What happens to colloidal particles in a liquid medium? And how to stabilize it?

"Colloidal particles: What are colloidal systems, give an example,--"

  Milk, bear foam, paste, blood, ---

"what happens to colloidal particles in a liquid medium."

  I understand the q as solid in liquid so a gel. Examples about gel are "agar, gelatin, jelly and opal" according to my lecture slides. The electrostatic forces are in some sort of middle phase: not enough to repulse into liquid form but not strong enough to form liquid either.

"How to stabilize colloidal systems in a liquid medium."

  Wikipedia about stability (here)

    "The stability of a colloidal system is the capability of the system
    to remain as it is. Stability is hindered by aggregation and by
    sedimentation phenomena, that determine phase separation."

  Now different things to consider are:

  Electrostatic stabilization

    "In a stable colloid, mass of a dispersed phase is so low that its buoyancy or kinetic energy is too weak to overcome the electrostatic
    repulsion between charged layers of the dispersing phase."

  steric stabilization

    "particles in polymers which prevents the particle to get close in the range of attractive forces."


Why would there be a spike in coverage within a gene in RNA seq data?

Without knowing how your libraries have been prepared and sequenced it is hard to tell if that is due to a technical or biological source.

However, there are a few bias sources in RNA-seq (which aren't an issue in DNA-seq)

One of them is that if you used a "random-hexamer" protocol, they're known to not be so random after all. See: Hansen KD, Brenner SE, Dudoit S. Biases in Illumina transcriptome sequencing caused by random hexamer priming. Nucleic Acids Res. 2010;38: e131.

You might also have a contamination from other species that would present a sequence identity for that part more specifically.


If birds are dinosaurs, then are mammals reptiles?

Reptile is not a clade - it is a paraphyletic group because it does not contain all descendants (i.e. birds) of a common ancestor. Humans are amniotes like birds and reptiles but while birds and reptiles are sauropsids, mammals are synapsids. Humans are not amphibians either because amphibia is another paraphyletic group which is distinct from amniotes. Possibly some amphibians and amniotes share a common ancestor. Amphibians, sauropsids and synapsids can be grouped together under tetrapoda. So both humans and frogs are tetrapods but humans are not amphibians.

However, birds are dinosaurs and belong to a very specific sub-clade of dinosaurs called theropods. Both dinosauria and theropoda are monophyletic groups - i.e. they contain all the descendants of a common ancestor.

Extending this to bacteria. Yes you would group all living things (eukaryotes and prokaryotes) and can call them cellular living organisms.
However, animals (or any other eukaryotes) are not bacteria (they have diverged a lot). Moreover, extant bacteria are not precursors for all life. The precursor is called Last Universal Common Ancestor but we don't know much about it (at the moment it is a hypothetical organism). Eukaryotic evolution itself is a big mystery. So it would be  preposterous to call all lifeforms as bacteria.


It is confusing.  The septum pellucidium is a thin membrane separating the left and right lateral ventricles.  It contains white matter (nerve fibers), blood vessels and a few neurons.  It has traditionally been thought of as just a separating membrane, but the fibers running through it connect to the hippocampus and hypothalamus and so it is probably a relay to those structures.
Lateral to the septum pellucidium are the septal nuclei. The septal nuclei are NOT considered part of the septum pellucidium (or vice versa).  The septal nuclei are traditionally divided into two major subregions, the medial and lateral septal nuclei.  As you might have guessed, the medial nuclei are immediately adjacent to the septum pellucidium.   As the septum pellucidium is quite thin, the right and left medial nuclei appear to compose a single midline nucleus with the septum pellucidium running through it. The lateral nuclei are the ones a bit further out and it is these that are called the lateral septum. The septal nuclei may be further divided into caudal and ventral regions.  Many neuroanatomists group the most posterior parts of the septal nuclei into a third group, the posterior septal nuclei distinct from the lateral and medial divisions.
This is part of the problem.  Structures in the brain were named based of where they were and what they looked like since their functions were unknown. For example the hippocampus was given this name because it looked like the tail of a seahorse (genus Hippocampus), and the locus ceruleus ('blue place') looks blue. As we have learned more, some neuroanatomists have divided regions into subregions or sometimes lumped regions together based on their models of the proposed physiologic functions or neurochemistry of those regions. The subcortical 'limbic' nuclei, including the septal nuclei are among those most subject to these changing definitions,.  And as you might guess, different neuroscientists often disagree about these divisions.  Being human, they sometimes behave as though their definitions are THE definitions, or gloss over differences between sometimes unclear definitions.  Ideally, people splitting nuclei into proposed subregions try to propose clear definitions, but this is not always the case and these proposed definitions may not be accepted or used.  This can make it difficult for experts to know exactly what regions are being discussed, let alone people not long immersed in the field.  Over time however, fields tend to come to a consensus on terminology though for many brain regions this consensus remains elusive.  I hope this discussion makes the topic of the lateral septum a little more comprehensible, if only by validating your sense that the topic is confusing.
Here is a readable overview about the septal nuclei and septum pellucidium:https://www.neuroscientificallychallenged.com/blog/know-your-brain-septum
Check out the first reference here to discussing the neurochemistry of the medial septal nuclei from a chapter by Risold in the Rat Nervous system https://www.sciencedirect.com/topics/neuroscience/medial-septal-nucleus
In contrast look at the introduction of the following paper regarding the lateral septal nuclei:
https://bio.biologists.org/content/8/7/bio043554
"Whole-brain mapping of projection from mouse lateral septal nucleus"
And if you have access, you may be interested in
https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.13746
"Differential and complementary roles of medial and lateral septum in the orchestration of limbic oscillations and signal integration"
And here is a paper that describes development of the posterior nuclei as being different from that of the lateral and medial nuclei
https://www.nature.com/articles/s41598-018-30020-9


I can suggest three books, none of them cover all those aspects, though:

1) The Foundations of Ethology, Konrad Lorenz. The best introduction I know for the field of ethology. Lorenz is called by some "the father of ethology".

2) Sociobiology: The New Synthesis, Edward Wilson. The deepest study of animal societies I know of.

3) Evolutionary Ecology, Eric Pianka. If my memory is right, it says something about the Navigation and Biological Rythms part.


Does human eye lens have a magnification of its own?

The magnification by the lens of the eye is well understood.  This document, written by Dr. Glenn Chapman at Simon Frasier University in British Columbia, Canada, lays out some of the technical details.  The image below is taken from that document. I modified it slightly by enlarging the $s$ and $s'$ variables because they are important for this answer.

For a simple lens like that in our eyes, magnification, $m$, is calculated as

$$m= \frac{s'}{s}$$

where $s'$ is the distance between the lens and the retina at the back of the eye, and $s$ is the distance between the object and the lens. For the human eye, the distance $s'$ is about 24 mm, or just a bit under 1 inch.  For an object to have exactly 1:1 size ratio (no magnification or reduction), it would have to be exactly that same distance from the lens. That is, the object would have to be about 24 mm in front of our eye. The problem is that, unless you are myopic (nearsighted), you cannot focus on objects closer than about 25 cm (about 10 inches)

Most objects are much farther away from the lens than 24 mm. That means $s$ is a much larger value than $s'$, making $m$ a fraction less than 1. A value less than 1 means that our lens is not magnifying the object but instead is reducing or demagnifying the object.

As a simple experiment, hold your finger upright in front of your eyes at arms length.  Bring your finger closer and closer until you feel your eye lashes. Your finger looks smallest when it is farthest away from your eye. As you bring it closer ($s$ is getting smaller) your finger appears larger and larger. When your finger gets to about 24 mm, then $m=1$. When your finger touches your eye lashes, the distance is less than 24 mm, and the finger is magnified to larger than actual size ($s > s'$ and $m > 1$).

This also explains why distant objects appear smaller than closer objects. If you see a stop sign at 500 m and a stop sign at 100 m, the closer sign looks larger than the more distant sign.  But which is the actual size? Neither, because the lens changes the apparent size. The way to see the actual size is to stand with your eye about 24 mm away from the sign. Then, magnification will be exactly 1:1 and you'll know the true size of the sign. You just won't be able to focus on it.


What would be “Sternum-Intermediate” distance?

The article states:

  Markers (blue stickers, approximately 1 cm in diameter) were attached
  to a point approximating the suprasternal notch and an intermediate
  position on the dorsal aspect of the left breast. The position of
  these markers and the two nipples of the model were extracted from the
  point cloud scan of the breast model through manual digitising using
  Meshlab...Three straight line distances were analysed (1. internipple,
  2. sternum-to-right nipple and 3. sternum-to-intermediate marker).

One can infer that the sternum-intermediate distance is from the sternum to the intermediate marker on the dorsal aspect of the left breast. It is not, I believe, a widely measured anatomical distance, rather one 'invented' for the purposes of the study.


Why does hair know when it needs to stop to grow

That's an awesome question! Let me help you rephrase, as I don't have a direct answer; why does hair stop growing at certain lengths, and differentially at various locations on the body?

There are three stages to hair growth:

Anagen phase- growth
Catagen phase- transition
Telogen phase- rest
(then falls out!)

You're asking why and how the anagen phase stops, or more concisely, what processes cause anagen phase to cease and proceed to transition to a degenerated rest.

The indirect answer I have for you is this: there doesn't exist a definitive mechanism for how the the telogen phase is induced- that is to say that the process by which the hair-producing follicle "turns off" it's cycle to come to a halt has not yet been fully elucidated in the literature and remains a discovery to be made.

I hope I've helped you understand your targeted question


Why do fully grown organisms need protein intake?

Protein is polymerized amino acids.

Humans do not require protein intake, but certain essential amino acids are required.  These essential amino acids are usually obtained through protein intake, but intake of the free amino acids themselves would suffice.

Amino acids, in free or protein form, are lost from the body due to urination (see Diverse characteristics of the urinary excretion of amino acids in humans and the use of amino acid supplementation to reduce fatigue and sub-health in adults), perspiration, menstruation, ejaculation, tear drops (see Amino Acid profiles in human tear fluids ), skin exfoliation, hair and nail growth, nasal mucus (see Identification of human nasal mucous proteins using proteomics), and vaginal mucus (see Proteins of Cervical Mucus).  Additional loses can occur due to additional bleeding, lactation, child birth, spitting (and other activities causing loss of saliva), and coughing up mucus.

Synthesis of new proteins from amino acids is constantly required by the body (see NUTRITION AND PROTEIN TURNOVER IN MAN). Though there are chemical pathways to reuse amino acids, it is necessary for the concentration of each amino acid to be non-zero, and therefore some fraction is necessarily lost through excretion.

Beyond just direct excretion of amino acids and proteins, there is excretion of nitrogen-containing metabolites such as urea, uric acid, creatinine, ammonium salts and bilirubin.


The plant looks like something in the genus Bougainvillea. These plants are native to South America, but found as introduced ornamentals in many places.

The colored petal-like organs are bracts (see the Wikipedia link above). The entire structure is an inflorescence with the flower buds growing out from the surface of the colored bracts — you should eventually see those flowers open and you could then dissect them confirm that the usual flower structures are present.

This is a well labeled diagram:


What is the name of this big tree with look of banyan branches?


Which came first: The Chicken or the Egg?

Most theories about origin of life say that unicellular organisms were first and multicellularity (like chicken) evolved much later, so in that meaning egg (single cell)* was first. Also, almost all chicken ancestors lay eggs (primitive birds, non-avian reptiles, amphibians, fishes and so on...) so eggs existed much earlier than chickens.

*in the meaning of zygote. The development of chicken embryo starts in hen's oviducts, so it's not a single cell at the moment when hen lays it (Gilbert, 2000).


How long does it take for the Opioids listed in the Description to induce Analgesia when Administered via IV?

These are 'peak' values when administered via IV, with the exception of oxycodone. There will be some variation person to person depending on their opioid tolerance and any concomitantly administered medications.

Buprenorphine: 60m

Butorphanol: 5m

Fentanyl: 5m

Hydromorphone: 30-90m

Methadone: 1-2h

Morphine: 20m

Oxycodone: Not administered intravenously

Pentazocine: 15m

Sufentanil: 3m

Tramadol: 2h


Interplay of neuritic and synaptic growth

Short answer
Both short and long-distance synapse formation can occur.

Background
Short-distance connections can be made between adjacent cells (Van den Pol et al, 1988). Your 'common ancestor part' is a bit obscure to me. In the end, every cell is born out of a single one :)

Long-distance connections can also be made. For example after neuroneogenesis either during development or even in the adult brain, whole neurons can migrate from their origin to a new part (Kaneko et al., 2017), or axons can grow to find a new target distally, for example after neural injury (Purves et al., 2001).

References
- Kaneko et al., J Neurochem (2017); 141(6): 835-47
- Purves et al. (eds), Neuroscience (2001), 2nd ed. Sunderland (MA): Sinauer Associates
- Van den Pol et al., J Comp Neurol (1998); 399(4): 541-60


Can a macrophage differentiate back into a monocyte?

No, macrophages can not turn back into monocytes, usually once a monocyte travels around the bloodstream for 1-3 days, it then leaves the bloodstream and travel to a tissue where it will differentiate to a macrophage or dendritic cell. It undergoes a conformational change, this usually happens during inflammation as the macrophages travel over a chemical gradient, macrophages can still enter the bloodstream, however, they won't re-differentiate to a monocyte. So to answer your question directly, macrophages don't stay in the same tissue forever as their life span is pretty long(1-2 months) so most likely an inflammation will occur and force the macrophages to diffuse across the chemical gradient, but they usually patrol around the tissue area where they differentiated.

source: http://www.histology.leeds.ac.uk/blood/blood_wbc.php


The spleen is not the only organ which removes "old" erythrocytes, this happens as well in the liver and the lymph nodes. The whole process is termed Eryptosis, the Apoptosis of Erythrocytes. During the aging of erythrocytes sialic acid on their outer membrane surface is removed. This leads to the recognition by macrophages and phagocytosis of this cells by macrophages which are located in liver and spleen. For more information see this article: "Physiology and Pathophysiology of Eryptosis"

Polycythemia is the state when you have an elevated number of red blood cells, characterized by an increased Hematokrit level. This is caused by the over-production of red blood cells, which can be caused by an overproduction of hematopietic cells in the bone marrow (so called myeloproliferative syndrome, which are basically cancers), the exposure to permanently low oxygen-levels (this is what athletes exploit when the do training at high altitudes) or malignancies (usually lymphoma). It is also possible due to the mis-use of Erythropoietin (EPO) which induces the production of red blood cells. Another possibility for having too much red blood cells is the over-transfusion during a blood transfusion. For further information have a look into the Wikipedia. The article there is pretty complete and contains a number of references.


why has evolution favored sexual reproduction using two mates over sexual reproduction using three mates?

Let's break it down: The chance that two individuals of distinct gender meet at one location in space time is tremendously higher than for three. We could do some math here (assuming biased random walks of points in three classes on a 2d surface etc.) but that is not necessary I guess. As far as we know sexual reproduction evolved long before complex sensory systems and/or brains (namely 1250 million years versus 500 million years) that allow for active search behavior beyond chemotaxis. Therefore a random walk would be a reasonable first approximation for organism behavior to simulate the situation back then. Having two genders seemed to have been a good trade-off between the chance to meet and advantages in terms of mixing the genetic information. Note that this answer might not be valid for organisms being able to reproduce in both ways, sexual as well as asexual.


History of ideas about the form of the genetic code

Before it was established that there was a triplet, non-overlapping, comma-less genetic code* for what at that time were thought to be only 20† amino acids, there was uncetainty about:

The codon size (must be more than 2, but...)
Whether the codons overlapped (e.g. in a stretch ABCDEFG with triplet codons, whether ABC, BCD, CDE etc were the codons)
Whether there were ‘commas’ as demarcation betwen different codons

These and other problems were disscussed by Crick et al. in Nature (1961) 192 1227–1232. There is an introductory gloss of this on Scitable, with a link to free-view of the original paper.

Footnotes

*We now know there are variants on the standard genetic code, but all the codes have the characteristics mentioned.

†In addition to the standard 20 amino acids stop codons can be subverted in certain circumstances to encode selenocysteine and, in some bacteria, pyrrolysine.


ATAB contains a quaternary amine and a terminal carbon-carbon double bond. The polyacrylamide reaction links acrylamide by their double bonds forming the polymer. The double bond on ATAB can be incorporated into the growing polymer chain, and the quaternary amine holds a positive charge, making a positively charged polymer.

The immobilines mentioned are probably just a weak acid or weak base group with a terminal double bond like ATAB or acrlyamide. They get trapped into the polymer and if you pour the gel with a pH gradient, they pick up charges according to the pH. I haven't found a good concrete immobiline example, I can't access that second article you linked.

I am away from my good computer and cannot make chemical structures right now.


At least 25% of the original liver seems to be the minimum for regrowth.

The initial regrowth is due to proliferation of hepatocytes: they exit G0 and enter mitosis. The ECM dissolves and is remodeled; the cholangiocytes and SECs also divide.

If you want to read more, you can visit the Google books link above, and the preview lets you read several pages on liver regeneration in rodents.  (If it doesn't work, try changing the URL to your current location: books.google.com is US, books.google.ca is Canada, etc.)


Balance is tricky and depends on a lot of things, including, to some degree, your sight. Balance is achieved and maintained by a complex set of sensorimotor control systems that include sensory input from vision (sight), proprioception (touch), and the vestibular system (motion, equilibrium, spatial orientation); integration of that sensory input; and motor output to the eye and body muscles. Your vision helps you see where your head and body are in relationship to the world around you and to sense motion between you and your environment.

Very simply put, to blindfold someone is to take out the contribution of vision to balance. So, if the other systems involved in balance are off even a bit, blindfolding someone will interfere with their ability to keep their balance, even on two legs, let alone one.

Here are those systems in more detail.

Proprioception. In your joints, muscles, tendons, skin, and other areas, you have proprioceptors, that tell your brain where yoor aody parts (arms, legs, etc) are in relation to self in space. Because we live on a planet with  gravity, even if we are blindfolded, if we are standing correctly, our feet will sent our brain signals that will in turn allow the brain to judge our position in space with regard to gravity and we will keep our feet firmly planted on the ground in a way which will maintain us upright in a constantly regulated position (if we sense less pressure from the bottom of our right great toe, we will adjust by leaning forward and to the right a bit until out=r brain says, "ok, right there!" This happens from all the skin and joint proprioceptors responding at the same time. Notice that once vision is blocked, our bodies become relatively very still; we focus on our balance. We move tentatively.

As people age, they lose some of their propioceptive abilities. That's one of the reasons for falls in the elderly.

Inner ear. In our inner ear are the semi-circular canals, three on each side, which are oriented at ~90° to each other so we cover 3 dimensions. In these canals is fluid which sloshes about when we move our heads, change directions, bend over, etc. The fluid moving about is detected by fine hair-like projections on the sensory cells lining the canal called stereocilia - like a wave would be detected by your leg in shallow ocean water. These semicircular canals help us to remain oriented in space. Now, the semicircular canals are also attached to otolith organs - two chambers which are concerned with gravity. They have fine crystals in them - called otoconia - which move according to our head's position with relationship to "down", or gravity.

If we stand perfectly still (probably not possible without support), everything is read by the vestibular system (the semicircular canals and the otolithic organs) as normal, and we stay upright (there is a constant communication between our vestibular system and our brain). So, when blindfolded, we can stay upright even if we shake our heads, bend them forward or back, etc (within reason). As we age, things can degenerate in this vestibular system, which affects our balance, and results in more falls in the elderly. (Diseases in the young can also affect this.)

Vestibulo-ocular Reflex. A complicated system which reflexly coordinated input from your vestibular system and your vision in head movement. If someone suddenly turns your head, your eyes will move in the equal and opposite manner, that is, your eyes will stay focused on the object on which they were focused just before your head was moved. This system is what allows you to easily keep reading something while you shake your head from side to side (not the case if you move the print side to side).

When things start going wrong (in a very slow manner) with your vestibular or proprioception systems, your eyes can help compensate by orienting you to the horizon, etc., in a manner, correcting for some 'off' calculations in your vestibular system. Vision helps us to identify orientation with respect to gravity, determine direction and speed of movement, etc., to a much lesser degree than the other systems described but enough to have an impact. So, in people whose vision is failing, either their other systems have to be in really good working order (e.g. why young blind people aren't always falling over) or they have problems with falling.

The Human Balance System (easy)
Researchers find diminished balance in those with poor vision (easy)
Balance (easy)
Visual influences on balance
Baloh and Honrubia's Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Kevin Kerber, MD
Somatosensory Systems
Vestibular Occular Reflex


It looks like a dorsal view to me, like your book says.
It isn't a section at all, these are embryonic structures visible from the outside.
Maybe you are being misled by the orientation of the neuraxis differing among organisms? The head will develop at the anterior neuropore; the spine will develop down the middle. You are looking at what will be the back.
Here's another view from Gray's (downloaded from Wikipedia at https://en.wikipedia.org/wiki/Somite#/media/File:Gray20.png ):


Do species ever go extinct by becoming too successful?

yes, infectious bacteria are a good example, a highly destructive infection may often kill its host before it can spread the disease.  https://www.ncbi.nlm.nih.gov/books/NBK27114/


Negative feedback in the fructose metabolism in liver

The main reaction of fructose in liver is phosphorylation, catalyzed by ketohexokinase (UniProt P50053). In one paper with rats it was shown that fructose load can deplete the liver of nucleotide triphosphates (ATP, GTP) although ADP and GDP are inhibitors of the enzyme. This shows there is no effective regulation.

M. I. Phillips, D. R. Davies: The mechanism of guanosine triphosphate depletion in the liver after a fructose load. The role of fructokinase. In: The Biochemical journal. Vol 228, Nr 3, Jun 1985, p. 667–671, {{ISSN|0264-6021}}. PMID 2992452. PMC 1145036.


Did the first cell self-replicate or was it multiple first cells?

Good question. Simple answer here: we have absolutely no idea.

I would hazard a guess to say that the first proto-cell probably did not have the ability to replicate, so there must have been many proto-cells prior to the occurrence of the first true cell with the property to replicate itself with some degree of fidelity. Whether or not at some point cells existed that could be traced to two or more independent abiotic generations, that is unknown. The likelihood of this event is all we can talk about. I defer to biochemists working on this (still very open) problem, but I think it is honest to mention that they too have no idea, really. This is because, as we can surely appreciate, likelihood and outcome are two entirely different things. And unlikely events happen all the time. Each life form and individual is astonishingly unlikely, but historical contingency so happens to have brought us all here despite the odds.


This animal is moth larva. The images presented are blurry, but if there are no any dots on the larva my first suggestion is:

pantry/Indian meal moth larvae -

"They are a common grain-feeding pest found around the world, feeding on cereals and similar products."

(picture source)


The definition of carbohydrates as compounds containing $C$, $H$ and $O$ usually with the empirical formula ${C_m(H_2O)_n}$, is outdated.

More rigorous and a accurate definition would be Polyhydroxy Aldehydes and Ketones composed of Carbon, Hydrogen and Oxygen. Moreover, the nomenclature including Mono-, Di-, Oligo- and Poly- "Saccharide" is preferred over the now obsolete and too-general term "carbohydrate", since the etymological origin of the word "carbohydrate" is from the greek words Carbo- for carbon and hydor- for water which indicates that the carbohydrates are "hydrates" of carbon and have the empirical formula ${C_m(H_2O)_n}$, which is not always true. Instead "saccharide" is derived from the greek word for "sugar" and hence is much more accurate as it does not limit the definition to any empirical formula.

Apart from the polyhydroxy aldehyde or ketone characteristic of carbohydrate, they have a marked structural and functional variation from other biomolecules. This includes the absence of $S$ (as in proteins), $P$ and $N$ (as in proteins and nucleic acids), presence of Glycosidic bond (as compared to peptide bond in proteins, phosphodiester bond in nucleic acid, and ester linkages in fats or glycerides) and much greater structural uniformity as compared to other biomolecules.However, these characteristics are not absolute as is evident from the fact that several monosaccharide derivatives do contain $S$ or $N$ atoms. Actually, the entire group of amino-sugars (Hexosamines etc.) are usually classified under carbohydrates since they are primarily monosaccharide derivatives obtained through enzymatic amination.

These characteristics distinguish this class of compounds without having to assign a empirical formula to it.

ADDENDUM
Adding the clause compounds which can, on simple hydrolysis yield polyhydroxy aldehyde or ketones in the definition helps involve certain non-reducing sugars like Sucrose.


How exactly does symbolic language for apes work?

The best article I found was this one. In it it says among other things that:

Kanzi, an unusually intelligent Bonobo chimp trained at Georgia State
University, was remarkable in that he learned to use around 200
symbols on a portable electronic symbol board, a computer with buttons
in the shape of absolute arbitrary symbols rather than manual signs.
More interestingly, Kanzi learned how to use this board while watching
his foster mother, Matata, being taught by traditional reinforcement
methods. So Kanzi did learn how to use arbitrary symbols without being
taught, although he did observe direct reinforcement of each symbol
during the process and the symbols were taught one at the time.
The
evidence for the mastery of syntax is not so convincing. While
chimpanzees can learn to order their symbols to get what they want, it
is not clear that they have mastered syntax. The reason is that when
they initiate communication, even adult chimps often abandon the order
they have learned and phrases such as, "Fight mad Austin," a famous
utterance of Kanzi's friend Panbinisha. Here the order doesn't seem to
matter. Apparently Panbinisha was trying to express, "there was a
fight at Austin's and someone (Austin?) was mad". It is interesting
that even human children simply don't make such errors once language
acquisition begins, and certainly adult speakers would never utter
such strings. Notice it lacks any morphemes (-ing, at, I, she, -ed),
the hallmarks of grammar.

The trainer of Kanzi has published some materials but I do not know if they are available free online. You could probably send her an email and ask. The article goes on to state:

The maximum number of lexeme symbols (simple nouns, verbs, and
adjectives) is interesting, too. The brightest chimpanzees master
fewer than 200 of these symbols by adulthood. Human children know
about 50 by the time they are 18 months old, when they begin learning
nouns, verbs, and adjectives at the rate of about 5 per day. So the
maximum achievement in symbol acquisition among other primates is more
than matched by human children before the onset of language
acquisition. In fact, the type of phrases spoken by chimpanzees and
gorillas also resemble those spoken by children before they acquire
their first language: "give orange" or "give Bobby orange" (without
the pronoun me) are common expressions of children before the onset of
language learning around the age of two.
The results suggest that
while chimpanzees and gorillas are far more intelligent than anyone
had imagined during the first half of this century, they are not
capable of human language. Rather, they have a primitive version of
the semantic ability children use before that explosion of
language-learning around the age of two.

At least according to that article there is not much of a grammatical structure at all. The apes does not so much care about the order of the words either, even if the can learn a certain order, especially if they get something to eat if they do it right.


The exact numbers depend on the protein.
In my hands, I would say between the pAraBAD and a pLac-T5 you can expect some fold improvement and pAraBAD and a pT7 promoters you can expect about an order of magnitude… but there are two big caveats.
First, pET and other T7 driven plasmids do not work in K-12 strains (without the pTARA) so BL21 is generally used. BL21 is much better generally than K-12 strains (more primary metabolites cf. omics paper) for a lot of things including protein expression. The chaperone balance is difference, so you will get differences from that too —if you have used the TAKARA plasmid team you will have notice how quirky protein expression optimisation can be.
Second, if your protein has a cofactor you have a major problem. FeS clusters, PLP, heme or even O2 (for maturation of GFP, say) become rate limiting and overexpressing the protein can make it highly toxic and you might be in a bigger pickle than with a lower level promoter. In my thesis, I added pyridoxine to a pBAD expression, because it gave an improvement.

Footnote: If the expression levels are really bad, changing promoter might not be that great as the assumption of linearity might not hold.
If heterologous and not codon optimised, consider using pRARE.
If insoluble, consider using ethanol shock and the TAKARA chaperon plasmid team.
If oxygen sensitive, alas, doing expression and purification anaerobically.


Does Remdesivir cause bone marrow suppression?

From Off-Target In Vitro Profiling Demonstrates that Remdesivir Is a Highly Selective Antiviral Agent:

Overall, the cellular and biochemical assays demonstrated a low potential for RDV to elicit off-target toxicity, including mitochondria-specific toxicity, consistent with the reported clinical safety profile.

This isn't a very complete answer, but the wikipedia article doesn't go into detail or link references explaining the mechanism by which nucleoside analogues suppress bone marrow function. So I can't say if the assay results in my link rule out a suppression effect by remdesivir


Difference between genetic engineering and synthetic biology

My understanding is that synthetic biology is genetic engineering 2.0. The difference is in the approach. Whereas genetic engineering projects are usually ad hoc, synthetic biology aims to apply proper engineering principles such as standardisation, modularisation, and reusability. Synthetic biologists create and use libraries of standard parts that are characterised, so they can be easily reused in projects. A part could be a gene, a terminator, a promoter, etc.

Synthetic biology also has greater ambitions. The focus is on creating whole systems/circuits of genetic regulation. This means there is a need for computational modelling and understanding of how biological systems work. In this aspect synthetic biology is a sister of systems biology a bit like synthetic chemistry (engineering) is a sister of chemistry (science).

You could of course argue that it's just a marketing ploy to invent a new name for something that is just the next step in genetic engineering, but the differences in approach are quite large and a new name signifies it.

With regards to synthesised vs. PCRed DNA: It doesn't really matter which you use in synthetic biology. However, cheap synthesis is one of the technologies that enable easier synthetic biology. The idea for the future is that you will be able to synthesise whole plasmids and chromosomes instead of having to "cut and paste" DNA. When that happens physical parts repositories will be obsolete, but they will remain crucial in silico. Cheap synthesis is nice, but doesn't make or brake synthetic biology.


You could try DeVita, Hellman, and Rosenberg's Cancer: Principles & Practice of Oncology. It has detailed information on both biological and clinical aspects of cancer. Apparently, the publishers regularly release online updates to cover the latest developments in oncology.

Reference to the current edition:

DeVita VT, Rosenberg SA, Lawrence TS, editors. DeVita, Hellman, and Rosenberg's cancer: principles & practice of oncology. 11th Edition. Philadelphia: Wolters Kluwer; 2018. 2432 p.


Father with mutated mtDNA- why isn't his offspring at risk?

...would then be his offspring at risk? Why?

No. Generally speaking, fathers do not pass on their mtDNA (Mitochondrial DNA).

Why? Because the mitochondria present in oocytes (egg cell) is the mother's, as every oocyte directly inherits the mother's mitochondria when they are made in the reproductive organs. The mitochondria that the sperm from the father carry to the egg do not enter the egg cell or are destroyed in the process.

It's also worth mentioning that, in general, mtDNA does NOT reside in the nucleus of cells, but in the mitochondria itself. It is not condensed during cell division, it is not spliced during Meiosis II, and it does not undergo recombination with another cell's mtDNA. Instead, when a cell divides, each cell takes about half of the mitochondria present in the cell and maintains them. That way only the mitochondria present in the cell before division will be inherited by the daughter cells, and thus only the maternal mitochondria present in oocytes (egg cells) before sperm instigate cell division will be inherited by any offspring.


How is tolerance to an allergen developed?

The allergy shot in itself is a form of therapy called allergen immunotherapy (AIT). In it's essence, we're trying to get someone to develop immunologic tolerance to a given allergen such as pollen, okay! So how does it happen at the cellular level? (Assuming the treatment protocol is known)

Understanding The Mechanism Of Allergen Immunotherapy, as an article is kind of a broad overview. Thus there are phases to AIT that include early, intermediate and late phases. The process begins with a downregulation of mast cell and basophil activity, followed by induction of allergen specific Treg cells, a decrease in Th2 cells, and then a decrease in IgE production with an increase in IgG4/IgA.

Mechanistically, it doesn't look like it's well known how basophils and mast cells get regulated by AIT, but the theory is that the mechanism may resemble H2R (a histamine receptor) receptor activity during venom immunotherapy: H2R becomes highly upregulated after therapy start, and inhibits Fcε-R1 activation of mast cells and basophils, even in the presence of IgE (2, paywall on this one).

They provide an impressive table in Akdis & Akdis 2014 as to the role of immune cells in AIT:

So in the process of encountering the allergen, the immune system produces Treg cells as a result of dendritic cell antigen presentation. An inducible type of Treg called Tr1 is capable of abrogating the response of Th2 and Th1 cells through the secretion of TGF-ß and IL-10. They have a good table for this, too:

There's an effect in there due to TGF-ß exerting its effect on B cells that ends up inhibiting class switching to most other immunoglobulins except mucosal IgA. In conjunction with IL-4, IL-10 is capable of promoting the class switch of preceding B cells to IgG4. So the classes of Ig will largely become IgG4 and IgA in response to the allergen of interest. The B cells will also begin to produce their own IL-10, and in a way become a regulatory type of B cell, or Breg, that propagates the tolerogenic response.

And so the big conclusion: (1) the mast cells/basophils aren't as prone to causing anaphylaxis, (2) the effector cells specific for the allergen have actually shifted to populations of tolerogenic DCs, Tregs and Bregs, and (3) antibody production has shifted to IgG4/IgA from IgE. The net result is due to the repeated exposure to the allergen at some optimal concentration, but the key is they performed the treatment slow enough that the immune system had time to build up tolerance without going crazy. It's also likely that we don't know how long the system stays tolerant for after successful treatment.

It's much more complicated and if you can get past the paywall on source 2 there's really good, detailed info. I didn't want to go into a novel here, but let me know if you need clarification anywhere.


What is the best way to block cigarette smoke from the body?

You don't smell carbon monoxide in cigarette smoke. It's odorless. (And not exactly the part of cigarette smoke I would be worried about.)

You smell the other components of cigarette smoke. Which are not odorless.

Holding your breath and getting out of the smoke seems the way to go. Even better would be exhaling, then holding your breath until you are clear.[1]

Carbon monoxide, as well as other components of cigarette smoke like nicotine, are very good at getting into your blood stream quickly. Plus, when at rest, we inhale / exhale at only a fraction of our lung capacity. By (deeply) inhaling (your alternative course of action), you would just get more of the smoke into your lungs than you already have.

[1]: The trick with holding your breath is of course that, if you run out of breath while still in the middle of the smoke, you can't help but inhaling deeply...


Why does high pH result in the denaturation of DNA?

The pKas of (neutral) guanine and thymine are 9-10 (ref). At high pH (>~10), those bases will be deprotonated and exist as negatively charged conjugate bases. As the deprotonated species, part of the G/C and A/T hydrogen bonding networks are eliminated. In the figure below, green dotted lines represent the hydrogen bonds that explain the observed base pairing. Red dotted lines represent disrupted interactions.


What is the name of this plant? (found in a rock)

I have been looking into this for days, but this plant is difficult to identify without its flower. I reached out to a botanist at Dartmouth, who suggests that it is either one of two species-- a nasturtium (Tropaeoleum sp.) or a geranium (pelargonium). The leaves are what are called peltate, meaning shield-like with the stem attached directly underneath.

Source:

Botanist at Dartmouth
http://etc.usf.edu/clipart/48400/48426/48426_peltate_leaf.htm

On further research, specifically of peltate leaves, this plant looks more like Umbilicus rupestris, which is commonly found in southern Europe and grows in damp rock crevices!

Source:

http://en.wikipedia.org/wiki/Umbilicus_rupestris


Modern biology attempts to group organisms by clades, that is, into groups that contain all descendants of a particular organism and no others.  A clade may be associated with characteristics that most or all members of the clade possess, but those characteristics do not define the clade.  Previously it was common to describe biological groups by particular defining characteristics, but that has been largely abandoned because it often does not reflect true relationships.

"Plants" (or Plantae) is a term that can mean several different things, which are outlined in this Wikipedia table.  In short, it might be (approximately) the clade of "land plants", the clade of "green plants", which includes land plants and green algae, or the clade containing those plus the red algae and the glaucophyte algae.  That last clade, also known as the Archaeplastida, is thought to include all descendant species of the initial organism which initially established the symbiosis leading to chloroplasts (although not some organisms that acquired chloroplasts by secondary ingestion of archaeplastida).  It seems like you are most concerned with that third group.

Alectoria sarmentosa (witch's hair lichen) is not a plant by any of these definitions.  It is a lichen, which are symbioses of a fungi with a cyanobacterium or a green algae.  Green algae of course have chloroplasts.

Monotropa uniflora (Indian Pipe) is a member of the heather family and so is a plant by any of the above three definitions.  It does not have chlorophyll; my guess is that it likely has degenerate chloroplasts.

I think a separate question would be appropriate to inquire about the chloroplast remnants of non-photosynthesizing plants like Monotropa uniflora.


As Armatus notes, we don't know ALL human metabolites and the enzymes + metabolic reactions that produce them. Identifying small molecules is hard and metabolism is dynamic, it depends on what is being fed into the system.

The virtual metabolic human (VMH) is an attempt at compiling the information that we do know. You can read their paper here. The human build currently includes (and links together);

13 543 metabolic reactions
4138 metabolites
3695 genes (enzymes)

It also attempts to compile all known metabolic reactions that result from the gut microbiome, nutritional metabolic pathways and genetic diseases that alter metabolism. Everything is linked via stable identifiers which is a real challenge.

The human metabolic database (HMDB) is also very good. It contains more metabolites than the VMH as it includes many partially or poorly characterised metabolites. The HMDB is really useful if you are working to identify metabolites while the VMH focuses on how they connect to one another.


Alkaloid synthesis is energy consuming for plants and have complex metabolic pathway.

If their evolutionary history is not known with certainty, they have numerous uses and are often toxic to potential plant or animal aggressor.

Chocolate contain many alkaloids including caffeine and theobromine. But apparently do it with a different pathway and is the result of convergent evolution.

It is safe to assume these alkaloid protects cocoa plant in the same manner it protects coffee and that the benefits of such poisons allowed poisonous cocoa plant to become predominant.

However, alkaloids of chocolate are solely responsible for its bitter taste. (Cf. Wikipedia page "Alkaloids" for more info).
If bitterness is part of its flavour, we prefer its fats the numerous volatile compound gained during fermentations of the beans. According to this article published on academy.org :

  The distinctive chocolate flavor evolves throughout its production. Odorless, tasteless “precursors” form during fermentation, and these precursors react during roasting to form taste and aroma compounds.

Also many essential oils are poisonous to insects, fungi or bacteria. These properties are sometimes used by humans : for instance cinnamon oil is toxic to mosquito larvae


Is disease transmisson through milk consumption or meat consumption considered direct or indirect transmission route?

Direct transmission is through direct contact with the infected person with no intermediary or vector. The Ebola virus and AIDs virus are examples. Indirect would be malaria spread through mosquitos, plague via rats, etc. The common cold spread through droplets in the air could seem indirect, but because of the proximity required, the CDC website lists it under direct. The CDC will provide reliable information for a lot of questions regarding infectious disease.


What is the name of this spider I found in The Netherlands?

I believe you are looking at a spider mite of the genus Anystis or Tetranychus. Both of these have The Netherlands in their range.
Here is an info page on the two genuses, includes a map of observations and a gallery of photos that you can even filter to only view images from a certain range. You can also filter the gallery to group photos into species categories.
Anystis: https://inaturalist.ca/taxa/249515-Anystis
Tetranychus: https://inaturalist.ca/taxa/203334-Tetranychus


Is there such thing as a generic "metabolic type"?

That book was likely crap, but in short the answer is yes, probably there is a genetic basis in the metabolism, with human 'types' that could benefit from a personalized nutrition. The discipline studying these relationship is called nutrigenomics, and the main concept is similar to what is being told for personalized medicine. The bad news is that unfortunately this is not easy to identify, surely not from the form of your finger.


Geometric Interpretations of the DNA Double Helix

The standard text-book answer to this question is illustrated by the cover illustration of one edition of, well, the standard text book which I reproduce alongside an image taken from a teaching site of my own in which you can view several different aspects of the double-helix in 3D.

[Views of DNA looking ‘down’ the axis of the helix. On the book cover the bases are black filled shapes of purine and pyrimidine structures, in the image on the right the purines and pyrimidines are red and blue outlines, respectively, with the sugar–phosphate backbone shown in white.]
The regularity of the helix (constant curvature and torque) maximizes base stacking, which involves the π–π interactions of the purine and pyrimidine rings. This is important for maintaining the structure of the double-helix and hence facilitating its function. Base stacking is discussed in another question on Stack Exchange Biology, in that standard text, Berg et al. , and in a chemical article in Wikipedia.
Although concerning a single-stranded RNA rather than a double-stranded DNA, I take this opportunity to illustrate the biological significance of base stacking by considering the anti-codon loop of transfer-RNA. As is well-known (see e.g. this StackExchange Biology answer), there is frequently ‘wobble’ at the 5′ position of the anticodon loop, allowing certain non-standard base-pairs at the third (3′) position of the mRNA codon. As the image below shows, this can be partly attributed to the poorer base-stacking at this position in the anti-codon loop (G-34 in the illustration) compared to the other two positions, allowing greater flexibility.

[Anticodon loop of yeast phe-tRNA, created by the author from 1ehz.pdb]


How EGDS (endurance genetic distance score) is calculated?

In my opinion, there must be something wrong with the formula given in the paper. The rationale behind the conversion of $d$ into the range 0-100 is stated in the papera as follows:

  An EGDS9 of 100 represents an “optimal” endurance genetic profile,
  that is, all GS’s are 2. In contrast, an EGDS9 of 0 represents the
  “worst” possible profile for endurance genetic profile, that is, all
  GS’s are 0.

So what they are basically saying is that they want

$d_{max} = \sqrt{\sum_{i=1}^n(2-0)^2} = \sqrt{4n} = 2\sqrt{n} \Longrightarrow EDGS_n \stackrel{!}{=}
 0$

$d_{min} = \sqrt{\sum_{i=1}^n(2-2)^2} = \sqrt{0} = 0 \Longrightarrow EGDS_n \stackrel{!}{=}
 100$

So let's just define EGSD as the percentage of reaching the minimum possible distance:

$EGDS_n =100 \cdot \frac{2\sqrt{n} - d}{2\sqrt{n}} = 100 \cdot \left(1 -\frac  d {2\sqrt{n}} \right) = 100 - \frac {100\cdot d}{2\sqrt{n}}$

Which gives us a formula very similar to the given. (Actually their formula is just missing the squre root in the denominator).

Let's apply this formula now to the case of the other paperb in discussion:

$EGDS_5 =100 \cdot \frac{2\sqrt{5} - \sqrt{8}}{2\sqrt{5}} \approx 36.754$

Not quite 40.8, but closer. Now, what if we assume the people in the other paper used this formula but made a mistake when calculating d, getting $d = \sqrt{7}$?

$EGDS_5 =100 \cdot \frac{2\sqrt{5} - \sqrt{7}}{2\sqrt{5}} \approx 40.839$

Interestingly, the other score 33.8 comes from apparently calculating

$EGDS_4 =100 \cdot \frac{2\sqrt{4} - \sqrt{7}}{2\sqrt{4}} \approx 33.856$

In their table, there are actually five rows but the last row has no value in its column?

I would say these are just bad papers, IMHO.

References

a Meckel, Yoav, et al. "Practical uses of genetic profile assessment in athletic training–an illustrative case study." Acta Kinesiologiae Universitatis Tartuensis 20 (2014): 25-39. (http://ojs.utlib.ee/index.php/AKUT/article/view/11961)

b Ben-Zaken, Sigal, et al. "Genetic profiles and prediction of the success of young athletes’ transition from middle-to long-distance runs: an exploratory study." Pediatric exercise science 25.3 (2013): 435-447. (https://www.ncbi.nlm.nih.gov/pubmed/23877193)


The 2-4% of Neanderthal genes refer to alleles, as you guess.  If, for a super simplified example, a human genome has

ALLELE_1__ALLELE_2__ALLELE_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7

and the Neanderthal equivalent had

ALLeLE_1__ALLELE_2__ALLELe_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7

(note the two lower-case 'e's), then they are 97.1% identical (67/69 characters), but if we sequenced a human and found

ALLELE_1__ALLELE_2__ALLELe_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7

then we might infer that "ALLELe_3" came from Neanderthals and that that genomic region was 14.2% Neanderthal (1 of 7 alleles).

(Obviously with only 7 alleles there would be other interpretations, but I don't feel like typing out 10,000 alleles right now.  You can see how you'd get enough information in a longer stretch of DNA.)

This is exactly the same as when you say "Half of my DNA is from my father and half if from my mother."  Obviously (one hopes) your parents were both human, and their genomes were virtually identical, but it's still possible to identify -- through allelic variation -- which segments came from which side.


Definition of "Effective population size"

Short answer: The effective population size of a population is the corresponding population size of a idealized (fisherian) population that would function in the same way with respect to genetic drift and inbreeding as the focal population under interest.

Long answer, below.

Definitions:

Heterogenity: the probability that two randomly sampled alleles in the population are identical (identical by descent).

Census Population Size: The census population size ($N$) is the number of individuals in the population.

Fisherian population

A fisherian population is an idealized population of size $N$, where all individuals mate at random, there is no selection, there is no population structure, there is no mutation and generations are non-overlapping. There probably are no perfectly fisherian populations in nature!

Genetic drift causes a decrease in heterogeneity. As the genetic drift is a function of the population size (see this post) this decrease of heterogeneity is a function of the population size. The heterogeneity at time $t$ is:

$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$

, where $H_0$ is the heterogeneity at $t=0$. You can verify by yourself that as $t$ increase , $H_t$ decreases. Also, as $N$ decreases, $H_t$ decreases. In other words, the longer you observe, the more heterogeneity gets lost and the smaller is the population, the higher is the loss of heterogeneity.

Effective Population Size

Let Pop_A be a real population. The effective population size ($Ne$) of Pop_A is the size of an idealized fisherian population that would have the same loss of heterogeneity than Pop_A.

You can read the above sentence twice to make sure you understand it. It basically is the definition of the concept of effective population size.

In other words: Let $N$ be the population size of Pop_A. If Pop_A is a perfect fisherian population, then its loss of heterozygosity through time is given by:

$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$

If Pop_A is not a perfect fisherian population, then it's decrease in heterozygosity is greater than the one given by the above formula. The decrease in heterozygosity of Pop_A corresponds to the decrease of heterozygosity of an idealize fisherian population of a different size. This size is called the effective population size $Ne$. So, we can rewrite the loss of heterogosity through time of Pop_A as:

$$ H_t = H_{0}\left( 1-\frac{1}{2Ne} \right)^t$$

(Note $N$ has been replaced by $Ne$)

, where $Ne$ is the effective population size of Pop_A.

Usually $Ne < N$, meaning that a real population undergoes more genetic drift than does a fisherian population of the same census size. There are many reasons that may yield a real population to have a higher drift than it would be expected with the same census size but respecting the assumptions of the fisherian population. Below I discuss three reasons:

Examples

Unequal sex-ratio

Think as a first example of a population where the sex-ratio is extremely biased to the point of having one male for 99 females. In such population, half of the alleles of a given locus at the next generation will come directly from the father. In such situations, the genetic drift is much higher than what would be expected from a fisherian population of size 100. Therefore $Ne<N=100$. To calculate $Ne$ when the sex-ratio in unequal you can use this formula:

$$Ne=\frac{4N_mN_f}{N_m+N_f}$$

, where $N_m$ and $N_f$ are the census populatino size of males and females respectively. You can verify that when $N_f = N_m$, then $N_f + N_m = N = Ne$.

Variation in population size through time

If your population size varies throughout a given time (a year for example) and that at time $t=3$ (a given period of the year) the census population size is given by $N_i$, then the effective population size is:

$$Ne = \frac{1}{\frac{1}{t}\sum_{i=1}^t\frac{1}{N_i}}$$

This is particularly relevant for insects for example which population size varies a lot between seasons.

Selection

Think now of a population where there is a great variance in fitness (there is selection). In such population, maybe all offspring will be produced by only a tenth of the current population. As a result the effective population is ten times smaller than the census population size.

You can probably find all these informations from wikipedia: http://en.wikipedia.org/wiki/Effective_population_size

Let me know if the concept of the effective population makes more sense to you now.


What physical evidence exists that shows motor proteins "walking" within a cell?

Since you chose kinesins as an example class of motor proteins, I will also stick to them. In general, the movement mechanisms of kinesins are well studied and the general structure of kinesin proteins, that is a dimer, is known by crystallography (see Kull et al. (1996) for the structure publication).

Even before that, the movement of single kinesin molecules in discrete steps of approx. 8 nm was shown by Svoboda et al. (1993). To resolve single molecules, they used optical trapping interferometry (see this practical guide to optical trapping by the Princeton University for more detailed information). Four years later, Schnitzer and Block (1997) were able to show that that for every step of approx. 8 nm lof a kinesin molecule, one ATP is hydrolysed. Visscher et al. (1999) used molecular force clamps to study ATP and load dependent characteristics of single kinesin molecules.

So far, it appears to be that kinesins move by a 'hand-over-hand' mechanism: Yildiz et al. (2004) labelled single heads of kinesin dimer molecules with a fluorophore and found that their data are congruent with a step of approx. 17 nm followed by a step of approx. 0 nm which indicates that the two dimer hands alternate in movement.

See also the review by Hirokawa et al. (2009) for a general overview of kinesin movement.


Why we need a plasmid for r-DNA technology

A plasmid has a site necessary for replication of genetic material know as the origin of replication (ori) since gene of interest (GOI) is just a segment of DNA it only posseses the sequence of interest and lacks an ori site, due to this it will not be able to replicate by itself. Replication of GOI is important for product formation in r-DNA technology (mostly protien) as when the host cells divides the GOI is duplicated and is transferred to both daughter cells. This way the number of recombinant cells will increase hence producing more of the final product.


How to identify the subspecies/breed of a bee

I am not sure about apiculture, but in academic research it is typical that people use microsatellite markers for identifying subspecies of bees. Microsatellite are repetitive regions of the genome that are useful in at identifying different species/subspecies, as well as for generating pedigrees and paternity analysis. Different species/subspecies have different numbers of repeats in a particular microsatellites, and these differing number of repeats are heritable. People use microsatellites because they are cheap, easy to run and reliable for identifying species/subspecies. Because there can be many different alleles (or different numbers of repeats) at a given microsatellite locus, so you only need relatively few microsatellites in total to identify individuals.
An example can be found in this paper. They used 7 microsatellite loci and could reliably identify between different African and European sub-species. It is worth a read of the intro:

Recent population genetic surveys in human (Bow- COCK et al.
1994;DIRIENZO et al. 1994) and other mammals (GOTTELLE et al. 1994;
TAEOR et al. 1994) and in bumble bees (A. ESTOUP,M. SOLIGNAJC. ,M.
CORNUET and A. SCHOLL unpublished results) have shown that
microsatellites are highly efficient at differentiating
populations or groups of populations. In this paper, we investigate their
usefulness for honey bee population studies by adressing the
following specific questions: Are the three evolutionary branches
inferred from morphometry and mtDNA confirmed by microsatellite
data? Are microsatellites useful for differentiating sub-species and
populations within subspecies? How does the pattern of variability of
these markers vary between branches/subspecies/populations and which
factors may be invoked to explain it? Is it possible to assign a given
colony to its population of origin from microsatellite data and how do
the individuals from this colony cluster within the population?

References:
Estoup A, Garnery L, Solignac M, Cornuet JM. Microsatellite variation in honey bee (Apis mellifera L.) populations: hierarchical genetic structure and test of the infinite allele and stepwise mutation models. Genetics. 1995 Jun;140(2):679-95. PMID: 7498746; PMCID: PMC1206644.


Is there any reason an arbitrary DNA sequence such as 5'-ACACACACAC-3' would not exist in nature?

You must first understand a few things:

What are proteins made of
What is DNA made of
What is the relationship between DNA and proteins

From DNA to proteins

DNA is transcribed into RNA which is then translated into protein. The protein, then has some effect (e.g. could be an enzymatic effect) such as affecting the level of sugar in the cell, digesting some lipids or affecting the expression of other genes.

More information on Khan Academy > Central Dogma

What is DNA made of?

DNA (or at least the genetic code) is made 4 different molecules which are called nucleotides. We abbreviate their names by the letters A,T,C and G.

What are proteins made of?

Proteins are made of amino-acids. There are ~20 different amino acids.

Genetic code

For the interest of your question it is now essential to understand how does the succession of nucleotides A,T,C,G in the DNA is reflected in the protein. This is called the genetic code.

We call a series of three nucleotides, a codon. AAT is a codon for example. Each codon (except special codons) correspond to a specific amino acid. This correspondance is called the genetic code. Here is the universal genetic code (where the T has been replaced by U because RNA contains U instead of T)

Consider for example the codon UAU and AUU (where only the order changes) The first one codes for the amino acid Tyr while the other codes for Ile. So yes, the order matters.

Information theory

Globally speaking, for any information the order of a sequence is of fundamental importance! More information on Khan Academy > Information Theory.


Are there any (chemical) processes occuring inside a seed while it's in a dormant state?

We can consider two processes that a seed might care about:

(1) Ordinary chemical reactions that just happen in the cytoplasm of the seed cells. It's very hard to stop chemistry! Even in the freezer, chemical reactions occur (slowly). This is why long-term storage of biological specimens is generally in an ultra-cold freezer (-80C). Chemical reactions could degrade DNA and proteins and prevent seed germination, so seeds take steps such as drying to reduce the chemistry going on. But, clearly this just slows down the reactions, as seeds of all types gradually lose their ability to germinate (some faster than others). Spore-forming bacteria are the most successful organisms in this regard: they drastically dehydrate the interior of the spore and surround it with a highly protective coat, and there is evidence that some can literally remain viable for millions of years.

(2) Seed metabolism: enzymatic reactions and the normal biochemistry of the cell. "Dormancy" means in part that seed cells shut down processes like transcription and translation and minimize their metabolism. But, research suggests that the metabolic activity of seeds is not zero - among other things, there are active enzymes that are involved in repairing damage to DNA and proteins.


Gas bubbles are foamed by electrolysis of water, generating bubbles of hydrogen gas on the negative electrode and oxygen gas on the positive electrode.

As for the foam itself... I am guessing there is some form of detergent in the buffer. Some electrophoresis buffers do contain detergent.


What could independent investigators learn from the first (known) copies of the virus from Wuhan, if they had (physical?) access to these samples?

I'll take a shot at this. It's my impression that most of this is political rather than scientifically grounded.  There are reasons to want physical samples of viruses (rather than just genomic sequences), e.g. if you want to do experimental (in vitro or in vivo) studies on a particular virus strain. (It might be theoretically possible to edit the genome or reconstruct the genome of an earlier strain, but it's much easier if you have the desired viral strain in hand.)
Based on this Financial Times article (which may or may not be accessible without a subscription/accepting cookies)

Mr Pompeo added the Chinese Communist party had still not shared virus samples with anyone outside China, impeding efforts to understand how it emerged.
A researcher at Wuhan Institute of Virology, who declined to be named, told the Financial Times earlier this month that China had not shared samples of the live virus with the WHO as the country “had already published plenty of information” such as the genetic code of coronavirus.

It does seem that almost all of the research on the origins of SARS-COV-2 is based on genome sequences rather than on phenotypic studies (i.e., in vitro and in vivo studies of actual viruses).
I don't think viral samples would actually be very useful (that's why I said at the beginning that I think most of this argument is political rather than scientific). In principle I guess you could use the viral samples from an early stage  do experimental infections in different animal species, but I don't know that any researchers actually want to do that, and I don't think there's been enough phenotypic evolution in the last few months that the early-epidemic viral samples would behave that differently from current samples ... it's also likely that researchers could study the effects of particular mutations (observed in genomic sequence) by modifying viral samples they had in hand.
To take an example from an earlier pandemic, researchers have done experimental studies in mice to show how particular mutations influenced the virulence of earlier flu strains. This is an example where it's useful to have an actual virus rather than just the genome - but in this case the virus was actually reconstructed from knowledge of the genome ("two isogenic recombinant chimeric viruses were created with an influenza A/WSN/33 virus background containing the PB1 segment from the HK/156/97").


What is the gas inside a Capsicum pepper, and how does it get there?

To answer your question of what the gas is, how about the glowing splint test for oxygen! I guess it might work with a recently snuffed out match too. Cut a plug in the the pepper but leave it in place until you have the glowing match ready, then quickly open the plug and hold the match into the opening. It should relight if it is oxygen and you may hear a popping noise.

As for whether the surface tension is preventing the flow of air, you could try adding some detergent (washing up liquid or soap) to the water to break the tension and see what happens.

However, I have found an article suggesting the environment is, compared to the standard atmospheric concentration anyway, low in O2 and high in CO2 in two different pepper cultivars.1

  Samples withdrawn from the fruit locule over time show that CO2 ranges between 0.5% and 3% (5000–30,000μmol·mol–1) (Fig. 2, top) while O2 ranges between 18% and 20% (Fig. 2, center), compared to the composition of standard atmosphere (400μmol·mol–1CO2; 21% O2)

1 Blasiak, J., Kuang, A., Farhangi, C.S., and Musgrave, M.E. Roles of Intra-fruit Oxygen and Carbon Dioxide in Controlling Pepper (Capsicum annuum L.) Seed Development and Storage Reserve Deposition. J. AMER. SOC. HORT. SCI. (2006) 131(1):164–173.


The tanning response to UV occurs in two phases:

The immediate response begins at exposure to UV-A, reaches a max at 1-2 hours, and fades between 3 and 24 hours.
This article speculates that this is due to the redistribution of melanosomes rather than additional melanin production.
The delayed response is more durable, occurring by repeated exposure to UV-B, as well as as UV-A and visible light. "It is a gradual process in which the skin starts darkening 48–72 h after irradiation, reaches a maximum ∼3 wk after exposure, and the skin does not return to its original melanin content until ∼8–10 months later."
This source says this is due to additional melanocytes, melanosomes, and more melanin, in general.

Both processes are influenced by genetic factors.

Source for the initial points, which also contains interesting details on the enzymes involved in these processes.


Replication doesn't start at the very end of a chromosome, so there is no problem with leading strand synthesis. It's probably easiest to see if the other half of the image was there:

Forgive the lion; plain white paper seems to be in short supply. Also my writing. Too much tea this morning. Hopefully you can see that leading strand synthesis can continue right to of the end of the chromosome as the fork progresses. The leading primers at the replication origin can be replaced once the first Okazaki fragment from the other replication fork is synthesized.

There is, however, a problem, aptly termed the end replication problem, with lagging stand synthesis:

The dots just mean the chromosome continues in that direction. Important to notice is the lagging strand RNA primer at the end of the chromosome. When this is removed, there is apparently no way to synthesize DNA there. Repeated replication cycles progressively shorten the chromosome and cause the Hayflick limit to cell division (the number of times a cell can divide before dying). To solve this problem, some cell types express an enzyme called telomerase. This is an RNA directed DNA polymerase that adds deoxyribonucleotide repeats to the 3' end of a DNA strand, using its own internal RNA template, to prevent information loss.


Why minimum infective dose of a virus is not just 1 particle?

From Merriam Webster:

  the smallest quantity of infective material that regularly produces infection

(emphasis mine)

The word "minimum" here is not meant as a strict minimum it is meant as a statistical bound, the absolute probability for which depends on the types of tests done and their inherent accuracy/inaccuracy.

Reasons that this "minimum" is greater than 1 could include:

Probability that a given particle actually finds a suitable host cell, enters the cell, and replicates; failures can occur at many stages along that chain
Rate of immune system reaction/response. At low exposure levels, the immune system may detect and clear the infection at a rate faster than it can spread, such that the infection stays asymptomatic. Some vaccines use weakened or low doses of pathogens specifically to evoke an immune response. The intent is that the weakened pathogen will not spread fast enough to overcome the immune response and will not produce a full disease.
Clearance of the infectious agent before it reaches symptomatic levels. This probably applies more to bacteria but I don't see why it couldn't also apply to viruses. I think the best example is exposure to bacteria that cause gastrointestinal infections like E.coli or Salmonella. Small numbers may grow and multiply in the gut, but they grow slowly if they aren't present in a high enough concentration and they may pass through the gut before causing any noticeable symptoms.

The minimum infective dose can also vary from individual to individual or due to environmental factors (for example, see this paper).

Some additional references:

Leggett, H. C., Cornwallis, C. K., & West, S. A. (2012). Mechanisms of pathogenesis, infective dose and virulence in human parasites. PLoS pathogens, 8(2), e1002512.

Ward, R. L., Akin, E. W., & D'Alessio, D. J. (1984). Minimum infective dose of animal viruses. Critical Reviews in Environmental Control, 14(4), 297-310.

Yezli, S., & Otter, J. A. (2011). Minimum infective dose of the major human respiratory and enteric viruses transmitted through food and the environment. Food and Environmental Virology, 3(1), 1-30.


Why doesn't cellular, replicative senescence (or the hayflick limit) constrain the normal development of an organism?

You pretty much have answered your own question. It is a math problem. Cells are burning up their telomeres during fetal development onward but the cells are multiplying exponentially in number.

But biology is a bit messy, embryonic stem cells do have telomerase activity and their telomerase are maintain. So the clock doesn't start counting down immediately.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360127/

Temporal wise hES cells are around 4–5 days post fertilization, at which time they consist of 50–150 cells. https://en.wikipedia.org/wiki/Embryonic_stem_cell.

So you don't quite start with an n of 1 cell. But of an n of 50-150 (in humans)... before you start to see telomere shortening. With that head start those 50 doubling can make a lot more cells. By my guestimate with excel ~1.69E17 cells ~320 tons. More than enough you to last a life time.)


Your question comes down to the definition of the units you state in your question - mutations genome-1 generation-1. In my opinion the answer is your choice (2).

How are mutation frequencies measured? Usually it is a case of scoring the appearance of a mutant phenotype as an indicator of underlying mutational events (see Drake,JW (1991)A constant rate of spontaneous mutation in DNA-based microbes. Proc. Natl. Acad. Sci. USA 88:7160-7164 for a detailed explanation.) Since, as you say, DNA replication is semi-conservative, the two daughter cells of a bacterial cell division each inherit one old DNA strand and one new DNA strand and so have the same probability of sustaining a given mutation. The overall mutational frequency has to be an aggregate of what has happened in both of them (and in all other cells in the population) since there is no way of distinguishing between them. In terms of your question the answer is (2) and this is why the mutation rate is normalised per genome.

In practice this figure is arrived at as follows. Suppose that you study a 1 kb gene, gene X, and measure the rate of spontaneous mutation in that gene (by some convenient assay) as 1 mutation per 107 cell divisions (again see the Drake reference for details). Assume also that the bacteria have a genome size of 2 x 106 bp.  Since each cell division equates to the creation of one new genome we get:

mutations per gene X per generation = 1 x 10-7

mutations per bp per generation  = 1 x 10-7/1000 (because it is a 1000 bp gene)

mutations per genome per generation = 1 x 10-7 * 2 x 106/1000

mutations per genome per generation = 0.0002

Now this is an underestimate because not all mutations will create a detectable change in phenotype. Drake uses a correction factor of 3.12 for this.

true mutations per genome per generation = 0.0002 * 3.12 = 0.0006 or 6 x 10-4

These were made-up numbers. See review in Drake JW et al.(1998) Rates of spontaneous mutation. Genetics 148: 1667-1686 for real examples.


Do the right-handed people tend to use the right side teeth of their jaw to chew food more often than the left-handed people?

Individuals have not only hand dominance but also a dominant foot, eye and ear. There has also been a belief that this sidedness applies to chewing as well. However, the short answer is that no one is sure, but that it may be related to handedness. I only looked at studies done after 2000.

One large study[1] found a questionable to weak correlation, not consistently maintained through different dentition (baby teeth, mixed, and permanent). A slightly smaller study showed a correlation; in 78% chewing side preference correlated with other tested lateralities (footedness, handedness, eyedness and earedness).[2] Another similar sized study found none.[3]

A small 2012 study found that there was a preference for right sidedness when chewing hard food (73.68%) and for soft food (57.89%) but failed to correlate this with hand/other-sidedness.[4] Another small study tested for sidedness, finding that 55% of subjects did not have any side preference, 30% preferred to chew on right and 15% preferred the left side, and this was reproducible in 90% of subjects only with almonds (a medium hardness food) as opposed to jerky or asparagus. Unfortunately they did not measure sidedness. Their findings were that chewing-side preference is not a fixed characteristic, and texture seemed to affect sidedness.[5] A review article determined that a person's dental condition to a large extent dictates how they chew.[6]

The studies were mostly designed very differently, making good comparisons difficult. I think it's safe to say it's possible but not known with certainty.

[1] Absence or weak correlation between chewing side preference and lateralities in primary, mixed and permanent dentition
[2] Chewing side preference as a type of hemispheric laterality
[3] Relationship between chewing side preference and handedness and lateral asymmetry of peripheral factors
[4] Chewing side preference in first and all mastication cycles for hard and soft morsels
[5] Chewing-side determination of three food textures
[6] Adaptation of mastication in response to the characteristics of the individual or the food


What is this plant that spontaneously sprouted in my balcony?

It looks like a raspberry, or some other kind of similar berry plant (blackberry etc.). The triple leaves and the habit of the plant are characteristic. Birds will often eat them and "deposit" the seeds randomly around the Earth.

https://plantvillage.psu.edu/topics/blackberry/infos

Berry plants usually have thorns or develop them as they grow. If no thorns are present, then perhaps it is another type of interloping plant. Other plants do look similar. In which case, your photos are insufficient for more further identification.


The pronuclei fuse and decondensation happens and now the cell is called a zygote. There is a stage called the midblastula transition (MBT), until which only the maternal products (cytoplasmic factors such as RNAs, proteins and ribosomes) are used. After MBT the zygote starts expressing its own genes from both the paternal and maternal alleles. However, certain genomic regions are imprinted  which means that one of the alleles is epigenetically silenced. It can be either paternal or maternal.


Why is ab initio protein secondary structure prediction less reliable than alternatives?

Preamble

In the comments @CMosychuk linked the most comprehensive text on ab initio I have seen this side of the year 2000 (Lee et al., 2009). It agrees that you've raised a good point.

  It is important to acknowledge that ab initio prediction methods
  solely based on the physicochemical principles of interaction are
  currently far behind, in terms of their modelling speed and accuracy,
  compared with the methods utilizing bioinfor- matics and
  knowledge-based information.

This is a good real life example of different philosophical approaches of inductive reasoning and deductive reasoning (AKA top-down logic) behaving as one might expect. Each specific software has it's own problems and advantages and may not fit into the below categories. I'll grossly simplify each approach in crude categories and then broadly explain why errors crop up in them.

Below, we'll discuss ab initio and why it goes wrong and then the alternatives including why they're currently generally more reliable. We'll round up with how ab initio is probably going to become realistically involved in reliable protein predictions.

Ab intio.

Figure showing the broad pipeline difference between ab initio and homology modelling.Nara Institute of Science and Technology.

Ab initio often works on the premise that physical laws can be applied universally in biology. As you are most probably aware, biochemistry is far messier than chemistry and often those physical laws appear bent if not completely broken. The goal of ab initio is therefore to combine physical properties with some fudge factors to account for a complex system. Due to the complexity of the system never being fully modelled, ab initio predictions are limited to what your input is. There are also limitations pointed out in the 2009 article:

potential energy functions.
conformational search engines
model selection scheme

What you can see now is that ab initio is missing something that the others have: biological experimental empiricism. Without that inductive reasoning ab initio modelling is very vulnerable to assuming far too much and oversimplifying the system (This xkcd springs to mind).

Although perfect ab initio prediction is the "Holy Grail" of protein structure prediction, currently if there is homology which provides an experimentally known structure then that is often more reliable.

Ab initio is not completely without merit. For relatively short proteins (100 residues) the accuracy has improved over the last decade (Lee et al., 2009). From the above mentioned article:

  ...the physics-based atomic potentials have proven to be useful in
  refining the detailed packing of the side chain atoms and the peptide
  backbones.

Homology modelling.

This type of modelling is a safe bet provided that the MSA is available and reliable. The premise here is that if two proteins look similar enough at a sequence level, and you know the structure of one, then probably there is structural conservation as well. The problem is that obviously, those small changes in sequence, or other contextual differences like post translational modifications, localised pH differences etc. might mean that the protein folds differently.

Machine Learning.

Neural networks are a form of machine learning. Conceptually, these use the same assumptions as homology modelling, but on a larger more sophisticated scale (not necessarily an advantage). A good example of “machine learning” winning out in terms of homology clustering and secondary structure prediction is that of HHpred. An algorithm will make subsets of "if" statements. If a protein has a certain combination of "ifs" and "nots" then it's safe to assume other proteins with the same "ifs" and "nots" have similar structures.

You need to know a lot of information about the dataset that you put in, and also one needs to know which of that information is relevant. If these conditions aren't thoroughly complied with the categorisation results will just be amplified errors, arbitrary categorisations, missing categories, or a combination of those three.

It's worth pointing out at this point that most modern secondary structure predictors use a combination of homology and machine learning.

A reasonable ab initio approach.

More recently iterative optimisation based on vague experimental data has become the standard practice shifting ab initio from a top down approach to something more inductive. Kulic et al., 2012 is an interesting example of such a modern holistic approach. It involves an iterative optimisation of ab initio protein structures based on experimentally derived structures.

Another excerpt from the 2009 article.

  Thus, developing composite methods using both knowledge-based and
  physics-based energy terms may represent a promising approach to the
  problem of ab initio modelling.


Why Did 6 Great Ape Species Survive But Only 1 Hominid Species?

Determining why one species (or group of species survived) while others did not can be difficult to answer, but I can offer one possible explanation for the genus Homo: competition. Competition between similar species is one possibility. Consider for example gorillas or chimps. The two species of gorillas occupy different habitats so they rarely compete with each other for resources (food, water, shelter, etc.). The two species of chimpanzees have non-overlapping ranges (or minimally so) so again they do not compete for resources.

Chimps and gorillas do overlap with each other for parts of their range and even potentially use the same resources, although no competition for resources has been observed (see this primate factsheet and McNeilage 2001). The same applies for the orangutans, which lives on two different southeast Asian islands.

The genus Homo is an entirely different story. As you may know, Homo first evolved in east central Africa. The first species to leave Africa and disperse across Europe and Asia was Homo erectus. This migration out of Africa happened as early as aout 1.8 million years ago. Homo sapiens had not yet evolved. However, while H. erectus was establishing itself across Europe and Asia, populations still in Africa continued to evolve.

Modern Homo sapiens evolved in central Africa perhaps about 250-200,000 years ago and dispersed out of Africa about 100,000 years ago. Homo sapiens also dispersed across Europe and Asia. Both H. erectus and H. sapiens co-occurred across parts of their range. Some have argued (Stringer and Andrews, among others, I believe but I'll have to be at work before I can verify ths reference) that H. sapiens outcompeted H. erectus, leading to its eventual extinction by competition. They occurred together and used the same resources, so H. sapiens could have caused the extinction of H. erectus. This has been called the replacement hypothesis. The later evolving species (H. sapiens) replaced the earlier evolving H. erectus.

However, Templeton (2002) has argued that the two species interbred so the species became integrated rather replaced (if I am interpreting him correctly).  While I don't dispute the possibility of interbreeding, I am skeptical of Templeton's complete dismissal of replacement.

Complicating the picture is H. neanderthalensis. Genetic evidence published by Green et al. (2010) suggests that Neanderthals diverged from H. sapiens (in central Africa) between 800,000-500,000 years ago and also dispersed out of Africa.  They also provided evidence of interbreeding between H. sapiens and H. neanderthalensis in Europe.  Modern H. sapiens may also have outcompeted H. neanderthals.

All of this was occurring during the Pleistocene ice age. Europe was experiencing repeated bouts of extensive glaciation. Thus, it is also possible that climate change caused or contributed to the extinction of H. erectus, H. neanderthalensis, or both.

In summary, the processes that led to the extinction of other species of Homo are complex and likey interactive. Competetion among species is, in my view, well within the realm of possibility but would be extremely difficult (if not impossible) to test. Climate change is also a very likely contributing factor. There are several other hypotheses but I have tried to hit the major highlights.  The debate is certainly not settled.

McNeilage A. 2001. Diet and habitat use of two mountain gorilla groups in contrasting habitats in the Virungas. In: Robbins MM, Sicotte P, Stewart KJ, editors. Mountain gorillas: three decades of research at Karisoke. Cambridge (England): Cambridge University Press. p 265


What is an "open system" when it comes to PCR machines?

In an open system, "mRNAs are detected because of their property of being expressed in the tissue sample isolated for study. This approach is in contrast to what are called closed-system approaches, in which the mRNAs to be detected are selected as candidates in advance of analysis; a contemporary example of a closed system would be a gene “chip” hybridization experiment." [Sutcliffe, J.G. (2001) J. Neurosci. 21:8306-9. “Open-System Approaches to Gene Expression in the CNS”] https://doi.org/10.1523/JNEUROSCI.21-21-08306.2001


"How do transport/carrier proteins rotate during facilitated diffusion?"

They don't. The explanation in the PDF you linked...

  Figure 11.1 shows an extracellular molecule bound to the transport protein; the transport protein then rotates and releases the molecule inside the cell.

... is an oversimplification, to say the least (you could simply say that this is plain wrong). What really happens is way more complex.

We call it conformational change.

According to Alberts, Molecular Biology of the Cell (2002):

  Each type of carrier protein has one or more specific binding sites for its solute (substrate). It transfers the solute across the lipid bilayer by undergoing reversible conformational changes that alternately expose the solute-binding site first on one side of the membrane and then on the other. (emphasis mine)

This is an image that explains way better the process, from the same chapter in Alberts (the legend provides a detailed explanation):

Figure 11-11A model for the molecular mechanism of action of the bacterial lactose permease (A) A view from the cytosol of the proposed arrangement of the 12 predicted transmembrane helices in the membrane. The loops that connect the helices on either side of the membrane are omitted for clarity. A glutamic acid on helix X binds H+, and amino acids contributed by helices IV and V bind lactose. (B) During a transport cycle, the carrier flips between two conformational states: in one, the H+ -and lactose-binding sites are accessible to the extracellular space (1 and 2); in the other, they are exposed to the cytosol (3 and 4). Unloading of the solutes on the cytosolic face (3 → 4) is favored because the lactose-binding site is partly disrupted and a positive charge contributed by an arginine on helix IX displaces the H+ from the glutamic acid on helix X. (A, adapted from H.R. Kaback and J. Wu, Accts. Chem. Res. 32:805-813, 1999.)

Thus, as you can see, we have conformational states: one of them exposes the binding site to the extracellular space, while the other one exposes the binding site to the cytosol. Just like what happens when an enzyme changes conformation, the 3D changes in the protein structure are quite small, and it's hydrophobic regions keep in the same place in both states.

Source: Alberts, B., Johnson, A. and Lewis, J. (2002). Molecular biology of the cell. 1st ed. New York: Garland Science..


Excellent question. The answer is that, in general, there is a higher rate of mutation in spermatogenesis compared to oogenesis. This is because there are more cell divisions during spermatogenesis, which allows for opportunities for mutation.

In addition, repeat diseases like Huntington’s sometimes have a phenomenon known as anticipation. This is when the disease gets phenotypically (and genetically) more severe with each successive generation. The exact molecular basis of this is not completely understood, but it is just well known that DNA polymerase tends to make more mistakes in large repeat regions, causing an expansion of the repeat. Anticipation is not linked to gender, I just wanted to point out that these repeats are prone to mutations that will expand the repeat and cause disease

You can see anticipation in this graph. This example is for Fragile X. The higher the repeat number in the parent, the greater the chance the child develops the disease. The parent doesnt have the disease, but what happens is the repeat mutates and gets expanded to the point where the disease will develop.

So, put these two facts together and you have your answer. A male's sperm tends to have a higher overall mutation rate, and the region responsible for Huntingtons is already prone to disease causing mutations as it is. The result ends up being the disease gets ‘inherited’ more often from the father

Picture from here


What, if any, is the difference between covalently closed circular DNA and plasmids?

As a descriptive term, we can take covalently closed, circular DNA (cccDNA) at face value: any DNA that is circular, with the ends joined by covalent bonds, can be described as cccDNA. Thus, plasmids are a type of cccDNA, but not all cccDNA are plasmids. Textbooks and lecturers describe plasmids as cccDNA for the purposes of DNA topology. This usage also appears in literature. cccDNA can also refer to circularized viral DNA, which is another type of episome. Note that the linked to papers are merely examples of how the term is used, not authoritative definitions.


As others pointed out, the question is not clear.. but yes, in general you use a primary antibody recognizing your peptide of interest, e.g. an antibody made in mouse, and then a secondary antibody recognizing your primary antibody, in this case an anti-mouse. The secondary antibody will obviously be made in a different animal than mouse (e.g. in goat), because mice cannot develop anti-mouse antibodies!
I hope I understood your question.


Why is Cysteine and Tyrosine used to calculate a sequence isoelectric point?

Every amino acid has a different isoelectric point: a pH where they do not carry electric charge. This isoelectric point depends on the side chains:

By glycine the side chain $-H$ is neutral (while the amino and carbonic acid groups are not) so the IEP is 5.97.
By lysine the side chain $-(CH_2)_4\mbox{-}NH_2$ is alkaline $[R\mbox-NH_2 + H^+ \rightleftharpoons R\mbox-NH_3^+]$, so it will have a more alkaline IEP 9.74 than glycine.
By glutamic acid the side chain $-(CH_2)_2\mbox -COOH$ is acidic $[R\mbox -COOH \rightleftharpoons R\mbox -COO^- + H^+]$, so it will have a more acidic IEP 3.22 than glycine.

Every side chain has more or less contribution to the IEP of the amino acid. In your question

the side chain of cysteine $-CH_2\mbox-SH$ is a weak acid $[R\mbox-SH \rightleftharpoons R\mbox-S^- + H^+]$ so the IEP is 5.07
the side chain of tyrosine $-CH_2\mbox-Ph\mbox-{\scriptsize (p)}OH$ is an even weaker acid $[R\mbox-OH \rightleftharpoons R\mbox-O^- + H^+]$ so the IEP is 5.66

And every amino acid has more or less contribution to the IEP of a protein.

References:

Table of pKa and pI values
Amino Acids with Acidity Values
Introduction to Proteins; Amino Acids, the Building Blocks of Proteins
Electrospray Mass Spectrometry


You can analyse a single chromosome. All the bioinformatics tools I know, allow that. Consider only the reads that map to the desired chromosome (or any segment of the genome). However, most next-gen sequencing experiments sequence the whole genome and not just a single chromosome. You'll just end up losing information by not considering other chromosomes.


Why is the Patellar reflex not triggered when the tendon is extended slowly?

This effect you are observing has to do with the nature of the afferent neurons (Ia fibers), which carry a signal into the spinal cord and synapse onto motor neurons directly.  See this text (scroll down to section 1.10) for a diagram.  At their other end, these Ia fibers penetrate into the muscle and wrap themselves around the body of the muscle spindles, "[which] are specialized receptors that signal (a) the length and (b) the rate of change of length (velocity) of the muscle."

Because the main role of these spindles is to monitor the muscles for very rapid changes in length, the neurons have a static range which is optimized for these quick jerks (rather than firing over a wide range of velocities).  When you are stretching the muscle slowly, the Ia fiber is not building up a sufficient depolarization to fire off an action potential.


best book for a comprehensive introduction to biology for a computer science graduate interested in undertaking research in bioinformatics

Welcome to Biology and welcome to Biology.SE!

It is hard to answer such a question as the domains you describe are very vast.

If you want a book in an introductory book to biology, then you want to read this post and this post.

If you are more interested in population genetics and molecular evolution then this post will interest you. Still talking about evolution I'd like to attract your attention to this post for the second suggestion in the first answer:  Yang, Computational molecular evolution

You'll probably want to have a look at the post A free book/resource for learning genetics?.

Book recommendations for algorithms used in evolutionary biology and Introductory book in genetics might be a post of interest as well.

Unfortunately I don't know any of the two books you cite so I can't quite give you advice for them. molecular biology of the cell is a very common book among first year biology. It sounds like a potential good reading for you. I know nothing about molecular biology of the gene except what I just read about it on Amazon.

I am hoping one will give you a better criticisms about very general books about molecular biology.