Can you disconnect sensation from the brain without destroying muscle functions?

Even if it were possible to selectively destroy sensory (afferent) nerves alone, the individual would not be able to walk/move normally immediately afterwards, because there would be no environmental stimuli with which to orient one's actions.

Two of the senses people often overlook are balance (or spatial orientation) and proprioception (where the body parts are with respect to each other and the physical world). (Some people lump the two; it's easier to think of them independently, because they really do quite different things.)

Proprioception (and closely associated kinesthetics) is possible because of nerve signals from skin, tendons, muscles, and joints. This gives us the senses of limb position and movement, the sense of tension or force, the sense of effort, the sense of gravity.[1]

  Patients (lacking proprioceptive feedback) made large directional and amplitude errors when performing a reaching task without visual feedback....The errors were associated with differences in velocity and acceleration for movements in different directions.[2]

Basically, without proprioception, you could not touch your little finger to your thumb without visual input, let alone actually perform more complex voluntary movements successfully.

The vestibular system exists through input from three semicircular canals located in the inner ear on each side. The canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).

  Three sensory systems, vestibular, visual, and somatosensory/proprioceptive, serve our sense of balance. Each of these systems provides unique sensory information to the brain where it is integrated (often in complex ways) to produce a final motor output to muscle groups for maintaining gaze, head and body posture, and controlling static and dynamic balance.[3]

Without these systems, we would be completely unable to get or stay in a standing position. We certainly could not walk.

So, long story short, the answer is no. Not only is it surgically impossible, but if it were, you would not have a coordinated, working body left. Eventually even speech would be affected (as proprioceptors on the mouth are involved in speaking).

[1] Proprioception From a Spinocerebellar Perspective
[2] mpairments of reaching movements in patients without proprioception. I. Spatial errors
[3] Anatomical and Physiological Considerations in Vestibular Dysfunction and Compensation


Resources of all known biochemical pathways?

You can find biochemical pathways on KEGG pathway for example.

  KEGG PATHWAY is a collection of manually drawn pathway maps representing our knowledge on the molecular interaction and reaction networks for:
  1. Metabolism
      Global/overview   Carbohydrate   Energy   Lipid   Nucleotide   Amino acid   Other amino   Glycan
      Cofactor/vitamin   Terpenoid/PK   Other secondary metabolite   Xenobiotics   Chemical structure
  2. Genetic Information Processing
  3. Environmental Information Processing
  4. Cellular Processes
  5. Organismal Systems
  6. Human Diseases
  and also on the structure relationships (KEGG drug structure maps) in:
  7. Drug Development

To illustrate the information you can find there, here is a screenshot:

If you click on kegg atlas, you get an atlas with all metabolic pathways. You can zoom in to great detail en click for further links.

If you click on glycolysis or oxidative phosphorylation for example, you will get linked to the following page (see picture). In these detailed schemes of the metabolic pathway, each intermediate can be clicked on, leading to a more detailed page.


Are bleach solutions still routinely used in biochemistry laboratories to rid surfaces of bacteria, viruses, certain enzymes, and nucleic acids?

I'm a research post-doc working in a US-based microbiology research lab. We still use a relatively low-concentration bleach solution to decontaminate most liquid cultures before disposing of them, but most of our surface and equipment decontamination is accomplished with alcohol (either ethanol or isopropyl alcohol (IPA)). We do work with some organisms that are not effectively killed by alcohol, such as C. difficile. C. difficile makes endospores which are very resistant to alcohol-based agents, but they are readily killed by bleach.
So after working with C. diff and other spore-forming bacteria we decontaminate with commercial wipes containing a stabilized sodium hypochlorite solution at a little less than 1%, which isn't even enough to give off a strong bleach odor. On metallic surfaces and some kinds of rubber, we follow up with an alcohol wipe to prevent corrosion from the bleach.
We do have other sporicidal agents that are used for specific applications where bleach isn't suitable, but most of them are much more harsh (requiring use of respirators), require a longer contact time, and have a substantially shorter shelf life at the effective concentration (sometimes just days or hours, vs. months with bleach).
Bleach is also good for destroying DNA and RNA in clean areas used for PCR setup, but there are some commercial products specifically designed to do this along inactivating nucleases that might degrade a sample, so I personally use those products. (Note that ethanol and IPA solutions can actually precipitate nucleic acids, leaving them behind after the solution evaporates.)


Does anyone know if there is a term to describe the following process?

The two terms of main interest to you
Cellular noise

Cellular noise is random variability in quantities arising in cellular biology. For example, cells which are genetically identical, even within the same tissue, are often observed to have different expression levels of proteins, different sizes and structures. These apparently random differences can have important biological and medical consequences
Cellular noise was originally, and is still often, examined in the context of gene expression levels – either the concentration or copy number of the products of genes within and between cells. As gene expression levels are responsible for many fundamental properties in cellular biology, including cells' physical appearance, behaviour in response to stimuli, and ability to process information and control internal processes, the presence of noise in gene expression has profound implications for many processes in cellular biology.

There is also the term developmental noise.

Developmental noise is a concept within developmental biology in which the phenotype varies between individuals even though both the genotypes and the environmental factors are the same for all of them. Contributing factors include stochastic gene expression and other sources of cellular noise.

Developmental noise is often sounds like a synonym of cellular noise, but it is supposed to include more processes that are causing phenotypic variation then cellular noise. For example, it is common to consider "micro-environmental variation" as being part of developmental noise and not of cellular noise.
The way your phrased your question
In your question you describe only sources of cellular noise. However, you end up saying Hence, cloned organisms are not identical, even if their DNA were identical. I just want to highlight that, there are other reasons than cellular noise for which two clones differ. These include micro-environmental variance, physiological noise, epigenetic variance and macro-environmental variance (often just called environmental variance). Note that I had never encountered the term "physiological noise" before, I just made it up but I wanted to highlight that noise also happen in among cells processes, not only within cells processes.
Intro to quantitative genetics
For a short introduction to quantitative genetics and the different sources of phenotypic variance (genetic variance, environmental variance, developmental noise, etc..) and how the concept of heritability fits into this discussion, please have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?


Wim Hof Method claims Alkaline Blood is Good. Contradictions? Counterproof?

The Wim Hof method unfolds its health effects by hormetic stressors, respiratory alkalosis is one of them (a minor one). The WHM does not follow the pH theory, even though Wim himself gave ambiguous statements in older interviews about this. There are many people who misinterpret the WHM breath work as plain hyperventilation, which is very wrong. It involves a hyperventilation phase in preparation of a hypoventilation phase. This is similar to apnea protocols. The hyperventilation phase itself can mediate minor health effects. As it is not a chronic practice but relates to a few minutes per day, the stress of respiratory alkalosis is very likely within the hormetic range, hence beneficial. The WHM does NOT advocate continuous hyperventilation, which is known to be linked to chronic disease (exceeding the hormetic window).

The clinical trials of the WHM are peer reviewed and well conducted. However, people tend to mix Wim's interviews with the clinical evidence, which is obviously bad. The major paper (group study with control group) is this one: https://www.pnas.org/content/111/20/7379.full.pdf

It clearly shows the anti-inflammatory effects and increased leukocytosis of the breath work (intermittent hypoxia) and also shows that blood pH correlates to the respiratory rate, more precisely blood CO2 levels as expected. Those are normal blood gas dynamics, nothing woo woo pH stuff and no serious scientist would attribute the health effects of the method to the temporary blood pH fluctuations seen from a short hyperventilation phase, especially not when far more dominant and better documented effects on hormonal adaptations can be discussed instead. Some practitioners get quite enthusiastic about urine pH measurements, which are VERY high after the breath work, however all this indicates is normal kidney function in response to temporary respiratory alkalosis, nothing fancy at all. The body increases bicarbonate outlet via the kidneys (renal compensation) when blood CO2 gets too low (hyperventilation) to maintain blood pH homeostasis. the pH strips measure this bicarbonate. Another misconception is that the reading would correlate to progress or health, while it actually just correlates with hyperventilation intensity/duration. It is quite annoying how many misconceptions about simple physiological details float around the web, primarily due to the success of the pseudoscientific pH theory and alkaline diet. I guess some people just got rich with that crap...

Understanding the WHM means understanding hormesis and the stress response in the first place. The whole idea is comparable to physical exercise: stress the body enough to become stronger but not so much to take damage.


Reading the specified Wikipedia article about Centrosome, actually explains why centrioles are NOT IMPORTANT for the PROGRESSION OF MITOSIS.

To better understand what wiki meant, let us look at both centrioles & centrosomes.

According to Biology Pages for Centrioles and Centrosomes >>

Centrioles are built from a cylindrical array of 9 microtubules, each of which has attached to 2 partial microtubules.
The Centrosome

is located in the cytoplasm usually close to the nucleus.
It consists of two centrioles — oriented at right angles to each
other — embedded in a mass of amorphous material containing more than
100 different proteins.
It is duplicated during S phase of the cell    cycle.
Just before    mitosis, the two centrosomes move apart until    they
are on opposite    sides of the nucleus.
As mitosis proceeds,       microtubules grow out    from each
centrosome with their plus ends       growing toward the    metaphase
plate. These clusters of microtubules    are called spindle
fibers.

So, now we know that during mitosis, the nuclear membrane separates and the centrosome nucleated microtubules (parts of the cytoskeleton) can associate with the chromosomes to fabricate the mitotic spindle.

Understanding the conceptual working of centrosome, the Wikipedia article states >>

  Interestingly, centrioles are not required for the progression of
  mitosis.

  When the centrioles are irradiated by a laser, mitosis
  proceeds normally with a morphologically normal spindle.

  In the absence of the centrioles, the microtubules of the spindle are
  focused by motors allowing the formation of a bipolar spindle. Many
  cells can completely undergo interphase without centrioles.

Therefore, even in the absence of centriole, centrosomes develop Astral microtubules which just exist amid and quickly before mitosis. Astral microtubules are characterized as any microtubule beginning from the centrosome which does not interface with a kinetochore.

Astral microtubules are not required for the movement of mitosis, but rather they are required to guarantee the devotion of the procedure. The capacity of astral microtubules can be by and large considered as assurance of cell geometry. They are totally required for right situating and introduction of the mitotic spindle assembly, and are in this way required in deciding the cell division site in light of the geometry and extremity of the cells.

An important note from the the Wikipedia article >>

  Unlike centrioles, centrosomes are required for survival of the
  organism. Acentrosomal cells (i.e. cells without centrosomes) lack
  radial arrays of astral microtubules.

  They are also defective in spindle positioning and in ability to
  establish a central localization site in cytokinesis.


You take a population of fish and put them in a new environment (another planet even). Will they evolve?

Yes they would evolve as long as they don't get extinct. It sounds very likely that they would very quickly get extinct though.

Note, however that they were already constantly evolving while being on earth whether or not their environment was stable or changing through time. Evolution is not a thing that occurs only when the environment is changing. Stabilizing selection, genetic drift and mutations affect the allele frequencies too, not only directional selection.

General comments on the post

I don't quite understand the relationship between the first paragraph and the second paragraph.

The first paragraph suggests a few misunderstanding of evolutionary processes. I recommend that you have a look at a free online introductory course of evolutionary biology such as Understanding Evolution by Berckeley University for example. Typically, if some concepts I used in the second paragraph above were unknown to you, then you definitely want to have a look at Understanding Evolution


Agarose vs agar? Why do DNA gels use agarose only and how do you obtain agarose from agar?

The answer to the first part of your question can be found on Wikipedia:

  Agar is a heterogeneous mixture of two classes of polysaccharide:
  agaropectin and agarose. Although both polysaccharide classes
  share the same galactose-based backbone, agaropectin is heavily
  modified with acidic side-groups, such as sulfate and pyruvate. The
  neutral charge and lower degree of chemical complexity of agarose make
  it less likely to interact with biomolecules, and, therefore, agarose
  has become the preferred matrix for work with proteins and nucleic
  acids.

This page compares the result of using agar gels to that of using agarose:

The second part of your question: here's a patent, although I have no idea whether this method of agarose purification is widespread.  Propylene glycol purification of agarose does seem to pop up a lot.  I think people who  purify their own agarose use that method, but I am not sure if biotech companies have other methods.

EDIT: it's propylene glycol, followed by ethylene glycol, that is commonly used, but PEG has been used at least once.


Biological significance of correlation between the radius of gyration and number of layers of convex hull of protein structure

From reading the paper, I don't see any obvious biological significance. The abstract says:

  Proteins exhibit intriguing diversity in their three-dimensional conformations that enables them to perform different functions

Which is great, but there is no connection in this paper between conformation and function - not surprisingly as this is a large part of structural protein analysis!

The way I look at this work is similar to the idea of a "descriptor" from the field of Cheminformatics. The radius of gyration is a descriptor, and so is this hull number. The author claims a correlation between these two descriptors, so... is one easier to calculate than the other?

This is interesting work, but I'm not sure at this point what the significance of hull number is for protein structural analysis. However I can say that the correlation between these two descriptors is not biologically significant - it's just a geometric relationship that would presumably hold for any set of 3D points.


When analysing phosphoproteins via Western blot, why is total protein level of the target protein recommended as an internal loading control?

It is because you don't know how your treatments affect the expression of the total specific protein; perhaps it down- or up-regulates the amount of protein being made, but the relative proportion of phosphorylation doesn't change. For example:
Imagine you have 4 samples from different treatments of which you have loaded an equal amount of total protein (lets say 50 ug total, note that this is too much to load on a WB for accurate quantitation; usually you want less than 10 ug). You run a western blot and find the following numbers (completely made up BTW) for the specific protein. In this scenario, 1 is untreated control.

10 ug
20 ug
10 ug
20 ug

You then try the phospho-specific antibody and get the following

1 ug
2 ug
3 ug
1 ug

What does that tell us about the 4 treatments?
Well, it tells us that 2 is up-regulating the total protein, but the relative proportion of phosphorylation is the same. In 3 phosphorylated protein is up-regulated (3x) but not total protein and in 4 total protein is up-regulated but phosphorylated is down-regulated (0.5x).


Why do bacteria adapt quickly to antibiotics but not to much more common threats?

Antibiotics usually target a single protein (most commonly components of the ribosome machinery). If you have a large population of bacteria, there are bound to be cells with mutations in the gene encoding for the target of the antibiotic that render the antibiotic ineffective. Microbes also have drug efflux systems that can help with resistance to antibiotics. Temperature on the other hand has broad lethal effects from disrupting the cell membrane to damaging DNA and affecting the reaction rates of vital enzymes so that it's impossible to adapt in such a short time by gaining a few mutations.


What are the sources of energy that alcohol provides?

Ethanol is converted into AcKoA, which can be "burned" in the Krebs cycle or can be used to build fatty acids.

By chronic alcohol consumption there is another pathway involving MEOS which converts ethanol to AcKoA as well.

  Are they more likely to turn into fat (as in beer belly) than blood
  glucose?

It won't turn into glucose, just into fat.

Note:

It is suspected that in extreme cases, like low glucose diets and starvation there is an AcKoA -> glucose pathway.

2011 - In Silico Evidence for Gluconeogenesis from Fatty Acids in Humans

So in theory it is possible to convert ethanol to glucose, but there is not enough evidence of that yet. Normally this conversion (if it exists) does not happen, or it has a very low rate...

  What compounds in alcoholic beverages (edited) give energy?

Mostly ethanol and sugar. E.g. sweet wine contains a lot of sugar, not just ethanol...


Wear two sets of gloves.  First, use nitrile gloves, not latex for this. 4mm or thicker is a specification I would recommend to avoid tearing.  Latex will bind too well to itself and tear easily with increased friction etc (same logic behind not using two condoms).  Also, use a coat with an elastic cuff on the sleeve.
So here's the breakdown

Put on first set of gloves
Put on coat over gloves.  Decon if needed for application.
Put on second set of gloves.
Science
Take off second set of gloves.
Decon as needed for your health
Take off coat
Take off first set of gloves

I can find sources for this, but I've been doing ABSL2 and BSL3 for a while, and they always go through this in safety training.

Edit: My internal nagging to site got the better of me, so some examples that recommend double gloving:

http://oehs.vcu.edu/chemical/labsafe/perchloricacid.pdf

https://extranet.fhcrc.org/EN/sections/ehs/hamm/chap3/section6.html

http://orsp.umich.edu/policies/um/committees/BRRC/ADDITIONAL_PRACTICES_revised_8_7_14.pdf

http://ehs.columbia.edu/carcmutguide.html

I could go on, but I think you get the idea.


Why there aren't any pandemic diseases by prions?

I think that you could argue that some prion diseases do form epidemics or outbreaks. In some cases it does appear that people have referred to BSE/vCJD as pandemics. There is even some journalism on the topic, and see also here.
Infection by prion from the environment does occur at some rate, and it is true that it is these prions are the more transmissible. See Table 1 in that linked paper for more information; it appears that the discovery of prion excretion through e.g. feces is relatively recent.
For less transmissible variants it is true that you usually have to directly ingest a fair amount of prion from (i.e. eat) an infected individual to be affected, which is a harder means of transmission because it implies cannibalism (which is not that uncommon biologically, but still).


Do ants also use the Earth magnetic field?

Hard to say, but for at least one ant species (see below) it seems to be an orientation cue for (relatively short-distance) migration (even if you're only going a few meters, it can be important to walk in a straight line!). At present it seems we know something about the proximal mechanisms of magnetoreception, and a little bit about the observed behavioural patterns, but don't have much more than informed speculation about the ecological/evolutionary advantages of this form of spatial orientation.

Searching "ant magnetotaxis" gets to this article on magnetotaxis in the migratory ant Pachycondyla marginata:

  The influence of geomagnetic field changes on the behavior of ants has been studied in the species Solenopsis invicta (Anderson and Vander Meer, 1993), Formica rufa (Çamlitepe and Stradling, 1995), and Oecophylla smaragdina (Jander and Jander, 1998) ... Another migratory insect species is the ant Pachycondyla marginata, which has very peculiar habits: a diet of living termites and migration in a preferential direction (Leal and Oliveira, 1995). These habits make such a migratory ant very attractive for the study of biomineralized magnetic materials.

From Leal and Oliveira 1995 ref above:

  Migration by P. marginata colonies lasted over 2 days and covered distances of
  2-97 m (n=48).

Selections from Acosta-Avalos et al. 2001 Naturwissenschaften:

  abstract: Migrations during the dry/cold season are significantly oriented 13 degrees with the magnetic North-South axis, while rainy/hot migrations do not exhibit a preferred direction. This result is discussed considering the hypothesis that P. marginata ants may use the geomagnetic field as an orientation cue for migrations in the dry/cold season.

  Given that colonies resume nest relocation late
  in the afternoon of the second day, most of the migratory
  process takes place under darkness conditions.

  On  the  other  hand,  nest  relocations  in  the  dry/cold
  season can be considered as typical migrations.

  The  use  of  geomagnetic  cues  is  more  commonly  associated with darkness conditions, as reported for mole rats
  (Marhold et al. 1997) and also proposed for bumblebees
  (Chittka  et  al.  1999).  As
  P.  marginata
  ants  start  the
  migratory  process  in  the  afternoon,  they  can  use  any  of
  those  cues  in  their  orientation  during  the  migratory
  journey. However, it is intriguing that they prefer an axis
  around the North–South axis to migrate. The only possible
  cue  to  give  this  information  under  all  conditions  is  the
  one  provided  by  the  geomagnetic  field.


Quick overview of how to capture microscope images of histology plate or fluorescent plate

For fluorescent microscopy images, wondering if I actually need a fluorescent microscope, or if I can make do with a regular optical microscope.

You need a fluorescence microscope. You need to be able to excite your sample with a narrow wavelength of light, and then image a different wavelength of light that is emitted. You need mirrors, emission and excitation light filters for that. You also need to understand the process. If you don't, having software to do the 'thinking for you' such as overlaying the different color channels is a nice thing, but then it's another requirement.

  If I need a fluorescent one, wondering if there is anything else needed, like special lighting or special materials for tagging the cells, which seems like it might require extra stuff like centrifuge and who knows what else.

Samples can sometimes have autofluorescence (e.g. the chitin that makes up the cuticle of insects is autofluorescent) but most samples are not. Almost always a fluorophore is used to stain the specimen for something. These can be cheap or very expensive, depending on what you want to stain. This really depends on your sample and how it is prepared. And know that most 'good' samples' are dehydrated or are treated by chemical fixation, which requires chemicals you cannot usually find at a local pharmacy. It depends on how ambitious you want to get as an amateur microscopist!

Also, you won't need a centrifuge.

  For the histology slides, wondering generally what it takes to do that too, if I can get by with a regular microscope.

You can get by with a regular upright widefield microscope for sure. If you perform the sectioning well (making thin slices of your sample) then even basic microscopes will produce fascinating images, provided your lighting is good. It helps to have a condenser or a nice lamp and some thin and clean glass slides for well illuminated images.

  Maybe fluorescent microscopy requires advanced biotechnology of some
  sort, which is sort of what I'm wondering, what the basics are.

It requires a little bit more optical work. I would stay away from it unless you are serious, because it takes quite a bit more work and equipment to make it minimally workable. Normal microscopy is certainly a lifetime of fun if you have the desire to find interesting samples and work to make them good for imaging.

Addendum: the principle of fluorescence microscopy is quite simple but aligning everything is actually quite difficult if you are an amateur with no specialized tools. Here is the principle only, notice how the input and output must be aligned and the small objective lens has to transmit both excitation and reflected light:

And here is an example of a basic lab stain for two elements of the cytoskeleton (actin in red and microtubules in green) and a DAPI-type stain for nucleic acids (that shows you the DNA-rich nucleus in blue). The crispness of the image really depends on the use of at least two or three lasers (not epifluorescent illumination, i.e. "lamp nearby") to produce the necessary and specific narrow excitation to separately image the different channels. The light detectors are in black and white (for increased resolution), and only in post-processing are they color-coded to make the image pretty.

For a start I would begin with the basics! Pollen, cells on the inside of your cheek, blood, a single onion layer (...is a monolayer of cells, perfect for imaging), anything else you find and can think of! And find yourself a nice stain, or a nice dye or ink that is partially permeable. The world is your proverbial oyster at this point.


Is there an evolutionary advantage for coconut oils to be rich in saturated fats?

This is entirely speculation, but the part of seeds that is pressed for oil(the endocarp) is enriched in saturated fats and long fats in ocean-going fruits. The coconut is 91% saturated fats, the oil palm is about 50%, etc. The tamanu or 'ballfruit' produces monounsaturated long-chain fatty acids in the endocarp, about 75% C18 oils, mono- or di-unsaturated.The calabash is astonishingly 20% saturated and 78% C18 oils, and is also sea-distributed(these seeds are called disseminules).

It's not a totally straightforward correlation. Peanut oil is 75% C18+ and 15% saturated and the oil palm mesocarp is only 50% saturated, but the endocarp is 81% saturated fats.

There's an additional consideration here: longer chain fatty acids are slightly more energy efficient per unit mass than shorter chain ones.

Without better data on energy density or spoilage rates on different blends of long-chain fats I can't conclude conclusively that spoilage and energy density are why disseminules tend to have longer-chain oils and more heavily saturated fats, or even that they definitely do. But it looks like they do, and that would make sense.


Is natural selection a tautology, and therefore not truly falsifiable?

I think @Remi.b's answer is great and really the only way to answer your questions is with a comprehensive introduction to evolution. However, I wanted to address the tautology issue more directly.

First, the "survival of the fittest" seems like a tautology with "natural selection" because it is not a description of how natural selection works, rather, it is a phrase meant as a synonym for natural selection, to help describe the result to someone unfamiliar with the phrase.

Let me use an analogy: it would be like if you were a very new learner of English, and I told you "Joe's truck has more mass than an elephant!"

If you aren't really familiar with the term "mass" in English, this phrase could be confusing. So I explain instead that "Joe's truck is heavier than an elephant." If you know the word "heavy" this is easier to understand.

However, there is a tautology there! the car is actually heavier because it has more mass, but that does not make either phrase untrue or untestable: it's just another way of saying the same thing within a context (i.e., those statements are the same if they are exposed to the same gravity).

The testable hypothesis that natural selection makes is that, given 2 things: 1) a population where individuals have traits that give them different chances of survival, and 2) some way for offspring to inherit traits from their parent(s), then the population over time will consist of individuals who are more likely to possess the traits that gave a high chance of survival.

Following this, should the environment change in some way such that a different trait is now beneficial, that trait will increase in prevalence.

There are way too many experiments to summarize here that show 1), 2), and a combination of 1) and 2), as well as experiments that show that indeed, when you have 1) and 2) you get natural selection.


What is the role of potassium acetate in plasmid extraction?

The alkaline lysis method of plasmid purification involves the addition of sodium dodecyl sulfate to lyse the cells and sodium hydroxide (a strong base) to denture the DNA. Potassium acetate is then added for two reasons:

The acidic acetate buffer neutralizes the solution and allows catenated plasmids to renature.
Potassium dodecyl sulfate is poorly soluble in water. Adding potassium to solutions of dodecyl sulfate precipitates it, thus facilitating its removal.


How long would it take for a change to the DNA would take effect?

OK, let's set up a specific hypothetical situation so we have some details: A virus (we'll call it Human Nasty Virus 1 (HNV-1)) can infect T cells (a type of white blood cell in the immune system) by binding to a certain receptor on its surface, which we'll call the Nasty Virus Receptor (NVR). Scientists have found that HNV-1 absolutely needs a certain protein sequence in NVR to bind, as people with a certain mutation lacking that sequence are completely immune to HNV-1 infection.

You sign up for a clinical trial using gene editing to specifically remove that DNA sequence from the NVR gene. Once that changed gene is transcribed and translated into protein, it is expressed on the surface of the cell, and HNV-1 can no longer bind.

T cells are derived from stem cells that live in the bone marrow. In order for the gene therapy to work, doctors will need to perform a bone marrow transplant - they will remove a sample of bone marrow, give it to the scientists for the gene editing process, then reinject the edited cells back into you. The editing process involves subjecting purified stem cells to a process called CRISPR, allowing them to grow in culture for a while, then screening the cells to select only those where the editing was successful. The successfully-edited cells are separated, cultured some more to expand their numbers, then given back to the doctors, who put them into your body, either into the bloodstream or directly back into the marrow.

So now you have your edited cells back inside you - how long will it take to become immune to HNV-1? Well, the honest answer is that, in the absence of ablative chemotherapy (see the bone marrow transplant link above for more info) prior to reinjection of the edited stem cells, you may never become completely immune. Here's why: Unless all of the bone marrow stem cells in your body are destroyed before reinjecting the edited ones, you will still have fairly high numbers of what are called "wild-type" or un-edited stem cells and mature T cells in your body, and those stem cells will continue making new wild-type T cells. Additionally, there are already wild-type T cells in circulation and in secondary lymphoid organs such as lymph nodes and the spleen, and some of these cells can be very long-lived (months to years). If for some reason you decide to undergo complete ablative chemotherapy to essentially destroy your immune system, the reinjected stem cells will eventually repopulate everything and you'll be immune to HNV-1, although you will have potentially lost your immunity to everything else you've ever been exposed to, unless the chemo is done in such a way as to preserve your immune memory cells.

This is actually a best-case scenario, as we were working with cells that can (relatively) easily be removed from the body, edited, screened, and reinjected. If you were trying to cure a genetic disease that affected solid tissue like the muscles (see Duchenne muscular dystrophy for an example), you obviously wouldn't be able to remove all the muscles and edit them ex vivo, you'd have to do the editing in the body, most likely using a viral delivery system for the editing machinery. The viruses wouldn't infect every single cell, and the editing wouldn't work in every cell that got infected, so the best you could hope for would be a partial cure. For some diseases, this may be enough, and many companies are working on this from various angles. There are also other options besides CRISPR-mediated gene editing that have higher success rates in vivo.

Finally, getting back to your original question of how long it takes from DNA alteration to expression of the gene product, the answer is that it depends on the gene and the context. In the case of our hypothetical situation earlier, as soon as the NVR gene's DNA is edited, the new sequence begins to be transcribed and translated into protein. There is still some wild-type protein left over initially, so it depends on the transcription rate of the gene and the turnover of the existing protein. Some proteins have an extremely long half-life, on the order of years or decades (or more!), while some degrade within minutes to hours of being synthesized.


What are the negative consequences of a narrowed biodiversity to the planet?

From an ecological sense, cycles of living beings are intertwined. Breaking cycles affects life being able to live, reproduce, and die in a manageable way. Insects, animals, and plants help feed each other and help them reproduce. Fewer insects are less of a food source for animals and can't pollinate plants as much. Reduced animal populations are less of a food source for scavenger insects and don't feed plants through manure or decay after death. Fewer plants means less food and protection of insects and animals from predators. Predators overload on newly-available prey and their populations crash. It all intertwines.

From an environmental sense, the results of a narrowed biodiversity include putting more carbon into the atmosphere. In addition to warming the planet and the ocean, the ocean acts a carbon sink, acidifying in the process. This damages existing sea life that can only live within a certain pH and temperature range without sickening or dying. Some fish are trying to migrate and are dying off, due to lack of food where they are headed.

From a medical sense, burning down forests is stupidity. There are drugs that are naturally found in their rare plants, which have been developed into medications that save lives, e.g. Paclitaxel or Taxol. Only 1% of remaining rainforests have been explored for these plants and their compounds and we're stupidly burning them up. Nature has evolved many useful remedies, but we'll never know about the ones we destroyed, and that means more sickness and death.

For people obsessed with money, that medical sense translates just as well into pharmaceutical products and the resulting loss of jobs and profits.

All of these factors are linked together, hand-in-hand.


Are stem cell lines cryogenically preserved or commercially available like HeLa cells are?

This is too long for a comment, so I have to write it in here:

Mostly this is because other cell lines are more practical in the lab.

Stem cells are much more tricky to maintain - especially if you want to keep their stem cell properties. They only grow very slow, tend to differentiate when they get too much stress, cellular signals and so on and need special media (these need to be defined, so that they are not containing factors which promote differentiation for example).

For everyday experiments (like expression profiles, experiments on the effects of certain substances on the growth, gene expression or whatever of cells) "normal" cell lines are much more suited as these are much easier to keep in the lab using standard media. Additionally,experiments can be more easily repeated and reproduced, since these cells should behave always the same.


What would be the scientific name of this worm

If you would have read the text from the source of that image (which by the way you didn't mention, I did a Google Image search and edited your question to include it), you would have known that what is seen in the picture is not a living thing, it is a latex fishing lure:

  Product Description: Sandworm/Ragworm 8″ size, sure fire fish catching lures. Costing less than live worms, but lasting much longer, never be without worms again.

Source: http://www.seafishingtackle4u.com/softbaits/ragworms-latex-lures/


Why are fertilizers with polonium 210 used when growing tobacco?

According to RADIOACTIVITY IN CHEMICAL FERTILIZERS by Milica M. Rajačić, Nataša B. Sarap, Marija M. Janković, Jelena D. Nikolić, Dragana J. Todorović and Gordana K. Pantelić at the Institute for Nuclear Sciences "Vinča", University of Belgrade, Belgrade, Serbia, and the relatively short half-life of polonium, it appears that primordial metals are the only hazard in fertilizers:

  Natural radioactivity results mainly from primordial radionuclides,
  such as 40K and the radionuclides from the 232Th, 238U and 235U series
  and their decay products. Terrestrial radioactivity and exposure due
  to gamma radiation depend primarily on the geological conditions and
  appear in different quantities in the soils of each region in the
  world. 1 [...]

  Fertilizers usually employed in the agriculture contain traces of
  heavy metals and relatively high concentrations of naturally occurring
  radionuclides. Phosphate containing fertilizers have been used
  worldwide to increase the quantities of the micronutrients, which are
  being continuously taken off from the soil due to farming activities.
  At the same time, the use of such fertilizers is the main
  anthropogenic source of the uranium input in the environment (about 73
  % of the total input of uranium) 2. [...]

  A total of 140 samples of different types of fertilizers were measured
  for their radioactivity content using gamma spectrometry technique in
  order to assess the implications of extended use of fertilizers on the
  concentrations of natural radionuclides in cultivated soil. The
  obtained data show that the activity concentration of naturally
  occurring radionuclides in fertilizer samples were 87 Bq/kg, 4860
  Bq/kg and 220 Bq/kg for 226Ra, 40K and 238U, respectively, which
  exceeds the activity concentration in soil by an order of magnitude.
  As it was shown in the paper, the use of fertilizers has a negligible
  effect on Raeq and D in soil due to dilution of fertilizer used on the
  large amounts of cultivated soil. However, the long term application
  of these fertilizers can have the effect of an accumulation of
  radioactivity in soils that can be harmful for the health of farmers
  and consumers of the products. [...]

  1: Akhtar N. Radionuclide pollution due to fertilizer use in some
  saline soils of the Punjab and their potential risk assessment on
  human health. Department of Physics Bahauddin Zakariya University
  Multan, Pakistan, 2006. 2: Stojanović M, Stevanović D, Milojković J,
  Mihajlović M, Lopičić Z, Šoštarić T. Influence of soil type and
  physical–chemical properties on uranium sorption and bioavailability.
  Water Air Soil Pollut 2012;223:135-
  144.

Artificial fertilizer is cheaper than regular fertilizer that also contains long-term nutrients, but also contains Po-210:

  Among all carcinogenic substances contained in tobacco smoke, Polonium
  210 (Po-210), with a half-life of 138 days, is one of the most
  dangerous, by exerting a devastating, chronic, slow and progressive
  carcinogenesis activity. The main source of Po-210 in tobacco is
  represented by fertilizers (polyphosphates) containing radium-226
  (Ra-222) which decades to plumb 210 (Pb-210). Through the thricomes
  Pb-210 is concentrated in the tobacco leaves, where it turns to
  Po-210, which at the cigarette combustion temperature (800-900 degrees
  C) reaches the gaseous state and it is absorbed by the micro particles
  released into tobacco smoke. Thus, smoke becomes radioactive in both
  its gaseous and corpuscular components and reaches the airways, where,
  particularly at the branches level and together with other substances,
  it exerts its carcinogenic activity, especially in those subjects with
  impaired respiratory mucosal clearance. The carcinogenic risk/one year
  lifetime of a smoker of 20 cigarettes per day is equivalent to that of
  undertaking 300 chest x-rays. It is calculated that Po-210 may be
  independently responsible of 4 lung cancers every 10,000 smokers.
  During cigarette's combustion, tobacco smoke is also released in the
  air, contributing to serious health risks for those exposed to passive
  smoke.


Does this leaf belong to carissa macrocarpa?

This plant seems to be Carissa carandas. With the thorns placements besides leaves, I was sure that this plant belonged to genus Carissa. Taking advice from Bryan Hanson, I searched for the plants in the same genus in my locality(Hyderabad, India). The white flowers and their rosy stalk made it easier for me to search. I found out that this is a common plant in country side and is used in many dishes. Thanks Bryan for pointing me in the correct direction.


Following DNA replication during S-phase of the cell-cycle, are all genomic regions subjected to the same stringent level of DNA-Repair?

So far, the known mechanism of DNA repair is to recognize mismatches or damaged nucleotides by enzymes surrounding DNA rather than by scanning along DNA. Therefore double check could not happen under such conditions.


How much of the human body is processed sunlight?

I think that Carl Sagan said it best:

  The nitrogen in our DNA, the calcium in our teeth, the iron in our blood, the carbon in our apple pies were made in the interiors of collapsing stars. We are made of starstuff.

The current view of cosmology is that every atom that isn't hydrogen, helium, or lithium was created in the fusion furnace in  the hearts of giant stars. These heavy atoms were then spread about the place by supernovas.

However, there's a lot more to the matter that makes up living creatures than just the atoms. The vast majority of the free energy that allows for the creation of intricate organic molecules with complex patterns of chemical bonds (e.g. protein, DNA, etc.) does indeed originate with our sun.


What differentiates diseases like Covid-19 and Polio from the common cold

There is not really an inherent difference between these viruses.  Polio is a run of the mill enterovirus - some of its closest relatives are "common colds", while others are less pleasant - see https://www.slideshare.net/TarekMahbubKhan/enteroviruses-and-polio for some examples.  Note that some "common cold" viruses have uncommon but nonetheless devastating polio like effects; a leading culprit for acute flaccid myelitis (polio-like paralysis) was the common cold enterovirus D68 ( https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(18)30094-X/fulltext but I haven't checked for updates lately).  But for that virus, damaging replication in nerve tissue is at most a rare complication rather than a frequent one.

Coronavirus has long been known for several strains of "common colds"; they were just not as frequently deadly.  Unfortunately, we did not see the "cold and flu season" as a demonstration of defenselessness against viral outbreaks, and did not use the opportunity to practice exterminating them.


Perception of distant lights without glasses

This phenomenon is known as bokeh.

You are right in the hexagonal shape being produced by the iris (of the camera), and from this, it is clear why this happens: The iris blocks out some of the light travelling into it, and a shape approximating that of the camera's iris aperture is projected onto the CCD.

The same thing happens for the eye. The iris will block out a portion of the light, causing the bokeh to approximate the shape of the iris aperture (aka the pupil), which is roughly circular for humans. Animals with non-circular pupils will perceive differently shaped bokeh. If the lens suffers from astigmatism, it will also result in non-spherical bokeh being projected onto the retina.

This stackexchange link goes into greater detail on Gaussian blur vs bokeh.


Minimum amount of RNA for cDNA conversion and qPCR

Two answers follow:

Technical experience of many: it should be no problem to have the same protocol with a twice-lower starting concentration, without making any adjustments whatsoever. The suggested 1ug is very much on the safer side of things, 2-fold fewer transcripts makes almost no difference. Maybe at 1 or 2 orders of magnitude (10 to 100s) less will you run into problems or a need to correct your reactions.
Scientific orthodoxy: the most scientific piece of advice anyone can offer you would be to try it both ways and compare your results using qRT-PCR. I'm guessing both approaches will show very similar results.


There is evidence that copper pots have antibacterial effects when used for storing drinking water (Sudha, et al. 2012), so the copper coins will probably have a similar effect.

The easiest way to test this at home would probably be to buy a test kit from an online vendor - these are relatively inexpensive.

Some Googling produced this website [appslabs.com.au], which has some tests for common types of bacteria. There are undoubtedly others too, if these don't sound suitable


Are there any known rules that neurons always follow while transmitting/receiving signals?

Short Answer:

"Always" is always a dangerous term in biology.

Longer Answer:

  What does a neuron do if it does not get stimulated/receives no signal for a long time. Will it die ... or try to find new connections that might send signals?

What neurons do when they aren't stimulated depends on the neuron and phase of development. Typically, thresholds for spiking will decrease, but it's also normal for cells to atrophy and die: neuronal death is a critical part of development, and loss of synaptic connections and some neurons is the most obvious feature of human brain development during adolescence, rather than birthing new neurons or growing new synapses.

  What does a neuron do if it is over-stimulated?

Overstimulated neurons may die, they may also reduce the efficacy of their inputs either by increasing their thresholds or reducing synaptic weights by removing postsynaptic receptors. Calcium is an important mediator of these signals - you could read about its role in long term depression for example (this has nothing to do with 'depression' in mental health, just reduction in synaptic weight). There are also short-term effects that limit overstimulation of particular pathways, with many acts on the pre-synaptic rather than post-synaptic cell. Neurotransmitter is held in vesicles, and after release, there are fewer vesicles available for the next release event. Presynaptic terminals also often have autoreceptors that cause negative feedback and limit subsequent transmission.

  What does a neuron do if it receives a signal -> does it broadcast it to all of its connections, or only 1

Of all your questions, "does it broadcast it to all of its connections" has the simplest answer: biological neurons almost always broadcast to all of its forward connections in response to any sufficient input (just like most artificial neural networks). However, the release probability at any one synapse is typically <1. Therefore, a given cell can make much higher-fidelity (and also higher-amplitude) connections with another cell by the number of contacts. If a typical cortical neuron makes only one synaptic contact with another cell, there will be a high rate of failures of transmission between the two cells. It's common for stronger connections to involve up to hundreds of individual contacts, just between two cells.

  Can a neuron send out a new signal without having received a signal from anywhere else

Some neurons are spontaneously active. There are various types, but the most familiar are the ones thought of as intrinsically oscillating. An example are the sinoatrial node cells of the heart (although these are not really neurons, they act a lot like neurons; there are similar cells that are neurons that control respiration). There are also some CNS cells.

  How does a neuron know if it has done his job "well". How does it get positive feedback.

This question is the most complex of all the questions you asked, entire textbooks and journals are needed to answer it, and it isn't at all possible to answer here. I'll just say that many of the learning rules used in artificial networks are not biologically plausible, they are simply computationally efficient. Biological neural networks use a lot more recurrent activity than artificial ones do, and a lot of the feedback like this occurs within that recurrent network. Biological networks are also built to do a variety of computations, and learning rules that apply in one may not apply in another. For example, pattern separation versus pattern completion require completely different learning rules.

However, the very general principle of updating synaptic weights in response to errors or outcomes does hold between artificial and biological networks.


Do voltage-gated calcium channels affect neuronal conduction speeds?

Most of the time, calcium is not the most important ion in terms of active propagation of an action potential along an axon. It is usually sodium and potassium which play the key roles here. In most living things the concentrations of ions for the intracellular and extracellular solutions are similar. For an action potential, you usually have an influx of sodium followed by an efflux of potassium. The sodium influx depolarizes the membrane and the potassium efflux re-polarizes it. The speed of conduction is determined by the membrane resistance and its "leakage". That is to say, how easily can a single travel along an axon? This is determined by the diameter of the axon, the greater the diameter, the faster the conduction. The leakage refers to ease with which ions leak out of the axon as the signal is propagating. Insulation via myelin sheaths help in preventing this, and, less leakage, the greater the signal at the next propagation site.

Calcium is the most important ion for the transmission of a signal from a pre to post synaptic cell. Without calcium, you have no neurotransmitter release. This is because the influx of calcium triggers a series of events involving the snare complex which eventually leads to vesicular release of neurotransmitter in quantal units. If you remove calcium from the extracellular solution, you will have no neurotransmitter release. If you block the calcium channels, you will have no neurotransmitter release.


This is an "aphid lion", a larva of a lacewing (family Chrysopidae). They eat aphids and other small animals, not blood, but are capable of biting humans. Here is a text about that (seems reasonable even with the silly title). It also says that "When a lacewing larva bites a human, it’s likely that any persistent itch or redness is due to the saliva injected at the site of the bite" so that would explain your pain.


I always add the Taq to the mastermix. First it makes the handling easier and it avoids pipetting steps which can cause contamination and can also be forgot. Then the enzyme is very stable and will even tolerate room temperature without problem. Since we are going to heat this 30-40 up to 95°C, so this is clearly not problematic. Since the reaction mix is cooled, you reaction will not start. And even if it does, there wouldn't be much amplification due to the low temperature.

I usually add everything which is the same for all reactions to the mastermix (this can include the DNA as well). If I use more than one DNA I split the mastermix in half. This way you are not going to make different pipette errors for the template, which is especially important for realtime-PCR. I usually dilute the primers slightly so I can pipett bigger volumes (simply use a part of the water used to balance the PCR reaction). You can also premix primer pairs, if you want, I have never seen problems doing this.


The article "Dental Anatomy of Rabbits and Rodents" (Crossley et al. 2010) provides a basic review of rodent teeth, as there are over 1700 species.  But, in general, the teeth are constant replaced due to abrasion.

What the mechanism is for continual dental growth in rodents are, in part, discussed in the article "Tooth organogenesis and regeneration" (Thesleff and Tummers), where they state

  During the cap and bell stages the lateral sides of the epithelial bud start enveloping the underlying dental mesenchyme, and from this point onwards the leading edge of the epithelium is called the cervical loop. The basal epithelial cell layer of the loop bordering the dental papilla is known as the inner enamel epithelium and the part facing the dental follicle is known as the outer enamel epithelium. The core of the loop is populated by loosely arranged stellate reticulum cells and a thin layer of stratum intermedium cells facing the inner enamel epithelium This cervical loop structure is maintained in continuously growing teeth and constitutes the epithelial part of the adult stem cell niche (Harada et al., 1999; Tummers and Thesleff, 2003: Tummers and Thesleff, 2008)


Is there any evidence that soft tissue can be preserved for 65m+ years and if not what hypotheses exist to explain it?

Schweitzer et al. (2007) studied soft tissue preservation in a number of specimens, including an 800-1000 year old moas, 300,000 year old mammoth and mastodon, and 65 million year old *T. rex. and Triceratops. The oldest specimen was a 78 million year old Brachylophosaurus. Their goal was to try to find common environmental conditions that favor soft tissues preservation in fossils. As of this study, they have not been able to identify a single common environmental factor that seems to favor soft tissue preservation. They did note, however, that the specimens from which they could extract soft tissue (with varying success) were from fluvial sandstone environments, meaning sandy rivers. They (so far) could not extract soft tissue from terrestrial mudstone or marine environments.

Note that Schweitzer et al. did successfully extract soft tissue from the mastodon. The conditions required for mummification are probably not conducive to soft tissue preservation.  Here is a good blog article on one of Schweitzer's previous studies of soft tissue preservation.

The importance of extracting soft tissue from fossils cannot be overstated. Based on Schweitzer's work, her and her colleagues (Organ et al. 2008) were able to develop a phylogeny that incorporated both mastodon and T. rex. The used the amino acid sequence from collagen, a protein that is abundant in soft tissue. She and her colleagues repeated the analysis (Schweitzer et al. 2009) and included Brachylophosaurus, a hadrosaur. As predicted by morphological and other evidence, the mastodon was most closely related to modern elephants and the two dinosaurs were most closely related to modern birds and alligators.

Here is the phylogenetic tree derived from Schweitzer's 2009 study. Mammut is the mastodon. Brachylophosaurus and T. rex are the two dinosaurs.

Literature Cited

Organ, C.L. et al. 2008. Molecular phylogenetics of mastodon and Tyrannosaurus rex. Science 320: 499.

Schweitzer, M.H. et al. 2007. Soft tissue and cellular preservation in vertebrate skeletal elements from the Cretaceous to the present. Proceedings of the Biological Society of London B: 274: 183-197.

Schweitzer, M.H. et al. 2009. Biomolecular characterization and protein sequences of the Campanian hadrosaur, B. canadensis. Science 324: 626-631.


Strange Exoskeleton Found in Maine: What is It?

It seems to me the ootheca of a mantis before larvae eclosion. You can read more about it here.

.jpg


What is the name for when genetic deviation results in an organism that doesn't work?

If you are referring to the mutation
I think the word you are looking for is lethal.
A lethal mutation is a mutation that causes the death of its carrier. Now there are recessive lethal and dominant lethal. For dominant lethal mutations, all heterozygotes are inviable. For recessive lethal, only double mutant homozygotes are inviable.
If you are referring to the individual
An individual that is not able to survive and reproduce is said to be inviable (I already used the term above). However, the reason for it is not necessarily genetic.


Does science have an explanation of how the first "common ancestor" formed in evolution?

Darwin's theory of evolution (and the modern theory of evolution) explains how the current diversity of life developed. Remember, the title of Darwin's book is On The Origin of Species, not the origin of life.

As for how the current diversity of life developed, or how species originate, the theory of evolution states that life forms change and diversify gradually, and species arise and differentiate from related species, via the processes of random mutation at the time of reproduction and natural selection. The ToE is a complex set of theories with many different semi-independent aspects but that's what it basically comes down to.

Clearly all this requires life, or imperfect reproduction at least, to exist; it says nothing about the first life, and it cannot say anything about it because given what we know of the processes that lead species to arise and life to diversify and aquire its form, those processes cannot possibly have been in play when going from abiotic stuff to the first living systems.

In other words, the Theory of Evolution is how life develops once it starts existing; it would work equally well if the first life appeared via natural chemical processes or was created by alien tinkerers or the result of a time paradoxical sandwich dropped in the wrong place on primordial Earth. The study of how life could start existing is usually called "abiogenesis".

The issue isn't actually as clear-cut as it may seem, since there is a very wide unknown space between what we consider the most archaic forms of life, and any entity that could plausibly arise via purely abiotic processes; every theory of abiogenesis does assume that a lot of the features we consider essential to life must have arisen after some kind of replication appeared, meaning those features would have evolved. So there definitely is some evolutionary biology involved in investigating abiogenesis, and maybe if we ever solve abiogenesis it will be folded into the ToE (like I said, the ToE is actually a complex set of theories and observations, not one single thing. So while our understanding of what the theory says and can say currently excludes abiogenesis, our understanding and definition of the theory could evolve). But we haven't, and it currently isn't.

You need to edit your question however, because it is completely unclear from the title or text that you are asking about abiogenesis. Your question sounds like it's about embryonic development or biochemistry. Those are the current instances we have of organisms forming; whatever processes were at work in creating the very first life, well for one thing maybe we wouldn't want to call whatever that was an "organism", but more to the point those processes cannot happen today. The atmosphere is wrong and too full of oxygen, there are organisms everywhere vaccuuming up whatever resources those original biochemical processes might have used, basically there is likely no chemical environment on modern Earth that's anything like the chemical environment life originated in.

To answer your question though, abiogenesis is currently an unsolved question, so no, Science does not have an explanation of how the first organisms formed. But if you want to have an idea of how things could have happened, what the challenges are in figuring things out, and what things Science currently considers likely or impossible, there is a lot of active research in the field and many different hypotheses. The Wikipedia page for Abiogenesis has a fairly comprehensive rundown on this.

This video describes one of them (my favorite and the first I've found actually convincing, I have no expertise whatsoever to base this on but I plug it anyway; if nothing else it gives an appreciation for what kind of things the researchers in this field look at when thinking abiogenesis) :

https://www.youtube.com/watch?v=av98Brx23_4

(disclaimer: youtube throws up an error for this video for me right now but I've watched it before, I don't know if the video's down or if the problem's on my end)


Do siblings have a bias toward believing they look different from each other?

You are not completely wrong but not completely right either. Some siblings tend to think they are less similar to each other, even twins. It may or may not have scientific reason, but it has sociological reason behind it. Every people in our society want to have their own separate identity and they do not want themselves to be compared with others even with their siblings.It might be also due to the result of fact that, siblings pass times with each other so often that they notice distinct differences in both their characteristics and look while ordinary people, looking at them for the first time, can not notice the differences. This is related to the reason why we can not sometime recognize people from any particular race or ethnicity at first look.


I suspect your problem is grasping what is a deleterious recessive allele. Wikipedia and textbooks explain it much better but I will try to illustrate with respect to your question.

  I have to merge somebody else's code into my code, there would be a heck of a lot of merge conflicts and errors.

Problem with this analogy is that when merging code both variants are written by people. People tend to write code that works on its own. This is not the case for DNA since mutations are usually random and more often than not result in gibberish. Better analogy would be maybe combining information from two coppies of the same data to overcome bit rot.

  Since the regions chosen during meiosis is random, shouldn't a similar DNA from sperm and egg resulted in a more stable genetic code since they are similar?

Lets consider two made up genes A and B.

A is a dominant functional version of A gene involved in development of hand. In very abstract (code-like) way it could be read as: "If at the end of hand initiate 5 fingers"
a is a mutated nonfunctional version of A gene. In very abstract way it could be read as: "If at the end of hand initbzngers". It produces nonfunctional protein. In biological terms "a" is called deleterious recessive allele.
B is a dominant functional version of B gene involved in development of brain. In very abstract way it could be read as: "If in neuron keep junctions together"
b is a mutated nonfunctional version of B gene involved in development of brain. In very abstract way it could be read as: "If in geuron keep junctions together". It never produces the needed protein.

Now lets consider cross between two dissimilar individuals:

father AaBB X mother AABb

Following Mendel's laws they produce progeny:

AABB - has at least one functional copy A and B gene and thus develops fine.
aABB - has at least one functional copy A and B gene and thus develops fine.
AABb - has at least one functional copy A and B gene and thus develops fine.
aABb - has at least one functional copy A and B gene and thus develops fine.

now let's consider cross between two similar individuals:

father AaBB X mother AaBB

Following Mendel's laws they produce progeny:

AABB - has at least one functional copy A and B gene and thus develops fine.
AaBB - has at least one functional copy A and B gene and thus develops fine.
aABB - has at least one functional copy A and B gene and thus develops fine.
aaBB - fails to properly develop fingers.

  cells basically create copies of DNA all the time in our body. ... Why does inbreeding cause genetic defects, but cell division in one's own body does not?

During normal cell division AaBB cells should produce only AaBB copies which have at least one functional copy A and B gene and thus are fine.

Big picture

In a real population imagine every individual has tens of thousands of genes and each of them can be made nonfunctional by random mutation. The nonfunctional copy often does not have effect since the individual has another functional copy. When two non-related individuals procreate, chances are mutations they carry are in different genes and their progeny are fine as illustrated above. When related individuals procreate chances are thay both have the same deterious mutation(s) and not all their progeny will be fine.

  But bed bugs for instance, have managed with inbreeding without any problem (goddamned creatures!).

Species for which inbreeding is normal have much less recessive deleterious mutations prevalence in populations for simple reason. If new deleterious mutation appears the inbreeding leads in two generations to aa homozygots that die or fail to procreate and the "bad" mutations are selected out fairly fast. Inbreeding is normal state for some species. Today inbreeding-resistant species are descendants of individuals who have survived many generations of inbreeding.


DNA test to prove that two grand-grand-children descend from same grand-grandparents

Yes testing for relatedness of grand-grand children is possible. (Ignoring some very unlikely, but theoretically possible cases.)

Grand-grand children are still highly related genetically, and this degree of relation is also shown in standard consumer grade commercial DNA testing kits (such as 23andme, where you could link to other people and see their degree of relatedness to you – even further beyond grand-grand children - or where you could even search for relatives, whom you may not know personally).


Is there a correlation between incidence of type 1 diabetes and vitiligo?

It has been associated with polymorphisms with the CD4 gene, which is usually implicated in type I diabetes. The wikipedia article for vitiligo also mentions studies for the NALP1 gene. NALP1 is expressed at high levels in T cells and Langerhan cells, white blood cells that are involved in skin autoimmunity.


Although a definitive ID will likely never be possible with such low quality photos, you probably have a Western Tent Caterpillar (Malacosoma californicum).

According to the USDA Forest Service, mature larvae are about 2 inches (4.5-5.1 cm) long and are highly variable in color and markings.

This insect is the most variable of the North American species of Malacosoma, in which six subspecies and several unclassified forms have been recognized.

Although this species eats primarilly trees and shrubs (e.g., see here and here), the Minnesota DNR suggests that garden plants can also be targeted.

Cocoons are of white silk dusted with a white to yellow powder. Your image appears to show that.

The Western Caterpillar is found throughout western North America:

 [Source: USDA Forest Service]


How are subspecies defined, in contrast to species?

Generally speaking, different species can't interbreed. For example, a giraffe can't mate with a gorilla.

Occasionally, very closely related species do interbreed - e.g. lions and tigers breeding in zoos. But the offspring are generally infertile.

Subspecies can interbreed, but they seldom do simply because they're separated from each other.

For example, consider the brown bear and the wolf, each of which have vast ranges embracing a wide variety of habitats. A subspecies adapted to a montane environment isn't likely to breed with a subspecies adapted to a desert environment. Of course, it would have been virtually impossible for a Eurasian wolf subspecies to interbreed with the wolf subspecies that lived in Newfoundland prior to its eradication.

The separation doesn't have to be geographic. Subspecies can sometimes evolve physical or behavioral differences that inhibit them from breeding with other subspecies.


Why does botulinum toxin seem to be more dangerous to humans than to other mammals?

Because of that, I assume botulinum toxin is more dangerous to humans than many animals.

Couldn't find too many examples but, there are some things to consider (according to [1]):

there are seven distinct types of toxin with variable action among animals
different dose / effect intensity ratio between toxin types
toxins A, B, E and F cause disease in humans
toxin C and D are more common to birds, cattle, horses

And here are some numbers:

cattle median lethal dose: 0.388 ng /kg [2] of C type toxin
mouse median lethal dose ( 12.88 times more than cattle): 5 ng/kg [2] of C type toxin
human median lethal dose: 1 ng/kg [1] of A type toxin

When it comes to carcasses toxicity, there are some papers to consider:

Smith GR, Turner A. Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type C. Epidemiol. Infect. 1987 Jun;98(3):345-51. PubMed PMID: 3297745. - Persistent toxicity at 20 and 37 degrees Celsius even for a long time. No toxicity at 16 degrees Celsius
Smith GR, Turner A, Till D. Factors affecting the toxicity of rotting carcasses containing Clostridium botulinum type E. Epidemiol. Infect. 1988 Jun;100(3):399-405. PubMed PMID: 3288491. - Maximal toxicity at 30 degrees Celsius that is lost in time.

  are they better in avoiding harmful substances based on more suited olfactory sense?

Not if we are talking about nonproteolytic B, E and F type bacteria. Indeed, Clostridium botulinum, proteolytic type A, B and F types produce odor [3].

  Or are we just more afraid?

I don't see how fear could (significantly) influence pharmacodynamics and pharmacokinetics of the toxin.

References:

CIDRAP - Center for Infectious Disease Research and Policy. Botulism. Available from http://www.cidrap.umn.edu/infectious-disease-topics/botulism
Moeller RB, Puschner B, Walker RL, Rocke T, Galey FD, Cullor JS, Ardans AA. Determination of the median toxic dose of type C botulinum toxin in lactating dairy cows. J. Vet. Diagn. Invest. 2003 Nov;15(6):523-6. PubMed PMID: 14667014.
P. Kendall. Botulism. Colorado State University Extension. Available from http://www.ext.colostate.edu/pubs/foodnut/09305.html


Is there a difference in how Gas is produced which determines if it becomes a burp or flatulence?

The gas expelled as a burp originates from the stomach. It is either gas swallowed together with food or gas that was dissolved in the drink. One prominent example for the latter is sparkling water where $\ce{CO2}$ is dissolved in the water at high concentration as carbonic acid ($\ce{H2CO3}$). Because of the acidic environment in the stomach the equilibrium between carbonic acid and $\ce{CO2}$ gas is shifted. Consequently $\ce{CO2}$ accumulates and needs to be expelled as a burp.

The gas expelled as a fart is mainly produced by microorganisms in the intestine and usually contains a lot of methane which makes it flammable.


Does the number of nodes determines the rate at which a neural signal is transmitted?

The number of nodes is a trade-off between speed of conduction and reliability. The fastest transmission would be where nodes are spaced at roughly the maximum distance to trigger sufficient depolarization at the next node - however, small changes in ionic concentrations or channel densities could lead to failures, so in practice the nodes are typically a bit closer.

The slowest transmission would be to have no saltatory conduction at all.

(I mean these to be general principles; one could probably design a hypothetical system with very close nodes that is actually worse than having no saltatory conduction, and there is probably a perfect edge case where nodes that are spaced at the maximum distance are slower because of membrane time constants)

The reasons for this are: that travel between nodes is very fast, regeneration at nodes is comparatively slow. However, there is a maximum distance for reliable transmission, so we can't simply have one long stretch containing no nodes in between.

edit: references were requested. This was off the top of my head so I would suggest any introductory neuroscience textbook, Purves is a preferred one of mine, but this will run you significant $ if you are not/have not been a student in a neuroscience course. The Wikipedia articles for https://en.wikipedia.org/wiki/Node_of_Ranvier and also for Saltatory Conduction both look good to me, though they do not address the specific issue in detail. This brief Neuron review is more appropriate to the specific question asked, though I am not sure people without an academic library subscription will have free access: http://www.sciencedirect.com/science/article/pii/S0896627300803232


What animals stop other members of their species from mating and why?

As the comments suggest, I think a little basic reading so you understand the definitions involved here might be appropriate.  The questions are a bit anthocentric, and I think that's why folks with a bit more biological culture might be concerned about the answers.

Alpha type structures can be found in all sorts of animals.  Sperm competition, where many males simply mate with the female and let the sperm work it out are also v common from snakes to mice to primates.

Its hard to say without you asking a more specific question, but the essential question is whether the competition occurs between the animals themselves or between the intermixed sperm of the males inside the female.  If that sounds gross, that's a typical reaction if you are not a monkey, snake, duck or mouse to name a few.  Different species choose different social roles in mating and for reasons that may be difficult to divine.

For animals in an alpha troop modality, the alpha male will eventually get older or weaker and the younger ones will have their chance to mate.  There is always tomorrow.  That's my very brief answer.

It might be worthwhile to take some time to read some about this - a page of response to your questions is not going to really answer your questions.  (I say this having answered several of them :).  I would recommend "The woman that never evolved" by Sarah Hrdy.  As a feminist in the 70s Hrdy decided to do a survey of primate male/female roles in mating, to try understand how human men and women became who they are (and who has not wondered this?).  This book will give you an idea of how so many different animals have come to different roles and possibly why.

Since I have a little time today, I'm adding a couple of tangential references:  Mice sperm have responded to sperm competition so much by evolving hooks on their heads and chain up together and swim together which enhances the chances of paternity.  Ducks are quite different.  they have a lot of forced copulation, but female choice of mate is still quite influential.  Duck vaginas are very complicated, with corkscrews and dead ends to make it difficult to copulate without 'consent'.


Why are nosebleeds easier to get in the winter?

The vast majority of bloody noses in healthy individuals arise from one specific area in the nose (on either side): Kiesselbach's plexus.

In the mucosa of the nasal septum (the cartilagenous structure separating the nose into two sides), there is an area where several arteries "meet", giving it an exceptionally rich vascular supply, called Kiesselbach's plexus. It is on the anterior surface, and exposed to dry air and trauma.

Bleeding typically occurs when the mucosa erodes for any reason, and the capillaries and venules (and sometimes arterioles) become exposed and subsequently break. The result is the familiar bloody dripping of a nosebleed.

Have you noticed that your lips chap more in the winter? Dry air and cols temperatures do that. The mucosa of your nose also dries out and suffers some damage. Not like your lips, but damage none the less. Damaged nasal mucosa is more susceptible to tears/trauma/erosion. If it happens in an area of rich blood supply, you get a nosebleed.

Anything that helps with the integrity of the nasal mucosa is going to help reduce nosebleeds. One can

run a humidifier in dry weather
avoid irritating by touching the nose or blowing nose too often
apply a very light layer of petrolatum or Bacitracin ointment to the inside of the nose covering Kiesselbach's plexus at night so the nose-breathing doesn't dry out your nose
use nasal saline spray to moisten and soothe the nasal membranes (don't rub the tip of the spray bottle against the nasal membranes, though)

*more serious or recurrent bleeding needs medical attention to rule out  other conditions that are associated with frequent nose bleeds.

Epistaxis


A question concerning the strength of synapses

What you are describing is exactly how long-term potentiation/LTP (or depression/LTD, for that matter) is measured electrophysiologically.

Here's an example from a 1988 review by Nicoll et al:

Nicoll, R. A., Kauer, J. A., & Malenka, R. C. (1988). The current excitement in long term potentiation. Neuron, 1(2), 97-103.

The x-axis is time in minutes, the y-axis is a measure of synaptic strength: the slope of the local field potential response to simulation of a particular pathway. You could also measure an EPSP internally, measure voltage with a voltage-sensitive dye, etc.

At the point marked "tetanus", a long train of pulses is delivered that is known to cause LTP. Afterwards, you see an increase in synaptic strength that is maintained for many minutes.

It's also possible to perform these experiments over longer time scales, with different paradigms, in the presence of various drugs that influence LTP, etc. Different protocols will give different durations of LTP.

These sorts of plots are ubiquitous in the LTP/LTD research field, so if you read any papers in that area you are likely to come across many similar presentations.


Could a sperm be altered to contain a female's genetics?

You might be interested in this article. In this study they created haploid ES cells from artificially activating an unfertilized oocyte and growing the haploid cells. These cells, when introduced in the ICM, give rise to viable chimeras.

In another study, haploid androgenetic ES cells were created by injecting a sperm into an enucleated oocyte. These cells also are capable of creating offspring when fused with another oocyte. [See this post also]

Also, since these cells can be cultured, they can be genetically modified. However, they undergo spontaneous diploidization and lose reproductive potential after a few rounds of division. This is related to the alteration of epigenetic status of these cells on certain imprinted loci. Others have also indicated the importance of both paternal and maternal imprinting in the viability of embryos which might be a problem in oocyte-oocyte derived hES cell fusions (See cross references). [Check this article too].

It can be concluded that oocyte$-$oocyte-hES fusions are not observed because of same imprint status (Also mentioned by Chris in the comments). AD-hES also lose their paternal imprints on prolonged culture (but retain maternal imprints). It is to be ascertained if paternal imprints are more unstable compared to maternal imprints under these conditions. It may be possible to optimize the culture conditions such that oocyte derived hES lose their maternal marks: would that lead to incorporation of paternal marks post-fusion is debatable.


How long can you keep sheep eyes in formaldehyde before dissecting?

Formaldehyde is a preservative, and is used to prevent decay. As long as the tissue is completely perfused (and there shouldn't be any issues with eyes that I'm aware of) it can be kept essentially forever. Have fun!


If senescent cells are removed by the immune system, how can they contribute to ageing?

In an healthy individual, senescent cells are likely removed by the immune system.  However, as we age, our immune system becomes impaired and may no longer be able to kill senescent cells.  Senescent cells can then accumulate and promote age-related diseases.


Back crossing is the process by which a hybrid organism is crossed back (backcrossed) into a pure organism. Let's see an example

Organism 1 is heterozygous for a single gene (e.g. a hybrid), which has alleles that we can call $A$ and $a$. We can write that organism's genotype.

Organism 1 Genotype: $Aa$  (100% chance)

Right now, there is a 0% chance that organism 1's genotype is $AA$.

Goal: increase probability that organism 1's genotype is $AA$

One way to achieve this goal is to cross Organism 1 with another organism, let's call it Organsm 2, that is has a homozygous (e.g pure) genotype of $AA$.

So if Organism 1 is crossed with Organism 2 and produces a new Organism 3 what is its genotype? Well, we're not sure.

Organism 3 Genotype: $AA$  (50% chance)

Organism 3 Genotype: $Aa$  (50% chance)

Now we do the same thing again, to get Organism 4

Organism 4 Genotype: $AA$ (75% chance)

Organism 4 Genotype: $Aa$ (25% chance).

This effect keeps compounding, until there is a very high chance that the final organism has a pure (e.g. $AA$) genotype.


Pharmacologically, can tricyclic antidepressants have a side-effect profile similar to neuroleptics?

Torticollis can occur for several reasons, one of which is a side effect of certain drugs. Rather than highlight one specific drug it is perhaps better to talk about the mechanism of action by which this occurs.

Torticollis in a drug induced form is classed as an extrapyramidial side effect. Classically results from some medications which have anti-dopaminergic effects. The neurotransmitter dopamine is important for the regulation of movement. Different medications have different degrees of anti-dopaminergic effect. To complicate things further there are several different types of dopamine receptors and different drugs have different effects depending on their action on these receptors.

Classically drugs that have been associated with extrapyramidial side effects are some of the antipsychotics but there are case reports of this with trycyclics http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489096/ however this appears to be a very rare, see http://www.sciencedirect.com/science/article/pii/S0924977X97004057.

The paradoxical treatment of torticollis might be dependent on the cause of the condition.  Tricyclic anti-depressants have anti-cholinergic effects, i.e. they block the effects of the neurotransmitter acetylcholine. This neurotransmitter works in opposition to dopamine in the basal ganglia (part of the brain responsible for movement control) as such might be used when the dystonia is as a result of doperminergic disregulation.

If you are at all concerned that you may be suffering side effects of any medication, then I highly recommend that you go and discuss this matter with your doctor. The above  is a simplified explanation of some of the reasons why these side effects may occur. It is not intended as information for the purposes of self diagnosis and treatment.


complete DNA transfer across different organism zygotes

Unfortunately the answer is no. Similar experiments of cross species nuclear transplants into enucleated oocytes have been attempted. Rat nuclear transfer into activated denucleated mice oocytes, rabbit oocytes etc.

The primary stumbling block appears to be incompatibility between mitochondria proteins derived from the donor nucleus and proteins derived from the host mitochondria. Mitochrondria proteins are encoded from two DNA sources, the genome within the nucleus and the genome within the mitochondria. While mammalian mitochondria proteins are very similar, there are differences. These small differences between species appears to be enough to kill a developing embryo if there is a miss match.

Attempts have been made to replace both host nucleus and host mitochondria. However complete replacement of host mitochondria has not been successful. Partial replacement of host mitochondria (mouse oocyte as host and rat nucleus with rat mitochondria as donor), appears to marginally prolong the life span of embryo. But death is still the outcome.

PS: nuclear transfer between subspecies and very closely related species does produce viable clone.  Coyote (Canis latrans) using dog (Canis lupus familiaris) oocytes. (Bos gaurus) adult nucleus donor cells and bovine (Bos taurus). My guess is that if a hybrid is possible between the two species, nuclear transplant between the two species should be possible


What is the name of this berry producing tree?

This is some type of Sumac in the genus Rhus. Probably either Rhus glabra (Smooth Sumac) or Rhus typhina (Staghorn Sumac). The berries of those two species are supposedly not poisonous. But they are closely related to other poisonous plants such as poison ivy and poison sumac. Poison ivy and poison sumac are in the genus Toxicodendron, but used to be in the genus Rhus.

A photo of Smooth Sumac


Does the tannin level in plants go down or up after they die? Or does the tannin level stay the same regardless?

Well maybe I'm confused, but do plants not produce tannins? If they do
  does the production of the tannins stop after death?

That depends on how you define death. Tannin is secondary product, so I don't think the plant cells will produce more tannin when they are starving probably because of cutting off the leaves, roots, etc... when the plant dies. The plant won't bother to degrade tannins (I guess it does not even have the pathway necessary to do that), because it is a defense mechanism against insects, mammalians, etc... and not an energy storage material. Tannins can be degraded by microbes, heat, UV radiation, chemical reactions, etc... So if you can't protect the tannins from all of these then they will degrade. (Note: you can't, all you can do is slowing down the process.)


Yes, it's Steatoda, probably nobilis, the False Widow.  The white band curving around the front of the abdomen is a good Steatoda diagnostic, and the light-colored abdominal pattern is pretty variable in this species - only hints of it here, but the pointy front end and the bits of a skeletal 'shield' pattern are there.
The spider is pretty harmless, although it is supposed to sometimes give a bite that's like a very mild Widow bite.  Not at all dangerous, but a little more potent than the usual harmless spider bite.

Below are a couple of pictures of nobilis, showing a range of markings:

Here is a citation describing the effects of S. nobilis bites that's not a fear-mongering tabloid story:

https://www.researchgate.net/publication/320623444_Envenomation_by_the_noble_false_widow_spider_Steatoda_nobilis_Thorell_1875_-_five_new_cases_of_steatodism_from_Ireland_and_Great_Britain

The images were taken from a random survey of Steatoda nobilis images from the internet, as a broad selection was desired.  However, this note (below) discusses some of the features I mention, along with photographs that support my comments.

https://cisr.ucr.edu/european_spider.html


Regular expressions are not commonly used for DNA or Protein analysis, but many people use Hidden-Markov-Models (HMMs).

If you are looking at protein domains, you can find many HMMs here:
http://pfam.xfam.org/


Will the heart keep beating if it's separated from the body?

Short version
The heart  has the ability to beat independently of the brain as long as it has oxygen. The heart will eventually stop beating as all bodily systems begin to stop working shortly after brain death. Remember the heart can beat, but your diaphragm and lungs wont. hence the cardiac muscles undergo asphyxiation and die off. However, immediately after death, there is enough oxygenated blood in the body to keep thing moving for a while

Long version
There is a simple explanation why.

As you know every muscle in the body has to receive stimuli from the neuromuscular junctions (and subsequently the nervous system) in order to contract.

The heart is a bit different in that it is not regulated by the brain, but the regulatory mechanisms lie within the heart itself. The heart conductive system contains a special group of cells called the pace maker cells (SA node) that fire at regular intervals and cause the heart to beat.

  Each heart beat is triggered by an electrical pacemaker - a group of cells in the heart that have the ability to generate electrical activity. They cause electrical impulses to spread over the heart and make it contract.
  The largest natural pacemaker of the heart is called the sinoatrial or SA node and is found in the right atrium. From it, specialised groups of cells that carry the electrical charge lead off to the rest of the heart.

(Taken from here)

The brain regulates the rate of the heart beat sure, but it does not send the signals that cause the heart to beat in itself.

In short, even after disconnection, the SA node still sends the impulse down the AV node and purkinje fibres that spread out across the cardiac musculature and cause them to contract, causing the heart to beat. This will continue for a while till they run out of energy and stop.

You can read more about it here:Wiki


Importance of knowing GC Content of an organism

Interesting question. The GC-content seems to evolve over time and it also seems that the GC-content of coding regions is higher than for the surrounding non-coding regions (see reference 1). If there is a specific function for this higher GC-content or not is (if I understand this right) debated among the groups which do research in this field. Have a look at the references (and probably also their references) to decide on this:

Both selective and neutral processes drive GC content evolution in
the human genome.
Integrating genomics, bioinformatics, and classical genetics to
study the effects of recombination on genome evolution.
Recombination Drives the Evolution of GC-Content in the Human Genome
GC-Content Evolution in Mammalian Genomes: The Biased Gene
Conversion Hypothesis
Contrasting GC-content dynamics across 33 mammalian genomes:
Relationship with life-history traits and chromosome sizes


It looks to me as Potter Wasp (or mason wasps), the Eumeninae, are a cosmopolitan wasp group presently treated as a subfamily of Vespidae, but sometimes recognized in the past as a separate family, Eumenidae.

Since there is no more info provided and image is not sharp I cannot be 100% sure.


How effective are restriction enzymes in protecting bacteria?

Note that a given bacterium will probably have more than one restriction enzyme, so the viral genome probably won't ever run out of targets. Even if it did, restriction enzymes could suffer mutations that may change the specificity. When you talk about microorganisms, it's more accurate to think in populations rather than individuals, since the colony would be able to grow again if they have at least one cell. Viruses need a certain density to spread, so even if the bacteria cannot defend against, it may be able to survive simply because the virus run out of hosts before some cells can be infected. This is even easier if the bacteria have some kind of resistance form.

Moreover, restriction-modification systems aren't the only defense line against viruses. Many bacteria have a system called CRISPR-CAS that acts like an immune system, inserting RNA fragments into the bacterial chromosome and using them as "antibodies" by hybridization. In this context, you can assume that restriction-modification systems, alongside other nucleases they usually carry, act as an innate immune system, while the CRISPR-CAS would be an analog to acquired immunity.

Diagram of the CRISPR-CAS system. Source.

Furthermore, not every environment has the same viral density. Some habitats may be protected against viruses by some means, like the gut microbiota (the carbon intake goes through the stomach acid and tons of hydrolases, which is very destructive for viruses); while some others may have an incredible amount due to lack of biodiversity and high cell densities (this is the case of most extreme environments). E. coli, as a gut bacteria, would probably have enough with only restriction-modification enzymes (In fact, while it have a CRISPR system, it seems to be repressed), while many others will need more defenses.


What is the difference between meristem and bud?

I looked in Taiz and Zeiger. Plant Physiology 5th ed and this is what I found:

Plant growth is concentrated in localized regions of cell division called
meristems. Nearly all nuclear divisions (mitosis) and cell divisions
(cytokinesis) occur in these meristematic regions. In a young plant, the
most active meristems are called apical meristems; they are located at the
tips of the stem and the root (see Figure 1.1). At the nodes, axillary buds
contain the apical meristems for branch shoots.
The root and shoot apical meristems formed during embryogenesis are called
primary meristems. After germination, the activity of these primary
meristems generates the primary tissues and organs that constitute the
primary plant body.
Most plants also develop a variety of secondary meristems during
postembryonic development. Secondary meristems can have a structure similar
to that of primary meristems, but some secondary meristems have a quite
different structure. These include axillary meristems, inflorescence
meristems, floral meristems, intercalary meristems, and lateral meristems.
Axillary buds are secondary meristems; if they are also vegetative meristems, they will have a structure and developmental potential similar to that of the apical meristem.

So, briefly, I could say that meristems are localized regions where undifferentiated cells reproduce themselves and originate new plant tissue. Axillary buds contain secondary (formed after embryogenesis) meristems. This meristem can behave like an apical meristem if it becomes vegetative i.e. either apical dominance disappears or it is excised and subcultured elsewhere.


Confusion regarding seedless grape and the normal process of germination

The seedless grape technically has a seed, but the seed has no hard outer shell and is microscopic/invisible. These seeds aren't viable. Technically you could isolate out the seed tissue from the grape and grow it in specialized germination medium, but that process also works for any other part of the grape plant. Hooray cuttings! Certainly the seedless grape would not grow if you put it in the ground.

The fruit part of the seeded grape is 'bait' to get animals to ingest the grape and carry the seeds within inside their digestive tracts. The goal is distance, but the surrounding feces provides bonus nutrients. The fruit is not designed to feed the seedling grape, but instead to act as bait for herbivores. The grape is mostly sugars and water, which makes them excellent bait but not amazing plant food. Plants can make sugar from the sun and pull water from the ground, but nitrogen and phosphorus are harder to come by.

Contrast fruit (which are for animals) with coconuts, which are examples of large fruit storing lots of calories for the seedling itself. The coconut flesh isn't as sweet as fruit, and it's much harder to get at.


To construct the G-matrix you need additive genetic variances and covariances for all traits, so you normally need results from breeding experiments (e.g. phenotypic midparent-offspring data), that you can do parent-offspring regressions on. Don't know any good online sources but see Balding et al. 2007 p. 534ff for some info. I've seen methods that claim that the G-matrix can be estimated directly from phenotypic data from unrelated individuals (e.g. Zintzaras 2011) or from genomic info e.g. SNPs (Vattikuti et al. 2013), but are not familiar with these and do not know how reliable they are.

A clear background on using mixed models to estimate the G-matrix, including examples/tutorials, can be found in Wilson et al (2009).

Or did you have something else/something more specific in mind?