Difference between negative allosteric regulation and non-competitive inhibition

There Are Two Similar but Distinct Types of Noncompetitive Binding.
Starting from a pharmacological perspective, there are 2 definitions of "noncompetitive" binding that have similar macroscopic effects but differ slightly in their molecular mechanisms. Depending on which definition you use, noncompetitive ligands can bind either orthosterically or allosterically. Aspirin at cyclooxygenase and alanine at pyruvate kinase have both been referred to as "noncompetitive" (see below), despite aspirin binding orthosterically and alanine binding allosterically. Both types of inhibition involve depression of the maximum response, efficacy or enzyme activity. In other words, they reduce $y_{\mathrm{max}}$, $E_{\mathrm{max}}$ or $V_{\mathrm{max}}$. This is described in (Lippincott. (2015). Illustrated Reviews Pharmacology. 6th ed. p. 34). Similarly, (Goodman and Gilman. (2011). The Pharmacological Basis of Therapeutics. 12th ed. p. 46) gives an operational definition of noncompetitive antagonism as that which depresses the maximal response to the agonist but the molecular mechanism of action "really cannot be inferred unequivocally from the effect". The two types of noncompetitive molecular mechanisms are (1) irreversible antagonism and (2) allosteric antagonism. Lippincott claims that both of these mechanisms are "noncompetitive" antagonism. Textbooks trump Wikipedia on credibility so I'm afraid to say that Wikipedia may have been leading people astray for years by saying that noncompetitive ligands can only bind allosterically. Due to this confusion, I think it's better to avoid the term noncompetitive entirely and opt for "insurmountable" inhibitor if the mechanism is unknown, or "irreversible/allosteric inhibitor" if the mechanism is.
Type 1: Irreversible Antagonism
Goodman and Gilmans' definition in the previous paragraph notes that the effect is for "a slowly dissociating antagonist" (i.e. an irreversible antagonist). This is mirrored in (Rang and Dale. (2015). Pharmacology. 8th ed. p. 11) and (Katzung. Basic and Clinical Pharmacology 11th ed. p. 31), which define noncompetitive antagonism as irreversible antagonism. Rang and Dale also makes the point that the term is ambiguous with other meanings of noncompetitive. Rang and Dale claim that aspirin is a noncompetitive antagonist at cyclooxygenase. It may be an irreversible antagonist but it's certainly not an allosteric one, as it modifies the orthosteric binding site. Another "noncompetitive" drug in this class (according to Rang and Dale) is phenelzine, which irreversibly binds MAO.
Type 2: Allosteric Antagonism
Not to be confused with negative allosteric modulators, (Goodman and Gilman. p. 46), (Rang and Dale. p. 17), (Lippincott. p. 34) and (Katzung, p. 32) all give a second definition of noncompetitive antagonism as antagonism at an allosteric site. This antagonism may be reversible or not but as the agonist can't displace the antagonist, it is insurmountable in all cases. Rang and Dale give the example of ketamine at the NMDA receptor, which depresses the maximal response by binding in the channel (an allosteric site) but doesn't bind irreversibly. For ligands relevant to enzymes, alanine and ATP allosterically (yet reversibly) bind pyruvate kinase. So this would cause insurmountable inhibition of pyruvate kinase activity but not irreversible inhibition. Various authors, such as (Mustafa and Hochachka, 1970) refer to this as "noncompetitive" inhibition.
Interestingly, I can't find any exogenous ligand that is both reversible and allosteric. It seems that allosteric antagonists are more relevant to receptors and transporters than enzymes. To make it even more confusing, Katzung claims that benzodiazepines (BDZ) act noncompetitively, since they bind allosterically. But this doesn't fit with any other definition of noncompetitive binding since BDZ is a positive modulator. Also interesting is that hexamethonium at the nAChR fits the definition of "noncompetitive", regardless of which one you use. It is an irreversible blocker at an allosteric site.
Marangoni, on p. 70 of Enzyme Kinetics: A Modern Approach, also points out the difficulty in distinguishing between irreversible orthosteric and reversible allosteric inhibition. Using an irreversible inhibitor is equivalent to removing some enzyme from the system, so $V_{\mathrm{max}}$ drops. But at the same time, an allosteric inhibitor causes insurmountable inhibition (reduces $V_{\mathrm{max}}$). Neither type of inhibition alters the affinity of the substrate for the active site of the enzyme (apart from the irreversibly inhibited enzymes with no affinity) so $K_m$ is left unchanged. The figure below, from (Jahangirvand et al., 2016), shows the antagonism of catalase by cimetidine on a Lineweaver Burke Plot. A glance at this graph tells us that $V_{\mathrm{max}}$ is depressed, while $K_m$ is unchanged, so we could (arguably) call this noncompetitive inhibition. But this would not tell us the molecular mechanism of the inhibition.


How do major and minor grooves arise in the DNA helix?

First the MAJOR groove. This can be considered by forgetting that the two DNA strands are separate and thinking of them as merged together like a rope or an electric cable in my diagram below. The cable is wrapped around an axis, which can be thought of as an imaginary rod. One could wrap the cable tightly round the axis so it was always in contact with itself and no space in between (as on the extreme left), or one can wrap it round less tightly with space in between (subsequent images). The latter is what happens and the space left by the wrapping of the rope is the major groove (because it's wider than the minor groove we come to next).

So to your question, what causes this winding to be the way it is — which is to say what causes the particular pitch of the DNA helix? This is presumably the most thermodynamically stable conformation, maximizing the strength of the hydrogen bonding between the bases (most linear, not too close or too distant) and minimizes steric and electric replusion (the phosphate backbone is negatively charged).

Next the MINOR groove. We now have to consider that our 'cable' is actually two strands of DNA — a sugar phosphate backbone with the paired bases in the centre. Although the bases are in the centre, the space between the two sugar-phosphate strands is not completely occupied. This creates another groove - the minor groove - less wide and of quite different origin to the major groove, but still able to accomodate certain small proteins. As it happens, this is the case with the electric cable analogy illustrated. The cable is two electric wires, but they are encased in the same plastic inuslator.

So to your question, what causes the minor groove? This is just the three dimensional shape of the DNA double-strand which reflects the molecules that make it up. The large phosphate groups can be considered like wide tubes at either side, whereas the bases between the strands are flat and so lead to a groove, irrespective of whether it is wound into a helix or (in one's imagination) stretched out.

(The 'major' groove is exaggerated in size compared to the 'minor' groove in the cable analogy, but I hope it illustrates the difference between the two.)


The Hawk-Dove game: why is the average payoff half of the difference between reward and cost?

One hawks gains 10, the other loses 5. So together, they gain only 5 (=10-5). On average, they gain 5 / 2 hawks = 2,5


How does RNA transcription determine which half of the DNA to use?

I'll keep this short and simple. The direction of transcription (which determines which strand is used as the template) is controlled by the promoter, which is a region of specific DNA motifs at the 5' end of a gene. RNA polymerase binds to the promoter, which orients it on the correct strand and in the correct direction, after which it can proceed to transcribe the gene.

That great little animation is from this website.


Are there species which is debatable if they should be classified as animals or plants?

No, there are no such debates. Plants and animals diverged over a billion years ago. Animals are defined by the unique molecules that are secreted by the cells, and fill the intercellular matrix, like collagen. Plants have unique cell walls, chlorophylls a and b, and plastids. The unique characteristics of plants are given here: http://www.bio.miami.edu/dana/160/160S10_10.html
Although there may be animals like sponges that don't seem to move around a lot, or corals that have symbiotic relationships with algae, simply "behaving like a plant" does not make them plants. Similarly, there are plants that move and trap insects. But taxonomists would never confuse them with animals.


What implications has the missing 2'-OH on the capability of DNA to form 3D structures?

To make sure I'm not comparing apples and pears, my (attempt to) answer the question will be broken into two parts: comparison of single-stranded nucleic acids and double stranded ones.

Single stranded DNA and RNA

Both DNA and RNA can form single-stranded complex tertiary structures in which the secondary structure elements are associated through van der Waals contacts and hydrogen bonds. The presence of a 2'-hydroxyl group makes ribose ring prefer different conformations than deoxyribose in DNA. Also, since 2′-OH moiety is both a hydrogen donor and acceptor, it provides RNA with greater flexibility to form 3D complex structures and stability to remain in one of these conformations. As Aleadam notices, this paper shows that tRNA and its DNA analog form similar tertiary structures though tDNA is not as stable as tRNA:

  Therefore, we submit that the global conformation of nucleic acids is primarily dictated by the interaction of purine and pyrimidine bases with atoms and functional groups common to both RNA and DNA. In this view the 2-hydroxyl group, in tRNA at least, is an auxiliary structural feature whose role is limited to fostering local interactions, which increase the stability of a given conformation.

These authors also show that at least one loop in the tDNA analog is more susceptible to cleavage by a restriction endonuclease. In this region the tRNA has a water molecule hydrogen bonded to 2'hydroxyl group.

I was not able to find more of such interesting comparisons in the literature.

Double stranded DNA and RNA

Both DNA and RNA can form double-stranded structures. Again, sugar conformation determines the shape of the helix: for DNA helix it's usually B-form, whereas helical RNA forms A-geometry under nearly all conditions. In RNA helix we find the ribose predominantly in the C3’- endo conformation, as 2'-OH stericly disfavors the C2'-endo conformaion, necessary for B-form geometry.

Physiological significance

dsRNA and ssDNA often provide a signal to the cell that something is wrong. dsRNA is of course seen in normal processes like RNA interference but it can also stop protein synthesis and signal viral infections (cf. double stranded RNA viruses). Similarly, ssDNA is much more prone to degradation than dsDNA, it often signals damage of DNA, or infections from single stranded DNA viruses and induces cell death. Therefore, due to their functions, under normal conditions DNA 3D structure is mostly a double-stranded helix, whereas RNA has a single stranded, "protein-like", complex 3D structure.


What's the difference between the neuroendocrine system vs endocrine system?

Neuroendocrine systems can be defined as the sets of neurons, glands and non-endocrine tissues, and the neurochemicals, hormones, and humoral signals they produce and receive, that function in an integrated manner to collectively regulate a physiological or behavioral state.
The neuroendocrine system is the mechanism by which the hypothalamus maintains homeostasis, regulating reproduction, metabolism, eating and drinking behaviour, energy utilization, osmolarity and blood pressure. (Source)

The central neuroendocrine systems serve as an interface between the brain and many of the peripheral endocrine systems. This chapter discusses the hypothalamic control of anterior pituitary systems regulating stress, basal metabolism, growth, reproduction, and lactation. Each of these systems involves one or more hypothalamic releasing or inhibiting hormones, released from hypothalamic neurons that terminate in the portal capillary vasculature that projects from the median eminence at the base of the hypothalamus to the anterior pituitary gland. There, the hypothalamic hormones act upon subsets of anterior pituitary cells to regulate pituitary hormone release and downstream physiological functions. Other hypothalamic neuroendocrine cells control water/salt balance, and lactation/parturition, through the release of vasopressin and oxytocin from nerve terminals that arise in hypothalamus and project to the posterior pituitary gland. Together, these hypothalamic neuroendocrine functions enable the central nervous system to respond rapidly to internal or external environmental change, and to maintain a response through endocrine hormonal transducers. (Gore, 2013).

The endocrine system is a group of glands and other structures that release internal secretions called hormones into the circulatory system.

Endocrine organs are richly vascularized ductless organs that produce hormones. The epithelial cells of the organ secrete their hormone product directly into the bloodstream where, upon binding with specific receptors in target organs, cellular functions are affected. The endocrine systemincludes not only the endocrine glands (pineal, pituitary, thyroid, parathyroid, and adrenal) but also single cells and small clusters of cells in the thorax and abdomen known as paraganglia. This chapter addresses the thyroid, parathyroid, adrenal, pituitary and pineal glands, and paraganglia. In addition to size differences, several features of endocrine tissues differ between rodents and humans, and often between rodents. (La Perle & Dintzis, 2018).

Question 1

When it comes to the brain, are the neurosecretory cells located in the hypothalamus or the posterior pituitary gland or both?

Neurosecretory cells are found in the hypothalamus. (Source)

There are two types of neurosecretory cells: magnocellular cells and parvocellular cells. Magnocellular cellsare large cells, having long axons that terminate in the neurohypophysis (also known as the posterior pituitary). Magnocellular cells release the hormones vasopressin and oxytocin to the general circulation; we will talk about the physiology of these hormones in Conjoint 403.  The parvocellular cells are small cells, with shorter axons that terminate at a capillary-rich bulge at the base of the hypothalamus known as the median eminence.

Question 2

Is the hypothalamus and the posterior pituitary gland classified as neuroendocrine glands...

No

...and is the anterior pituitary classified as an endocrine gland?

Yes.
The following is from: https://courses.lumenlearning.com/boundless-ap/chapter/the-pituitary-gland
(emphasis mine)

The posterior pituitary (or neurohypophysis) comprises the posterior lobe of the pituitary gland and is part of the endocrine system. Despite its name, the posterior pituitary gland is not a true gland; rather, it is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary gland.

The pituitary gland is an endocrine gland, about the size of a pea, that sits in a small, bony cavity at the base of the brain whose secretions control the other endocrine glands and influence growth, metabolism, and maturation.
While the pituitary gland is known as the master endocrine gland, both of its lobes are under the control of the hypothalamus: the anterior pituitary receives its signals from the parvocellular neurons, and the posterior pituitary receives its signals from the magnocellular neurons.
The anterior pituitary, also called the adenohypophysis, is a major organ of the endocrine system, and is the glandular, anterior lobe of the pituitary gland.
The anterior pituitary gland secretes 7 hormones: follicle stimulating hormone, luteinizing horomone, adrenocorticotropic horomone, thyroid stimulating horomone, prolactin, endorphins, and growth hormone.
The posterior pituitary gland does not synthesize any hormones.  Hormones known as posterior pituitary hormones are synthesized by the hypothalamus, and include oxytocin and antidiuretic hormone (ADH), also called arginine vasopressin or vasopressin (Liu, 2007). The hormones are then stored in neurosecretory vesicles (Herring bodies) before being secreted by the posterior pituitary into the bloodstream.
With regard to neurohormones mentioned in question 3, neurohormones are hormones that are produced by neurosecretory cells and released by nerve impulses (e.g., norepinephrine, oxytocin, vasopressin).
This is the part which can be confusing. Whilst ADH and oxytocin are released from the posterior pituitary gland, which is an endocrine gland, the hormones are produced by neurosecretory cells within the hypothalamus and they are stored in and released from neurosecretory vesicles within the posterior pituitary gland. Therefore they are classed as neurohormones.
References
Gore, A. C. (2013). Neuroendocrine systems. In Fundamental Neuroscience (Fourth Edition) (pp. 799-817). doi: 10.1016/B978-0-12-385870-2.00038-X
La Perle, K. M. D., & Dintzis, S. M. (2018). Endocrine system. In Comparative Anatomy and Histology (pp. 251-273). Academic Press. doi: 10.1016/B978-0-12-415759-0.00058-3
Liu, K. D. (2007). Hyponatremia and Hypernatremia. In Critical Care Secrets (Fourth Edition) (pp. 285-290). doi: 10.1016/B978-1-4160-3206-9.10044-8


Two brown-haired people have two children, P and Q. P has blond hair. Q has brown hair. What is the probability that Q is heterozygous?

Assumptions: Blonde hair is Homozygous Recessive and that the traits are strictly Mendelian.

The parental generation must be both heterozygotes as at least one child is Blonde (bb). So your cross is Bb x Bb.

Your square is going to look like this:

           _B_            _b_

_B_         BB           Bb

_b_         bB           bb

So of the question is:

  What is the probability that Q is heterozygous?

The PhD is INCORRECT. They probably just made a simple Punnet Square in their head and forgot the caveat that you have to exclude "bb" because Q is not Blonde. The possible allele combinations for non-Blonde offspring from a Heterozygotic cross are only BB, bB, Bb.

Therefor the probability that Q is Heterozygous is indeed 2/3 (bB, Bb).

It's not uncommon for PhD students - who are often deep into their own research - to gloss over details and possibly give incorrect answers because the information hasn't been relevant to them for years (most traits aren't Mendelian, strictly recessive or dominant, and rarely involve a single allele), so give them some slack unless they were being a jerk about it. =)


Why is contractile vacuole absent in parasitic protozoans but present in free living protozoans?

No, you are wrong. Parasitic protozoans too have contractile vacuole, for example trypanosoma.
Also Wikipedia says:

  Not all species that possess a contractile vacuole are freshwater organisms; some marine, soil microorganisms and parasites also have a contractile vacuole


The genetics of pigmentation is relatively complicated, as the pathway for the pigmentation (regulation of the pigment production, ratio between the melanins, maturation, trafficking and distribution of the melanins from the melanocytes to other cells) is quite long and also subject to different regulations. All the mutations found to date (at least to my knowledge) affect single parts of this long process (so for example MC1R mutations are affecting whether eumelanin is made, while Rab7 and Rab27a is most likely involved in the distribution of the melanosomes). Not all gene functions in this network have been understood so far.

Population studies have shown that the three main ethnic subgroups (west-africans, asians and europeans) have developed independently from a common ancestor with different (and independent) mutations in each arm. See the figure from reference 1 as an illustration, it also shows the genes involved in each arm:

Pigmentation is a protection against UV light, so there is a strong selection against mutations in areas with high UV light (west africa for example). The general theory is that in areas with less UV light the skin got lighter to allow the production of vitamin D (for which you need UV light). If you want to go through the single genes and their influence on pigmentation, please have a look at this Wikipedia page, which gives a good explanation. Also have a look at the references.

References:

Unpacking Human Evolution to Find the Genetic Determinants of Human
Skin Pigmentation
The genetics of pigmentation: from fancy genes to complex traits.
Molecular genetics of human pigmentation diversity
Human pigmentation genetics: the difference is only skin deep
The etiology and molecular genetics of human pigmentation disorders


Do any plants grow leaves beneath the ground?

It is a known phenomenon. A good example of the same can be observed in Philcoxia minensis.

This plant is predominantly found in sandy areas of Brazil and its underground leaves photosynthesize using sunlight energy through the relatively opaque sand particles.

These leaves also play the function of trapping and digesting nematodes underground supplementing nitrogen in the leached soils. This article [with pdf] explains this mechanism in detail.


Deciduous trees are those which shed their leaves once a year at the time of winter season and later grow new leaves, plants those keep their foliage throughout the year are called evergreens. Deciduous trees usually have broad leaves e.g., ash, beech, birch, maple and oak. There is a confusion exists over the dominance of trees in rain forest, but most of the resources suggests broad leaf evergreen trees as the most dominant. But deciduous trees are equally important because the difference may be negligible.

Deciduous trees shed their leaves usually as an adaptation to a cold or dry season. Evergreen trees do lose leaves, but each tree loses its leaves gradually and not all at once. Most tropical rainforest plants are considered to be evergreens, replacing their leaves gradually throughout the year as the leaves age and fall, whereas species growing in seasonally arid climates may be either evergreen or deciduous.Reference

The dominant plants in the tropical rain forest are broadleaf evergreen trees. Unlike evergreens that grow in colder parts of the United States, those of the tropical rain forest have no protection against cold weather or droughts.Reference

Adaptations of Deciduous trees

Broad green leaves capture sunlight needed to make food through photosynthesis.
They cuts off the supply of water to the leaves and seals off the area between the leaf stem and the tree trunk, as sunlight and water become scarce, the leaves are unable to continue producing chlorophyll and this produce vibrant colors in the leaves.
In winter, they simply loose their leaves and seal up the places where the leaves attach to the branch. Losing their leaves helps trees to conserve water loss through transpiration.
In spring the trees grows back their leaves and start the cycle once more.

In the spring, deciduous trees begin producing thin, broad, light-weight leaves. This type of leaf structure easily captures the sunlight needed for food production (photosynthesis). The broad leaves are great when temperatures are warm and there is plenty of sunlight. However, when temperatures are cold, the broad leaves expose too much surface area to water loss and tissue damage. To help prevent this damage from occurring, deciduous trees make internal and physical adaptations that are triggered by changes in the climate.
Cooler temperatures and limited sunlight are two climatic conditions that tell the tree to begin adapting. In the Fall, when these conditions occur, the tree cuts off the supply of water to the leaves and seals off the area between the leaf stem and the tree trunk. With limited sunlight and water, the leaf is unable to continue producing chlorophyll, the "green" stuff in the leaves, and as the chlorophyll decreases the leaves change color. The beautiful display of brilliant red, yellow, and gold leaves, associated with deciduous forests in the fall, is a result of this process. Most deciduous trees shed their leaves, once the leaves are brown and dry.
Reference


Hot spots on the human body caused by cell phones are caused by the EMF/RF (ElectroMagnetic Frequency/Radio Frequency) emitted from the phones (or any mobile wireless device). (There is much conjecture about the safety of  these frequencies and whatnot... That is not what I am here to talk about).

In this case, the term hot spot does not refer to you being a WiFi hot spot! It simply means that since the frequencies are similar to that of a microwave, you will absorb them and they will cause heating internally. These areas will remain warm for a time - whether you can feel it or not, some people can, some can't. Shown here is a thermal image of someone who recently used a cell phone and one who had not.


"Air sac" and "air cell" in a chicken embryo

According to Atlas of Chick Development by Ruth Bellairs and Mark Osmond, a book I'm using for my developmental biology course :

  Air space  is the space between the two shell membranes at the blunt end of the egg. The chick pushes its beak into this space shortly before hatching and takes its first breathe of air.

Besides allantois is the extra embryonic membrane and the space enclosed by it is allantoic cavity.

Here label 2 is Allantoic cavity.


In the Lineweaver-Burk Plot, why does the x-intercept = -1/Km?


If I sent a bag of rice to the bottom of the ocean and brought it back, could I eat it?

Depends on the container.  The bottom of the ocean has three main properties that would affect the rice:

Water
Salt and floating materials
Pressure - at the bottom of the Mariana Trench, the pressure is 1000x that standard atmospheric pressure at sea level.

Rice is absorbent.  Depending on the container, if it is permeable to water, then both seawater and pressure will affect the rice.

Rice + Water = soggy rice with a different texture than cooked rice.

Rice + Brine in Seawater = soggy rice that absorbed salt and fine particulate materials from the surrounding water.  (Cooking this would probably taste just like using seawater to cook rice.)

Rice + Intense pressure = the water, salt, and other materials would be absorbed on its way down more quickly due to the increased pressure, and any air within the grains would be replaced with water as the grain is compressed.

I do not believe it would work at all like a pressure cooker does due to the cold temperature; I am fairly certain that it would be only the grainy soggy rice - cooked rice is different from dry rice because of changes to the starches by the heat when cooking (and obviously the absorption of water).  The rice itself is a starch, so the carbohydrates would not likely respond differently to the pressure in the absence of heat.

I am curious if anyone might come up with anything on the chemistry of carbohydrates under pressure at near-freezing temperatures - whether any chemical bonds may be altered (like deformation of the beta-1-4 glycosidic linkage).  That's beyond my level of chemistry/physics knowledge.

But the duration of the journey would likely result in mush by the time it came up.  There are not many nutrients to white rice in the first place, other than the carbohydrates, so the nutrient change would be what it gains in the brine.

If I am missing something, please point it out.  But I believe this is the extent of the effects on the rice.

However:

If your rice were in a sealed container capable of withstanding the pressure without collapse or leaking, I am fairly certain that the rice would arrive back to the surface completely unchanged.  Humans are able to go down to the sea bottom in specially designed vehicles.


Why doesn't crossing over happen in mitosis?

It can actually on very rare occasions however, it is also highly problematic and generally creates deleterious mutations and can inactivate genes. Depending on the location of the cell and the cross-over within the genome, it can also contribute to the formation of cancer. For instance, in the case of retinoblastoma, if there is one mutated copy of RAS on one chromosome and a normal copy on the other and mitotic crossing over occurs, then you can potentially remove the protective nonmutant copy of RAS from one of the daughter cells. This cell is then one step closer to becoming tumorgenic.

Thus, one reason this may not occur ordinarily is to reduce the chance of causing such a cancer. As for why it does occur on the rare times it does, I am not certain as of the time of writing this.

Reference: The Biology of Cancer, by Robert A. Weinberg


Does the Petri dish lid orientation on workbench affect aseptic technique?

DISCLAIMER: I am a computational biologist and haven't touched a Petri dish since I was an undergraduate biology student.

I would expect that the best thing to do would be to place the lid face down.
When placed so on the bench, it is only the tip of the lid that comes into contact with your (presumably sterile-ish) bench. If you place it face up, the interior of the lid will come into contact with the air of the lab. Despite the presence of the bunsen, I would expect that to gather more contamination.

Since the lid is larger than the dish itself, the lip of the lid never touches the dish. Therefore, if the lip of the lid touches the bench and becomes contaminated that is not a big problem since that contamination should be blocked from spreading to the actual culture. If, on the other hand, the lid were placed face up, the interior of the lid (which hangs just above your culture when closed) will have come into contact with possibly contaminated air and could then cause contaminants to drop onto your culture.


How do you check how many cones you have in your eye?

One of the two confirmed cases of tetrachromacy was confirmed genetically:

From this Popular Science article:

  Based on Antico's genes, Jameson has determined that Antico's fourth
  cone absorbs wavelengths that are "reddish-orangey-yellow, but what it
  appears to Concetta is uncertain at the moment," she added. Since the
  tests aren't calibrated for this wavelength, empirically demonstrating
  tetrachromacy is still really difficult.

Color vision is connected to the X chromosome and mutations in the X chromosome cause less or more color vision.  In the above case, the theory that people with 2 mutated X chromosomes could have four cones instead of three was tested.

This image from Scitable by Nature Education articles simulates regular vision on the left and tetrachromatic vision on the right:

As far as how to test to see how many cones you have, there are some online test that may or may not be very reliable.  This Metro news article has a test produced by Professor Diana Derval, author of "DesigningLuxuryBrands: The Science of Pleasing Customers’ Senses.  However, due to the limitations of computer screens it would not be reliable to test for tetrachromacy.


Using autoclaved store-bought distilled water for labwork?

Yes, distilled water would be absolutely fine for your needs. You really don't need ultrapure water except for the most sensitive of applications. You also don't need to autoclave the distilled water before making things like media/buffer/etc; instead you would autoclave/filter them after you make them.

You can take a look at this document for an overview on different grades of water.


Mode of Enzymatic Inhibition via R-Allele

Bhattacharyya M, Martin C, Smith A. 1993. The importance of starch biosynthesis in the wrinkled seed shape character of peas studied by Mendel. Plant Mol Bio 22(3):525-531

Abstract:

  The wrinkled-seed mutant (rr) of pea (Pisum sativum L.) arose through mutation of the gene encoding starch-branching enzyme isoform I (SBE1) by insertion of a transposon-like element into the coding sequence. Two isoforms of starch-branching enzyme have been documented in the developing pea embryo. The second isoform, SBEII, is expressed towards the later stages of embryo development while SBEI is expressed highly in the early stages. Due to mutation of SBEI the total amount of starch and the proportion of amylopectin, a branched starch polymer, are greatly reduced in the wrinkled (rr) line as compared to that in the wild-type, round (RR) line. Consequently, the level of sucrose in the rr line is nearly two fold that of the RR line. Increased sucrose concentration in the developing embryos of this mutant line causes increased uptake of water and thereby increases the cell size and fresh weight. During seed maturation in these mutant seeds a greater loss of water occurs. As a result, the wrinkled seed phenotype develops. Besides this morphological variation, the mutation also causes changes in the amount of lipid and of one storage protein, legumin. This review article discusses the role of the SBEI enzyme in causing such metabolic changes in the developing embryos with the implication that metabolism can play a central role in plant development.

These authors claim that the mutant protein is not present in peas, so the wrinkled phenotype is not due to an inability of the protein to bind its substrate (amylose and amylopectin - the linear and branched components of starch, respectively) but rather its complete absence. The mutant is due to an 800 bp transposon insertion into the coding sequence of SBE1. If it was expressed, it would be reasonable to expect that it wouldn't be able to bind its substrate. The authors also discuss mutations at other loci that have been shown to be responsible for the wrinkled phenotype, but it is believed that these are relatively newer and would not have been observed by Mendel.


Are eukaroytic promoters located in the 5' UTR region?

Most promoter elements are not a part of the mRNA sequence. They are upstream (towards 5') of the transcription start site. However, a certain class of promoters called downstream promoter elements (DPE) can overlap with the geneic region. These elements have been reported to lie at 29-33bp upstream of the transcription start site and widely employed, in Drosophila [1]. Mapping of DPEs has been done for mouse human genes as well [2]. However, a detailed analysis supported by good sequencing data is yet to be done.

So, though DPEs are present in the transcript, I am not sure if they are retained in the exon. This can be confirmed by mapping the splice sites but this analysis is not presented in these papers.

You can see from the below figure [3] that most first exons in humans are big enough to harbour the DPE.


At what temporal scales do forest structures change?

This question is too broad. What type of temperate forest?

The European Environment Agency recognized dozens of temperate forest types:
 Acidophilous oak and oak‑birch forest types
 Mesophytic deciduous forest types
 Beech forest types
 Mountainous beech forest types
 Broadleaved evergreen forest types
 Floodplain forest types
 Non‑riverine alder, birch or aspen forest types

Community types will experience different patterns and rates of change based on numerous properties including climate, edaphic conditions, stand density, species pools, specific species characteristics, land use history, etc.

See Wright & Fridley (2010)
-Rate at which woody species colonize and dominate old fields decreases significantly with latitude.

Rates of woody succession were highly correlated with both annual temperature...and measures of soil fertility

See Fridley & Wright (2012)

suggest that climate plays a relatively minor role in community dynamics at the onset of secondary succession, and that site edaphic conditions are a stronger determinant of the rate at which ecosystems develop to a woody-dominated state.

See Peet & Christensen (1980)

Examined thinning rates based on initial stand densities -- found rates to be higher in denser stands and later densities became similar regardless of initial density (after 40 years).

Further compounding all of this are issues such as invasive species, shifts in herbivore pressure, plant pathogens/pests, etc.
Also, it's hard to find European forests w/out some type of historical major human influence.

From Parviainen 2005:

Latest estimates show that there are about 0.3 million ha of virgin forest (0.4 % of the total forest area) left in strict forest reserves and other protection areas in the temperate zone of Europe.

So given all of that, it's hard to definitively nail down specifics to answer your question.

Each of these above characteristics/variables/issues will influence both individual growth rates (i.e., tree diameter and height) as well as population and community dynamics.

To answer your question a little more directly:

As shown in the paper linked above (Peet & Christensen 1980), stand density rates vary dramatically based on initial stand densities and succesional stage; high-density stands can see HUGE loss of stems/ha in < 40 years, while low-density sites might see very little change.

Diameter distributions can change drastically, but will likely take multiple decades to shift to the "late-succesisonal reverse j". However, this is strongly dependent on frequency and magnitude of disturbances -- large canopy-clearing disturbances such as major wind events will accelerate this shift in distribution.

Species composition can certainly shift fairly quickly (1 or 2 decades), but typically only in transitional stages of succession or due to major disturbance. Late-stage successional forests (i.e., "mature forests") will typically see very little change in species composition in this time frame, but again so many facotrs will influence that. Because of changing climates, mass introductions of invasive species (both competitors and pathogens), etc., forests appear to be changing more rapidly. [See Israel (2011)].

Overall, forests change continuously, with most processes occurring on the time-scale of decades. However, this depends on scope b/c understory plants can change from year to year, while canopy trees can live for centuries. Noticeable shifts in community composition and biomass are visible on decadal timescales, but only long-term evaluation will demonstrate the effects of past disturbances. The takeaway, then, is that forests chnage on multiple time scales and as a result of many variables; as a rsult, one can never consider a forest as a static community or as a climax type.

However, we have more long-term data sets available and numerous advances in sampling methods that are aiding our ability to understand forest change across time scales. So we are just now beginning to truly understand some of the phenomena on a deeper level.

I'd recommend you start with an overview of the topic:

van der Maarel & Franklin (2013) should provide a number of citations for you to follow:

covers the composition, structure, ecology, dynamics, diversity, biotic interactions and distribution of plant communities, with an emphasis on functional adaptations;
reviews modern developments in vegetation ecology in a historical perspective;
presents a coherent view on vegetation ecology while integrating population ecology, dispersal biology, soil biology,
ecosystem ecology and global change studies;

Citations
 - Fridley, Jason D., and Justin P. Wright. 2012. “Drivers of Secondary Succession Rates across Temperate Latitudes of the Eastern USA: Climate, Soils, and Species Pools.” Oecologia 168 (4): 1069–77. doi:10.1007/s00442-011-2152-4.
 - Israel, Kimberly A. 2011. Vegetation change in Duke Forest, 1977 – 2010. University of North Carolina at Chapel Hill Masters Thesis. 120 pp.
 - Parviainen, J. (2005). Virgin and natural forests in the temperate zone of Europe. Forest Snow and Landscape Research, 79(1-2), 9-18.
 - Peet, Robert K., and Norman L. Christensen. 1980. “Succession: A Population Process.” Vegetatio 43 (1): 131–40.
 - van der Maarel, E. & J. Franklin. 2013. Vegetation Ecology, 2nd Edition. Oxford University Press, New York, New York. Pages 28-70.
 - Wright, Justin P., and Jason D. Fridley. 2010. “Biogeographic Synthesis of Secondary Succession Rates in Eastern North America.” Journal of Biogeography 37 (8): 1584–96. doi:10.1111/j.1365-2699.2010.02298.x.


Would a colony with only one male and female collapse?

Populations founded by a single pair are quite common in the lab

The Drosophila Genetic Reference Panel, one such example of high artificial inbreeding, is a series of inbred lines where the researchers mated brother and sister flies for 20 generations to form the lines, which means they will be highly inbred. When you do these though you often lose many of the initial lines because of inbreeding depression. Inbreeding depression is reduced fitness as a result of increased homozygosity in the lines - deleterious mutations are more frequently expressed. I have tried to find the number of initial pairs they used to make the ~200 DGRP lines but come up unsuccessful, but I've heard it was around 1500 pairs, although that may be well off the mark*.

What would happen to your mice?

Just like the DGRP lines, there is a high risk that the population would collapse. However, if they do get through a few generations of inbreeding, and are kept in steady conditions (i.e. selection doesn't change once the lines are formed), then they have an ok chance of persisting. If you started with multiple founder pairs then there's a better chance you will still have some (very inbred) mice in a few generations. The success rate will depend on the frequency of deleterious mutations and strength of their effects.

What is inbreeding?

Inbreeding is increased homozygosity in the population than would be expected under random mating. For example, if the frequency of two alleles ($A_1$ and $A_2$) at a gene are $p = 0.1$ and $q = 0.9$ respectively, the expected frequency of $A_1A_1$ homozygotes is

$p^2 = 0.1^2 = 0.01$

the expected frequency of $A_2A_2$ homozygotes is

$q^2 = 0.9^2 = 0.81$

and the expected frequency of heterozygotes is

$A_1A_2$ is $2pq = 2 \times 0.1 \times 0.9 = 0.18$

If the true frequency of heterozygotes ($A_1A_2$) is less than 0.18, then there is inbreeding.

Is there a benefit to inbreeding?

Well inbreeding can be a good thing. Imagine all of those lines that did not collapse. It is possible that a population formed out of those would have higher fitness than the original population, because deleterious mutations may have been purged (lines carrying deleterious mutations are more likely to collapse). So a highly inbred population can prosper. However, that population would also have lower genetic variance. Genetic variance places limits on the potential for adaptation, low genetic variance means low potential to respond to selection. So, if selection is not constant, then inbred populations are more likely to go extinct as they are unable to adapt to novel scenarios.

Inbreeding in nature

One classical example of high inbreeding in nature is in cheetahs, where it is beleived they went through a strong genetic bottleneck ~10,000 years ago. The problems faced by cheetahs today really highlights the problems of high inbreeding because they are struggling to adapt. Genetic bottlenecking is a  serious long-term problem for many species including the Javan rhino, the Kakapo, Mountain Gorillas, and others; even if we can stop poaching and habitat loss wiping out these species in the short-term, they will struggle to adapt to changes in the climate etc..

  "As a species, cheetahs have famously low levels of genetic
  variation. This can probably be attributed to a population bottleneck
  they experienced around 10,000 years ago, barely avoiding extinction
  at the end of the last ice age. However, the situation has worsened in
  modern times. Habitat encroachment and poaching have further reduce
  cheetah numbers, consequently snuffing out even more genetic variation
  and leaving cheetahs even more vulnerable to extinction."

* Supporting material from the DGRP paper would suggest that it was indeed formed from 1500 isofemale lines.


Is my Y-chromosome the same at 78 as it was at 18?

By and large, yes.  Some telomeres might be shorter, but the rest of the sequence will not change.  Certainly, any regions used for ancestry testing will be stable.


Background correction when reading ELISA with TMB substrate

Using different wavelength for reference give some advantages. You can measure a baseline of each well. All well might not have the same baseline because each well might not be the exactly same as others. In addition, you could make scratches on it, you might touch the bottom, or you get some dirt from your bench. And this can be corrected by A540 in your case. So, variations at a lower range are not much concerned. Sometimes, even if you choose a wavelength where the absorbance seems not to change after reaction, there might be a small change. This is not concerned ether, because both absorbances are concentration dependent unless states in solution do not change (froming complexes or something like that).

But still, you get high background from samples showing 1.4 or more at A450. I do not have experiences for this substrate, but you might want to think several possibility:
1)You might get bubbles on the top of your solution in the wells,
2)You might not get accurate values because OD is too high,
3)The solution might get precipitates
4)This may be a very less possibility, but some secondary reaction occurs.

For 2), 3), and 4). You might want to check linearity by drawing a standard curve, and avoid to use the range deviating from the liner relation.

PS
I should've mention that you would check the specification of your plate reader. OD=3 could be way to high to measure it. Because light intensity decreases to one thousandth though 1 cm light path at OD=3. It is very hard to measure such weak lights exactly. Probably many specifications of plate readers say you could measure ODs up to around 2, but some people think it is ideal to measure ODs up to around 1.


Can an upper forearm amputee correctly control the Median and Ulnar nerves

Yes, severed nerves still convey neural responses from the brain.

In fact, nerve potential recordings in the ulnar and median nerves of the stumps of arm amputees have already been successfully applied to control arm prosthetics (Jia et al. 2007; Kuiken et al., 2007.


Why is it sometimes difficult to resuspend E. coli in P1?

This is particularly an issue when you do maxipreps and the pellet is 200x the size of the pellet from a miniprep. The reasons why? Maybe you're pelleting at too high of a g-force (pure speculation). Alternatively, you could be growing the cells too long. I typically miniprep after a 12 hr culture. If you're seeing any darker colors in your pellet, you have a significant amount of dead cells. Those dead lysed cells will spill out their genomic DNA which is very viscous.

For maxipreps, you can't break up the pellet merely by pipetting up and down a few times and calling it a day. What you can do is swirl the side where the pellet is and breakup the clumps. Alternatively you can use a different pipet tip (for an extensive discussion on this very topic see Pipetting damage to cells). I change to a P200 for my minipreps and pipetting only the area around the pellet seems to do the trick for me. For maxipreps I use a P1000 which is better than using a 5mL syringe.


Why is there sperm mitochondrial suicide?

Maternal inheritance of mitochondrial DNA is very well conserved, although some species, such as some mussels, show paternal inheritance.  As for why or what the advantage is, some of it is due to basic logistics: sperm cells have ~100-1000 mitochondria, egg cells have 105-106, so male contributions are largely washed out.  Plus, most mitochondria in sperm are toward the tail, which does not always or necessarily get inside the egg.

For a more selection-based mechanism of the actual destruction, think about what sperm do.  They are small packets of energy that do nothing but race until they die.  That's it.  Energy production, which occurs in the mitochondria, produces reactive oxygen that can damage genomes.  The mt-genome in the egg is far less likely to be damaged.

Additionally, I might look to chromosome uniformity.  Heteroplasmy does occur now and again, and it's not usually a good thing.  Mitochondria are very important, so it makes sense to have an all-or-nothing approach, lest any deleterious genomes persist.


single units vs ensemble recording for signal detection

First spike latency or similar measures when looking at ensembles only tells you about the latency of the least affected unit when you are talking about latency increases, or the most affected unit when you are talking about decreases.

For example, if you record from 30 cells on a multiunit cluster and the latencies of 29 of them increase but 1 does not change, you might conclude no effect on latency.

Also, changes in detection probability can be harder to recognize in multiunit recordings. If a pharmacological manipulation increases or reduces activity overall, including at distant sites, this might change your threshold of which cells' spikes you can accurately detect as spikes by increasing or decreasing the noise floor.

For example, if your threshold decreases, you might be recording spikes from ~20 cells in your control condition, but then sample from ~50 in your pharmacological manipulation. Note that in this circumstance the total number of spikes you record might actually go down, but you would underestimate the affect because you don't know how many cells you are actually sampling from.

Of course there are problems with single cell recordings too. Sometimes it's really the ensemble activity that matters more, in that case the single units aren't as informative. You also have the problem of tracking accurately a single unit throughout a pharmacological intervention, which can be problematic depending on the time course of the manipulation (electrodes drift, cells die) or if the manipulation itself affects spiking properties (it may be more difficult to ensure you have the same cell if spike widths or amplitudes change).


What do you call that part of the muscle that connects directly to the bone?

The tendon is the part of the muscle that connects directly to the bone.

  A tendon (or sinew) is a tough band of fibrous connective tissue that usually connects muscle to bone and is capable of withstanding tension. Tendons are similar to ligaments and fasciae; all three are made of collagen. Ligaments join one bone to another bone; fasciae connect muscles to other muscles. Tendons and muscles work together to move bones.

The image was taken from the wikipedia link.


genetic difference subpopulations vs movement rate

[..] if a geneticist finds no significant difference between 2 subpopulations that have temporal spatial overlap

This isn't clear. Significance difference between what? What statistical hypothesis are you testing for which one would found no signicant difference (accepted the null hypothesis). Are you maybe thinking about a t-test between testing difference between the average phenotypic traits?

  it might be that they are still almost closed (no connection). Is this right?

Do you mean no gene flow (aka. no migration)?

  Can I deduce anything about the individual exchange rate between populations and the genetic similarity/difference?

"Individual exchange rate" is typically "called migration" or "gene flow".

At some extend, yes you can. But the question is really broad and will be hard to answer in the general sense. I will just provide a very common methodology here.

You can compute $F_{ST}$, a statistic of population divergence. A very good paper explaining the math of $F_{ST}$ is Nei (1973). I recommend computing $F_{ST}$ following Weir and Cockerham (1984). Then, if you can assume a finite island model (equal migration rate $m$ between any two population) and a constant and known population size $N$, then

$$F_{St} = \frac{1}{1 + 4N(m+\mu) \frac{d}{d-1}}$$

, where $d$ is the number of demes (number of islands)This equation can be found at many places. Slatkin (1995) is a very good paper but note that its final solution differs a little bit from the one I presented (by a square term) for reasons explained in Charlesworth (1998). You can solve for $m$ and plug the observed $F_{ST}$ and $N$. Note that depending on the markers used, $\mu$ will be negligible in comparison to $m$.

You might want to have a look at the very related post How could one calculate the gene flow between two populations?


Why doesn't mitochondrial DNA accumulate damage over successive generations?

If it was the case that we were inheriting damaged mtDNA, we would be inheriting ageing from our parents which in itself is not advantageous in terms of evolution.Considering that the germline mitochondria is purely maternal, nature has evolved a way to switch off the mitochondria of oocytes, and keep it in a simple state, mainly to serve as a template. This template is essentially error free, as the levels of ROS generated, is very low.

Mutations in DNA (mitochondrial or nuclear) in most cells in the body can be harmful to the health of the individual, but will have no influence on the next generation. The genes which we pass onto the next generation are separated off during early development into special ‘germ line’ cells which form sperm and eggs. Great care is taken to minimise the risk of mutation to these genes – genes in germline cells act as a blue print for the next generation. This is essentially why aging is not heritable, and it is a system that works pretty well.
Research has uncovered a rather elegant solution to this problem – those mitochondria that will be passed to the next generation are maintained in an inactive state.Mitochondria are only inherited through the maternal line – every mitochondria in your body came from your mother, and this is true for most animal species. The mitochondria in sperm are generally discarded at some point prior to fertilisation.
Membrane electrical potential, a measure of the activity of the electron transport chain, was reduced in oocytes compared to both sperm and the surrounding tissue. Further, ROS production was 50- and 100-fold lower in the eggs of fruit flies and zebrafish respectively. Finally, they confirmed that oocyte mitochodria in both species exhibit a simpler structure, indicative of reduced activity. So, it seems that in both fish and flies, the mitochondria in egg cells represent little more than a blueprint, ready to be passed on to the next generation error-free. By deactivating ovarian mitochondria, the fidelity of information is ensured across generations, and aging is not heritable.

Taken from: http://blogs.ucl.ac.uk/gee-research/2013/11/11/damage-and-fidelity-the-role-of-the-female-germline-in-mtdna-inheritance/
You can read the article here: de Paula, Wilson BM, et al. "Female and male gamete mitochondria are distinct and complementary in transcription, structure, and genome function." Genome biology and evolution 5.10 (2013): 1969-1977.


What is the significance of running an uncut plasmid on electrophoresis gel?

It is used to determine whether the unused/excess amount of plasmid has contaminated the  final solution of the desired recombinant DNA  or not.
Electrophoresis is performed on the "Blank"(uncut) plasmid to define its bands.If the electrophoresis result contains the bands of both "blank" and recombinant DNA , it shows that your solution is not 100% pure.


Phylogeny: Hybridization between different species sharing same genus?

Hybrids are not considered named species of either of their progenitors, but classified as hybrids of both. So they would be called Capsicum chinense x baccatum.


There is no difference in base pairing between different kinds of organisms. Humans, animals and bacteria all share the same fundamental mechanisms as they all use DNA. Which bases can pair is determined by the chemistry of the individual bases.

The bases in DNA form the following hydrogen bonds when they are paired:

If you would try to combine other bases than the canonical Watson-Crick pairs, the hydrogen bond donors and acceptors wouldn't match. You need a donor/acceptor pair at each position.

There are different base pairs possible, but these situations don't really occur in DNA but in RNA. You can find G/U wobble base pairs and even base pairs that use different parts of the bases than the canonical base pairs, e.g. Hoogsteen base pairs.


Probably a domestic hybrid of a mallard.
From Cornell:

If your duck has large patches of white where you didn’t expect it, think domestic duck.

Mallards (Anas platyrhynchos), which have the identifiable green head in the wild, are only 1 of 2 species of ducks that have been domesticated. So it would be no surprise if a strange looking mallard was in fact, well,  a mallard.
Again, according to Cornell:

Another common form [of the domestic/hybrid mallard] is the bibbed version. It has a sort of normal body and head plumage, and a white chest.

Also:

The passion for weird plumage in domestic ducks does not stop with white, but can go the other way too.  Some breeds are darker than normal Mallard plumage

These descriptions both match your specimen quite well.
Although your picture is low quality, it appears to me that the posterior feathers of your specimen also are not straight. Again, quoting Cornell:

Watch for the little curled feathers on the back of the male, above the tail.  Only the Mallard and its domestic descendants have those.

Finally, most hybrid ducks that come from some domesticated origin tend to be larger than  non-domesticated specimens since early domestication efforts emphasized large size for food (vs simply plumage for appearances). Your image has no relative scale, so I cannot comment on whether this applies to your specimen or not.
In terms of a specific "name" for such a hybrid?
I did find evidence that some people refer to domestic-hybrid mallards like your dark-plumage, white-bibbed mallards as "manky mallards", though I'm not sure how ubiquitous this is. For example, see here and here.

Though 10000birds.com claims non-domesticated birds can also occasionally develop bibs similar to those seen on domesticated descendants.


Value of r (intrinsic rate of natural increase)

NCERT shows per capita value is divided by 1000, not hundred (%). So the data you see is 22.50 per thousand! So, the per capita rate is 22.50/1000 = 0.02250 that is almost equal to 0.0205 given in book!

To make you understand better, remember that GDP and per capita GDP is different, the same way birth rate or death rate is calculated per 1000 but when we ask per capita we have to actually divide it by 1000.

Now in 2016 , it is 0.01019 i.e. 0.0102

I hope you understand!!


What is a simple protocol for staining cells in suspension?

You will get a lot of false-positives using the following method, and a real transfection of a fluorescent protein is always the way to go, because then you will prove that the transfection was really successful.

That said, you could try to use DAPI, followed by fluorescence microscopy or flow cytometry. DAPI is a very bright stain for DNA and cannot pass an intact cell membrane. If the cell membrane is disrupted, e. g. by necrosis, DAPI will enter the cell. I have never seen anyone trying to prove electroporation this way, but it will be worth a try. It could be that the time is too short for DAPI to enter the cell, so you'd need to tweak your setup.

I'd try the following: Prepare a cell solution with DAPI (something like 5 µM concentration should do). Split the solution into two electroporation cuvettes, perform the electroporation with one cuvette, leave the second one untouched as a control. After the electroporation, analyse the samples MOMENTARILY (means: within a few minutes) using a flow cytometer (if possible).

As for the cells, you could use anything. I suggest eukaryotic cells because they are more easy to visualize than bacteria. However, you would need a laminar flow hood for aseptic handling of cells. In theory you could also use bacteria, which are more easy to handle, but I'm not experienced with immunofluorescence in bacteria.


Why does high-voltage mostly shock a person, and even small current kill?

These statements are not true, simply speaking. Currents as little as few microampers can kill a person if, for example, applied directly next to the heart. A few seconds of 220V can kill a person even if the current is in miliamper range (Biksom, cited below, mentions 4s at 120mA). However, it is true that it is not the voltage alone that kills, that there are other factors (most importantly, the effective current, which, however, normally increases with voltage).

Look, Ohms law states that R = V / I (resistance equals to voltage divided by current). Given a constant resistance, a higher voltage produces also a higher current, full stop. Given a voltage of, say, 24 V, and the resistance of our bodies being 1000 - 4000 Ohm, the current will not exceed 6 - 24 mA. Note that in case of 220V this largest current would be less than ten times these values, so well below 1A! Yet, this is sufficient to kill an adult.

What's more, extremely high voltage can actually break the skin and effectively lower the skin resistance, which results in an even higher current (see formula above).

So where does this popular knowledge come from? Well, we know that things like electric sparks can have very high voltage, but are harmless. They are harmless not because the current is low, but because the duration and the total energy is low, since the total energy is given by power (in watts) times seconds, and power P = V * I (voltage times current).

Also, it comes from anecdotical evidence, since being shocked by thousands of Volts and survive can make you famous... precisely because it is extremely rare to get into contact with a high voltage line which can supply a steady flow of the current and survive.

Another reason became apparent in the comments: confusion between the factual current of the jolt one is getting and the nominal amps on the fuse. The former is given by the resistance and voltage; the higher the voltage, the higher the current. However, an 1A fuse is likely to blow quicker than a 10A fuse, thus cutting the line before the current penetrates our body to reach the heart and bring it into fibrillation.

It is a similar story with lightnings: duration is extremely short, but more importantly, in most of the cases the lightning did not run through the person who survived -- because if it did, they would be dead (also, see this fascinating bit). It either run over the skin, seeking the path of the lowest resistance, or through a material nearby.

Also, high frequency currents are less likely to penetrate the skin.

Literature links:

Biksom, "A review of hazards associated with exposure to low voltages"


Incubation time of Antarctic Phosphatase in lab

For 5' extensions or blunt ends, incubate the sample for 15 minutes at 37 degrees Celsius.

For 3' extensions, incubate the sample for an hour.

https://www.neb.com/protocols/1/01/01/vector-dephosphorylation-protocol


What does ophthalmologist see in your eye?

The name of the instrument is ophthalmoscope. It is used to determine the health status of your retina. Retina is the one of the few places in the body where you can observe the blood vessels directly.

The link also includes a picture of what your eye looks like from doctor's point of view.


NRAS is indeed a molecular switch, as part of the MAP-Kinase signaltransduction pathway it acts in controling the signal which goes downstream and finally will cause the expression of genes. In the case of NRAS this includes genes for proliferation, which is important for tumors. In principle, this looks like shown on this figure (from here):

RAS (this is the same for all three RAS family members) needs to be activated so it can signal downstream, this happens, when GTP is bound to the protein. Since permanent activation is obviously not a good idea, RAS itself has an intrinsic, but slow GTPase activity, which is activated by GTPase-activating proteins (GAP) and will eventually cleave the terminal phosphate group group from the GTP to make GDP + P. GDP bound RAS is inactive. GDP stays bound to the RAS protein and needs to be exchanged against GTP by Nucleotide Exchange factors (NEF) to activate RAS again.

The general principle is shown in this figure (from here):

Mutations in RAS proteins occur in 98% of the time in three locations (see reference 1): In codons 12, 13 and 61. All three mutation affect the ability of the protein to break down GTP by abolishing the intrinsic GTPase activity by the GAP (see reference 2). This leads to the accumulation of RAS protein which is permanently bound to GTP and therefore activated, subsequently activation transcription of genes for proliferation (amongst others). This process can lead to the formation of cancer.

Your questions:

The conversation of GTP to GDP does not lead to cancer. This process stops the activation of RAS proteins. It is the permanent activation which causes the problems.
You have the mutation in the KRAS gene, which is the origin of the problem. The wrong activation is of course done by the KRAS protein.
GEFs facilitate the exchange of GDP to GTP, the break down of GTP is supported by the GAPs. The mutation hinders the GAP to fulfill their role, so they are useless in the mutated form of the protein.
The other way round. If RAS proteins are bound to GDP, they are rendered inactive, unless a GEF exchanges it again to GTP.

References:

RAS isoforms and mutations in cancer at a glance
Guanosine triphosphatase activating protein (GAP) interacts with the
p21 ras effector binding domain.


Has the gestation (pregnancy) period for humans always been 9 months?

human gestation period

According to the link gestation period doesn't vary much between great apes.

I don't see any signs that human are becoming "more complex". In fact human babies are uniquely underdeveloped compared with other mammals (large brain size, upright posture)


What kind of shiny bronze beetle is this?

The plant helped identifying the beetle: This is a rosemary beetle (Chrysolina americana), which feeds on rosemary,  lavender and thyme. See here and here for some more information.


What are the functions and differences between axons and dendrites?

This reference is a bit basic, but lists the functions and differences between axons and dendrites.  Specifically, dendrites receive signals from other neurons, to the cell body; whereas, axons take signals away from the cell body (essentially 'input-output').  A diagram of the parts and the processes is below:

(Image source with additional information)

This Youtube tutorial is a nice visual description of both, and how they function within a neuron.


Is the SHC014 chimeric coronavirus "eerily similar" to Covid-19 in anything but a journalistic sense?

The "similarity" of this specific chimera was addressed in a recent paper concerning the lack of evidence that SARS-CoV-2 is lab-grown:

  Another claim in Chinese social media points to a Nature Medicine paper published in 2015 [7], which reports the construction of a chimeric CoV with a bat CoV S gene (SHC014) in the backbone of a SARS CoV that has adapted to infect mice (MA15) and is capable of infecting human cells [8]. However, this claim lacks any scientific basis and must be discounted because of significant divergence in the genetic sequence of this construct with the new SARS-CoV-2 (>5,000 nucleotides).

Liu, S. L., Saif, L. J., Weiss, S. R., & Su, L. (2020). No credible evidence supporting claims of the laboratory engineering of SARS-CoV-2. Emerging Microbes & Infections, 9(1), 505-507.

The "eerily similar" nature seems at most to be something well recognized by virologists, particularly in the wake of SARS: coronaviruses circulating in bats could become dangerous to humans if mutations occur in key parts of their genome or recombinations occur with other coronaviruses in bats or intermediate hosts. That's more or less what happened with the first SARS and more or less what happened with SARS-CoV-2, as best as can be told right now.

I'd also take a bit of umbrage at the language used in that article:

  this new coronavirus was found so potent it could infect and replicate in human airway cells naturally

seems like a bit of fear-mongering. Any virus that affects humans can "naturally replicate" in human cells: the author could have merely written that instead of calling it "so potent".


Since you suggest they come from a plant, they might be dried aphids. These insects usually feed on plant sap, and I already noticed some tiny, white, and apparently dead ones on plants.

As suggested in the comments, these are actually not dead aphids, but only the cuticle they leave after moulting, or ecdysis.


What is the distance between the 3' 18s rRNA (the Kozak consensus sequence) and the A-site of eukaryotic ribosomes during protein translation?

Kozak consensus sequence (KCS) is present near or overlapping with the start codon. I am not sure what you mean by distance between that and A-site. Start codon is localaized at P-site at the time of translation initiation. Distance between start codon/KCS and A-site at initiation is same as distance between P- and A- sites (I guess ~20Å). A-site keeps moving during translation and hence the distance keeps increasing. Crystal study is available; See here.

See this figure from the abovementioned study for the relative positions of start-codon, P-site (exit) and A-site (entry).


Found the answer in the PeptideProphet paper: number of tryptic
termini (NTT)

  This number, which can be 0, 1, or 2, measures how
  many of the peptide termini, on the basis of amino acid sequence,
  are consistent with cleavage by trypsin.


Why is extracellular measurement of action potentials so different from intracellular?

I'm going to mostly duplicate my answer to another question Neural signals amplitude since it's exactly the same as this one, but it has no upvotes so I can't vote as duplicate. Once I get an upvote either place I'll vote to close the other.

In the first figure, those voltages refer to the difference between the inside and outside of the cell (i.e., -70mV means the cell is 70mV more negative than the outside).

You can't possibly measure that potential difference from outside of a cell. When you do extracellular recording, like in the second figure, you are measuring spatial differences in ion concentrations that occur due to ions flowing in and out of cells. For example, when a cell fires an action potential, lots of positive ions flow into the cell; this makes the area just around the cell slightly more negative than an area further away. The magnitude of this potential as measured depends greatly on your recording configuration, the type of signal you are recording (i.e., population activity or just a single cell; synaptic currents versus action potentials), how close your electrode is to the signal you are recording, and where your ground is (or position of both of your electrodes if you are doing a bipolar recording).

Also, in this second recording, either the voltage is reversed (i.e., the electrode near the cell is taken as ground), or it is actually measuring return currents in the dendrites of the cell; otherwise, the action potential would be in the opposite polarity (downward first, then upward) compared to inside the cell.

Although it varies, in most cases the signals you record extracellularly are on the order of microvolts to a couple of volts.

Lastly, in the quote you reference, the line before it was:

  The total harmonic distortion (THD) of our amplifier stays
  below 1% for input signals smaller than 7.3 mV peak-to-peak.

That article is describing an amplifier system for recording extracellularly (potentially for a brain-machine interface). They are saying that one type of distorting noise is not a problem in their amplifier at the input voltages you would expect in an extracellular recording of spikes or local field potentials, which indeed would usually be less than 5 mV. This amplifier would not be suitable for recording intracellularly.


What is the meaning of a 1,4 bond between sugars?

Amylase breaks the bond between two sugar molecules in a chain (the chain is called starch).

The type of bond is called a glycosidic bond which is just a covalent bond between sugar molecules.

The "1.4" bond you are talking about is normally written "1,4" or "1-4"; you could interpret it as "1 to 4" because it is referring to a bond involving the first and fourth carbons of the sugar (they aren't bonded directly, there is an oxygen in between); they are just numbered that way so that (bio)chemists can talk about the molecule - see this other Q&A from Chemistry about the numbering of the carbons of glucose.


The methods should be equivalent, given the same data. Using phylosignal's demo:

library("picante")
library("phytools")

set.seed(5)
randtree <- rcoal(20)
randtraits <- rTraitCont(randtree)

phylosignal(randtraits[randtree$tip.label],randtree)

phylosig(randtree, randtraits[randtree$tip.label], method="K",test=TRUE)

phylosignal returns:

         K PIC.variance.obs PIC.variance.rnd.mean PIC.variance.P PIC.variance.Z
1 1.430635          0.01147             0.4631411          0.001      -2.662701

and phylosig:

$K
[1] 1.430635

$P
[1] 0.001

Both give K = 1.430635 and an identical P-value.

Mathematically, it shouldn't matter if you shuffle the trait values or generate a null distribution of K. To get a null distribution for K, you have to shuffle something, and the tip values are probably being shuffled. You could check the code to be sure. An analogy is that, when doing a randomization for an ANOVA-like test, you can either shuffle the observed values or the group membership. Either way will give the same answer.

As for interpretation, Brownian motion is the simplest model for trait evolution, implying no direction, optima, rate changes, etc. K = 1 when the observed variation equals the expected variation. If K is greater than 1 then neighboring tips tend to resemble each other more than you would expect, suggesting a deviation from Brownian motion.


Which ionic channels of Pacemakers can work in very low frequencies in extrasystole?

I think none.
It is so specific frequency range that the possible sources are

autonomic nervous system and
some reflex arch.

Also, the frequency is logically low with autonomic triggering.
My conjecture is that sympaticus starts up extrasystoles.
I think it must go through some reflex arch to be so specific.


Why should you use an annealing temperature about 5°C below the Tm of your primers?

You want to have primers which bind under the conditions of the reaction only to your sequence of interest. If you go too far off the optimal annealing temperature (5°C below the Tm is indeed a relatively good choice in my experience), your will affect the PCR efficency and thus the yield of your reaction.

An annealing temperature, which is much too low allows annealing of your primers to other sites than your intended target with partial annealing or internal base mismatches. This leads to unspecific amplification and lower yields.

If the annealing temperature is too high no primer binding can happen and you will get not PCR product. Alternatively, partial binding can also lead to misprimed products, although this is much less likely than getting no product at all.


Gel electrophoresis is a basic lab method to get size info about nucleotide fragments, although one might need to chop up larger DNA to be able to apply this method. The wikipedia page covers the topic well, thus I'd suggest reading it. I'll just give a short outline:

Nucleotide fragments are loaded into a gel (agarose or acrylamide).
The gel is put into a static electric field
Nucleotide fragment move to the positive end, because they have negative charge
larger fragments migrate slower than smaller fragments
standardized DNA ladder can be used to get approx size.

UV fluorescent dye is used to stain the fragments.

Another way, is to check closely related species. Among closely related species it is a fair assumption that they have similar genome size. You can also hybridize the unknown DNA to a DNA of such close relative to see how much of them are similar and you can also make estimates based on the size of the hybridized regions.


Both are ways for an organism to adapt to the environment, but enantiostasis focuses on maintaining functionality while homeostasis focuses on maintaining a stable internal environment.

For example, if the organism has to deal with changing salt concentration in water, it can do it in two ways:

Homeostasis : the organism will adapt itself so that its internal conditions do not change despite the change in the external environment (the focus is on not changing these conditions). This could mean stopping or reducing other activities because of this adaptation, but, in this example, the internal conditions (salt concentration inside the organism) will not change.
Enantiostasis : the organism adapt itself so that its functionality is preserved, at the possible expanse of stable internal conditions. This could mean the salt concentration in the organism will change, but the organism's functions will not stop or be reduced because of it. Enantiostasis can be realized either by avoiding external changes (for example, absorbing more water when the salt concentration is high and less when it's low) or tolerating it with a wide range of possible conditions.

(Source : detailed explanation on this subject as a commentary on a university course)


Is there random assortment in metaphase II?

Metaphase I

Your understanding of the metaphase I is not entirely correct. In normal (human) metaphase I homologous chromosomes separate. Therefore, sister chromatides go together. More precisely sister chromatides are kept together at centromere. You have only two possibilities for each chromosome:

<-AA   aa->

or

<-aa   AA->

If we multiply the two possibilities for all 23 chromosome pairs it leads to correct number  223 of possibilities.

There can be one or more crossovers between two or more chromatides but the fate of crossovered chromosome arms is determined by the fate of centromere they get connected to.

Your diagram of random assortment, if I understand it correctly, allows for more than 2 possibilities for chromosome pair:

<-Aa   Aa->
<-aa   AA->
<-AA   aa->
...

And it would lead to incorrect number of possibilities (more than 2)23

Metaphase II

In metaphase II sister chromatides separate as they would in mitose. Yes, there is random asortment of which chromatide goes left and which goes right. With your notation it could look like this:

<- A   A'->
<- b   b'->
<- C'  C ->
<- D   D'->
...
<- w'  w ->

However, as I said earlier, some chromosomes can crossover more than once, so you can have thinks like:

<- g''   g'->

or

<- F'''   F ->

or

<- h'    h'->

Inverse meiosis

For every rule in biology there is an exception. Some species have inverse meiosis. This means they do it in reverse order. In metaphase I they separate chromatides and in metaphase II they separate homologous chromosomes.


Assessing beta diversity variations with time

Rather than Mantel, I would suggest doing a procrustes analysis. I didn't know much about it (and still I don't) but a reviewer required it for a paper I submitted, so I used the implementation in vegan package. You can also give a look at this nice tutorial
The idea of procrustes is similar to Mantel's but it should perform better for this case.
I don't what to say about the second question, sorry!


Why are aminoglycoside antibiotics particularly effective for aerobic gram negative bacteria?

Anaerobiosis is incompatible  with effective intracellular accumulation of aminoglycoside antibiotics such as streptomycin and gentamycin.

After an initial binding step involving outer membrane lipopolysaccharide the kinetics of the uptake of aminoglycosides exhibit two energy-dependent processes (EDP I AND II). EDP I  is the slow, rate-limiting stage and is dependent upon the membrane potential ΔΨ, but the details of the process are unclear. EDP II is more rapid and may be triggered by membrane changes arising as a result of translation errors caused by the antibiotic accumulated in EDP I since protein synthesis inhibitors block the transition from EDP I to EDP II.

EDP I requires  a threshold value of ΔΨ, and there is evidence that this threshold often cannot be achieved under anaerobic conditions.

This summary is based on information in this review from 1987.  I haven't been able to find any more recent information.


Large nocturnal butterfly with red and black hindwings

That is a moth, in the family Erebidae. It is in the genus Catocala. Wikipedia has a nice page on Lepidoptera of Poland. https://en.wikipedia.org/wiki/List_of_Lepidoptera_of_Poland
including all the Catocala there.


Question about production of CFTR protein

CFTR (cystic fibrosis transmembrane conductance regulator) is an integral glycoprotein of the plasma membrane, and mucous is rich in secreted glycoproteins. All proteins are made on ribosomes: CFTR will be cotranslationally inserted into the ER membrane while secretory glycoproteins are cotranslationally sent across the same membrane into the lumen of the ER. In the ER the initial glycans are added to specific amino acid residues. The folding of all proteins is carefully monitored by chaperones in the ER to avoid misfolded proteins reaching the cell surface. Various folding factors also come into play, including peptidyl proline isomerase and protein disulphide isomerase.

Proteins destined for the cell surface leave the ER in COPII-coated vesicles (CFTR will be in the vesicle membrane, secretory glycoproteins in the vesicle lumen) and are targetted to the Golgi where the glycosylation process is completed. Another round of vesicle transport gets the proteins to the cell surface - when these vesicles fuse with the inner surface of the plasma membrane the vesicle content is secreted into the surroundings, while the vesicle membrane proteins enter the plasma membrane.

The classic example of a CFTR defect, resulting in cystic fibrosis, is due to the ΔF508 mutation - the loss of a single amino acid results in misfolding, and the defective protein is held in the ER resulting in loss of CFTR function at the cell surface. Overcoming this retention is one of the targets for CFTR therapy, because if the ΔF508 protein does manage to pass through the secretory pathway to the cell surface it provides sufficient channel function to abolish cystic fibrosis symptoms.

I haven't cited any references here because this is all standard biochemistry/molecular cell biology textbook stuff, so should be easy to confirm.


Depending on the stage of cell-cycle you are interested in, people often use the size/morphology of the cell as an indicator. Then you select cells with a cell sorter.

Another option is to specifically tag some cellular molecule that can give an indication as to the relevant stage and then sort the cells based on the tag. This does not necessarily have to be cyclins - for example if you are only interested in S/G2 you could tag the DNA or maybe histones.


I would like to know what this insect is please

That is a planthopper, order Hemiptera, suborder Auchenorhycha, Superfamily Fulgoroidea. It looks to be in the Genus Phrictus. Very similar to a picture I saw on the web of Phrictus diadema.


Is global life expectancy normally distributed?

Let's see!

I took the most recent WHO data from here and did a quick an dirty analysis in R. Here is the histogram as well as a normal distribution with the same mean and standard deviation as the actual data:

Does not look very normally distributed. In fact, the shapiro test confirms this impression:

Shapiro-Wilk normality test

data:  df$life_expectancy
W = 0.94141, p-value = 4.338e-07

Edit

Commenters requested to weigh the life expectancy by population size.Well...the result is pretty ugly:

Apparently, the large populations of China and India produce disproportionally high bars. However, keep in mind that we are using averaged values which means that all the variation within countries is not represented by the histogram. We would actually have to have data on individual ages of death for a random sample of the world population to finally settle the question. :/


First, and I cannot stress this enough, you should not go seeking out human pathogens if you don't have the appropriate equipment to handle it at the right safety level.  That goes for all pathogens, even ones you might find around your house.

In a professional lab, you might get samples from collaborators, clinical samples, vendor, or really an number of other professional resources.  A well respected vendor as an example is ATCC, but the general public wouldn't be able to "shop" there.

But you really don't need to go far to get a whole host of microbes to study, you can grow them all at your house.  The basics of bacteria culturing can really be broken down to three steps: (1) get a source of bacteria, (2) put some of the bacteria in an environment where they can grow easily, and (3) harvest them to do something useful with them.

(1) Is fairly easy, bacteria are everywhere.  You can swab nearly any surface of anything in your house and come up with microbes (note you might also get some mold/fungi).  In this case (3) is easy as well.  Once you have culture you can streak it across a slide to view it under a microscope (you could also use several proper mounting techniques).  After all, looking at microbes under a microscope is the real goal here!

The only part of this plan that will take some real elbow grease is making your own culture dishes at home, but it's not as hard as you might think.

Making your own culture dishes:

1) The "plates" themselves.

  I recommend getting the smallest Tupperware like containers your can
  find that are microwave safe, dishwasher safe, and really make a good
  seal (water tight at the least). They really don't have to be big, and
  you will make your life easier if you buy a bunch to match. They need
  to be super clean. After running them through your dishwasher at home,
  put them all in a boiling pot of water until you are ready to pour in
  your "medium." A mid-low simmer will work

Note that you won't probably be able to have perfect sterile technique at your house, but you should try to do what you can.

2) Your "Medium" or Broth

  I highly recommend using pectin as your gelling agent if you can't get
  your hands on some agar. After that comes plain unflavored gelatin,
  but I recommend pectin. You can get it at almost any grocery store and
  my recipe is made assuming that. You can determine how much you want
  to make, just scale up the ratios. I'm going to list things as rough
  volume by volume so you won't need a scale.

  i) Make the powder first:

  45mL of pectin;
  4 bouillon cubes ground as finely as you can (you can get different
  types and results depending on if you start with vegetable, beef, or
  chicken. I recommend starting with vegetable.);
  125mL of refined white sugar;
  Additives (more on this later)

  ii) Mix the powder into 500mL of water.

  Before you mix in the powder, heat the water to 50-75oC (mid low heat), but not boiling. Mix the powder in while stirring until
  dissolved.

  iii) Bring the mixture up to a boil. Let it boil for about 2 min,
  stirring all the while.

  iv) Cover the pot and let it cool for 4-5 min.

  You by no means want it to cool down to room temperature, you just want
  to get it a little below boiling. If you are at 55oC or below it's
  definitely time move on.

  v) Dip/fill your "plates" 1/3 full of media using clean/sterile
  utensils and seal while hot but not boiling.

  You may have noticed this seems an awful lot like canning, and that's
  because it is. Again you want to be as clean as possible in this step
  and of course try not to burn yourself on anything.

  vi) Let your media plates set and chill over night in the
  refrigerator.

  You really probably only have to wait a few hours if you are anxious
  to get going. You are going to want to store the plates that you are
  not using in the refrigerator anyway. Also if you made a bunch of
  plates, let the cool on a counter before you put them in the fridge so
  that you don't raise the temp of your fridge too much.

  Remember the thing about additives? You can play around with adding
  different amounts and different types of salts, vitamins, food, or
  other items to see how they affect the cultures you get to grow. All
  kinds of fun there. First go round, leave them all out.

Now you have your own home made culture plates! The above recipe was empirically tested by my childhood, and repeated by my son's. Not all pectin from the store may be equal, this is with Ball Classic (I have no relation to the company). I'd love to know people's results in trying it, because I might need to re-think how/what I'm doing to get it to work.

Go around your house swabbing things with sterile swabs (you can get these at a drug store), and then streak them out on plate. While it will be a little different with a swab and homemade plate, the idea is similar to what is done here.

Leave your plate in a warm wet place, but not in direct sunlight. Ideal temp is going to be around 37, but you can leave them above and below that and still get things to grow. On top of our dryer is where I leave them.

After a day or so you should have colonies you can streak out on a slide and look under a scope. You will find all kinds of things this way. If you want a more formal way to put things on a slide, you can check out dry and wet mounting from a Google search.

You are actually quite likely to run into E.coli if you sample enough "areas" this way. Obviously don't eat or huff the stuff that ends up growing. Maybe you can post some fun pictures of this if you try it.

As pointed out in the comments, if you successfully get bacteria to grow, then you will need to successfully get rid of them.  I should point that a good set of rubber gloves (that you can bleach and wash after use), or disposable gloves are a really good idea when handling plates that have grown bacteria.

Clean Up

First off, I want to clearly say that this stuff can clog a pipe.

If you tried to grow something on a plate, and you didn't get a colony that you can see with the naked eye (note some microbes might make CLEAR growths) you can probably just scoop the gel into the trash.

Note that I said probably.  If you swapped any part of your body, waste, or that of an animal you must decontaminate even if you didn't see anything grow.  On the plus side decontamination is easy.

If you did see something grow, or you otherwise need decontamination:

First make a 20% bleach solution in a large Tupperware like container (probably don't want to do this is a nice metal pot, but could do it in a junk one).  You can go as low as 10% bleach solution if you sure your bleach is NOT a cheap already watered down brand (like something bought at dollar store).  But just to be sure, I recommend 200mL of bleach in 800mL of plain tap water.

Drop your plates and lids into the bath (with the lid off) and let it sit for 10-15 min.  Then, working under/in the bleach solution with your gloves on, use a fork/spoon to get out the medium (it will be like thick jello).  Do this for all your plates, and you can do more than one at a time this way.

Once you have all the medium out and floating in the bleach, take the plates out and put them in the dishwasher.  Strain out the bleach/medium/funkiness you grew through a cheap colander (I recommend dishwasher safe plastic like PP).  Put what get's caught in the colander in the trash and take the trash out.  Wash the plates, lids, colander, and large container you used for the beach bath.

Slides

Slides present extra caution because they can break or shatter to create sharp edges.  For the most part, if you cover your sample with a cover slip, and seal it with nail polish, you can actually keep your slides indefinitely with little risk.  If you do decide to dispose of them, they should first go into a thick Ziploc bag (use an expensive freezer guard type bag for this) or into a Tupperware you don't mind throwing away.  If you never sealed your sample to your slide, you should also decontaminate the slide in bleach first (as above, with extra caution to not cut yourself).

If you are sophisticated enough to get microscopic photos of the microbes you see, by all means post them up and we'll try to ID them as best we can (many look very similar, and we use genetic or protein markers to get a true ID).


Can this image be the result of a Western Blot?

I do not think that a publication quality blot should have such an artifact, but I was able to find something similar by purposely over blotting (not the same as over exposing) a gel.  If you use too much primary, secondary, or developing reagent, you can get your HRP signal to "burn in" a membrane where you get a distinct "negative band."

By negative band I mean a region that is more clear/white than background. This happens mostly when you have way too much secondary antibody.  Normally when this happens, the CENTER of the band burns in first so you would see a white center with dark edges.  And that's only when you are imaging the membrane as it is burning in.  Often the whole band is white.

After going through the westerns of grad-student who is working with me, I found this image:

It came with the clear notation that it was burned in and disregarded (said student was learning how to do Westerns at the time).  It's a GAPDH blot for those that care.  When this does happen, it's obvious because you can then see the band with your naked eye on the membrane.  Again this would be a reason to not publish the blot.

The image could have non-maliciously been edit via compression, screens, filters, etc as mentioned by others in the comments.  This is the only way I can think of to experimentally have a similar image.  Ether way I don't think the image should be reported as is.


Is DNA actually like source code repository?

I think this analogy is not actually that bad, but you are making some incorrect conclusions from it especially regarding 'junk' DNA and which parts of a repository DNA holds (which shows the limits of analogy!). Think instead of the DNA of an organism as a single local copy of a particular commit.

There is no remote to compare to and no list of historical changes, each organism just has its own local copy of the most recent source that can sometimes be merged with other local copies via sexual reproduction or horizontal gene transfer.

What you need to drop from the analogy

Get rid of any thought of a master branch or ideas that the repository contains backups of previous versions. These thoughts will only mislead you.

This statement:

  original DNA was not erased, but backed up every time new mutation (commit in software SCCS) appeared.

makes little to no sense in biology. There is no backup, except in that each organism is a branch of it's parent(s) source.

Where the analogy could work

Genomes of different species are all branches from some original source code. Therefore, you find a lot of commonality when you compare even very distantly related life, especially in the most key libraries that are involved. There is a ton of conserved sequence in the basic machinery for replicating DNA and producing proteins, for example.

This is why your statement:

  This explains why human DNA is mostly so similar to dog DNA, fish DNA etc. Because we all evolved from same primitive cells! Base of our "repository" was same!

is mostly correct.

Length of source

Your analogy has gotten some criticism for your conclusion:

  Theoretically, the more primitive organism is, the shorter DNA it should have.

but I would argue this is actually a way in which your analogy works, yet your conclusion from it does not. Software development involves both adding new code and deleting obsolete code. Lines of code is a poor measure of how primitive some code is. Biology shows this well: all life is equally primitive in terms of years of existence, and single-celled organisms are much more advanced in terms of numbers of generations. If organisms contained some log of all the past changes (which they do not), the repository would be way way bigger in bacteria than in animals because of that large number of generations.

Summary

In summary, analogy can be helpful to wrap your head around some information, but be careful in taking it too far. Sometimes analogy is good for generating new hypotheses and for guiding your learning, but you need to verify those hypotheses in the actual biology (see Richland and Simms 2015 for one take on the usefulness of analogy as an educational tool).

I disagree strongly with the comment by @SPr stating "The analogy between the genome and source code repository is unhelpful and poor": even the imperfection in an analogy can be very helpful in that they help you build a relational map of the world by finding where analogies work and where they conflict.

Richland, L. E., & Simms, N. (2015). Analogy, higher order thinking, and education. Wiley Interdisciplinary Reviews: Cognitive Science, 6(2), 177-192.


What is the scientific and common name of this bug?

Definitely appears to be Pentatomidae (as others have pointed out) due to shield-like, broad bodies. With over 4500 species and larval stages demonstrating significant variability even within species, ID can be difficult without knowing specific fauna, size, habitat, etc.
The OP doesn't list a size, but because OP is viewing under a scope, I assumed this is a fairly tiny species.
I came across this similar-looking unknown species (simply labeled "PK03") of the genus Eysarcoris

 Credit: CBG Photography Group, Centre for Biodiversity Genomics
The Eysarcoris genus is present in India (e.g., see indiabiodiversity.org with example of "two-spotted sesame bug")
A similar species well known throughout Europe is Stagonomus venustissimus (previously classified as Eysarcoris):

 Credit: Jose Manuel Sesma (2016); appears to be originally posted here
I cannot say if either of these species is correct (doubtful), but I think they are closer than the other provided answer.
I'll update if I find anything specific.