply happens to be an efficient way to get a ribosome to start translating. The closer a sequence is to the consensus Kozak sequence, the more efficient it is, because the probability of translation initiation is higher.


Can nervous disorders be cured? Will enough research be the answer?

Yes, levodopa type treatments for parkinsons.

epilepsy:
In 2017, 116 children were randomly assigned to undergo epilepsy surgery or receive medical treatment. After 12 months, 77% of the children who had undergone surgery were seizure free compared with 7% who received medical treatment.

Check news and histories of advances in neuroscience and neurology.

Every year drugs improve, it's best to stay objective in the face of mind dysfunction, meditate.


When female mosquitos bite to suck blood, they need to overcome the body reaction against it. So when they found a bood vessel, they inject their saliva into the wound. This saliva contains substances which affect blood clotting and platelet aggregation (so the blood will stay liquid which is essential for sucking) and a vasodilatory substance (which widens the blood vessel and prevents contraction of it). The exact composition depends on the exact mosquito species.

These "foreign" substances cause a local immune reaction which results in the release of histamine in the skin. The itching and also the red skin and the swelling are a result of the histamine release. See the Wikipedia article on mosquitos for more information.

If you are interested in a deeper look on the composition of the mosquito saliva have a look at these two articles and their references (if there is help needed in getting the articles, let me know):

Role of arthropod saliva in blood feeding: sialome and post-sialome
perspectives.
Toward a description of the sialome of the adult female mosquito
Aedes aegypti.

Since the substances affect the blood coagulation cascade, there is some research going on if and how this can be used clinically. See this article for an overview or have a look at the original publication here ("Unique thrombin
inhibition mechanism by anophelin, an anticoagulant from the malaria vector")


Many of the statements in your question are false, including your ideas about waste products.

Ultimately, fats, just like carbohydrates, end up as water and carbon dioxide if they are used in cellular respiration for energy. The reaction path is different, but the ultimate reaction products are the same as you would get from burning fat in a fire: reaction with atmospheric oxygen oxidizes the reactants to carbon dioxide and water.

This is the reverse process of photosynthesis, where carbon dioxide and water react to form sugars, with oxygen as a byproduct.

The mass leaves the body as exhaled carbon dioxide and as metabolic water through the urine, vapor in exhaled air, etc.


Evolutionary explanation to why we have such large memory capacities?

We don't have large memory capacities.
If anything I would have asked the opposite, why is our memory so bad and unreliable considering how large our brains are. Even with this gigantic brain we struggle to remember a few phone numbers. Here's how our short term memory compares to monkeys: https://www.youtube.com/watch?v=zsXP8qeFF6A&ab_channel=BBCEarth . I have no explanation as to why humans are so bad at this, this amount of data should be nothing for a brain of our size.
As for long term memory, I'm not really convinced it is that large really, it seems to me people in general in ten years.. have forgotten pretty much everything. Occational glitch.. occational stuff, and even that is usually vague and full of wrongs.
And when people cram for exams.. take the best students ten years later and see how much they still remember, it will be just a tiny fraction.
What do you mean by "filling up their memory capacity"?
Are you expecting some sort of a state where the persons hard disk is full and nothing.. nothing new can be learned? That state doesn't make any sense, the brain is always deleting from memory plus it would make more sense to have the memory slowly deteriorate, rather than fall off a cliff into no functionality at all.
We don't remember anything. We always feel like we are going to remember the now for so long and all but we don't. And we have this bias because we don't remember what we don't remember, which is nearly everything.


Based on the overall apparence and the distinctive metallic patches on the wings it looks like a moth from the subfamily Plusiinae (Looper moths). I'm not familiar with North American moths, but after a quick check at species found there Megalographa biloba (Bilobed looper moth) seems likely, and this species is also found in California.

(picture from wikipedia)

Also see the pictures at Bugguide.net.


Maximum biologically possible age for a human being?

Even in perfect environmental conditions we would age. Living is associated with a myriad of deleterious processes, both random and deterministic, which are caused by imperfectness, exhibit cumulative properties, and represent the indirect effects of biological functions at all levels, from simple molecules to systems. Here is a good read on this topic https://www.ncbi.nlm.nih.gov/pubmed/27060562

Even if nothing else was wrong (which is not the case) the accumulation of intracellular and extracellular junk which our systems are unable to dispose of (lipofuscin, amyloid beta, etc) would eventually kill us. https://en.wikipedia.org/wiki/Senile_plaques

As for the maximum age - nobody we know of made it past 125 years yet. https://en.wikipedia.org/wiki/List_of_the_verified_oldest_people


It was moistening its respiratory and osmoregulatory organs:

Woodlice as all other terrestrial arthropods face the major challenge of preserving water balance. In their case the two systems that immediately suffer from desiccation are osmoregulation itself and respiration. In woodlice these two functions are carried out mostly by the pleopods: modified leaf-like appendages on the ventral side of the hind body part ("tail") (see here and here some annotated photos and drawings of ventral side of woodlice).

To maintain these structures in moist state woodlice have a number of adaptations, one of them being the ability to "pick up water from external sources via uropodal dipping, with the water moving upwards by capillarity" (see here). Uropods are the tiny rod-like appendages on the tip of the "tail", and dipping of the uropods is exactly what you were observing.


Is the sense for salt depending on the electrolyte level in our body?

Is this possible or am I just hallucinating?

Certainly possible, but I'd peg the mechanism closer to Sensitization or De-sensitization of the neurons involved so that when you finally ingest some salt the sensation is different. The sodium and chloride levels of the ingested material wouldn't have a direct effect on the level of De-/Sensitization, but rather how low your stores are or how long you've gone without.

  So, I imagine it like this....

What you broadly described is how regular sodium receptors work. They will work that way regardless of what you've been doing, and doesn't really explain an increase or decrease in your ability to taste salt - the signals will fire either way.

Check out the action of the Capsaicin receptor and how it changes sensitivity over short periods of time. I'm betting the phenomenon you're describing will be closer to this (an increase or decrease in the number of sodium receptors in response to the abundance of salts or lack-thereof) than an immediate mechanism from the drink itself.


What are the features on a microscope one needs in order to do lab work?

It sounds like you need a microscope for standard microbiology lab tests. At a minimum, any standard wide-field/brightfield microscope would work. If most of your histology work involves colorimetric stains (e.g., H&E, gram staining), you don't need any fluorescence capability. If you are working with a lower budget, look at the new lines of LED-based miroscopes, which dramatically drop the cost (I think around $10,000).

If you plan on doing a high volume, in particular of fixed histology/cytology slides, then you may want to invest in some of the automated slide scanner microscopes. They have a small benchtop footprint and can be programmed to image large areas automatically, for later analysis.


How suddenly does lactose-intolerance onset?

Disclaimer: I am not medically qualified, and this answer must not be construed as being medical advice of any kind.

Primary adult hypolactasia is the most common cause of lactose intolerance. The majority of the world's population have this phenotype.

In these individuals, at weaning, there is a reduction in the level of the enzyme lactase, which is responsible for digesting lactose to galactose and glucose in the small intestine. Undigested lactose can create symptoms via osmotic effects (causing diarrhoea) and because it is metabolised by bacteria in the colon, producing gas and thus abdominal bloating.

About 35% of adults have a genetic variant in an region upstream of the lactase gene which results in the expression of lactase continuing into adult life. These individuals are lactose tolerant. This trait is most common in Northern Europe.

According to references cited in

  Ingram, CJE et al. (2009) Lactose digestion and the evolutionary genetics of lactase persistence Hum Genet (2009) 124:579–591

(I have removed citations from the passage for clarity.)

  "most lactase non-persistent individuals can tolerate small amounts of lactose (as in tea or coffee), and some can consume a lot without ill effects. Variation in the composition of the gut flora between individuals, as well as a psychosomatic component may account for some of the interindividual variation in symptoms."

The clear implication is that there is a lot of variation in the tolerance of lactose amongst those lacking the lactase persistence trait. Given the contribution of the gut flora to the symptoms these could presumably vary as a result of, for example, antibiotic treatment. Also I imagine that the effects of undigested lactose could be synergistic with some other gut disturbance.

Added in response to comment from the OP:

In someone with the (common) genotype that corresponds to 'no persistence of lactase' the possibility of showing symptoms will be present from a young age. Apparently there is a lot of variation in the severity of symptoms. If an adult suddenly exhibits symptoms then I am suggesting that this could be due to an interaction of non-persistence with some other gut disturbance - I imagine this could happen quite quickly. Alternatively I suppose that a change in diet could trigger symptoms.


Are there known downsides to removing UV mutation hotspots to prevent some skin cancers (Genetic sunblock)?

Short-wave UV light (UVB and UVC) causes transition mutations at dipyrmidine sequences (ref.). In the work presented on KNSTRN quoted by the OP the authors report that 19 from a panel of 100 squamous cell carcinomas (SCC) contained a mutation in KNSTRN (and furthermore three of these contained no other mutation across the six genes that were analysed (Fig. 1b)). Normalising for ORF length this makes it the 3rd most recurrent mutated gene. It would seem therefore that it a fairly important mutagenic target. In a broadened set of SCCs they found a total of 29 KSTRN mutations, and of these 13 were Ser24Phe (TCC>TTC) mutations, which they refer to as a 'hotspot'.
Accepting the arguments in the answer from @Chris it is still interesting to consider how one might remove such a hotspot. The normal amino acid at this position is a serine. Here is the human codon useage for ser, obtained from here:

TCT 14.6%
TCC 22.0%
TCA 15.0%
TCG  6.0%
AGT 11.9%
AGC 19.4%

It would seem therefore that it would be theoretically possible to edit the Ser24 codon from the UV-sensitive TCC to AGC, essentially eliminating this 'hotspot'.
This, of course, doesn't answer the question - are there downsides to this? I already selected a synonymous codon with a similar frequency of useage so that shouldn't be a problem. However here is an example of a synonymous codon substitution which has an effect upon splicing of the LMNA gene resulting in muscular dystrophy, and the paper cites several other examples of this. (I haven't actually checked to see where the Ser24 codon lies in relation the exon-intron boundaries in the KNSTRN gene.) No doubt there are other mechanisms by which my proposed edit could have unwanted effects. It would have to be tested carefully, and so we come back around to a cost-benefit analysis - would it be worth developing this editing idea (even if it were feasible as a therapy) given that there are clearly many paths to SCC not involving this specific mutation.


Spruce growing high up in a maple trunk: Can a partially rotted trunk completely sustain another tree?

Note  This answer makes the presumption that the crotch in the maple's trunk is indeed a breach through its bark, and does reach the inner woody tissues.

The heartwood of most trees consists of the dead connective tissues, xylem, which surrounded the cells that once formed the living layer of phloem under the protective bark.  That connective tissue itself mostly cellulose, and is a polymeric chain of glucose i.e. sugar molecules bonded and linked in such a way as to make them indigestible to most lifeforms.
Certain bacteria and fungi, among others, are able to do so, and they are among the first responders in the decomposition scene.  When these microbes, often present in the gut of various insects, are able to break down the woody fibers into forms that permit their re-use by other plants, the detritus is comprised mostly of carbohydrates, alcohols, carbonic acid, and water.  Phosphates and various other trace elements which were present in the cells of the woody tissues are released also.
Later, visiting birds and mosses will further augment the ecosystem, adding nitrates and various salts — potassium, sodium, chlorides, and the like.

Another thing that needs to be considered is the drainage.  Where does the excess water go?  Pressure on the capillaries inside the xylem of the maple should be able to channel some water downwards, but not much will exit through the roots.  I've never heard of such a thing.  The hole in the maple will widen and exacerbate, deepening the rotted area, but it will be acidic and somewhat saline due to the lack of drainage.

Can it completely sustain another tree?  As the ecosystem flourishes, probably; unless the new tree has special requirements for the pH or salinity of its soil which are not maintained by the rotten wood, then it should be able to gain enough nutrition in the form of nitrates, phosphates, and water, but not all of that will come from the other tree directly.

The branches of a tree will only grow so large as can be sustained by their root system, of course.  The limited space in which this little sapling has taken root will result in the less than maximal form that you see in the photographs.

So, in conclusion, that spruce will probably not thrive by any means, but it will manage to survive.  Spruces do favor more acidic soils — lower pH — than many other trees, so it has that going in its favor.
That much is obvious, I suppose:  ten years, and it no larger than a four–year shrub.

There is a problem if all this occurs inside a tree which has not fallen, however.  Usually, the outer bark of a tree protects it from such decompositional actions, because the inner woody tissues of most trees do not contain adequate chemicals to deter insects and fungi from chomping or ‘mycelizing’ their way through the heartwood.
Eventually, the maple will either need to be cut down or will be weakened enough that it will collapse.


It is hard to tell from the image, but using this species key for Polistes wasps, it is reasonable to conclude that your wasp is either P. metricus or P. fuscatus.

If you look at this image of a P. metricus female, you can see the dull reddish markings on the abdomen:

On your image, you can see the same markings on the abdomen, at a different angle:

Based on these markings, your wasp is most likely Polistes metricus. You can read more about this insect here and here.

Here is a link to the image I modified.


Divide the plate into equal sectors. Count one sector as accurately as you can then multiply that number by the number of sectors. This assumes the colonies are roughly equally distributed.


Fossil record of previously thought extinct animals

The formation of fossils is exceedingly rare. A number of unlikely events must all line up for us to find one. So there would be no reason to expect that we would find a fossil of anything but the most common and easily fossilized organisms. The probability of NOT finding a fossil is much greater than finding one.


Often artificial neurons are created with conventions that zero is "rest" and 1 is "threshold". The unit starts at 0, and when it reaches 1 it will send an input to all of its targets and be reset back to 0.

This isn't exactly how real biological neurons work, but its a reasonable approximation in some contexts (and can do real world computations).

Most of the inputs to a unit are variable, so you add some voltage to the neuron based on the synaptic weight. For example, one input with a weight of ".2" would move the cell 1/5th of the way to threshold by itself.

When people talk about a bias input, they are referring to an extra "always-on" input with a small synaptic weight. This can maintain a rest greater than 0 in a leaky integrate-and-fire cell; this allows for some more biologically relevant forms of inhibition (negative synaptic weights) to have an influence on the unit, by offsetting the bias input and pushing the voltage back to 0.

More often, I am familiar with using a bias input in networks that are not leaky. These networks just integrate until they reach threshold (although they may or may not get negative inputs). For these networks (or for a leaky network where the bias current is substantial relative to the leak), adding a bias input ensures that the network won't stochastically "fall asleep" due to a period of low activity. If the bias current is equivalent to ".02" units per cycle, for example, you would guarantee that the cell would fire once every 50 cycles with no other input.

There are some real excitable tissues that show similar behavior, but not due to a real bias input. Rather, there are intrinsic channels that slowly depolarize a cell. Some examples are in cardiac myocytes and the sinoatrial node making up the heart's "natural pacemaker", as well as in brain circuitry that controls breathing. The bias input is sort of a "made up" construct that is functionally, but not mechanistically, correlated with real biology.


How did the endoplasmic reticulum come to be?

Found the following on wikipedia. Seems pretty self explanatory:

  The Golgi, ER, and lysosomes are likely to have evolved as a result of
  the plasma membrane going through invagination. An increase in the
  overall volume of a cell would require the plasma membrane to fold in
  order to maintain a constant surface area to volume ratio. These folds
  may have led to the specialization of internal membranes to maintain
  communication with the environment. In the first stages of eukaryotic
  cell life, the membranes may have been interconnected and attached to
  the plasma membrane. Later on, as their functions diverged, the
  membranes may have become separate structures


Using Canonical Correspondence Analysis on matrices with missing data

First, you cannot fully analyze pair-wise correlations between your environmental variables with NA values, and therefore cannot fully discount including covarying variables. If this is the case, you will not be able to know which of the covarying variables is responsible for any trends in your data.

Second, I don't believe CCA will work with NA values -- you will either have to eliminate the observations containing those missing values or fill them in with column averages. However, both of these methods will have an impact on your results, so move forward cautiously.

Third, I wonder if CCA is even the way you want to go. nMDS (non-metric multidimensional scaling) is much less constrained than CCA. Additionally, it doesn't suffer from as many assumptions/limitations as CCA.

From McCune & Grace (2002):

  The following two questions can be used to decide whether CCA is appropriate: (1) Are you interested only in community structure that is related to your measured environmental variables? (2) Is a unimodal model of species responses to environment reasonable? If, for a specific problem you answer yes to both of these, then CCA might be appropriate

However, missing environmental data is still a problem in nMDS.


Why isn't Bubonic Plague as virulent as it once was?

The identification of the Black Death with plague is now fairly well-established - see this paper (open access) in which PCR and protein detection were used to detect the presence of Yersina pestis in human skeletons from plague-related mass graves across Europe.

Outbreaks of plague do occur in rural environments, see this WHO page for some details. The WHO plays a role in responding to these outbreaks, as long as they are notified by the relevant countries. Plague infections respond well to antibiotic treatment.

There has also been a recent outbreak in Madagascar. According to the epidemiologists we are still in the midst of the 3rd plague pandemic, which started in China in the mid 19th century.


It's just so much more convenient to have the enzymes ready without having to thaw them. The main reason you freeze enzymes is to keep them active, if you figure out a buffer that keeps them unfrozen without compromising activity, that is a huge increase in convenience.

Not having to thaw the enzymes before use saves a lot of time, if you can manage to keep the enzymes active in those non-freezing conditions that is a clear advantage.

Glycerol also stabilizes proteins in solution, and multiple freeze and thaw cycles can negatively affect enzyme activity for some enzymes.


Chlorophyll is organic, not living, which is a fancy way of saying that it contains carbon. As for your question about boiling, it depends on whether or not the heat from boiling will disrupt the chemical bonds and destroy the molecule. According to Wikipedia, chlorophyll a will melt at around 117°C (I'll assume that chlorophyll b is similar), which is higher than the boiling point of water, so if the temperature is strictly maintained, the chemical should stay intact.


M-type potassium channels by muscarinic receptors

Closing of the channel through muscarinic receptors involves activation of phospoholipase C and depletion of membrane phosphatidyilinositol-4,5-bisphospate which is needed for the channel to stay open. Once the channel is closed,  potassium, which is a positive ion accumulates inside the cell eventually depolarizing it or lowering its threshold for activation. Thus, blocking the extrusion of K ions results in excitation of the target neuron.

See this for more:
Brown, D. A., and Constanti, A. (1980). Intracellular observations on the effects of muscarinic agonists on rat sympathetic neurones. Br. J. Pharmacol. 70, 593–608.


The evolutionary origin is alleged to be recent: Other animals do not have a preference for dissonance and consonance.  (McDermott & Hauser, 2004).

Humans have new auditory regions in the brain for predicting and processing speech, and processing the emotions conveyed in the voice. The human voice mostly has harmonics in the 3rd and 4th note due to the properties of the vocal tract. There have been some basic studies of the 12 notes of the piano as represented in the human voice, which concluded that the "consonant" sounds from chords and melodies correspond to the the sound of the human voice.

This article suggests that dissonant/amusical frequencies are uncommon in natural ecology, because of the way physical objects resonate. Bird melodies are atonal and not particularly dissonant or consonant.

Some people may suggest that animal alarm calls are more dissonant than mating calls, especially those that are made to scare you like a cat hiss, a gecko scream, baby marmots which are separated from their mother, a rabbit being eaten.

Actually, many studies have identified brain regions used for emotional processing, the same that react when they see a beautiful or unnerving image, by MRI tomography and also from people who have had strokes which make them non-reactive to music, and people with amusia known as amusics.

  They also
  found an increase in frontal-midline (Fm) theta power
  for consonant music, indicating greater coherence of
  neural firing in certain population of neurons. This is
  interpreted as reflecting activation in the anterior cingulate cortex (ACC), which has been implicated elsewhere in processing pleasant music (Blood & Zatorre
  2001). The ACC’s role in emotion is also supported by
  its inputs from other key emotion-related areas, such as
  the amygdala, hippocampus, and parahippocampal gyrus (Devinsky, Morrell, & Vogt, 1995).

There are a lot of studies on the topic, this is a well written summary of recent research.

Musical sensory stimulation is a fascinating topic with complex ecology and brain quirks, it's best to research the topic individually to find which aspects of music do what to the brain:

Music rhythms vs cardio/breathing/cerebral rhythms, individual sound consonance/dissonance, and complex auditive patterning of sounds found in rhythmic chords and melodies. The conflict-resolution of harmonies are what you are referring to regarding the sequence of notes, there are studies on musical expectation, it's a sub-field of consonance/dissonance neuroscience.


Are there ways to speed up the growth of plants?

Yes.

The research team, led by the Durham Centre for Crop Improvement Technology, and including experts at the University of Nottingham, Rothamsted Research and the University of Warwick, have discovered that plants have the natural ability to regulate their growth independently of Gibberellin, particularly during times of environmental stress.
They found that plants produce a modifier protein, called SUMO that interacts with the growth repressing proteins.
The researchers believe that by modifying the interaction between the modifier protein and the repressor proteins they can remove the brakes from plant growth, leading to higher yields, even when plants are experiencing stress.[1]

Bacterization is the process by which bacteria applied to the soil and plant parts. Under certain conditions yields were able to increase 10 to 13 percent. However, not all results were able to be reproduced so this is something you can look into more as well. [2]
Another option is to artificial increase the amount of CO$_2$:

Over the years there have been numerous laboratory experiments which conclude that increases levels of CO2 result in increased plant growth no matter how that plant growth is quantified. Sylvan Wittwer in Food, Climate and Carbon Dioxide tabulates the results. [3]

Lastly, you can look into genetically modified organisms (GMOs) which is a hotly debated topic.
With a Google search, you will see that that there are numerous articles on methods to increase plant growth, to numerous for me to give a blurb about them all. Therefore, I linked a few that seems promising as well as interesting.


Linkage between chromosomal loci and the Hardy-Weinberg principle

Linkage is a physical reality

Linkage refers to the physical presence of several loci on the same chromosome. Two loci that are said to be in close linkage mean that they are locataed relatively close to each other on the same chromosome.

Linkage disequilibrium is a statistical reality

If two alleles at two different loci are found on the same haplotype than expected by chance (that is more often than the product of the respective frequencies), then there is an statistical association between these two loci. We refer to this statistical association as linkage disequilibrium (abbreviated LD). If there is absence of statistical association, then the two loci are independent and we talk about linkage equilibrium.

Let's consider two bi-allelic loci. We will call the two loci A and B and the two alleles A0, A1 and B0, B1 at loci A and B, respectively. Let $p_{AB}$ be the frequency of the haplotypes that contains both A1 and B1. Let $p_A$ and $p_B$ be the frequencies of the alleles A1 and B1, respectively. Then LD between the loci A and B (called $D_{AB}$) is defined as

$$D_{AB} = p_{AB} - p_Ap_B$$

There are other related mathematical definitions of LD than $D_{AB}$, such as $D'_{AB} = \frac{D_{AB}}{D_{max,AB}}$ and the correlation of coefficient among the two loci $r_{AB}$.

Linkage disequilibrium and Hardy-Weinberg equilibrium

You will note that, knowing whether or not each of the two loci are in H-W equilibrium (or respecting the assumptions of H-W equilibrium; see this post) tells you nothing about LD among these two loci. For example, two loci can both be at H-W equilibrium but be in LD (or in linkage equilibrium). Similarly, two loci can both be at H-W non-equilibrium but be in LD (or in linkage equilibrium).

Linkage and linkage disequilibrium

Various things can affect LD. In theory, there is no need for linkage to have linkage disequilibrium. A strong epistatic interaction for early life survival between two loci (whether or not they are in the same chromosome) can eventually cause  LD. However, most of the cases of known LD probably concern pairs of loci found in tight linkage. There is a diversity of processes that lead to LD and reviewing them would be outside the scope of this answer.


What happens to blood after a person dies?

After death, blood normally coagulates unless the deceased has ingested certain medications or chemicals (e.g. anti-coagulants).

According to this article, normal clotting time is 3-15 minutes: http://www.angelfire.com/sc3/cjrp/forensicsofdeath.html

However, this probably applies to external wounds, like cuts. When a person dies, the blood pooled internally would probably take longer to coagulate. You might find the answer by typing blood + coagulate + forensics into Google.


How can heart disease cause dizziness after eating?

Dizziness after eating, which can lead to falls and passing out, is called postprandial hypotension, and as the heart is indeed responsible for responding to hypotension by increasing it's rate - which can be seen in any number of clinical scenarios from blood loss to standing up too suddenly - failure to do so, for any reason including heart disease, can result in continued hypotension, which is experienced by most of us as dizziness.

Postprandial hypotension (PhTN) is defined as a fall in systolic blood pressure (SBP) of ≥ 20 mmHg occurring within 2 hours of a meal. This hypotension (hTN) can result not only in dizziness, but  may also cause syncope, falls, weakness, angina pectoris, and stroke.

Because PhTN is particularly common in older hypertensive patients, and older patients tend to have higher incidences of heart disease, it was initially thought heart disease was the cause. However, that didn't explain why some young people without heart disease have PhTN.

In truth, the mechanism of PhTN is not fully understood.

Normally after a meal, blood supply to the gastrointestinal (GI) tract increases, starting with increased flow through the left gastric and celiac arteries, followed by the mesenteric artery, which is more prolonged. Observations indicate that the postprandial hyperemia progresses along the GI tract in association with the movement of ingested food. The magnitude (25–200%) and the duration (3–7 h) of the hyperemia appear to depend somewhat on the composition of the meal. The increase in GI blood flow means there's less blood to circulate in the rest of the body (relative hTN). Normally this is corrected for in various ways.

Baroreceptors (nerve cells within arteries near the heart and in the kidney) are sensitive to rises, falls, and the rates of change in BP, but are especially sensitive to sudden falls in BP, which results in decreased baroreceptor firing. Autonomic Nervous System responds by increasing sympathetic outflow and decreasing parasympathetic (vagal) outflow. Sympathetic outflow leads to vasoconstriction (increased systemic vascular resistance, or SVR), increased HR (tachycardia) and increased force of contraction on the heart (positive inotropy). This leads to a partial restoration of arterial pressure. In people with PhTN, any abnormality at any point in the system will result in an insufficient rise in SBP to overcome the fall.

Therefore possible contributors to PhTN include inadequate sympathetic nervous system compensation for meal-induced GI blood pooling; impairments in baroreflex function; inadequate postprandial increases in cardiac output; impaired peripheral vasoconstriction, as well as abnormal responses to GI hormones released during digestion.

  Dysautonomic patients with postprandial hypotension fail to maintain systemic vascular resistance after a meal. This impairment in vascular response to meal ingestion may underlie the development of PhTN. Power spectral analysis suggests an impairment in the postprandial autonomic modulation of HR in healthy elderly and dysautonomic subjects, possibly predisposing to hTN when vascular compensation is inadequate.

Heart conditions that might result in an inadequate response to PhTN include low heart rate (bradycardia), heart valve problems (decreases cardiac output), heart failure (decreased ejection fraction equals cardiac output), patients with atrial fibrillation (decreases cardiac output because of inadequate filling of ventricles), heart attack (decreased ejection fraction), heart muscle disease (cardiomyopathy), severe left ventricular hypertrophy, people with HTN on medications which cause a lowered heart rate, etc.

Therefore, Postprandial Hypotension is an important hemodynamic abnormality in patients with cardiac diseases as well as autonomic nervous system abnormalities such as can be seen in Parkinson's Disease, diabetes mellitus, and others.

Postprandial Hypotension: Epidemiology, Pathophysiology, and Clinical Management
Association of postprandial hypotension with incidence of falls, syncope, coronary events, stroke, and total mortality at 29-month follow-up in 499 older nursing home residents.
Postprandial hypotension. Pathophysiological mechanisms and clinical implications in different disorders.
Postprandial hypotension in response to duodenal glucose delivery in healthy older subjects
Postprandial Hyperemia
Arterial Baroreceptors


What organism has the longest Hayflick Limit?

The Hayflick limit is generally associated with telomere length. Human telomeres are a little on the long side as species go, but are not extraordinary. Many species of mice, and other rodents, have far longer telomeres than humans, for example, and obviously have much shorter lifespans. There's also such a thing as a "mega-telomere", found in a number of bird species, which can hundreds of times longer than human telomeres.

There's only a vague correlation between telomere length and a species' lifespan.  See Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination for a starting point.  Telomeres are a part of the longevity story, but probably a fairly small part.

That said I don't see an explicit statement that those species with very long telomeres have a higher Hayflick limit. I assume this is because the Hayflick limit is an ultra-simplistic and not very useful description of a very specific set of conditions, but I don't know that for sure.


GWAS: why is replication in another cohort so crucial?

As an elaboration of my comment.

Summary: Replication is required in GWAS studies to account for non-random technical biases.

An example of such bias is, for example, a chip used for genotyping giving consistently incorrect genotypes for a locus. In this situation adding more subjects will not correct for this effect and therefore the only solution is to genotype additional subjects with another method (e.g. another chip or experimental protocol). Another source of non-random technical bias is at the phenotype measurement level. You might want, if possible, to measure the phenotype using other techniques to make sure that bias will be corrected.

A replication cohort does not need to be huge and the actual size needed will largely depend on the effect size of the SNP seen in the discovery cohort. A "power-to-detect" calculation would help in predicting the cohort size needed. For a SNP to be significant, it must pass Bonferroni correction but as you can run a statistical test at the candidate site only the correction will be usually not very astringent (i.e. you might run association tests on "only" a few dozens or hundreds SNPs).

Historically GWAS replication was also required to correct for population structure but as the tools evolved substantially (e.g. the use of principal component analysis) and the cohort sizes are now substantially bigger compared to the first GWA-studies, this is less a concern. What was required is to sample independently other subjects from either the same or a different population.

For your situation what you could do is to split your cohort into a discovery and a replication panel, genotype your subject in the replication panel using an independent technique, eventually do the same with the phenotyping and replicate you candidate SNPs. The replication panel needed is usually must smaller than the discovery cohort for the reasons stated in the previous paragraph.

For your last question about the meta-analysis. Yes this could also be a way to go but be careful that you will still need a replication cohort to validate SNPs found this way therefore resulting in the exact same problematic you described.

I hope this help!


What kind of red/green/black, spiny caterpillar is this?

Looks like a greenish variant of Hemileuca maia – the Buck Moth, which according to here does occur in Oklahoma. This source also suggests that touching the caterpillar (or its relatives) is a bad idea...

 Source: statebystategardening


Are there macrophages in the blood vessels and within the blood stream?

Usually, monocytes and neutrophils are present(there are other cells like Lymphocytes and other leukocytes), the only time a macrophage will be present is when inflammation occurs, I suspect this is due to the large size of the macrophage, it would be difficult for it to travel in the bloodstream, as it is quite big, compared to the small size of a monocyte. During inflammation, vascular dilation and permeability increase, which makes it easier for cells and proteins to diffuse across the endothelium.

A source that macrophages are present in all tissues: https://www.researchgate.net/publication/227897252_Macrophages_in_the_embryo_and_beyond_Much_more_than_just_giant_phagocytes

A source that talks about all the leukocytes and lymphocytes present in the blood normally: http://www.histology.leeds.ac.uk/blood/blood_wbc.php


Why are there seven entries for Pimpinella dioica in the Catalogue of Life?

While any large database may have errors that can lead to multiple entries (sensu har-wradim's answer), I think most of the multiple entries detail the taxonomic history associated with that species. Your link to the sponge Haliclona digitata provides a clear example. First, dismiss the H. digitata (Schmidt, 1862) entry. As clearly stated, it is a synonym for a different species of sponge, Tedania anhelans.

The remaining entries are all links to various homonyms of H. digitata. Skimming through the World Porifera Database entries (via the "Online resource" links), provides the necessary information. Lendenfeld's use of Chalinorhaphis is the original description. It is the senior homonym, meaning the specific epithet (digitata) has precedence over junior names. The junior names include Adocia digitata (Baer) and Gellius digitatus (Koltun). It was probably Tanita & Hoshino that transfered digitata to the genus Haliclona but I cannot verify this without seeing the article.

The taxonomic history can also be tracked for Ichneumon varius, but the linked databases don't hvae as much detail as the Porifera database for H. digitata. Still, it suggests that the description by Pontoppidan in 1763 is the senior homonym, and the subsequent uses by Cuvier, Gmelin and Muller are junior homonyms.

This is also what I think har-wradim is alluding to for Pimpinella dioica. Unfortunately, the Umbellifer database seems to have little detail in this regard.

The Catalogue of Life provides a convenient mechanims to begin a thorough search for the taxonomic history of a species.


Does the Parasympathetic Tract of Colon Sigmoideum Travel with Nervus Vagus and its Nucleus Dorsalis Nervi Vagi?

I found the following from Wikipedia:

  Pelvic splanchnic nerves are the primary source for parasympathetic innervation [for Sigmoid colon].

The non-cranial nerve is extending the scope of the cranial nerve by a synapse between the two neurons. The neurons are transmitting the electrical impulse from one neuron to another.
So this way the splanchnic nerve does not need to be with CN 10 in the region of impact.

The parasympathetic tract of colon sigmoideum can travel with nervus vagus by having a synapse between pelvic splanchnic nerve and CN 10. I verified this from my professor.


Is a bone marrow transplant limited by sex?

Short answer: Yes. Because in almost all cases of organ transplant, the organ recipient will be administered immunosuppressive drugs.

There is some literature on the effect of sex on the outcomes. I have included two hints here.

from: http://www.nature.com/bmt/journal/v35/n6/full/1704861a.html

The impact of the donor gender on outcome in HLA-identical sibling donor hematopoietic stem cell transplantation for multiple myeloma was studied in a retrospective registry study of 1312 patients (476 male to male (M → M); 334 female to male (F → M); 258 male to female (M → F); 244 female to female (F → F) reported to the European Group for Blood and Marrow Transplantation (EBMT). The best overall survival (OS) from the time of transplantation was found in F → F (median 41 months) with no significant difference between other groups (median 25 months in M → M, 18 months in F → M, 19 months in M → F) despite a significantly higher nonrelapse mortality in F → M. This was due to a significantly lower relapse rate (REL) in F → M compared to all other groups. Before 1994, OS was poorer in F → M than in M → M, which improved to similarity from 1994 onwards (median 29 months in M → M and 25 months in F → M). The reduced REL contributed to this improvement in F → M indicting a sex-specific graft vs myeloma effect. Therefore, a female donor is as good as a male one for male patients, while for female patients gender disparity is a negative factor for outcome.

from: https://www.broadinstitute.org/news/1386

"It's been clear for some time that bone marrow transplants involving a female donor and a male patient pose a higher risk of GVHD," said Bradner. "This ‘sex mismatch' arises from genes that are carried on the male-specific Y chromosome and are therefore present in males but not in females..."


Does the pyloric sphincter contract after ingesting only liquid?

NO IT DOESNT CONTRACT AFTER INGESTING LIQUID

1)The pyloric sphincter always remain  tonically contracted even in an empty stomach.However this tone of the pyloric sphincter is insufficient to prevent the passage of liquids to the duodenum.Thus almost all the liquid intaken in an empty stomach passes immediately to the small intestine.

2)Filling of the stomach triggers an enteric reflex that increases the tonical contraction of the pyloric sphincter.When fluids are taken then,their rate of passage to the duodenum is considerably reduced.(Although little is slowly absorbed into blood from the stomach).

REFERENCE:TEXTBOOK OF MEDICAL PHYSIOLOGY(GUYTON AND HALL)

3)As the small intestine is the seat of absorption,delaying passage to it delays large amount of alcohol absorption into blood.This not only delays its effect in the body but also fascilitates the persons capability to intake more alcohol.(This varies considerably in different persons but the central physiology is this)

REFERENCE:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1705129/


Preferred criteria for new bee colony location

According to Thomas Seeley, in his book, Honeybee Democracy, he gives the following as important criteria for honeybees when selecting a nest site when a bee colony moves to swarm:

Larger volume (the minimum nesting capacity was found to be around 14 liters with more preference to nests with a capacity of approximately 30 to less than 100 liters)
Relatively small entrance (10 to 30 centimeters squared)
Nest with the entrance located near the floor of a tree cavity
Direction of the nest entrance (south facing for thermoregulation during the winter)
Nest height (preference given to higher nests for colony defense)
Remnants of previous honeycombs (saves work and energy in building the nest structure)

Interestingly enough, bees did not necessarily display a preference for the shape of the entrance, the shape of the nest, the draftiness or dryness of the nest cavity (they are able to plug and waterproof nests).

Flower/nectar/food availability is not necessarily a direct factor as this changes quite frequently throughout the seasons and honeybees are not able to leave their honey stores (which are necessary to sustain the colony throughout the winter) or take them with them every time the colony has trouble finding food. Honeybees have a complex and efficient system for optimized location and sharing of food sources, therefore distance is not as large a factor.


When designing rtPCR primers always check the extensive and well validated  taqman library for the ABI system, the primers for the region you want are already well characterized:

http://www.lifetechnologies.com/order/genome-database/details/gene-expression/Hs01072897_m1#more-information-section


Which comes first, PCR or Gel electrophoresis?

PCR comes first. If PCR works right, then a specific product will be amplified. But you cannot see it in the little plastic Eppendorf PCR tube. That is what the electrophoresis is for. After you run PCR, you run the products on an agarose gel to visualize it (with the help of some flourescent dye). The agarose gel is just to see if the PCR worked.


What is the relationship between migraines and histamine?

Yes, this is true.
Histamine is thought to induce the enzyme Nitric Oxide (NO) Synthase.  NO is then available to act locally on the vasculature as a vasodilator.
NO binds to guanylyl cyclase in vascular smooth muscle cells, which leads to the production of cyclic GMP, which in turn forms phosphorylated protein kinase G. PKG phosphorylates Ca2+ channels, slowing the influx of calcium into the cell, which leads to smooth muscle relaxation, and vasodilation, which leads to migraine.
The only silver lining is that there is a check in place: with the binding of histamine to H3 receptors on c-fibers in the central nervous system, feedback inhibition prevents the further release of histamine from these sites.
References:

Akerman S, Williamson DJ, Kaube H, Goadsby PJ. (2002).  The role of histamine in dural vessel dilation.  Brain Res. 956(1):96-102.
Gupta, S., Nahas, S.J.,Peterlin, B.L. (2011) Chemical Mediators of Migraine:
Preclinical and Clinical Observations.  Headache: The Journal of Head and Face Pain, 51(6): 1029–1045.


Genetic information is the heritable information used by organisms to guide their self-assembly. It's why traits can persist across generations. DNA is, by far, the primary material used (by life) to encode genetic information, but it's not the only one. RNA is a pretty common alternative to DNA.

If we're looking to Wikipedia, this is actually referred to (in passing) on many pages about genetics. They usually link to the page on the best known edge case, RNA viruses:

  An RNA virus is a virus that has RNA (ribonucleic acid) as its genetic material. This nucleic acid is usually single-stranded RNA (ssRNA) but may be double-stranded RNA (dsRNA). Notable human diseases caused by RNA viruses include Ebola hemorrhoragic fever, SARS, influenza, hepatitis C, West Nile fever, polio, and measles.

While viruses fall into a weird middle ground between life and inanimacy, they still all need genes, and many of them use RNA for that. Side note: retroviruses get their name from the fact that they use reverse transcription to synthesize DNA from an RNA template.


Anomaly in growth of fungus in Potato dextrose broth.. turbidity is not seen in one flask

Several explanations are conceivable. Knowing what type of fungus you are working with and how exactly you proceeded to inoculate the cultures could help narrowing down the possibilities.

Here are some possible explanations:

Since you inoculated six liquid cultures from the same stock culture, the process might have been too long. Let me explain. Most fungi are strictly aerobes and do not tolerate well even short lack of oxygen. So, as I can guess, while you were inoculating the dextrose broths one after the other, the stock culture just remained unaerated on your bench. Since it can take a few tens of minutes to prepare everything and to proceed to the inoculations, it is possible that while you were doing so, the physiological state of the fungi just kept deteriorating, to such a point that one of the last inoculations did not contain enough viable cells to initiate a growth in the broth.
You might have forgotten to shake the stock culture just before taking the sample used in order to inoculate the broth. So it is possible that all the biomass in the stock culture was sedimented and you just inoculated your broth with the supernatent.
Also, a classic mistake is to mix up some of your broths. You think that you have inoculated all six broths with the stock culture, but maybe you unintentionally skiped one, or maybe you inoculated the same broth twice.


The major reason for this is because H20 can cause hydrogen bonding. Hydrogen bonding is what allows for plants to transport "this electron source" from their roots through their stems an further.

The stronger polarity of H20 also allows for stronger interactions. Such as ionic interactions (not fully bound but 2 polar atoms interacting). This kind of ionic interaction also allows for other types of material interactions such as cohesion and adhesion.

Overall, aside from the discussion of abundance as mentioned above (which is a very good point), it also allowed the plants to grow in directions that were more advantageous (darwinian) for their survival.


Conserved acetylation sites in a given protein

You can use the NCBI subpage HomoloGene

Halfway down page on left you can choose to show Multiple Alignment as seen in this screenshot.

I think you will then see what you are looking for as in this screenshot:


ATP utilized in Glycolysis vs. Gluconeogenesis

This energy is not lost, it is dissipated as heat.

And this must happen because of thermodynamics -- the direction of the reaction is simply determined by the difference of energy between substrates and products, and it must be positive for the reaction to happen spontaneously.


If post transcriptional modification happens , how can a gene code for amino acids in a particular order?

"then shouldn't the protein produced be different every time? Shouldn't the order of amino acids be different? And if it is, doesn't that mean that the protein produced is different?"

It is not different every single time, but it is different depending on what kind of post transcriptional modification takes place. The proteome is larger than the genome thanks to this, genes can code for many different proteins thanks to post transcriptional and post translational modification as well.

So as I understand it, gene segment = same order of nucleotides = same primary mrna

post transcriptional modification to primary mrna = different mature mrna = different order of amino acids = different polypeptide chain (then different protein later on)

Hope this helps


Genomic DNA resuspension after ethanol precipitation

Just a thought, have you tried eluting the DNA in Molecular Grade Water instead of TE?

For DNA which are supposed to be used in downstream applications like sequencing or transformation, elution with Water instead of TE buffer is frequently done.
I agree longer genomic DNA can be sticky upon elution, but if by chance the DNA is not entirely dissolved when you add the eluant (you see some very small clumps of flakes instead of a homogeneous clear solution) , that may be because of the presence of low amounts of alcohol (organic solvent). That's why it is recommended that after aspirating the alcohol, you should leave the tube opened for ~10 minutes for the trace amounts of alcohol to dry out before you add the eluant.

Sorry if you have done these things already, just wanted to be sure.

Hope this helps!


Why are there exactly four nucleobases in DNA?

A now deleted answer put this down to an argument based on amino-acid coding in codons but, as pointed out by Konrad Rudolph in a comment, arguments based on codons cannot be correct because the 4-base system likely pre-dates the evolution of protein translation.

So why four?

I suggest that it comes from a combination of factors which make it a 'just right' fit for RNA-based replicators: more would be bad, and less would also be bad. The four bases are able to copy with high reliability because two features combine to exclude mis-pairings: there are two size classes - meaning any purine-purine or pyrimidine-pyrimidine pairing results in incorrect separation between the strands, excluding A-G and C-U bonds; and there are two classes based on number of OH-bonds - which limits the potential for A-C and G-U bonds. More bases must, inevitably, weaken the strength of these exclusionary approaches and increase the number of mispairings. RNA world replicators will have lacked the sophisticated repair and error checking mechanisms of modern lifeforms so this increase in mispairings would likely not be corrected.

Of course, a two base system would be even more capable of reducing errors. I suggest that the advantage of the four base system is that it allows for much more complex 3-dimensional structure to form in RNA and thus enabled a broader range of catalytic capabilities. I've only considered even-numbers because only even numbered systems could use the Watson-Crick style of base pairing.

I'd also suggesting reading Eörs Szathmáry's 2003 paper on this very question.

Addendum

A group in California has just published a paper in which they successfully added a third base pair stably into DNA. I think this could shed some light on why four - you can read about it here or get the full paper here (Nature, so pay walled).


Your plant looks like this one: https://es.wikipedia.org/wiki/Euphorbia_heteropoda. It could be this species or a close relative. I found it in the "Monadenium" section of http://succulent-plant.com/families/euphorbiaceae.html, so the exact species likely belongs to this (former ?) genus.

It seems difficult to find it on other versions of Wikipedia, which makes me think that Euphorbia heteropoda might not be its valid scientific name.

The leaf will likely fall, leaving a scar as can be seen on the older parts of the plant.

From the photos illustrating the Wikipedia article, it seems it can have more than one leaf at a same time.


The "truce of the watering hole" -- is it completely discredited?

Cleaning stations offer a pretty strong individual incentive not to attack, those that attack do not get cleaned and thus get riddled with parasites. Watering holes are just the opposite there is no advantage to not attacking and in fact a decent advantage for attacking, (a meal) many predators hang around watering holes just because the draw prey.

To put it another way the genes from lion A say hunt things at the watering hole, the genes from lion B say don't, Lion A is going to have more meals and thus more offspring than lion B therefore the genes to hunt at the waterhole will spread. Lion B gains no benefit from not hunting at watering holes that can offset the very large and immediate advantage lion A gets. This is a good general test to why group selection generally doesn't work, even if all lions were type B as soon as lion A occurs from a mutation it has a huge advantage and drives out lion B's genes.

There is quite a lot of evidence that predators often concentrate around watering holes, heck this is how crocodiles make a living. The idea that lions do not is an out dated and stems from early observations done only during the day (when lions are mostly inactive yet close to watering holes to hunt at night), spread by fiction writers and reinforced by advertising and poorly researched articles.

https://www.nrcresearchpress.com/doi/abs/10.1139/z77-235#.XkxeG2hKhPZ

https://academic.oup.com/beheco/article/23/5/970/232520

The Serengeti Lion: A Study of Predator-Prey Relations
By George B. Schaller

Seasonal Diet and Prey Preference of the African Lion in a Waterhole-Driven Semi-Arid Savanna


Is this sentence about RER correct on Wikipedia?

As stated in a comment, your understanding of protein translation in eukaryotes is not accurate. In order to provide a concrete reference that isn't wikipedia, I'll quote here from Biochemistry (2nd ed) by Voet and Voet (1995 / John Wiley & Sons) pg. 307:

  Cytologists have long noted two classes of eukaryotic ribosomes, those free in the cytosol, and those bound to the ER so as to form the rough endoplasmic reticulum (RER ...) Both classes of ribosomes are nonetheless structurally identical; they differ only in the nature of the polypeptide they are synthesizing. Free ribosomes synthesize mostly soluble and mitochondrial proteins, wheras membrane-bound ribosomes manufacture transmembrane proteins and proteins destined for secretion, operation within the ER, or incorporation into lysosomes ... These latter proteins initially appear in the RER

Pretty succinct and thorough description.

The wikipedia text you quoted is a bit shallow (on its own) and somewhat incomplete, but essentially correct. The RER isn't solely associated with synthesis of proteins destined for secretion, but this is one of the classes of proteins synthesized in association with the RER. It would be more accurate to say that proteins destined for transmembrane insertion, secretion, or certain other kind of 'special handling' are synthesized in association with the RER rather than free in the cytosol.

The details of how, for example, these different classes are targeted to the RER are fascinating but somewhat beyond the scope of the question. Well explained in the referenced text, though, if you're interested.


Confused about the calculation of BLOSUM matrix

Ok I'll try to go through it myself and see what happens.

First, we get the pair counts: $$ c_{ij}=\begin{cases} \displaystyle\binom{n_i}{2} & i=j\\ n_i n_j & i\ne j \end{cases} \;\;\;\;\;\implies\;\;\;\;\; c_{11}=1, c_{12}=2, c_{22}=0 $$ Clearly, the normalizer is just $T=\sum_{i\geq j} c_{ij}=3$ and $c_{ij}\equiv c_{ij}^{(1)}$ since there's only one column. Then our pair distribution is: $$ q_{ij} = \frac{c_{ij}}{T} \;\;\;\;\;\implies\;\;\;\;\; q_{11}=\frac{1}{3},\;q_{12}=\frac{2}{3},\; q_{22}= 0  $$
Hence, the occurrence probability per residue: $$ p_i = q_{ii} + \sum_{i\ne j} \frac{q_{ij}}{2} \;\;\;\;\;\implies\;\;\;\;\; p_1 = \frac{2}{3},\;p_2=\frac{1}{3} $$
and the expected pair frequency:
$$ e_{ij} = \begin{cases} p_i^2 & i=j\\ 2p_ip_j & i\ne j \end{cases}\;\;\;\;\;\implies\;\;\;\;\; e_{11}=e_{12}=\frac{4}{9},\; e_{22}=\frac{1}{9} $$
Now we can finally compute the odds ratios:
$$ r_{ij} = \frac{q_{ij}}{e_{ij}} \;\;\;\;\;\implies\;\;\;\;\; r_{11}=\frac{3}{4},\; r_{12}=\frac{3}{2}, r_{22}=0 $$
Computing the log-odds $s_{ij} = \log_2( r_{ij} )$ gives the same values as you get.

So why is $r_{11} > r_{12}$? Well, notice they have the same normalizer, i.e. $e_{11}=e_{12}$. So the difference comes from the fact that $ q_{11} > q_{12} $, the empirical pair distribution. Essentially, because of the way we computed $q_{ij}$, we consider there to be only one pair QQ but two pairs of QS.
I would also note that sometimes results are a little unintuitive for very small samples (data sparsity throws off the statistics essentially).


Is the human collarbone supposed to break?

This looks like a misinterpretation. Because collarbone is the only horizontal long bone of the human body [1], it is the first to fracture when falling on the shoulder.

Its fracture can affect many structures:

  The muscles involved in clavicle fractures include the deltoid, trapezius, subclavius, sternocleidomastoid, sternohyoid and pectoralis major muscles. The ligaments involved include the Conoid ligament and Trapezoid ligament [1].

It is indeed a shock absorber, but for the upper torso (some way or another any bone can be considered a shock absorber):

  The clavicle also serves as something of a "shock-absorber" for the upper torso. Physical contact from the side will be partially absorbed by the clavicle. Because of this function, the clavicle is a very commonly broken bone [2].

The fracture can lead to severe injuries:

  Displaced or comminuted clavicle fractures are associated with complications such as subclavian vessels injury, hemopneumothorax, brachial plexus paresis [...] [3]

References:

Wikipedia contributors, "Clavicle fracture," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Clavicle_fracture&oldid=615723256 (accessed July 30, 2014).
Erich Rosenberger M.D. Anatomy And Physiology (2009). Available from http://www.sciences360.com/index.php/anatomy-physiology-299-12859/ (accessed 30.07.2014)
George Mouzopoulos, Emmanuil Morakis, Michalis Stamatakos, Mathaios Tzurbakis. Complications Associated With Clavicular Fracture. Orthopaedic Nursing, October 2009, Volume 28, Number 5, Pages 217 - 224 - See more at: http://www.nursingcenter.com/lnc/cearticle?tid=938803#sthash.F09wonvJ.dpuf


Can someone identify this Brazilian bird?

These look very similar to the Guira cuckoo (Guira guira) which are found in this part of Brazil.

Source: https://en.wikipedia.org/wiki/Guira_cuckoo