Stress response has 2 main components:

Quick response, within minutes, is by the Sympathomedullary Pathway (SAM): hypothalamus > sympathetic nervous system > release of adrenaline and noradrenaline from the adrenal medulla > stimulation of the heart, dilation of the muscle arteries, constriction of the gut and skin arteries, glcogenolysis (the breakdown of glycogen into glucose) > more glucose available as a fuel
Delayed response, within hours, is by the The Hypothalamic Pituitary-Adrenal (HPA) System: hypothalamus > pituitary gland > ACTH > release of cortisol from the adrenal cortex > gluconeogenesis (formation of glucose in the body from other substances) > more glucose available as a fuel

Cortisol secretion from the adrenal cortex can be stimulated by things other than stress, for example, hypoglycemia, but hypoglycemia will simultaneously activate the sympathetic nervous system, which will trigger the release of adrenaline (Neuroendocrine Response to Hypoglycemia).

Some cortisol is also secreted along with aldosterone in response to hyperkalemia or hyponatremia (Vivo.colostate.edu), for example in SIADH (A Case of Transient Hypercortisolism Simultaneously Occurring With the Syndrome of Inappropriate Antidiuretic Hormone Secretion Induced by Olanzapine).

Cortisol can be also increased without stimulation of the sympathetic system in Cushing syndrome due to a pituitary adenoma or, rarely, other tumors that secrete ACTH or in adrenal adenoma, which secretes cortisol.


How are primary monoclonal antibodies for screening mutant cells made, physically?

Monoclonal antibodies are typically manufactured from a hybridoma cell line. If you are able to obtain hybridomas already made for your antibody (not very likely), or another antibody against your protein, then it's quite easy to produce the antibody yourself. The hybridomas secrete the antibodies into the media, so after growing a bunch of cells, you can purify the antibody from the media with a protein G column.

However, there are not very many hybridoma cell lines available. It's a lengthy and expensive process to make your own (several months and thousands of dollars), even with the help of a core facility/company. You would provide the facility with several milligrams of your protein, they would use it to immunize mice, then after 1-3 rounds of screening, you could obtain hybridoma clones.

There are some banks with hybridomas available for research, for example:

http://dshb.biology.uiowa.edu/

http://www.cellbankaustralia.com/ecacc-hybridoma/


It's a common misconception that pathogens "don't want to kill their hosts". In reality, pathogens don't "care" at all about killing their hosts. All pathogens "want" to do is transmit from one host to the next. (Taking out the teleogenic language: There's no natural selection on a pathogen to reduce virulence as such. The selection on a pathogen is for transmission.)

In some cases, transmission is optimized when the virus is less virulent. In other cases, transmission works just fine when the virus is highly virulent. Rabies is one of the latter cases.

If a pathogen is spread by, say, respiratory contact, then having a host that is ambulatory and seemingly healthy may allow the first host to contact many others, so reducing virulence may enhance transmission in that specific case.

If the pathogen is spread by sand fleas (as in myxoma in Australian rabbits), then rapidly killing the host is counterproductive, because fleas leave a dead body. But keeping the host healthy is also counterproductive because a healthy rabbit scratches away its fleas. Optimal transmission turned out to work with a virus that kills 50-75% of its victims, because that makes the host very sick for a long time, allowing the fleas to bite it unimpeded.

Rabies spreads by damaging the brain, making the host aggressive, and spreading through bites in saliva (among other ways, but that's an important one). Serious brain damage to the point of wildly abnormal behavior is really not compatible with a host living a long time, so optimal rabies transmission means very high host mortality.

Finally, humans are not natural hosts for rabies and rarely transmit the virus, so in any case there's minimal natural selection for any virulence changes in humans. But it likely wouldn't matter, for the reasons above.


Do biological facts determine when a human fetus is considered alive and human?

Life is generally distinguished from non-life by metabolism and growth. As such, a fetus is alive. The reference to "not...until 26 weeks gestation" that you've heard likely refers to viability.* With the most aggressive medical care, this is the approximate age when a fetus may be able to survive outside the womb.

The term human from a biologic perspective is a species label.** Given that a fetus is genetically indistinguishable (in broad strokes) from a post-natal human, I think it would be hard to argue that it is anything other than human.

Summary: Yes, a human fetus is both alive and human.

*Note that this use of the word viable is standard but deviates somewhat from the etymology of the word.
**I'm ignoring here other ancient species (homo-) which may be considered human but are irrelevant to the question.


Dopamine, norepinephrine, and serotonin are more commonly found during the attraction phase of a relationship.

All these chemicals stimulate the brain's pleasure center. But this stage only lasts 1.5 - 3 years [2]. That's why 'we no longer feel the initial feelings of love'.

Oxytocin and vasopressin seemed to be more closely linked to long term bonding and relationships characterized by strong attachments [1].

Attachment makes relationships last for years and decades. It is based on commitment and mutual friendship. Oxytocin and vasopressin are at higher levels [2].

The neurological process involved in the perception of heartache is not known, but is thought to involve the anterior cingulate cortex of the brain, which during stress may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest [3].

Image from Wikipedia [1]

References:

Wikipedia contributors, "Biological basis of love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Biological_basis_of_love&oldid=613867553 (accessed June 26, 2014).
Wikipedia contributors, "Love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Love&oldid=614240299 (accessed June 26, 2014).
Wikipedia contributors, "Broken heart," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Broken_heart&oldid=613979584 (accessed June 26, 2014).


"Prime" structure of DNA Double Helix: Confusion

A single, unwound strand of DNA runs 5' to 3', the video is correct. When wound properly, the strands run in reverse directions, 5' to 3' for the first, 3' to 5' for the other. That diagram is not helpful, though the post itself is quite good.


All the organisms shown in the figure reproduce asexually. (A) is Penicillium in which non-motile conidia are produced singly or in chains. Organism (B) is Chlamydomonas in which reproduction occurs by zoospores. In Hydra (C) and yeast (D), asexual reproduction takes place by budding.
Mutliple fission and Spore Formation are two distinct processes where in:

Multiple fission can be explained with the following diagram:

Multiple fission is a process of asexual reproduction in which a single organism splits up into multiple organisms or daughter cells of similar type under favourable conditions like availibity of food and suitable environmental conditions.

Spore formation can be explained with the following diagram:

Spores are tiny microscopic hard unicellular sexual bodies which are always suspended in air. Under suitable environmental conditions they settle down and grow into new plants. Above given is a structure of rhizopus(bread mould) reproducing through the process of spore formation. Each rhizopus consists of a globular structure at the top known as the sporangium which consists of spores. When the favourable conditions arrive then the sporangium bursts and the spores get suspended in the air. Soon they settle on the moist bread particles, leading to the formation of new rhizopus plants.


DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. However it is yet to be linked closely to mammalian moles.
Information here, states:

"Moles are overgrowths of skin cells called melanocytes, but the genetic factors involved in their development are not well understood."

The BRAF gene is one of the most well-studied genes involved with benign moles, if a mutation arises in this gene - there may be a production of an altered protein that causes melanocytes (melanin-producing cells located in the bottom layer of the skin's epidermis) to aggregate into moles.
I cannot answer why DNA repair does not occur. Maybe the cell cannot identify the mutation, maybe the cell cannot corrects the damage, or maybe it is also from environmental factors. This is an active area of research, but receives far less attention compared to cancer or heart disease.


HEPES is a particular chemical, not a mixture of chemicals so unless you have the ability to synthesise your own chemicals you cannot produce it without having the dry chemical preparation.


Difference between crossover rate and recombination rate?

Let's start with the second question.

  Is 'per base pair' and 'per locus' the same thing?

No, not necessarily. A locus (plur. loci) is a location in the genome. It can be of any size. A locus can be a single base pair or it can be 10 base pairs, or a whole gene or anything you want.

  'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing?

Recombination rate and crossover rate are not exactly the same thing!

Let's define two loci. Here is a drawing of two haplotypes (the maternal one and the paternal one). Let's represent the loci on the maternal haplotype with capitalized letters and the loci on the paternal haplotype with lower case letters

---A---------B---

---a---------b---

Let's Let's say that between these two loci there are on average 0.2 crossover per reproduction. The crossover rate is therefore 0.2.

Let's draw the two haplotypes after crossover(s) in a case with...

... 0 crossover

---A---------B---

---a---------b---

... 1 crossover

---A---------b---

---a---------B---

... 2 crossovers

---A---------B---

---a---------b---

... 3 crossovers

---A---------b---

---a---------B---

... 4 crossovers

---A---------B---

---a---------b---

You might see a pattern here! If the number of crossovers is even (including 0), then the association between the two loci is unchanged. If the number of crossovers is odd (including 1), then the association between the two loci is changed.

The recombination rate is the rate at which the association between the two loci is changed. Let $P(n)$, be the probability that there are $n$ crossovers betwee our two loci. The recombination rate is therefore $P(1) + P(3) + P(5) + P(7) + P(9) + P(11) + ...$.

To make a long story short, the recombination rate is the rate at which the number of crossovers is odd.


Have there been new discoveries concerning the perception of taste for the last 10 years?

I'm not quite clear on exactly what you're interested in, but the short answer is yes, there have been discoveries related to the perception within the last 10 years.
The example that comes to mind is the role of the cannabinoid 1 receptor in the sense of taste of lipids.  The full text of a good article is available online here.

Source:
Brissard L et al. 2018. Orosensory Detection of Dietary Fatty Acids Is Altered in CB1R−/− Mice. Nutrients 10(10): 1347.


What happens when someone is stung by a jellyfish?

The problem is that box jellyfish doesn't specify one jellyfish but a group of different jellyfish. Some of these are highly venomous - I pick here Chironex fleckeri, as this is often called "the most venomous jellyfish in the world".

Chironex fleckeri has long tentacles which are covered with millions of explosive cells called Cnidocytes which inject a dart with the very powerful toxin upon touch. It is therefore very dangerous to touch the tentacles with bare hands to remove them.

The toxin is a mix of different bioactive proteins which have cytolytic, cytotoxic, inflammatory or hemolytic activity. Case reports (you can find information in reference 3 about it) show that the tentacles "burn" though all skin layers causing immediate strong pain and lasting scars (if the victims survive) which tend to show signs of necrosis. The toxins itself paralyze the muscles of the heart and the respiration and also causes hypokalemia by hemolyzing red blood cells (one of the toxin acts as a membrane pore in the blood cells). This causes further problems and often a cardiac arrest. See reference 1 and 2 for details on the toxins. Especially 2 is interesting, as this is a PhD-Thesis on this topic with a lot of references.

Treatment depends on how severe the injury is - in severe cases an antivenom can be used. Besides this typical measures are CPR, giving oxygen and removing the tentacles (with appropriate protection). See reference 3 (good overview) to 5 for details on this topic.

References:

Chironex fleckeri (Box Jellyfish) Venom Proteins: Expansion of a
Cnidarian Toxin Family that Elicits Variable Cytolytic and
Cardiovascular Effects
The molecular and biochemical characterisation of venom proteins
from the box jellyfish, Chironex fleckeri
Chironex fleckeri (Multi-tentacled Box Jellyfish)
Jellyfish stings and their management: a review.
Cytotoxic and cytolytic cnidarian venoms. A review on health
implications and possible therapeutic applications.


Re-establishment of Hardy Weinberg Equilibrium After Selection

Revised to add complete solution

Before the owls arrive, 100 out of the 2500 mice are dark-colored. This ratio provides the frequency of the recessive allele

$$q^2 = \frac{100}{2500}$$

So $q$ is 10/50 or 0.2. This means that the frequency of the dominant allele $p$ is 1 - 0.2 or 0.8.

Knowing these frequencies, it is possible to calculate the number of each allele

$$AA = (0.8)^2 \times 2500 = 1600$$
$$Aa = 2 (0.8) (0.2) \times 2500 = 800$$
$$aa = (0.2)^2 \times 2500 = 100$$

Of the light-colored mice, 2/3 are AA and 1/3 are Aa. The same proportions hold after the owls leave, but the total humber has been reduced. The dark-colored mice are all aa.

$$AA = \frac{2}{3} \times 240 = 160$$
$$Aa = \frac{1}{3} \times 240 = 80$$
$$aa = 80$$

From these values, the total number of each allele may be calculated

$$A = 2 \times 160 + 80 = 400$$
$$a = 80 + 2 \times 80 = 240$$

These numbers provide the frequency of each allele post-selection

$$p = \frac{400}{640} \approx 0.63$$
$$q = \frac{240}{640} \approx 0.37$$

Applying Hardy Weinberg for the new equilibrium

$$aa \approx (0.37)^2 \approx 0.14 $$

which is, "approximately" 15%.


Even teachers are sometimes wrong. ;)

Chitin is a homopolysaccharide. This just means that it is made up of repeating units of the same monosaccharide - in this case that monosaccharide is N-acetylglucosamine. Other examples of homopolysaccharides are glycogen and cellulose.

The basic structure of chitin is shown below as a polymer of two N-acetylglucosamine units:

Homopolysaccharides can be linear chains or branched, as long as they are made up of just one type of sugar unit. A heteropolysaccharide is made up of multiple different monosaccharide units. Glycosaminoglycans would be an example of a heterpolysaccharide as they contain two different sugar units.


The key here is to recognize the distinction between a community as a whole and the individual species within that community. Just because individuals have the capability to self-perpetuate, doesn't mean that a community as a whole does.

For example, imagine an island with a whole bunch of caterpillars. Now imagine that you introduce a non-native caterpillar-infesting wasp. On the mainland, the caterpillars have evolved resistance to this wasp and so can fight off the infestation. But on the island, they never evolved that resistance, and rapidly succumb. Upon introduction of the wasp, you have a "community" of wasps and caterpillars. The caterpillars can reproduce, as they have been, so they're self-perpetuating within their species. The wasps can also reproduce by laying their eggs in the caterpillars, so their species is self-perpetuating. But the wasp infestation is killing caterpillars faster than they can reproduce, so the community is unstable. Over time, the population of both wasps and caterpillars will crash as all the caterpillars die off. Each species can self-perpetuate, but the wasp/caterpillar community, taken as a whole, does not.

That, in a slightly more complex way, is what happens with non-climax communities. The pioneer species change the environment in a way that permits other species to grab a toe-hold. These species are more suited to the changed environment, and thus push the pioneer species out.

For example, species which can survive in nutrient-poor soil grow and die in that soil, enriching it with nutrients. Now that the soil is no longer nutrient poor, faster-growing plants can grow in the soil, and push out those species which started there. Each individual plant can reproduce, but the community as a whole is changing from one which favors the nutrient-poor adapted plants to the nutrient-rich adapted ones.

It's only in a climax community where the members of the climax community create/maintain an environment which is most conducive to the climax community species. This is why it (the climax community) is being called "self-perpetuating". The community as a whole is maintaining an environment which favors those species which make up that community.

Wipe out the climax community species (e.g. through a forest fire), and you no longer have an environment which favors the climax community species. A new set of species comes in, changing the environment, which then allows other species to come in, changing the environment further, which then ...


There is a comprehensive 2012 review of the development of the mammary gland by Macias and Hinck which covers the poster’s question(s). I shall try to summarize the points they make regarding the development of alveoli and their role in milk secretion, ‘borrowing’ two of their illustrations to do so.
Development of mammary gland and role of hormones

At birth there is a rudimentary system consisting of a few rudimentary ductal system.

Until puberty this system grows along with the rest of the organism, under the same hormonal influences that affect other tissues.

At puberty oestrogen — in concert with growth hormone and insulin-like growth factor — accelerates the growth of this ductal system, and its branching is subsequently stimulated by progesterone.

It is only in pregnancy that alveoli form, with a continued requirement for progesterone (perhaps partially indirect) and a specific requirement for a prolactin — which is secreted both from pituitary and — as a different molecule, placental lactogen — from the placenta. The alveoli express the genes for the synthesis of specific milk proteins such as casein, α-lactalbumin and β-lactoglobulin.

[Lactating Mammary Gland: Alveolar cells shown in pink (nuclei blue and milk droplets white) with surrounding adipose tissue yellow]
Oxytocin does not affect the development of the mammary gland (as is made clear in the reference cited by the poster). After parturition it is released from the pituitary in response to the nervous stimulus of suckling and causes the myoepithelial cells around the alveoli to contract causing ejection of the milk.
It should be mentioned that the alveolar cells apoptose on weaning, being replaced by adipocytes. However new alveolar can develop from undifferentiated epithelial cells during a subsequent pregnancy.
Regarding the poster’s specific questions
Q1 The article doesn’t mention anything about development of mammary alveoli, though. How does that happen, then?
A1 The development of the mammary alveoli occurs during pregnancy, under the influence of prolactin/placental lactogen and progesterone.
Q2 I know milk formation primary requires prolactin, oxytocin and indirectly, oestrogen.(4) So does this process wait till pregnancy?(If yes, then the lobes and branches are devoid of any lumen, and they remain empty until pregnancy, which seems skeptical to me.)
A2 The poster’s statements are not completely accurate. Milk formation does not require oestrogen, and oxytocin only affects it in so far as failure to remove milk causes involution. The ducts are indeed devoid of the alveolar lumen until pregnancy, and return to this state on weaning. It is not clear why you are sceptical that this is so. The mammary gland development after puberty prepares the ductal network, but alveolar cells only arise when they are required. Pregnancy is quite long enough for them to develop.
Q3 Can lactation occur without alveoli formation?
A3 I would think not, although the situation regarding neonatal milk secretion (witch’s milk) is unclear because of the obvious ethical barriers to its study in humans. The increase in breast nodule size is suggestive of development. So my opinion is primarily based on argument. The formation of milk requires cells with a specific pattern of gene expression, i.e. of milk proteins and metabolic enzymes that are required for fat formation. It also needs a structure and organization that allows the milk to be secreted into a duct. That is what an alveolus is. Therefore I would imagine that in these circumstances the rudimentary mammary ducts of a new-born infant develop alveoli under maternal hormonal influence.
Postscript
This is a topic I worked on for my doctorate, but have not had contact with for many, many years. It was interesting reading the review — how the technology has changed! I also find it curious that the review makes no mention of corticosterone, as one of the earliest systems for observing alveolar development in vitro was in explants of mammary gland from pregnant mice cultured in defined medium with insulin, prolactin and corticosterone. Perhaps the corticosterone was mimicking what is now known to be the effect of progesterone in vivo.


Can we produce synthetic red blood cells lacking antigens?

Actually there are such particles. It is estimated that about 20% of the hemoglobin (HGB hereafter) is in HGB vesicles (HbV hereafter) formed by RBCs. So sure, it is possible to use small particles instead of RBCs, but these vesicles have major and minor antigens on their surface. According to some of the articles they cause other complications too by blood transfusions and they are destroyed by the immune system within 3 to 7 days. So they don't solve the problem.

In Vivo Volume and Hemoglobin Dynamics of Human Red Blood Cells
Artificial Oxygen Carriers (Hemoglobin-Vesicles) as a Transfusion Alternative and for Oxygen Therapeutics
Red blood cell vesiculation in hereditary hemolytic anemia
The red cell revisited--matters of life and death.
Red blood cell microparticles and blood group antigens: an analysis by flow cytometry
Hemoglobin-Vesicles as Oxygen Carriers
Physiological Capacity of the Reticuloendothelial System for the Degradation of Hemoglobin Vesicles (Artificial Oxygen Carriers) after Massive Intravenous Doses by Daily Repeated Infusions for 14 Days

HGB vesicles without major and minor antigens are not a perfect solution either (I think), because the immune system tends to attack such things. For example by viral infections the MHC1 levels are low (in cells with nucleus) to avoid T cell response and the NK cells does not like that, so they destroy such cells. I am almost sure something similar would happen with this kind of vesicles as well. At least afaik. the immune system checks not just the presence of these antigens, but their composition as well. So if a RBC is under stress, then it changes the antigen composition on its surface and the leukocytes destroy it if necessary. According to some of the experiments PEG can cover HbV antigens and increase immune compatibility, so having less surface antigens seems to be a better choice than having more.

Development of a Synthetic Blood Substitute Utilizing Hemoglobin Vesicles
Biocompatibility of Hemoglobin Vesicles, a Cellular-Type Artificial Oxygen Carrier, on Blood Cells and Plasma Proteins In Vitro and In Vivo
Artificial Oxygen Carriers, Hemoglobin Vesicles and Albumin−Hemes, Based on Bioconjugate Chemistry
Hemoglobin Vesicles, Polyethylene Glycol (PEG)ylated Liposomes Developed as a Red Blood Cell Substitute, Do Not Induce the Accelerated Blood Clearance Phenomenon in Mice

HGB vesicles have another problem. The HGB inactivates in them without reduction (metHb formation). Only Fe2+ HGB can carry oxygen. This can be solved with methylene blue according to this study.

Red Blood Cells Donate Electrons to Methylene Blue Mediated Chemical Reduction of Methemoglobin Compartmentalized in Liposomes in Blood
Inhibition of methemoglobin formation in aqueous solutions under aerobic conditions by the addition of amino acids

We cannot use free HGB either, because it would decrease the NO levels and lead to endothelial dysfunction. I think to small particles would have the same effect because of increased surface.

Mechanisms of Slower Nitric Oxide Uptake by Red Blood Cells and Other Hemoglobin-containing Vesicles
Microparticles in stored red blood cells as potential mediators of transfusion complications
Removal of Cellular-Type Hemoglobin-Based Oxygen Carrier (Hemoglobin-Vesicles) From Blood Using Centrifugation and Ultrafiltration

According to other studies RHSA-heme (serum albumin bound to synthetic heme) is another option. It seems to be safe if you replace only 20% of blood volume (of rats). I think a complete transfusion is not safe, because it would reduce the NO levels as we already discussed. I have not found an experiment which does complete transfusion.

Safety evaluation of an artificial O2 carrier as a red blood cell substitute by blood biochemical tests and histopathology observations.
Exchange transfusion with synthetic oxygen-carrying plasma protein “albumin-heme” into an acute anemia rat model after seventy-percent hemodilution

So there is ongoing research in the topic. There is progress, but none of the current solutions is perfect I think.


Looking for a cancer drug target database to guide sequencing of patient tumor DNA

Not sure if the exome sequencing is the way to go for this kind of tasks, especially if you have an idea of the mutations you might be looking for. Current arrays are pretty performant and are much more rapid and cheap.

For the data, you might consider having a look on The Cancer Genome Atlas. Otherwise Biological Networks might provide you the API for you if you aren't afraid of doing a little bit of Java to interface it with R.


I found this article on why frost increase soil fertility - specifically nutrient density in the soil.  101 years old!
The Occurrence of Bacteria in Frozen Soil
E. C. Harder  Botanical Gazette  Vol. 61, No. 6 (Jun., 1916), pp. 507-517
https://www.jstor.org/stable/2469064?seq=3#fndtn-page_scan_tab_contents
Relevant text pasted below.  In short: it is bacterial action and nitrogen fixation which contributes to soil fertility.  Freezing increases bacterial population and these metabolic activites.  The theory is that freezing kills bacterial predators on higher trophic levels (protozoans) but the bacteria live and thrive in the absence of predators.

An analogous hypothesis proposed by RUSSEL3 for increases in the number of bacteria after partial sterilization by heat, frost, or other means is that by such partial sterilization the protozoa are killed, thus permitting the unhindered development of bacteria which under normal conditions is held in check by protozoa.
BROWN and SMITH (loc. cit.) in their investigations dealt mainly with the physiological activities of bacteria under conditions of low temperature and frost, although they also made some determinations of the number of bacteria in frozen soil. Their principal conclusions regarding the ammonifying, nitrifying, denitrifying, and nitrogen fixing powers of frozen soils are as follows: (1) that "frozen soils possess a much greater ammonifying power than unfrozen soils"; (2) that "during the fall season, the ammonifying power of the soil increases until the temperature of the soil almost reaches zero, when a decrease occurs, and this is followed by a gradual increase and the ammonifying power of the soil reaches a maximum at the end of the frozen period"; (3) that "the nitrifying power of frozen soils is weak and shows no tendency to increase with extension of the frozen period"; (4) that "frozen soils possess a decided denitrifying power which seems to diminish with the continuance of the frozen period"; (5) that "during the fall season, the denitrifying power of the soil increases until the soil freezes, after which a decrease occurs"; (6) that "frozen soils possess a nitrogen fixing power which increases with the continuance of the frozen period, being independent of moderate changes in the moisture conditions, but restricted by large decreases in moisture"; and (7) that "in the fall, the nitrogen fixing power of the soil increases until the soil becomes frozen, which in almost ceases, after which a smaller nitrogen fixing power is established."


Are these statements about the effectiveness of condoms in preventing HIV transmission reconcilable?

Note that those three statements are also approximately equivalent to pregnancy risk in the context of vaginal intercourse:

Condoms form an essentially impermeable barrier to sperm
Sexual activities other than penetration carry a very low risk of pregnancy
The use of condoms has an annual failure rate around 15%, i.e. on average 15/100 couples using exclusively condoms will conceive in a year

There are dozens of sources that reconcile these issues, and it all comes down to the failure rate and misuse rate of condoms. Even the source you cite talks about this explicitly, so I'm not sure why you still have a question about it that isn't already answered there.


It appears to be a Banana Spider:

  ... a male Heteropoda venatoria, also called a Banana Spider. The female is a more robust spider with shorter legs. This is the spider that is responsible for the rumors that tarantulas come into the U.S. with bananas because they are often spotted emerging frrom a bunch of bananas in a fruit store in the North. This Giant Crab Spider is usually the culprit. The species is found in all tropical regions, its range extending clear around the world. It is very abundant in all tropical seaport towns, being transported in trading vessels. Its chief food is cockroaches. The female carries her eggs beneath her body. According to this site it is also called the Huntsman Spider.

https://www.whatsthatbug.com/2003/11/11/banana-spider-from-peurto-rico/


Magnetic-activated cell sorting vs. FACS

Magnetic-activated cell sorting (PDF download), or MACS, is a procedure developed by Miltenyi Biotec to separate cells from complex mixtures using antibody-coated magnetic nanoparticles. The antibodies are specific for certain cell surface markers, either expressed on your population of interest (positive selection), or expressed on undesired cell types (negative selection). After adding the antibody-coated beads to the cell mixture and incubating, the suspension is added to a special single-use separation column affixed to a magnet, to which the beads stick, while unlabeled cells flow through. If performing a negative selection, the flow-through is your population of interest and the bound beads and cells are discarded. If your cells of interest are bound to the beads (positive selection), the column is washed several times to make sure unbound or weakly-bound cells are washed through, then the column is removed from the magnet and the cell-bead complexes are eluted.

In fluorescence-activated cell sorting or FACS, the initial complex cell mixture is first labeled with one or more cell surface marker-specific antibodies that have been conjugated to fluorescent dyes. Cells can also be analyzed that express one or more recombinant fluorescent proteins in conjunction with a gene of interest, allowing for selection of cells without using antibodies. After incubation and wash steps, red blood cells are lysed, if analyzing whole blood. The reason for RBC lysis is shown below:

Without lysis, the RBCs overwhelm the cytometer, as they make up around 95% of the cells in human whole blood. White blood cells (leukocytes), on the other hand, only make up 0.1-0.2% of cells, and lymphocytes between about 15 to 50% of leukocytes.

The cell mixture is then analyzed on a cell sorter such as a BD FACSAria.

From: https://commons.wikimedia.org/wiki/File:Fluorescence_Assisted_Cell_Sorting_%28FACS%29_B.jpg

The cells pass in single file past one or more laser beams, which excite the dyes and cause them to fluoresce at a certain wavelength. The user can then use gating to select the combination and intensity of colors they are interested in, and when a cell meets the criteria, it is given an electrical charge, and electro magnets direct it into a collection container.

So what are the pros and cons of each technology? MACS separation generally is quicker than FACS staining, and a greater number of cells can be processed at one time (sometimes orders of magnitude more, depending on instrument and protocol). If you are, for example, looking to purify large numbers of CD4+ T cells from whole blood, MACS may be the better choice of the two (although I prefer the RosetteSep system for that particular requirement). MACS doesn't require a rather expensive dedicated instrument, although automatic platforms are available if needed. On the downside, most MACS-qualified beads are mostly only available from Miltenyi, so if they do not have beads with your particular marker of interest available, you will need to do the conjugation yourself, at the expense of time and possibly precious antibody while you optimize conditions. Fluorescent-conjugated antibodies are extremely common, and available from practically innumerable companies, so unless you are working with a self-generated antibody it's much more likely that you'll be able to find one for FACS quite easily. There are MACS beads that contain antibodies directed at certain fluorophores, so you can use flow antibodies for MACS, although optimization is likely still necessary. Finally, MACS separation is only an option for cells that have your marker of interest expressed on the cell surface.

One of the major advantages of FACS is multicolor staining (depending on the instrument you're using). This makes it much more straightforward to purify potentially rare populations that are only differentiated by their combined expression of a number of surface markers, necessitating multiple gating steps. If this were to be accomplished by MACS, you would need to go through multiple rounds of purification, something that could take longer than FACS, and not necessarily be feasible, as a certain number of cells are required for each MACS run. With FACS, these rare populations (which may only be tens or hundreds of cells per million) can be collected just as easily as more common ones. Also, as mentioned above, there are more antibodies available for flow/FACS than for direct MACS. Additionally, FACS allows for sorting of cells expressing GFP and relatives, letting you collect populations based on internal markers.


Can a human being live without any carbohydrates?

The Atkins diet is based on that. Without carb intake, however, the citric acid cycle (CAC) eventually basically stops and proteins will be utilized to be converted to carb intermediates to feed the CAC. Progressive and strict use of the Atkins diet will eventually kill you as the CAC is essential to life.

The idea behind Atkins is that fats will be used to feed the CAC, and that will happen until the carbohydrates that keep the cycle running are depleted. At that point one will develop ketosis and the CAC stops, and with it the production of ATP. Note that fatty acids can be fed into the CAC, but are not sufficient to keep it running; fats burn on a fire of carbs.


Identification of a small to mid-sized, yellow moth species found in India at monsoon season

This is likely a member of the Nygmiini moths. The Nygmiini are a tribe of tussock moths of the subfamily Lymantriinae (formerly called the Lymantriidae) of the Erebidae family

A specimen that closely resembles yours can be seen here, and copied below:

I have not found a definitive species for you, but will keep looking. I'd advise you try to do the same given this information.


The genome may be divided into two classes of sequences - those that code for proteins and those that do not. Those that do not code for proteins may be again divided into classes consisting of actively transcribed sequences that have biological activity (such as long noncoding RNA, microRNA, competing endogenous RNA and so on) and those that aren't.

These untranscribed noncoding regions may be involved in regulating the activity of protein coding and actively transcribed regions by binding to transcription factors or transcriptional coactivators/corepressors that control whether certain genes are expressed or not - this can happen close to the start of the gene (i.e, promoters) or far away (at enhancers). Distant enhancers can still affect gene expression because they and the genes they affect can be close together in three-dimensional space (The genome is folded in cells!).

Regulatory genomics is, simply put, the study of these regions, which are called genomic "features" and how they regulate genes. A great example of studies in this area are offered by papers published as part of the ENCODE project http://www.nature.com/encode/#/threads


Clonal and subclonal mutations in cancer

They don't really contradict each other; the clonality of neoantigens adds an extra layer over the overall mutational load ; but overall mutational load (and consequently overall neoantigen burden, because mutations in a fixed sequence context generate neoantigens at a certain rate) by themselves are also predictive.

Tumours with a high neoantigen burden tend to generally respond better anyway (See Snyder et al, NEJM , Rizvi et al, Science and Van Allen et al, Science) and also the fact that mismatch repair deficient cancers generally tend to respond.

So if you take high neoantigen tumours already (both lung and melanomas have extremely high mutation burdens), and then stratify them based on neoantigen clonality , you tend to further stratify patients by response associating with checkpoint blockade.

The whole point of McGranahan et al was to point out that it is possible to raise immune responses that target all the cells in a tumour, and that the ability to do this may dictate survival in general and checkpoint blockade response in particular, but only when antigen presentation and immune infiltration are intact. McGranahan et al note that clonal neoantigens do nothing in Lung squamous cancers because of depleted CD8 infiltration and MHC class I expression and there is other work (See http://www.pnas.org/content/113/48/E7759.abstract )

As for this bit

  Plus, probabilistically how likely it is for a certain cancer lesions
  to have lots of shared mutations? A totally genetically homogeneous
  lesion with no branches with a very high number of mutations.

That is quite complicated to answer; but as a general rule it is worth remembering that,  as the number of divisions and the number of mutations (and ergo prospective subclones) increases, for tumours to stay clonal it requires extremely strong selective sweeps so that at any given time a very small number of clones tends to predominate, and at least in untreated/pre-treatment tumours, there is the tendency for a lot of them to show effectively neutral patterns of evolution ( http://www.nature.com/ng/journal/v48/n3/abs/ng.3489.html )


Relation/difference between metabolism and cellular organisation

This paragraph appears to draw a distinction between "the sum total of all reactions in cells" and "some isolated reactions that occur in cells". The former is "metabolism" and one defining trait of life; the latter are "metabolic reactions" and can occur in a test tube, and if so they do not fit tidily in a living/nonliving distinction (the paragraph talks about "not living things" but "surely living reactions", which is one way of illustrating the confusion I guess).
As to whether "metabolism" and "cellular structure" are the same thing, I think it's not so much that they're literally the same thing but they're not really separable, are they. The cellular structure is made by "all the chemical reactions in the cell", and "all the chemical reactions in the cell" are mediated by the cellular structure. It's a bit like trying to separate out "a race" from "the people running in the race". You can have one or two metabolic reactions happening in vitro, but if you had all of them in your test tube, happening the same way they do in the cell, you'd have a cell.
The reality of course is that there isn't a single all-encompassing definition of "life", so don't try and nitpick things too much. Metabolism is important because it's what allows living things to do what living things do, thermodynamically speaking. Cellular structure is important because it happens to be the way all living things implement their metabolism, and arguably it is a necessary requirement for metabolism to occur (there are arguments for why you need a small space enclosed by a membrane for example). Other things are also important like reproduction (and other near-universal feature of life that is a basic thing living things do, and allows Darwinian evolution), being subject to Darwinian evolution (because that is the process that leads life to being optimized in the way it is, and able to do the things it does to begin with), sensing and reacting to its environment (all this stuff about "what life does", well, those are universal things life does)... That means you can have arguable examples like viruses, which I would expect your textbook to call "nonliving" because they do not have metabolism or a cellular structure, but some others might call "living" because they have genetic information, replicate, are subject to Darwinian evolution and share a common ancestor with all other known life. The labels are less important than the features one is discussing at any one time. I expect your textbook probably says something like this at some point.


Can someone identify this flowering bush from the US?

Polygonum cuspidatum, common name Japanese knotweed. A notorious invasive species.

It's actually a herbaceous perennial (those stems grew in just one season, and will die back to the ground at the first hard freeze), not a shrub. The red things are ripening seeds, not flowers.


The female breast is composed primarily of fat and connective tissue plus lobules and ducts for milk production and delivery.  The pectoralis muscles form a thin layer beneath the breast, as seen in the figure in the link. An athletic female can enlarge the size of the pectoralis muscle and the laterals muscles, just as male athletes can enlarge their "pecs" and "lats".

Exercise burns fat so athletic women often experience reduction in breast size. Of course, other factors such as diet and genetics also influence the effects of exercise on fat burning.

So, athletic females with enlarged lateralis muscles and pectoralis muscles may have a larger overall bust size but the cup size of their breasts might actually be reduced.


Evolutionary selection pressure for human hair patterns?

At least some of it is a side effect of the way human skin develops. Humans actually have the same number and density of hair follicles as great apes, it is merely that our hair develops as short vellum hair rather than the thicker, longer hair of great apes. This is a side effect of the same genes that control eccrine sweat gland development, turning on the genes causes the skin to develop more sweat glands at the cost of reducing hair thickness across the body. For humans, a primarily tropical species, having sweat glands was evolutionarily more useful than being hairy, so we largely traded hair for sweat glands. As a result, the distribution of hair across our bodied may be at least in part a side effect of where it would be most useful to have sweat glands. Hair is typically retained in the armpits and groin because it helps trap odors that may elicit sexual signalling.
Hormones may also play a role. Testosterone has been linked to changes in hair development, and may actually be related to male-pattern baldness.


This is a clematis, probably clematis vitalba.

This plant is native to Europe and Turkey. It also occurs on the westcoast of the USA and Australia/New Zealand, but it is probably introduced there. Source occurences

Picture from Dutch wiki:

Many clematis species have a very nice smell, and both the flower and the fruit are also nice to look at. That is why clematis species are grown in garden often, with countless varieties. They differ in color (most are white, pink or purple), in flower size and in flower time (spring/summer).


Does anyone know a good pancreatic-cancer metastasis cell line?

SUIT-2 cell lines are derived from the liver metastases of Pancreatic Ductal Adenocarcinoma. The subline S2-007 is highly metastatic. The other sublines are S2-013, S2-020 and S2-028 which have decreasing metastatic capabilities.

You can probably refer these articles for more info :
1. https://www.ncbi.nlm.nih.gov/pubmed/3102439
2. https://link.springer.com/article/10.1007/s10585-017-9840-3


How do legs of tiny insects/spiders like mosquito/Opiliones work?

Arthropods use basically the same system to operate their legs. Yes their legs are tiny, but so are their muscles.(Is it so hard to imagine everything is downscaled? Their digestive system is also much smaller, but they don't need to eat the same amount as we do either...)
In general it's just a kind of smaller-sized mechanism that is based on the same principles: use a muscle to create tension over a joint, and so move the appendages. The big difference is off course that in mammals the muscles work against an internal skeleton, and in arthropods the muscles attach to the inner surface of an external skeleton.


Is nutrient absorption different in Hypersensitive I patients?

The absorption is itself not different, but the rate of absorbed substances is different because of greater amounts of proteins in the allergic lymphatic circulation.
So less capacity stays for circulation of nutrients and so less absorption in time.


Why doesn't it feel suffocating when taking a shower?

Most likely a matter of relative perception.

For example, if you start with empty hands and pick up a 20 pound weight, you will perceive it as heavier than if you start with a 10 pound weight and then pick up a 20 pound weight.

Likewise, whoever's in the shower had plenty of time to get accustomed to gradually increasing steam, while you walked in and got the full blast immediately.


What neuro-motor diseases cause the lower esophageal sphincter (LES) to malfunction?

This is called achalasia. According to UpToDate, the mechanism for this diseases are generally unknown. What is known, however, is that the esophagus has a neural system called the myenteric plexus and if these ganglion cells in the esophagus are damaged in any way (e.g. physically, followed by Wallerian degeneration, or the primary process of degeneration after physical damaging of neurons), it can lead to lower esophageal dysfunction as these neurons regulate the inhibition of the contraction of this sphincter muscle. Dysinhibition leads to a closed sphincter.

Yes, you are right in that the vagus nerve is the primary route of the myenteric plexus to the central nervous system, so damage here might result in dysfunction as well.

Histological studies have reported fewer myenteric neurons in people with achalasia, and inflammatory cells in the region, perhaps suggesting infection or autoimmune etiology 1.

Additionally, from the UpToDate article, Chagas Disease has been associated with this disease. Chagas disease is a parasitic disease caused by the species Tropanosoma Cruzi, and these parasites multiply within cells, causing them to burst.

Check out pathophysiology of achalasia on websites such as UpToDate.

1 "Histopathologic features in esophagomyotomy specimens from patients with achalasia." Goldblum JR, Rice TW, Richter JE. Gastroenterology. 1996;111(3):648.

EDIT:

I answered the opposite, but the principles still apply. Here is a wonderful resource on this topic ("Physiology of esophageal motility," http://www.nature.com/gimo/contents/pt1/full/gimo3.html. It includes a diagram showing the vagal neural pathway and the main neurotransmitters responsible for each action (relaxation and contraction).


Notice the cell labeled "spermatid" is still attached to the Sertoli cell. Once released from the Sertoli cell, spermatids are called spermatozoa.
This process (release of the spermatid to form a spermatazoon) is called spermiation
EDIT
The text you added is still correct, but not well explained. Spermiogenesis is the development of the spermatid, the haploid 1N gamete produced by the second meiotic division, into a cell with a long flagella with a small amount of cytoplasm. Spermiation is the release from the sertoli cell. Both spermiogenesis and spermiation are involved in the development of a spermatid to a spermatozoon, but the specific point where we stop calling them spermatids and start calling them spermatozoa is release by the Sertoli cell, or spermiation, a substantial process in its own right. Both spermiogenesis and spermiation are important steps in the conversion of the haploid 1N gamete to a motile, free spermatozoon.


What is this spider, and what is this object that emerged from its rear end?

I do not know what species of spider this is, but I think the white ball is actually spider poop.  Unfortunately a quick search did not return many references, but here is a picture for comparison.

Spiders produce uric acid, which is a near-solid and excreted out white.  This is done to minimize water loss. These malpighian tubules drain into an pouch attached to the digestive tract, or stercoral pocket.  The uric acid waste from the is combined and eliminated together with solid waste from the digestive tract.  In your spiders case, this would be undigested insect parts (black) mixed with the uric acid (white).


Can someone identify this odd looking spider?

I agree with JulPal's comment from August.  It looks very much like a male Thiodina (now renamed Colonus) sylvanus.  As with many Salticids, the females look rather different, and it turns out that there is apparently a similar species of Colonus in the area, which can be distinguished in the field by the fact that the white mark on the carapace is not a block so much as a thick longitudinal line.
I attach an image from Tree of Life, with the link below:

http://www.tolweb.org/Thiodina_sylvana/5911


All somatic cells contain the same genome, then how does it knows that it should develop into a specific organ?

The answer to your question is not really know yet and there is whole scientific field dedicated to it: developmental biology. I'll try to explain the basics however:

Like you described the identity of a cell (its cell type; which organ it belongs to) is dependent on which of (actually) ~30000 human genes are activated (or read) in that cell. There are two fundamentally different ways this is done in cells:

Transcription factors:

These are proteins that bind to specific (regulatory) DNA sequences and thereby lead to the activation (or repression) of certain - usually nearby - genes. Since they are proteins, their own genes have to be activated in the first place, so we already at a 'chicken or the egg' type of problem. In principle proteins can 'survive' outside the nucleus of the cell for some time, but they are usually degraded within a few hours, so I guess the remaining factors from the mother cell are not very important (I have no idea if anyone ever checked this).
Additionally many transcription factors are not constitutively active, but are waiting for some outside (from the perspective of the cell) signal. These could be certain developmental signals, growth factors, hormones or environmental factors like nutrient availability (the list goes on ...). During embryo (& therefore organ) development not only the presence of these signals (morphogens), but also their intensity are a very important factor in determining the 'fate' of a given cell.

Epigenetics

The term epigenetics describes genetic regulation that does not happen on the sequence level. Instead the accessibility of the DNA is regulated through modifications of histones (which are part of the chromosomes) and the DNA itself. Thereby the cell can almost permanently shut down certain genes. Since epigenetics are also inherited during cell division, this regulation affects whole cell lineages and is therefore very important in regulating which cells are active in certain organs or tissues.


Are all Autoreceptors Downregulated by their Respective Endogenous Ligands?

Autoreceptors - are receptors of the presynaptic terminal.
α2 adrenoreceptors receptors are down-regulated due to repeated exposure.

Pharmacodynamic tolerance begins when the cellular response to a substance is reduced with repeated use. A common cause of pharmacodynamic tolerance is high concentrations of a substance constantly binding with the receptor, desensitizing it through constant interaction

This is a common occurrence - not just for autoreceptors but receptors in general.
But for your interest here is one for dopamine autoreceptors (Pay-wall).


There are linear and rotary molecular motors in the cells. Do any of them have a fixed or stable frequency or speed?

There are molecular motors but the frequency is a function of energy input (ATP); similar to the angular velocity dependence on amount of current in electrical motors.

The concept of molecular motor may not be suitable for a clock like device. There are clocks based on genetic circuits, which produce stable oscillations. Examples include the circadian clock, cell division, menstrual cycle etc.

Developmental events involve checkpoints and the timing is regulated by several factors such as number of cells, concentration of some protein etc. However, I haven't come across a master clock that integrates and synchronizes all these signals for precise developmental timing. That makes it an interesting area of research.


After how many generations descendant is not more related to ancestor, than to a random individual in an ancestral population?

There is an interesting way to look at this question. By definition, two individuals are related only if they have a common ancestor. (If you mean something else by it, please correct me. For completeness, I include the trivial case in this: that is, I regard you as one of your own ancestors.) So your question can be inverted: it is really asking after how many generations everyone in the ancestral population is your ancestor?

As indicated in the comments, the answer will depend on the specifics of the population structure, including its size. But a first stab can be taken in this way: you had 2 ancestors one generation back, 4 two generations back, ..., $2^n$ (not necessarily distinct) $n$ generations back. So you certainly cannot be descended from everyone in the ancestral population if less than $\log_2 N$ generations have passed. ($N$ = population size, which for simplicity I assume to be stable.) In a freely mixing population under the very simplest assumptions, you will eventually decay exponentially towards complete coverage with a half-time of one generation.

This is complicated by the fact that some lineages die out completely. For instance, some of the individuals in the ancestral population didn't have any children. Some had children, but no grandchildren, etc. Obviously none of them were your ancestors, so you will never be related to them (except through previous common ancestors), no matter how much time passes. In fact, as time passes, more lineages tend to die out. So, if you look back very far, you'll find that the entire current population has only a very small numbers of ancestors in the distant past. This is called coalescence, and is what people are talking about when they speak of "mitochondrial Eve", for instance.

So, in summary, it's complicated. It takes only a fairly small number of generations ($O(\log_2 N)$) before you're potentially related to most of the ancestral population. But over longer times ($O(N)$ generations) your relationship to the ancestral population actually goes down.


Is there a dominant gene for right-handedness?

There is a lot of information at OMIM  - too much to summarize here - regarding the genetics of handedness and links to which hemisphere of the brain dominates (in an individual), to schizophrenia (slight association with non-right-handedness), and to hair whorl patterns on the scalp. References are provided at the above link. Basically, hand skill appears to be a complex multifactorial phenotype with a heterogeneous background.


Regarding dimensions:

As per this image the length and breadth seems to be ~30-50 μm (area should be roughly around 900 μm²). The third dimension (thickness) as per this article can be assumed to be around 3-7 μm.

Regarding cell attachment:

Cells attach to extracellular matrix via integrins, which attach to ECM proteins like collagen and fibronectin. The matrix is a net of fibres and the cell is not specifically attached to a single fibre but rather "sits"(as you said) on the matrix [see the below image]. A single cell also simultaneously interacts with two different types of ECM proteins such as fibronectin and collagen.

During migration they move along the matrix using lammelipodia (actin filament polymerization in the direction of motion).

Fibroblast express ICAM1/VCAM1 (Inter/Vascular Cell Adhesion Molecules) under certain conditions such as inflammation and bind to T-cells and endothelial cells.


Is marriage with half-cousin's daughter more risky than marriage with others?

The medical term here is consanguinity, or a consanguineous union. The risks of consanguinity are well studied, and based on the principle that children born to parents with shared genes are more likely to be homozygous for recessive alleles. Population level measurements of specific risks for, e.g., fetal loss, major birth defects, or other problems vary depending on the population studied. Many of these studies look at first cousins, where typical numbers are between a 1-5% greater risk for major birth defects and 4-5% greater risk for late miscarriage or death of a child before age 10. The data on earlier fetal or embryonic loss isn't conclusive.  You can read more about this in the review I linked to at the end of this answer. The specific risk for a specific individual isn't on topic here, since it is a personal medical question. If you are looking for an answer to that question, I'd suggest scheduling a visit with a medical geneticist.

Your diagram depicts marriage between half first cousins once removed, with an expected shared percentage of genes of 3.125%, equivalent to second cousins, which fits the definition of consanguinity generally used in the medical literature and allows application of studies that use that definition. The fact that one of the potential parents in this marriage was also the product of a consanguineous union may increase the risk.

Consanguinity is an important risk factor for many birth defects and other diseases (see Cecil Medicine Chapter 41 and this review)


How do bile salts affect lipase activity?

Let us first clear out some basic concepts regarding lipase, colipase and bile salts. The pancreatic lipase has an optimum pH range of about pH 8.0 (Worthington). This can be understood easily by Le Chatelier's principle: as the reaction moves forward, there is reduction of pH (due to formation of fatty acids). So, a basic pH would help the reaction in moving forward. See this diagram (Worthington):

It can also be understood on the basis of lipase's optimum pH, which lies between pH 8-9. See the graph (orange line) (Chegg):

This optimum pH is brought about by bile salts. Bile salts are slightly alkaline, with pH range of about 7-8 (Britannica). This helps lipase in catalysing its reaction. Bile salts also help lipase by increasing the surface area of fat droplets. Bile molecules have a hydrophobic and hydrophilic part. The hydrophobic part is attracted towards fat while the hydrophilic part is attracted towards water. This helps stabilize fat droplets by emulsification i.e. breaking the fat droplet(s) into smaller parts. This also increases the surface area of fat droplets.

Now, the matter gets complicated when we talk about concentration. Since bile molecules contain hydrophilic and hydrophobic ends, they tend to form micelles with increasing concentration (just like soap). As long as its concentration is below critical micelle concentration, it will carry on emulsification and increase lipase activity. But when its concentration becomes more than the critical micelle concentration, it will form micelles and not carry on emulsion. This significantly reduces lipase activity by not only decreasing surface area, but also reducing pH to slightly acidic (Erlanson et al, 1973). This is where colipase helps. Colipase binds to the C-terminal, non-catalytic domain of lipase and stabilizes its active conformation and increases the hydrophobicity binding site (Verger et al, 1999). Colipase strongly binds to the ester bond of the triglyceride molecule, by which its hydrolysis by lipase becomes easy (Mansbach, 2011). Thus, colipase helps in overcoming the inhibitory effect or bile salts on lipase.


In which reactions of glycolysis is magnesium involved?

In the 1st step where glucose is converted to glucose-6- phosphate by the enzyme hexokinase, in the 3rd step where fructose-6-phosphate is converted to fructose-1,6-bisphosphate by the enzyme fructose-1,6-bisphosphatase and in the last reaction where 2 phosphoenolpyruvate is converted to pyruvate by the enzyme pyruvate kinase.. In this 3 reaction Magnesium is needed as they are ATP dependent reaction and Magnesium stabilises the ATP in this reaction and help the reactions to proceed faster.


Will DNA nanostructures be useful for medical applications?

I think biomedical applications are not an absurd perspective. More specifically, regarding your concerns:

(1) Unless the DNA is first internalized by cells, and then somehow enters the nucleus (both are not very likely, especially considering the small concentrations we're talking about here after dilution in a human body), you would still need the DNA structure to disassemble to become "available", and the strands to be long enough to be incorporated, which is usually not the case. And, of course, you would need some DNA integration mechanism to be at work, such as a recombination with genome sequences that happen to be very similar to the ones used to build the DNA nanostructure (which can be avoided during the design step). In other words, no, it's quite unlikely.

(2) Immune responses might actually be a bigger issue; in particular, some Toll-like receptors (TLR), that activate the innate immune system, can respond to DNA and RNA fragments. But immune responses may not be so problematic if the DNA nanostructures are used for short-term mission, like 1-shot delivery to a specific organ, in which case they do not need to stay around for very long. Additionally, this can be a useful feature; immune recognition can be used to direct the trafficking of nanoparticles to lymph nodes for example, where the efficieny of their payload (e.g. an immune modulator) could be maximized.


Can somebody be deaf to voices of some people only?

Although you loose the high frequencies in your hearing with age (20kHz and below), this is highly unlikely. The frequency spectrum of our voice is pretty much limited, which is also shown by the fact the for normal telephone, the spectrum transmitted is located between 300 and 3400Hz and the spectrum band between 300 and 3000Hz is named the "voice band". See here for some details.

According to reference 1 the "voice fundamental frequency" for men is between 85 and 180Hz (depending on the reference) and for women between 165 and 255Hz. These frequencies are close enough together to rule out specific hearing of male or female voices. Furthermore the frequencies even overlap.

What happens in age-related pathological hearing loss (also termed Presbycusis) is that voices generally get muffled due to losses in the spectrum and hearing intensity. See the Wikipedia link and also reference 2 for more details.

Reference:

The frequency range of the voice fundamental in the speech of  male
and female adults
Presbycusis


21joanna12, look into snRNPs.  These are parts of the splicosomal apparatus and some of them (the U1 and U2, U11 and U12 snRNPs) are also the guideposts that bind near the splice junctions at the end of introns.  These help guide the splicing apparatus to the splice sites. There are also proteins that bind RNA and interact with the splicing apparatus to switch alternative splicing, such as SP proteins.
https://en.wikipedia.org/wiki/SnRNP
https://en.wikipedia.org/wiki/SR_protein
https://en.wikipedia.org/wiki/Exonic_splicing_enhancer

Here's a recent review that might serve as an entry into the literature: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4232567/


Why Can Varied Species Live Together in Particular Ecosystems?

The answer should be B "Each spices occupies a different niche" because this is the only answer that reflects a model of species coexistence.  Niche theory proposes a mechanism that allows multiple species to occupy the same space and time any yet avoid competition for limited resources.  Briefly, the model says that a species niche is the total suite of resources that it requires to survice and reproduce and that coexisting species will limit their niche overlap to avoid competition (and its requisite reduction in fitness).  Species can limit niche overlap by preferentially using a subset of resources that are not shared with potentially competing species (this is called the realized niche) or by evolving a new niche that does not overlap with the competitor (this is called character displacement).

Note that your reasoning is incomplete because the question does not specify that the organisms listed are the complete set of organisms  in the community.  For example if the community contained another species of grass, then choice "C" would be false.  Most importantly though, habitat or trophic variation are not mechanisms of coexistence, so they should not be used as general hypotheses explaining coexistence.


Collective term for both exons and introns

How about "splicing fragments"? It might be easier to refer to them according to the mechanism of production.


Excluding the Exon, What Does the Rest of the Genome Do?

A few percent codes for RNA, like microRNA, long non coding RNA, shRNA ect. These RNA while not translated into protein do have a function.

Some RNA are ribozymes, catalytically active in their own right, but they do work with proteins. An example of such complex is the ribosome, where the catalytic peptidyl transferase activity that links amino acids together is performed by the ribosomal RNA
https://en.wikipedia.org/wiki/Ribosome

Then there are miRNA, that control gene expression by RNA mediated silencing.
https://en.wikipedia.org/wiki/RNA_silencing

Then there lncRNA... these long RNA can regulate gene activity by binding to transcription factors. So a cell can maintain a high concentration of transcription factor in an inactive state that can rapidly go into use once a signal is received. This is rather recent discovery.

About 45% of the human genome is composed of what is essentially viral parasites. While some of these viral genomes are full functional and encode endogenous viruses (this is why there is come concern about xeno tissue transplant). Most of these viral parasites have degraded somewhat, having accumulated mutations that either render unable to leave the cell, but still able to replicate and multiple in the genome (we call them transposable elements), or are completely inactive (repeat elements).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4124830/

Examples are
Alu element make up 10.7% of the human genome. It is rather old parasite... youngest expansion is about 30 million years old. Mostly inactive, although some Alu elements are still active.
https://en.wikipedia.org/wiki/Alu_element

Line repeats. ~17% of the human genome.

Some DNA is structural. The centromeric repeat array which may be several Mb long per chromosome (exact length is unknown due to variation between people and difficulty to clone and maintain for analysis). Here the DNA serves as a pad over which the kinetochore forms. This DNA tend to be transcriptionally quiet, few if any genes.

And there are pseudo genes... genes that are no longer active due to mutations.


What species is this large bug? (South India)

I suppose it's a whip scorpion.

  Whip scorpion (order Uropygi, sometimes Thelyphonida), any of approximately 105 species of the arthropod class Arachnida that are similar in appearance to true scorpions except that the larger species have a whiplike telson, or tail, that serves as an organ of touch and has no stinger. The second pair of appendages, the pedipalps, are spiny pincers, and the third pair are long feelers.

It is most common in India and Japan to New Guinea.


can somebody please Identify this queen ant?

There are 4 main families in France. Formicinae, Dolichoderinae, Myrmecinae ans Ponerinae. This is a an ant in the subfamily Formicinae because it is large and has only one segment between the thorax and the abdomen. You can deduce that because the thorax and the abdomen seem very close. This particular ants is a queen of the genus Formica (wood ants) from the general aspect. The presence of wings indicate this is a reproductive individual and because the eyes are small compared to the rest of the head it is a female. The color and the general shape and the size would allow any trained observer to identify the genus Formica, although no formal criteria can be seen on this picture. Formal criteria require inspection of the funicula, a part of the antenna, which cannot be seen on this picture. For references please visit http://antarea.org, http://cle.fourmis.free.fr and read Seifert - Ameisen Mittel und Nordeuropas. Lutra.


Why do cells divide (or copy themselves)?

The "Why" question

Why do organisms replicate?

Given that there is (extrinsic and also eventually intrinsic) sources of mortality, organisms that did not replicate just ended up disappearing. Those that did replicate eventually ended up giving rise to important lineages.

In other words, replication occurs because those who did not replicate disappeared. It is also because unique instance of things may disappear that you regularly backup your computer (if you do).

The "How" question

By what mechanism did early replication occur?

You actually did not really ask about it but here are a few words anyway.

The mechanism by which first replication occurred are mainly unknown as it is hard to investigate specific processes that occurred such a long time ago. The field that studies the origin of life is called abiogenesis. You might especially want to read the section on Self-enclosement, reproduction, duplication and the RNA world. You might also want to read about Autocatalysis.

I am afraid that a summary of existing hypothesis on early reproductive systems are 1) out of my capacity and 2) would hardly fit into the wish to receive a very (VERY VERY) easy explanation.


Can 1.5 gigabytes encoded in the human genome really account for the complexity of a human being?

This is a VERY hard question to answer; I think mostly because it is very hard to think about how the DNA actually encodes information.

The first important thing to note (and also the only direct answer I can give to your question), is that

(Yes) the human genome does encode all information to make a human being, but only in the context of a cell/organism that can read this genome.

Transferring this to the computer code analogy this means that if the genome is the source code for a program (or rather a couple of them), then the operating system (and also the actual hardware) that executes this code is the cell itself and the two parts have to match up in order to work together.

This is essentially a hen/egg problem: without the cellular machinery to read and operate on the genome the organism doesn't work, but at the same time the genome is the source of the everything that reads it.
If one would put the human genome into another (not closely related) species (or the egg cell of one), this would not form a human being, because the organism/egg cell can't read the instructions properly. (This is also the reason why hybrid animals like i.e. mules are often sterile - the genomes of their parental species are similar enough to be readable and make a working animal, but there are already enough differences to introduce problems).

This brings me to what i think is the actual core of what you're asking:

How can so much complexity be encoded in so little space/bits/... ?

and I don't have a clear answer for that (and neither have I ever seen one). There are, however, a few things one needs to consider

Emergent behavior is when seemingly very simple and limited rules lead to very complex structures. This happens all the time in nature and our body plans are no exception, it is however very hard to see or understand and even harder to consciously design from scratch. Nowadays, machine learning algorithm can get complex results from initial simple instructions, but only because they run 'a couple' of optimization steps inbewteen - evolution has done the same thing for millennia.

A second thing to keep in mind, is that code can be re-used. Programmers already do that (a lot), but usually they try to keep the code readable and make a clean copy for a new purpose. Nature / the genome most of the time doesn't do that and its been re-using and re-purposing pathways on any level for millennia. The reason that arms and legs are built very similar, or that essentially all animals are symmetric is that it's just easier to (re)use the same set of instructions a couple of times with slight alterations than specifically writing everything down.

Finally (as almost always), Randal Monroe explained pretty well, why just knowing the 'source code' of the genome doesn't mean we actually understand how it's doing what it's doing:

This answer's gotten pretty long now and I'm out of time to add sources - if anyone feels motivated to add something feel free to make/propose edits.


Inoculating agar plates with microbes suspended in sterilised water?

It would be great if you could provide more information with regards to what you have done already and what the problems were that you observed. That being said, yes, the "protocol" you found should work.

I am assuming that this is some kind of homework / school project so you don't actually need to know what organisms you are inoculating with and at what levels.

One thing I would recommend is that when you take your swab sample, wet your swab by dipping it into the sterilised water first and then swab a predefined area of about 10cm x 10cm (4in x 4in) very thoroughly before putting the swab back into the test tube. Once back in the test tubes make sure that you swirl the swab around for a sufficient length of time (~30s) and press the swab against the inside of the test tube to allow as much liquid as possible to run out of the swab. The last step is important in order to maximise the yield of bacteria, yeasts and moulds that you might find in your sample.


Does making yogurt from non-pasteurized milk work against possible disease bacteria?

In short, 'No.'

Yogurt, in and of itself, is the product of milk with specific strains of bacteria that are not particularly unique. Yogurt is just as hospitable to harmful bacteria as beneficial bacteria.

The two mechanisms which spring to my mind that would prevent infection by harmful bacteria in yogurt would be the following:

*The already dominant beneficial bacteria outcompete for the harmful bacteria, effectively limiting the capacity for harmful bacterial growth.

*The already present beneficial bacteria create extracellular products which damage harmful bacteria.

The second, if it happens at all, doesn't happen on a scale that I'm aware of. The first could happen, but I highly doubt it. It seems, to me, that it would be more likely to happen in cheese when most of the easy resources have been consumed, which in yogurt they haven't.

Yogurt, and all products stemming from milk, are inherently safer not because of any bacteria that take up residence, but because the mammary glands inside the animal producing the milk are effective filters for a variety of infections. Milk is a product that is constructed in the mammary glands, and the cells are selective about the output. Keep in mind, however, that it is by no means sterile. There are dozens of virii and diseases which can be imparted by breastmilk, and nursing women must adhere to guidelines concerning exposure to medications and diet. It's also possible for DDT and other compounds to become concentrated in breastmilk, resulting in harm to the child.

http://www.breastfeedingbasics.org/cgi-bin/deliver.cgi/content/Drugs/pre_pass.html

So, yes, while milk in and of itself is safer than other options, it is not risk free. A virus could easily infect the mammal or herd producing the milk for sale to humans, and only exhibit dangerous symptoms after the milk had been sold. This is why it's illegal to sell unpasteurized milk for human consumption in most U.S. states.


Is high metabolism linked to high evolutionary turnover?

Metabolism and evolutionary rates are linked, but not in the way you describe.

First consider that metabolism is intrinsically linked to body size. The larger an animal is, the smaller amount of energy per unit mass it takes to maintain that body. This can then be extended to many things about an organism, such as life span, gestation time, population growth, etc. (see Brown et al. 2004 for more detail).

Next consider that metabolism changes with temperature. Take an ectotherm (an organism who's internal temperature is the same as the ambient environment, traditionally called cold-blooded creatures) like a lizard, which will go thru temperature fluctuations throughout the day. It will have higher metabolism when the temperature is higher. A lizard living in a warm environment like the tropics will have an overall higher metabolism than a lizard of the same size living in a temperate climate. With that higher metabolism comes a different life span, gestation time, population growth, etc. even though their body sizes are the same.

When temperature is considered and corrected for, all organisms have attributes that scale directly with body size. A plant literally has the same metabolic rate as a lizard if they are a similar mass and live at the same temperatures. (Seriously, see the Brown paper).

Now onto evolution. Rates of evolution depend on many things, but primarily two. Generation time (the time for 1 generation of a population to reproduce) and mutation rates of DNA.
A longer generation time decreases the rate of evolution. For example a single celled organism reproducing every month will evolve faster than an elephant reproducing every decade.
Larger rates of mutation in DNA increase the rate of evolution. If DNA does not change then evolution cannot happen. So the faster DNA changes (thru mutation rates) the faster the potential evolution can be.

Generation time increases with increased body size/metabolism (Brown et al. 2004). Mutation rates decrease with increased size/metabolism (Gillooly et al. 2005).

With those two general patterns, one can say that the rate of evolution decreases with increased metabolism.

Now onto dinosaur evolution. You said that R. Bakker observed that dinosaurs had a higher rate of evolution than expected. With the hypothesis that a higher metabolism caused this. I'll assume they had the same physiological constraints as animals of today, which is reasonable considering they are ancestors of birds. Which everything I just laid out I would propose R. Bakker hypothesis is false, since a higher metabolism means a higher generation time and lower mutation rates, which would lead to decreased rate of evolution.

The latest science says that dinosaurs were endothermic (regulate their own temperature) up to a point (Witze 2014), so their internal temperatures were not as warm as mammals, but probably warmer than most fish and reptiles.
So when accounting for size they likely had lower evolutionary rates than mammals, and higher rates than fish, reptiles, insects, or other ectotherms.

Why then does R. Bakker observe higher evolutionary rates in the fossil record then? I can think of just a general reason why. The timescale of dinosaurs is on the order of 10's of millions of years. Much longer than the tiny amounts of evolution that we have observed in the past 100 years of science. There could easily be processes happening at those long time scales that we aren't considering.

References

Brown, J. H., Gillooly, J. F., Allen, A. P., Savage, V. M., & West, G. B. (2004). Toward a metabolic theory of ecology. Ecology, 85(7), 1771-1789.Link

Gillooly, J. F., Allen, A. P., West, G. B., & Brown, J. H. (2005). The rate of DNA evolution: effects of body size and temperature on the molecular clock. Proceedings of the National Academy of Sciences of the United States of America, 102(1), 140-145. Link

Witze, Alexandra  (2014). Dinosaurs neither warm-blooded nor cold-blooded. Nature. 2014 Link


Why do patients with type 2 diabetes not show the body wasting seen in type 1 diabetics?

The following is based on a conversation I had with a senior biochemist in my university who conducts grant-funded research on the relationship between diabetes and heart disease. It can be criticized for the paucity of external sources from which its veracity can be checked. However, although the question is based on a misconception I thought it should be addressed. Perhaps others could help improve the answer by supplying references etc.

The following points about Type 2 diabetes mellitus are relevant.

‘Type 2 diabetes’ refers to a disease which encompasses conditions
with a spectrum of severities.
This means that the description of it being “characterized by so-called ‘insulin resistance’” — alternatively expressed as cells being refractory to insulin — in fact means that there is a variation in the degree to which the cells are refractory. In many cases, although this leads to a higher blood sugar, it does not result in the complete breakdown of fat and muscle protein found in type 1 diabetes, where insulin is completely lacking.
Type 2 diabetes does not result in an increase in fat deposition and body weight. In many — but not all — cases it is caused by overweight.
In type 2 diabetes caused by overweight there is a gradual loss of fat. It is not apparent in a ‘snapshot’ of type 2 diabetics, many of whom have such large fat reserves that it will take a long time before these are broken down.
In severe type 2 diabetes the situation eventually becomes similar to type 1 diabetes as the beta cells of the pancreas can be destroyed. In these cases insulin injection is required.
Normally type 2 diabetes is controlled with drugs that reduce the glycemia — metaformin is currently the agent for the first line of treatment — and by lifestyle changes, especially in diet. (The treatment of type 2 diabetes was reviewed by Juan José Marín-Peñalver et al. in 2016 and considers their mechanisms of action etc..)


Binomial nomenclature: Why am I seeing different genera with the same species name?

Two different species can have the same species epithet if they belong to different genera ('species name' is referring to the full binomial name). Consider for example Pinus glabra and Ilex glabra

P. glabra

I. glabra

Two species can be have the same genus name (meaning they belong to the same genus) and will therefore necessarily have different species epithets (otherwise we would name them exactly the same way which would be very confusing). Consider for example Pinus glabra (again) and Pinus resionosa

P.glabra

P. resinosa

As a consequence, if two species share the same species epithet then it tells you nothing about how closely related they are. If they share the same genus name, then they belong to the same genus (except exceptions probably!).

For the above examples, the term glabra comes from "glaber" (latin) which means "Hairless". So the only thing you can tell from P. glabra and I. glabra is that they are probably both hairless when you compare them with their respective closely related species.


How do the brain and nerves create electrical pulses?

This is quite a big question! I'll try to outline the basic view.

First, let's review how neurons signal between each other. The canonical way for a neuron to send a signal to a downstream neuron is by generating an action potential, the "electrical impulse" you have heard of. This action potential causes the release of neurotransmitter at a point where the two cells are very close to each other called a synapse. The downstream postsynaptic cell receives the neurotransmitter signal and converts it into a small electrical signal. If enough of these small electrical signals happen in a short time, they sum together and are likely to initiate an action potential in the second cell and the cycle repeats all along the circuit.

How is the electrical signal generated? The basics of how this works was worked out most famously by Hodgkin and Huxley in 1952. The short story is that the plasma membrane is selectively permeable to ions. Let's build the concept from the ground up.

The toolbox

Imagine a sphere of plasma membrane that represents a simple neuron. For starters, we assume that this membrane is bare lipid with no membrane-associated proteins. Because of the hydrophobicity of the bilayer, charged particles cannot diffuse through the membrane.
The cell is bathed, inside and outside, in a solution containing many ions (charged atoms), including sodium (Na+), potassium (K+), chloride (Cl-), and calcium (Ca2+). As we noted above, these ions cannot go through the membrane without "help".
Now we add an ion pump protein into the membrane which will pump sodium ions out and potassium ions in. This particular pump, the Na-K ATPase, creates an excess of sodium ions outside the cell and an excess of potassium ions inside.
Now we add a potassium ion channel to the membrane. This protein creates a pore in the membrane that only allows potassium ions through. This particular protein's pore is always open. Now things start getting exciting...
What do the potassium ions do now that they can go through the membrane? Ions will move based on the forces created by their electrochemical gradients. The pump created a chemical gradient by putting excess K+ inside, so the K+ ions start to flow out through the ion channels. But K+ ions are positively charged, so when they flow out, positive charge starts building up outside and negative charge builds up inside. This electrical gradient opposes the chemical gradient, tending to pull the K+ ions into the cell while the chemical gradients pulls K+ ions out. The influx and efflux reach an equilibrium at the Nernst potential, where the electrical and chemical forces equal out. For physiological concentrations of K+ ions, the K+ equilibrium potential is about -80mV or -90mV. This means that K+ ions will flow until the outside of the cell is 80-90mV more positive than the inside of the cell. We started at 0mV, so K+ ions mostly flow out.
We now have a membrane potential, a difference in electrical potential between the inside and the outside of the cell at about -80mV (usually closer to -70mV or -60mV in "real life"). In particular, this membrane potential is the resting potential that exists when the cell is not active. We can simplify for now and think of the resting potential as being set by a resting permeability of the membrane to potassium ions, but not to sodium ions. We call this membrane polarized, and thus depolarization is when the membrane potential becomes more positive, and hyperpolarization is when the membrane potential becomes more negative.
Now, we add to the membrane a voltage-gated sodium channel, an ion channel that passes only sodium ions but is usually closed. The voltage-gating means that this ion channel is sensitive to the membrane potential. At the resting potential, the pore is closed and the membrane is still impermeable to sodium ions. When the membrane potential becomes slightly more positive, the channels opens and sodium ions can flow. This channel is also inactivating, so that when it opens it only opens for a short period of time, letting in a limited amount of sodium.
What way will sodium flow when we open this channel? Because of the negative resting potential (-70mV) and the excess of sodium ions outside due to the pump, both the electrical and chemical gradient will drive sodium ions into the cell. The sodium equilibrium potential is usually around +60mV.
To complete the machinery for generating an action potential, we also add a voltage-gated potassium channel to the membrane. It works just like the voltage-gated sodium channel that is also closed at rest and opens when the membrane potential becomes more positive. This channel opens a bit more slowly than the sodium channel does, but it does not inactivate.

Generating an action potential

Ok, so how do these parts come together to create an electrical impulse?

The cell sits at its resting membrane potential, with all of its voltage-gated channels closed. It receives a signal from an upstream cell that causes a slight depolarization. The action potential will initiate when the membrane potential hits the threshold potential.
At the threshold potential, the voltage-gated sodium channels open letting sodium ions flow into the cell. The sodium flux pulls the membrane from the resting potential (-70mV) towards the sodium equilibrium potential (+60mV). These values are far apart, so the driving force is large and the membrane depolarizes rapidly. This is the action potential upstroke.
The depolarization also activates the (slightly slower) voltage-gated potassium channels. The potassium ions flow out and drive the depolarized membrane (about +20mV at the action potential peak) back towards the potassium equilibrium potential (-80mV). At the same time, the sodium channels are inactivating so that sodium is no longer depolarizing the membrane. The repolarization rate is usually slower than the depolarization rate. This is the action potential downstroke.
The whole process of the action potential depolarization/repolarization cycle takes about 2-3 milliseconds in an "average" neuron. Once the cell reaches resting potentials again, the membrane is basically reset. The voltage-gated channels are turned off. The ion pump moves the potassium ions that flowed out and the sodium ions that flowed in. That patch of membrane is ready to fire another action potential!

As a final note, I'll mention that the voltage-gated sodium channel provides a mechanism for the action potential to propagate down the axon. The action potential is initiated in one location of the cell, and creates a depolarization. This depolarization causes the voltage-gated sodium channels in neighbouring regions of the membrane to open and generate an action potential cycle of their own. This is how an action potential travel down axons (and sometimes dendrites too).


In this context, that nomenclature means "cells which express PDPN"


What is meant by "the degree to which a gene is expressed" in an individual?

It is true that a gene is either being expressed, or not being expressed. However, the degree to which a gene is expressed can vary tremendously. "Degree of expression" basically means the number of times the gene is read by the transcription machinery, which (generally) correlates to the number of copies of mRNA present in the cell, which (generally) correlates with the number of protein molecules being translated. Essentially, the degree of expression of a gene corresponds to how much of the gene's product is being produced. (Of course, this being biology, things aren't always quite as simple as that, but this is the general trend.)

Here's an example. All nucleated cells express housekeeping genes that are required for the normal function of the cells. These are often involved in maintaining metabolism in the cell, sensing and processing nutrients, maintaining the cell's structure and shape, etc. These genes are expressed to a very high degree, meaning they are always "on" and being transcribed. On the other hand, there are many many genes that are not needed in "normal" situations, and are only turned on at certain points in development, during pathology, during a certain point of the cell cycle, or other similar situations. These genes have a very low degree of expression, and in fact may be turned off altogether in some cells.

So, the degree of expression can be described as the rate at which the gene is being transcribed. In a study like the one illustrated in your question, the number of copies of each gene's mRNA in the cell is quantitated, and compared to the expression of a housekeeping gene that should have the same degree of expression regardless of the sample. The relative amounts of each mRNA are then compared among individuals, and scored accordingly. This numerical score is then turned into a color for the purposes of generating the heatmap image.


Where to download confier (pine) or A. thaliana annotated reference RNA transcriptomes in full .gbk (GeneBank) format?

You can download the entire set of annotated RefSeq transcripts for a given genome assembly from NCBI Assembly portal.

Go to https://www.ncbi.nlm.nih.gov/assembly and search for Arabidopsis thaliana
Use the 'Download' button to pick 'RNA Genbank format' as the file type and 'RefSeq' as source to download all RefSeq RNAs annotated on this assembly in Genbank format.

Note, however, that the RefSeq transcripts in this file will be the ones that were annotated at the time of the release, June 2018, in this particular case. It is possible that additional RefSeqs have been curated for this species in the mean time, and those will not be a part of this file.


Are all functions of a human cell known?

As someone who has dabbled in both biology and programming, I assume you are referring to the theoritical ability  of functional programming to simulate organic behaviour from well defined input. From that point of view, our comprehension of the human cell behaviour is  currently near stone age level.
The astounding diversity of homeostatic and signaling parameters in our body makes a realistic simulation of human cell normal behaviour largely out of reach, so don't even think about patholgic states.

The more data we will acquire, the more precise our simulations will be. Currently, our data acquisition methods are too primitive, and clearly are not deterministic enough to base computed simulations upon them.

Of course, this answer reflects my own opinion, but I dare think that most of my colleagues will adhere to that view.


Absorption of glucose in small intestine

Na+ channel proteins would not be able to generate a concentration gradient, as they are passive transporters, not pumps. They essentially can only facilitate diffusion of Na+ down a gradient. The Na+/K+ pump is ATP-driven, providing active transport needed to establish or maintain a concentration gradient.


Difference between bacteria and bacteroids?

Bacteroids are the endosymbiotic forms of rhizobia (in the root nodules of leguminous plants).

Löhnis & Hansen (1921) J Agric Res 20: 543-556; emphasis mine:

  It is not superfluous to emphasize once more that persistence in
  calling these forms "bacteroids" is by no means to be recommended.
  They are true bacteria, not foreign bodies looking like bacteria, as
  Frank's pupil Brunchorst erroneously believed. To speak of a
  "bacteroid" growth of bacteria is no less absurd than it would be to
  speak of a "fungoid" growth of fungi.

https://naldc.nal.usda.gov/download/IND43966363/PDF

Gerson & Patel (1975) Appl Microbiol 30: 193-198; emphasis mine:

  Rhizobium is an aerobe, existing as a free-living bacterium in soil or
  as a partially anaerobic symbiont in the root nodules of leguminous
  plants. It is in the symbiotic form (bacteroid), which is frequently
  morphogenetically different, that nitrogen fixation takes place.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC365797/

MacKenzie et al. (1973) J Bacteriol. 113: 387-393; emphasis mine:

  [C]hanges [accompany] the transformation from the free-living rod
  forms to the nitrogen-fixing bacteroid forms. (...) During the
  transformation into the bacteroidal state the wall decreased in
  thickness, became less rigid, and developed a particulate surface.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC251641/