How body loses more fat in CO2 form than in sweating form?

If you exercise heavily, you can sweat enough where you have to drink to replace it. But on a normal day, you don't sweat all that much.
On the other hand, when you metabolize food, you essentially burn it. According to the Merck Manual,

Carbohydrates, proteins, and fats supply 90% of the dry weight of the diet and 100% of its energy. All three provide energy (measured in calories), but the amount of energy in 1 gram (1/28 ounce) differs:
4 calories in a gram of carbohydrate or protein

9 calories in a gram of fat

A typical diet is 2000 calories per day. If you get 50% of your calories from fat (shame on you!), that is 1000 calories of carbohydrate or protein, or 250 grams. It is 1000 calories of fat, or 111 grams. 361 grams total.
We will simplify. CH bonds contain little energy compared to CC bonds. H weighs little compared to C. We don't change much by ignoring H. There is some O and other stuff, but we will ignore that too. It will still be roughly right. So you burn about 361 grams of C.
For every C atoms you metabolize, you must breathe in 2 O atoms, and breathe out all 3 atoms as CO2. C atoms have an atomic weight of 12. O is 16. So CO2 is 44. Every 12 grams of C becomes 44 grams of CO2. So to burn 261 g of C, you breathe out 1324 g of CO2.
1324 g of water would be 1.324 liters. It is easily possible to sweat that much in a day, but you typically don't. You typically breathe out more CO2 than you sweat water.


How prevalent is Taq polymerase in adding 3' A overhangs to the PCR product?

I am not sure of a case where Taq doesn't add 3' A overhangs.

You could use TA cloning to clone your PCR product.  The basic principle is to use a vector with 3' T overhangs.  If you have a vector without these overhangs, you can use a terminal transferase + dTTPs to create them (or even Taq, but this is not as great because it adds a purification step to isolate the vectors with overhangs; terminal transferase is much more efficient).  You can then ligate your PCR product that has a 3' overhang.

Protocols for adding the 3' T overhangs to your vector are given in Zhou and Gomez-Sanchez 2000.


Smell samples the chemical composition of the environment, the groups of molecules you are sampling in those examples still exist in nature. It is like asking why being able to taste pizza would evolve, it doesn't, not by itself anyway, it is the inevitable result of being able to taste the things and conditions that make up pizza, carbohydrates, proteins, fats, oils, acids, bases, salts, etc. things that would be important for our ancestors to be able to detect.

With paint you are smelling volatile organic compounds, and many are important biological and/or hazard markers, some are related to rotting meat, others to infection, others to food sources, and others to natural toxic water sources. With burning rubber you have many different smell depending on the rubber, but in each case you are smelling a burning organic polymer which releases organic compounds which again would exist in nature.


What is the speed of blood in when flows through the fingertip?

This reference gives about 10-20cm/s in the major arteries and 5 cm/s in the major veins of the index finger in 5 male subjects, though there was a lot of variation.

The answer is going to be highly dependent on the level of the vasculature you are talking: through the largest artery or capillaries you will get different results, and different results in veins as well, and it will depend on many other physiological parameters.

Because it will vary greatly, even within individual vessels, you can't use the speed to estimate volume per time because the vasculature does not maintain a constant diameter; in fact, changes in vessel diameter are the major contributors to changes in flow volume.


How long do Ziehl-Neelsen stained samples keep?

This TB study might help you: external page
Briefly, they used 6 to 19 months old samples of mostly bad quality (due to their age). The last sentence of the quote below sounds promising though.

The 12,543 sputum smears stored at the national TB reference
laboratory for 6 to 19 months were stored at room temperature in a
wooden slide box without a cover slip. Most of them had lost their
stain reflecting the counterstaining with methylene blue. Restaining
of 436 doubtful slides by ZN gave disappointing results throughout [...]
After a 6 to 19 months storage of ZN stained sputum smears in a
non-air conditioned atmosphere, the bright red color of eggs due to
carbolfuchsin had virtually disappeared. [...] In such case, the ZN restaining of sputum smears allows to rediscover AFB that were discolored.

When I did this the last time, we used fresh and few months old samples which looked similar to the first of your images. Just have a look at the paper, I guess.


Correlation of non-coding DNA with coding DNA

If you have 2 different mutations (irrespectively of where they sit in regards to the final gene-product), and both correlate perfectly with a given phenotype, (and you have dismissed any other potential cause), you can not formally say, if the first mutation, or the second, or both mutations are required for your phenotype. (Though you can make educated guesses or rely on external information...)

Loss-of-function mutations do not have to be in the protein-coding region (but simply in one part of the genome, which is required for the expression of a gene towards a phenotype).

Polymorphisms can also be neutral - especially in artificially bred / selected animals, such as the wolf-like animals we now call labradors. You could easily envision a scenario where some neutral mutations was present in an individual, which would have a desirable / selectable mutation. If that neutral mutation is within a few 100bp of the selected mutation, it unlikely will have been uncoupled from the selected trait / mutation.


Let us say this myopic patient has amplitude of accommodation of 8D.  The patient accommodates 8D beyond far point, thus his near point is 1/6+8=0.07m (7.1cm).

If we compare the case with emmetropic eye with accommodation amplitude of 8D, the near point is 1/8=0.12m (12cm).

So, yes, near point of myopic person is different from an emmetropic one. But, you are wrong thinking that near point of "normal" eye is 25cm. The near point is age-and-lens dependent, thus near point is individual one and should be calculated considering amplitude of accommodation.

Look at this picture of age-related accommodation changes -

Look at the scheme of far/near points (near point here is just an example)


I believe it is because of the violets' propensity to collect mould. They seem to like warm, humid space, but in a closed-air type system, it is a breeding ground for mould.

There could be another reason as to why they die, but I would assume it would be an infection.


Primitive streak being only present in caudal half of embryo affecting gastrulation?

It would help a little in answering your question to know more about what organisms you are interested in, or the specific source that you are referencing, with e.g. the relevant quote.

For example, the primitive streak is specific to amniotes: avians, mammals, and reptiles. In other common model organisms such as flies or amphibians gastrulation happens differently.

Another thing to keep in mind is that gastrulation is a very large and structurally distending process, so it can't be really said to happen "only on one end" of the embryo. The whole embryo is going through gastrulation. We can however talk about the placement of certain gross morphological structures on the embryo. But really each cell is affected by gastrulation, whether it's immediately obvious under a microscope or not.

Looking at the Amniote section of the wiki page on gastrulation, it appears that the main morphological changes in gastrulation do occur on the caudal side - for amniotes.

However, in Drosophila, gastrulation involves the formation of an approximately homologous structure called the ventral furrow, which is obviously on the ventral side, extending most of the anterior-posterior axis. However the invagination event does actually happen on the dorsal/caudal side.

So, it's complicated, and it depends a lot on which organism you're talking about.

Update following response

Humans are amniotes, they follow more or less the normal amniote path in gastrulation according to the wiki link above.

An important note missing in my previous answer above is that gastrulation itself defines bilateral symmetry in embryos; prior to this establishment animal-vegetal is the only obvious axis. So we are kind of defining the rostral-caudal axis according to the formation of such structures as the primitive streak, which are formed during gastrulation.

So it's a little circular to say that gastrulation happens on caudal end only; as gastrulation includes the step that establishes the rostral-caudal axis. Without gastrulation that axis just doesn't exist.

Again, gastrulation is a process that happens to the entire embryo. It doesn't just happen in one area. Structures such as the primitive streak are just obvious clues that the process is happening. It might be proper to say that the primitive streak begins forming caudally (I don't know of exceptions, though I'm not an expert), but it would not be proper to say that gastrulation is a caudal process.


That is a mole cricket. Order Orthoptera, family, Gryllotalpidae https://en.wikipedia.org/wiki/Mole_cricket
I'm not surprised you live by a lake. They burrow in sandy soil or sand, often right up to the water's edge. They can fly, but spend most of their time underground. You do not need to save it, as it will find its way back to its home if you just let it go. They are not pests. They don't bite, or spread disease.


It is a torrent salamander. Most likely this is the southern torrent salamander (Rhyacotriton variegatus)


Humans genetic/phylogenetic "next relative" in central Europe?

I am not sure I understood the question. Is the following your question?

  Among all species living in central Europe, which one is the most closely related to homo sapiens?

Source of information

opentreeoflife.org (nice vizualisation on OneZoom.org) is one of the most update synthesis of existing research inn phylogenetic reconstruction. I base my answer in consideration of the tree on OneZoom.org.

Answer

Outside Homo sapiens, there is no living primates (or any other Euarchonta) in Central Europe. The sister branch of primates include Lagomorpha (Hares and Rabbits) and Rodents (mice, rats, squirrels, prairie dogs, porcupines, beavers, guinea pigs, hamsters, and capybaras). In other words, any Lagomorpha and any Rodents are all equally related to any Primate (incl. Homo sapiens). Their Most Recent Common Ancestor (MRCA) lived about 75 millions years ago.

Examples of species of lagormorpha and rodents that live in Europe include Mus musculus, Rattus norvegicus, Lepus europeanus and Sciurus vulgaris.

How about Hedgehogs?

Hedghogs are Insectivora and they are a sister group to all primates, lagomorpha and rodents. Their MRCA lived about 80 million years ago. So, no there are species currently living in Europe that are more closely related to us than hedgehogs.

Note

The term "next relative" does not mean anything! You might want to understand your understanding of phylogeny with an introductory course.


Identify this black dragonfly with bluish coloration along its flat top, yellow on it's mid-body and green on its head

This species of dragonfly is Brachydiplax chalybea. Colloquially known as blue dasher.
General information
More information


Keep in mind that the plasmid map is made by someone, and probably not perfect. They're also made by programs that let you annotate everything everywhere, even overlapping stuff.

In silico, I assume that the DsRed part and the Lacz parts were present, perhaps copied from some other plasmid map including annotation. After that, someone decided it was a good idea to annotate the complete ORF (in yellow).

What I think this means in reality (just guessing from the map, which is just coarse schematic picture): there's a part of Lacz still present in the plasmid (in pink, second lane) which is fused (in frame) to the DsRed gene (red). Together this gives the fusion gene marked in yellow. Also notice the part (terminator?) in pink that's in the third lane.


It is an actual insect, Lethocerus americanus, also known as Giant Water Bug. See:

Matches the colors, body shape and small eyes and head. And yes, they are very annoying. As expected from real bugs. You know, like the first one.


How common is bacterial mediated transformation? In plants? In animal cells?

In animal cells the process is called transfection, to differentiate from transformation which is the process by which cells become immortalized (cancerous). I'm mainly familiar with mammalian cells, and in these systems some reaction is required to open pores of some sort in the cell membrane to allow the genetic material to enter. Viruses can mediate cellular entry on their own, but I am unaware of any method that uses live bacteria (although this doesn't mean that some specialized method doesn't exist).


Satiety is complex, and there are several kinds of satiety, all of which come into play in different circumstances. Things that decrease or halt our eating are called satiety signals. Different satiety signals are put out by different substances (carbohydrates, fats and proteins) as well as by things like gut stretching and other signals. There is also a psychological component to override satiety signals (company during meals, appearance of food, cost, etc.). The best measure of satiety may well be when a person stops eating a given meal. In lab conditions, the meals are carefully calibrated, but people (and animals) can feed as long as they desire to (ad lib).

Historically, satiety was thought to be the end product of serum glucose, available energy based on body heat, fat utilization by the liver, and the generation of ATP and other energy-rich molecules by the liver and/or brain. For the most part, these hypotheses have not withstood the test of time.

Three major signals influence food intake: satiety signals, adiposity signals, and central effectors. For the sake of simplicity, I'll deal only with satiety signals. Satiety signals (SS) arise from the GI tract and related organs during a meal, and influence eating behavior by activating peripheral nerves passing from the GI tract to the brain, or by recognition by brain receptors.[1]

As food interacts with the lining of the stomach and intestine, gut peptides and other signals that coordinate/optimize the digestive process are secreted. The signals that inform the CNS function as satiety signals. Different signals are secreted in response to carbohydrates, fats, and proteins, and it's the specific mix of signals that informs the brain as to what precisely has been eaten.[2]

Cholecystokinin (CCK) is the most extensively studied gastrointestinal satiety hormone. It is secreted by cells in the duodenum and jejunum in response to ingested fat and protein in chyme (food plus gastric fluid). Giving CCK IV decreases ad lib meal size, while blocking CCK receptor sites will increase ad lib eating per meal.[3][4]

Carbohydrates and fats as the most effective stimulators of Glucagon-Like Peptide (GLP-1) and Peptide YY (PYY). IV GLP-1 decreases meal size by promoting early satiety.[5] Within the CNS, PYY is detectable in the hypothalamus, medulla, pons, and spinal cord.[6]

Enterostatin is a protein which is broken down into a digestive lipase and a five-peptide fragment (Ala-Pro-Gly-Pro-Arg (APGPR) in humans). The appetite regulating effects of APGPR in the brain are specific to high-fat or fat diets but not towards diets rich in protein or carbohydrate.[6][7]

Amylin decreases meal size in rats, probably through the same pathway as CCK. Oxyntomodulin (OXM) and pancreatic polypeptide (PP) are also meal terminators. Pre-prandial subcutaneous administration of OXM to overweight and obese humans over a 4-week period resulted in a significant reduction in body weight of 2.3 kg, compared with 0.5 kg for the placebo arm.[9]

This is a growing field, and there is more suspected, and more to prove. But one can see that there is no one measure of satiety.

[1] That satiety signals come from the stomach and beyond was shown by "fake eating", that is, diverting swallowed food from the stomach by creating a fistula. If food is allowed to enter the stomach, satiety signals are elicited; if not, eating continues for a long time.
[2] Gastrointestinal Satiety Signals I. An overview of gastrointestinal signals that influence food intake
[3] Gastrointestinal hormones and satiety
[4] Rats with spontaneous mutations of the CCK-1 receptor (called
OLETF -Otsuka Long Evans Tokushima Fatty- rats) eventually become obese
during their lifespan.
[5] Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2
[6] Introduction to Gut-Brain Interactions
[7] Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors.
[8] Amylin decreases meal size in rats
[9] Gut-Brain Interrelationships and Control of Feeding Behavior


Does a human body decompose in a completely sterile environment ?

No it wont. Unstable molecules like ATP will quickly degrade spontaneously. The stable ones like many proteins and lipids wont degrade spontaneously. Enzymes are essential to degrade them and are to be supplied extraneously.

  What happens in vacuum ?

Body will dry up :P


Relationship between toxicity of drugs and negative effects on brain

Short answer
The causes of death after heroin, cocain or cannabis overdose are mainly due to cardiac and respiratory arrest, and not to neurotoxic effects.

Background
The cause of death after a lethal overdose of your mentioned drugs are the following :

Cocaine (lethal dose: 30 mg - 5 g via mucus membrane (EMCDDA)): Cocaine-related deaths are often a result of cardiac arrest followed by an arrest of breathing (NIH). Cardiac effects are mediated via increased sympathetic output and a local anesthetic effect (Schwartz et al., 2010);
THC: (lethal dose: ~1000mg/kg i.v. in primates (Drug library)): No known cases of human fatalities. Toxicity appears as achypnea (rapid breathing), tachycardia (fast heart rate), ataxia, hyperexcitability, and seizures (Fitzgerald et al., 2013), but death seems mostly associated with respiratory arrest and cardiac failure (Drug library);
Heroin: (lethal dose 200 - 2000 mg i.v.(EMCDDA)): overdose often due to respiratory arrest (Anoro et al. 2004) caused by mu-opiate receptor activation in the brainstem (Karch, 2006).

Hence, heroin, THC and cocain are lethal mainly due to peripheral causes (i.e., cardiac and respiratory arrest). Although these effects are mediated, at least partly, through central mechanisms (i.e., occurring in the central nervous system and specifically the brain), the drugs themselves do not cause death because of neurotoxicity.

And a closing comment, with credits to @MarchHo - In general, neurotoxins do not cause death due to neural toxicity per se. Most notably even botulotoxin, being one of the most potent neurotoxins known, causes death due to respiratory failure (CDC).

References
- Anorro et al., Rev Esp Salud Publica (2004); 78(5): 601-8
- Fitzgerald et al., Top Companion Anim Med (2013); 28(1):8-12
- Karch, Drug Abuse Handbook (2006)
- Schwartz et al., Circulation (2010); 122:2558-69


Can herbs absorb harmful substances leached in water supply

You'd have to test it. Plant roots naturally pull poisons like heavy metals out of the soil through water. These are called metallophytes, and can even be classified into what're called hyperaccumulator plants. The use of plants to remove harmful substances from the soil, air or water is called phytoremediation.

The process of absorbing harmful substances, however, relies on the structure and size of the substances involved because the substances must enter cells. We know from elementary biology that cells only allow molecules of certain properties to pass their cell membranes. Since the filter additive in question is an unknown, it's hard to say if a plant would absorb it. It's also hard to say if it's harmful to you, or if it even gets into your water. Testing for a chemical of unknown behavior requires some analysis like mass spectrometry (fair example).


What effect has changing pH and salt concentration on protein complexes?

The formation of protein complexes or aggregates in aqueous buffers is determined by a number of factors: physical properties of the protein itself, pH, temperature, type and concentration of the used cosolvent (salt). Solutes are often roughly divided by type into chaotropes ('disorder-making'), which destabilise protein structures and kosmotropes ('order-making'), which stabilize them. [1, 2]

Chaotropic salts interfere with intramolecular interactions mediated by non-covalent forces such as hydrogen bonds, van der Waals forces, and hydrophobic interactions, which, at high cosolvent concentrations, results in protein denaturation.

Kosmotropic salts, on the other hand, cause water molecules to favorably interact, which also stabilizes intermolecular interactions in proteins. The salt molecules readily interact with water from the protein's hydratation shell and remove it from the protein surface, which produces thermodynamically unfavourable interactions that are reduced when proteins associate to form complexes. With increase in salt concentration the protein precipitation (salting out) increases.

Both cations and anions have been ranked separately by their capacity to precipitate proteins, to form a Hofmeister series [3, 4] (first set in 1888 but still hotly debated), e.g.:

SO42− > H2PO4− > CH3COO− > Cl− > Br−

At large salt concentrations protein solubility is given by the empirical Cohn equation [6]:

lnS = α − βc

where S is the protein solubility, c is the salt's ionic strength, α and β are empirical constants characteristic of particular salt.

Salting-out agents are very widely used in protein purification (to concentrate proteins eg. with ammonium sulfate), chromatography or crystalization.

The influence of pH on protein-protein interactions in solution works through altering of the electrostatic properties of protein surfaces. At pH equal to the protein's isoelectric point (pI), where its net charge is neutral, charge repulsions of similar molecules are relatively low and many proteins will aggregate. Very low and very high pH will case proteins to denature; during digestion, for instance, proteins are in extremely low and then extremly high pH that exposes their backbones for enzymatic degradation.

For more information, please refer to:

Martin Chaplin, Kosmotropes and Chaotropes, http://www.lsbu.ac.uk/water/kosmos.html
Zangi R. Can salting-in/salting-out ions be classified as chaotropes/kosmotropes? J Phys Chem B. 2010 Jan 14;114(1):643-50.
Pace CN, Treviño S, Prabhakaran E, Scholtz JM. Protein structure, stability and solubility in water and other solvents. Philos Trans R Soc Lond B Biol Sci. 2004 Aug 29;359(1448):1225-34; discussion 1234-5.
Shimizu S, McLaren WM, Matubayasi N. The Hofmeister series and protein-salt interactions. J Chem Phys. 2006 Jun 21;124(23):234905.
Zhang Y, Cremer PS. Interactions between macromolecules and ions: The Hofmeister series. Curr Opin Chem Biol. 2006 Dec;10(6):658-63. Epub 2006 Oct 10.
Ruckenstein E, Shulgin IL. Effect of salts and organic additives on the solubility of proteins in aqueous solutions. Adv Colloid Interface Sci. 2006 Nov 16;123-126:97-103. Epub 2006 Jun 30.


Braquio-abduction illusion explanation and references

It may be because, when we move our shoulders towards our the body, also know as abduction (Fig 1.) gives the central part of the body an elevation. when we rotate our arms more upwards (Adduction), the elevation will be lost.

So in other words, when we are making snow angels,

Start Normal position (hands near thighs) = Back and shoulders on ground
Middle position      (hands in middle)   = Back elevated and shoulders on ground
Final Position        (hands upward) = Back and shoulders on ground again.

Due to this motion, it seems as if the ground become concave.

Source:

Anatomical Terms of Movement

Articulating the Importance of Joints in Anatomy


Why is heart failure treated as more critical than kidney failure?

I don't know that one is treated as more critical than the other. Both are potentially life-threatening conditions.

One in five people over 40 will develop heart failure (HF). That makes it a very common disease of aging, and as more people survive other events (e.g. MI), it will continue to be prevalent, if not to rise.[1][2]

When a patient presents with heart failure (HF), whether it is to a PCP, an urgent care center, or the ER, it is treated.

In the US, the prevalence of CKD (chronic kidney disease) in people ages 60 and older approximately the same as of congestive heart failure (CHF): 18.8 to 24.5 percent. Between 1980 and 2009, the prevalent rate for end-stage renal disease (ESRD) increased nearly 600 percent, from 290 to 1,738 cases per million.[3]

When a patient presents with renal failure (RF), whether it is to a PCP, an urgent care center, or the ER, it is treated.

That makes both conditions much more common (and less emergent) in presentation than, say, anaphylaxis (life-threatening allergies).[4] Known rates or cases of anaphylaxis were 0.0004% for food (e.g. peanuts), 0.7% to 10% for penicillin, 0.22% to 1% for radiocontrast media, and 0.5% to 5% after insect stings.

Emergencies are emergencies, and are triaged for care based on risk, with standardized acuity scales that have five levels (e.g., 1- resuscitation, 2- emergent, 3- urgent, 4- less urgent, 5- nonurgent).[5] To claim that one is treated as more emergent than another, one would need to present evidence that, e.g. HF is rated as emergent more often than RF.

[1] Lifetime risk for developing congestive heart failure: the Framingham Heart Study
[2] Chronic Heart Failure: Contemporary Diagnosis and Management
[3] Kidney Disease Statistics for the United States
[4] Anaphylaxis in the United States
Considering the 1999 US population of 272 million, the population at risk for anaphylaxis from food is 1099, from penicillin is 1.9 million to 27.2 million, from radiocontrast media is 22 000 to 100 000, from latex is 220, and from insect stings is 1.36 million to 13.6 million. These calculations yield a total of 3.29 million to 40.9 million individuals at risk of anaphylaxis.
[5] Emergency Severity Index (ESI): A Triage Tool for Emergency Department


Quantifying DNA in a band on gel electrophoresis

All three methods could be used to measure the amount of DNA. However in practice, method 2 (estimation by dye brightness) typically works best in a normal workflow. It really depends on what you plan to do as your downstream application.

Problems with method 1:

Yield from gel purification methods is sometimes finicky and prone to loss.
Absorbance of remaining agarose can influence the results. DNA cleanup is a must.

Problems with method 2:

Quantification is difficult as you must estimate the band brightness against a known standard (add a known quantity of your ladder and use that for estimation).
Supercoiling of plasmids causes multiple bands to appear, so the estimation must be performed multiple times and then added (now it's less of an estimation and more a guess)

Problems with method 3:

Working with radioactivity adds a significant amount of safety protocols into a simple procedure
All products from radiolabeling must also be handled as radioactive material
Using an image has the same issue as method 2 where you're estimating instead of actually quantifying.
You could get more quantitative results from a scintillation counter, but then the products become more difficult to use because of purification from the scintillation fluid (maybe this is possible but I never tried it).
You're limited to procedures which would incorporate the radiolabeled nucleotides
If you do something like dA-tailing, then you're not quantifying the amount of DNA, but the amount of copies of a transcript.


Why was Darwin's Finch argument valid considering Weismann's argument?

Weismann's mouse tail experiment showed that mouse tail length is not inherited, if the change in tail length was caused by mutilations, and there was an absence of selection pressure.

However, Darwin's finches represented a completely different idea of evolution. In this case, the beak size of the finches did in fact change, but this was not due to mutilation. The beak sizes of the finches changed because finches with lower fitness due to their beak sizes were selected against, leading to the beak size changing over time.

If the mice were instead selected for tail length by preventing the long-tailed mice from reproducing, then it is indeed possible that the mice would eventually evolve to have shorter tails, or even absent tails.

Similarly, if the finches had their beak sizes reduced artificially but their fitness preserved (for example, by grinding down their beaks and feeding them soft food that does not require large beaks to break), the finches would not be expected to evolve smaller beaks.

It is not clear which method is the one through which the evolution of the overbite occurred. It could be due to a change in relative fitness, but a case can also be made in which fitness was not a large factor.


Why do humans transport glucose but not sucrose like plants?

Short answer digestion and absorption.

Animals have to digest sucrose into it's component sugars before it can be absorbed. Turning it back into sucrose afterwards would take energy and have no real benefit so it has had no reason to evolve.

The real question is why do plants make sucrose, and the answer is by living at a much slower pace,As you mentioned it is has slower uptake on the cellular level which is fine for plants but a detriment for more energy demanding animals. Stability is the other concern, sucrose is a lot more stable than glucose, animals are burning through glucose as fast as they can release it from storage so it doesn't matter how stable it is, whereas plants keep it around for longer and move it slower so it has a chance to breaks down on the way which would be a problem. Sucrose is more chemically stable than glucose and slightly more favorable osmotically (takes less water to dissolve the same energy value of sucrose than glucose) Both of these reasons make it more beneficial for plants to convert the sugars to sucrose, (if starch was water soluble they would likely only convert it to that.) They do this right at the end of photosynthesis then break it down just as it is being used in respiration so the energy investiture is minimal, while for animals they would be spending energy to break it down (digestion), then energy to put it back together, then energy to break it down again for respiration, its two extra steps for no benefit.

Just as a extra you can see why animals would evolve to break it down for absorption since as has been mentioned glucose is easier to absorb, whereas plants don't have to worry about extracting it from anything.


THYROGLOBULIN (19S) comes to a heavier position than ferritin (51S). Why?

Ferritin and iron-containing ferritin are different and the latter
would of course be heavier; it will therefore sediment faster.
Figure 3 of the third article uses thyroglobulin and ferritin as molecular weight markers. For your information thyroglobulin is 650kDa whereas ferritin is 440kDa. Also note that apoferritin i.e. ferritin that is not bound with iron has a sedimentation rate of 18S (from the same article that measures the sedimentation rate of iron bound ferritin - ref#2).

There seems to be some confusion regarding the sedimentation rate of ferritin. From this article:

  One molecule of ferritin can bind up to 4500 Fe2+ ions.
  When fully loaded with iron, the ferritin can increase in mass up to
  ca 900 kDa; it then has a sedimentation coefficient of 24S (Chasteen &
  Harrison 1999).

55S for ferritin seems dubious.


What can the timing of human urination tell about the human's physical condition and circadian rhythms?

The fact that urine output (enuresis) and other kidney functions are circadian is well known, just search on pubmed 'circadian urine kidney'. This can be due both to the fact that liquid consumption is less during the night and to the fact that hormones regulating kidney function like aldosterone and plasma angiotensin II are circadian.


Consuming animals by slaughtering vs injecting barbiturates?

For many drugs, the animal cannot be slaughtered for consumption within a certain time. Here are the slaughter withdrawal periods for some common drugs when used on cattle. There are also withdrawal periods for lactating dairy cattle, but I won't list them for brevity.

flunixin (NSAID) - 6 days
florfenicol (antibiotic) - 36 days intramuscular, 55 days subcutaneous
penicillin G procaine (antibiotic) - 10-14 days
tilmicosin (antibiotic) - 28 days
oxytetracycline (antibiotic) - 28 days intramuscular, 48 days subcutaneous
enrofloxacin (antibiotic) - 36 days, do not use in veal calves

More importantly for your question, I have found this report on pentobarbital used for euthanizing cattle. It says:

  Adequate measures should be taken to ensure that carcasses of animals treated with this product and the by-products of these animals do not enter the food chain and are not used for human or animal consumption.

Barbiturates are more dangerous than many other drugs and, furthermore, dead animals cannot metabolize them and they can be quite heat stable (ie won't readily decompose during cooking).


Why only water in liquid form is essential to live?

A layman's view of the problem :

Let's assume that water in liquid form was not necessary and organisms could survive on solid or gaseous water. What would some of the difficulties be to sustain such a life form?

Solid Form of water

How would the organism move without breaking or tearing itself apart? How would essential substances be transported from one part to another of the organism body?

Gaseous form

What would be the size of the organism? Gas has a much bigger volume than water.
In order to transport nutrient molecules within the a gaseous body, a huge air pressure needs to be generated. Also, how will gravity be overcome while transporting these molecules? A lot of energy will be required to maintain such pressures.

I guess nature (which always takes an optimal path) asked such questions and found that water in it's liquid form was the most suited to support life on Earth.

It need not be water alone. Other liquids may be able to support life as well. Only, we haven't discovered them yet. But whatever the substance, it's liquid form would seem to be an optimal solution for life.


If I understand correctly what you mean by "I would like to dilute my RNA to 100 ug":

Your RNA preparation is at 3.3 μg μl-1.

To add 100 μg to a reaction you need to add 100/3.3 = 30 μl

Then make the total volume up to 1000 μl with enzyme and buffer as appropriate.


The photo is not high quality, but the shape and size of the insect definitely point towards it being the nymph of some species of assassin bug (order hemiptera, family Reduviidae).
See this as an example:

Specifically, your specimen looks similar to one found in a home in Virginia.
The genus is likely Zelus, and based on it's greenish hue, I'd say it's an individual of the eastern US's most common species of Zelus, Zelus luridus (Pale Green Assassin Bug).

 Source: Christine Hanrahan

Nymphs are solid green, wingless, and with narrow bodies

The most reliable feature to distinguish this species from others is the pair of spines on the rear corners of the pronotum. These spines are long on the lighter colored individuals and shorter on ones that are darker. It can also be distinguished by dark bands on the distal ends of the femurs, but these can often be too light to be easily seen. [Source].


What is the statistical relationship between radioactivity and mutation rate?

According to this wiki page , the average background radiation is 3.01 milli-Sievert per year (including natural and artificial sources). This equals 0.301 rad.

I found a short letter to nature that says the average forward mutation rate in human is 2.6 * 10^-7 per locus per rad = 2.6 mutations per ten million bases. Also it say that this mutation rate is quite uniform among species. The size of the human genome is approximately 3.2 gigabases.
So doing a quick maths: (2.6*3.2*100)*0.301 = 250.432 mutations per year per human. This is an approximation because I rounded the size of the human genome to 3.2 gigabases. Also this doesn't mean that we actually acquire this amount of mutations because we have repair mechanisms.


What is the closest possible analogue to human cells?

What about Escherichia coli? Every undergraduate lab has easy access to plenty of E.coli culture methods and its stupid easy to culture. There are always HeLa cells as well if you really want the perfect analogue to human cells because, well, they are human cells. Other options would include:

a) HEK 293 cells (Human Embryonic Kidney 293 cells), which are nice for what you're looking at as they don't replicate out of control, but are still extremely easy to grow. However, they're generally used as hosts for gene expression and they're finicky when it comes to contamination and they don't really act like normal cells that would be hit by low level radiation (ie tissues that are closer to the skin's surface)

b) 3T3 cells which would be nice for you as they are contact inhibited cells, meaning they functionally keep growing into a layer one cell thick (a monolayer) which could be nice for you, especially if the low level rad you're testing is alpha emitting in which case you need a homogeneously thick cell layer.


What was the first gene(s) found to code for ncRNA

The first eukaryotic genes cloned were the 18S and 28S rRNA genes from the frog X. laevis as described here: http://www.genome.gov/25520303

And yes, they are definitely ncRNA genes.


Why are tumor suppressor genes recessive?

I was typing out an explanation, but then realized that this text book does a much better job:
Lodish et al. 2000. Section 24.2: Proto-Oncogenes and Tumor-Suppressor Genes in Molecular Cell Biology 4ed. WH Freeman
Proto-Oncogene:

Conversion, or activation, of a proto-oncogene into an oncogene generally involves a gain-of-function mutation. At least three mechanisms can produce oncogenes from the corresponding proto-oncogenes.

Point mutations in a proto-oncogene that result in a constitutively acting protein product
Localized reduplication (gene amplification) of a DNA segment that includes a proto-oncogene, leading to overexpression of the encoded protein
Chromosomal translocation that brings a growth-regulatory gene under the control of a different promoter and that causes inappropriate expression of the gene

An oncogene formed by the first mechanism encodes an oncoprotein that differs slightly from the normal protein encoded by the corresponding proto-oncogene. In contrast, the latter two mechanisms generate oncogenes whose protein products are identical with the normal proteins; their oncogenic effect is due to their being expressed at higher-than-normal levels or in cells where they normally are not expressed. However they arise, the gain-of-function mutations that convert proto-oncogenes to oncogenes act dominantly; that is, mutation in only one of the two alleles is sufficient for induction of cancer.

Tumour Supressor Gene:

Tumor-suppressor genes generally encode proteins that in one way or another inhibit cell proliferation.... Since generally one copy of a tumor-suppressor gene suffices to control cell proliferation, both alleles of a tumor-suppressor gene must be lost or inactivated in order to promote tumor development. Thus oncogenic loss-of-function mutations in tumor-suppressor genes act recessively.


Why does a caloric reflex test induce sideways movement of the eyes?

The horizontal (= lateral) semicircular canal isn't truly horizontal.  Have a look at this lovely image from Wikipedia, which gives a nice explanation.  If you keep track of the helicotrema of the cochlea there, which is on the lateral aspect, you can see that the horizontal semicircular canal connects with the utricle higher laterally than medially.
This is somewhat confirmed in Maxwell, 2016 Figure 1 which illustrates that the "horizontal" semicircular canal is only horizontal when the eyes are lowered by 30 degrees from a standard anatomical position.  (Bearing in mind that the two lateral semicircular canals are not coplanar, but diverge by 15 degrees).  That paper also confirms that buoyancy is a key mechanism in the caloric test.
Because the lateral end of the horizontal canal is higher, treatment with cold water will draw the endolymph away from it to the medial end, and hence away from the ampulla ("ampullofugal lymphokinesis").  The patient would feel they were turning laterally relative to the the position of the fluid (taken to be fixed in space).  This leads to two types of eye motion - the vestibulo-ocular reflex to maintain fixation by moving the eyes medially, and saccades to follow the position of the "moving" stationary object that the patient is trying to focus on by moving the eyes rapidly laterally.


Is glycolysis the beginning part of fermentation, or does fermentation follow glycolysis?

As @bpedit indicates in his comment, this is a semantic question — i.e. one regarding the meaning and usage of words. I will explain how I and others use these words and why. If you are convinced by my logic you will wish to use them in the same way, if not you are free to use them differently. However there is no ‘universal truth’ here, and if you are student I have no idea what your instructor thinks.

The problem is that ‘fermentation’ and ‘ferment’ (both as a noun and a verb) are old words, predating any understanding of the processes involved. Thus the Oxford English Dictionary quotes a relevant early example of the use of ‘ferment’ as a verb as follows:

  1663 Cowley Verses, to Royal Society iv, All their juyce did .. Ferment into a .. refreshing Wine.

From this, it is clear that the idea of the fermentation process is the conversion of some initial compound (the sugar in the ‘juyce’) to some final compound (the alcohol in the wine). This usage is still current in referring to the process of fermentation, for example a Google search brings up a BBC Science educational page which states:

  Beer and wine are alcoholic drinks made by fermentation reactions that use yeast to convert sugars into ethanol.

You may or may not be aware that term ‘ferment’ was historically used to mean what we now term yeast, and ‘Zwischenferment’, the obsolete German term for certain enzymes in yeast, is derived from this. So the original concept was merely of some biological conversion effected by yeast, although this has later been extended to bacteria and the idea changed to indicate metabolic processes capable of generating ATP anaerobically.

Part of the discrepancy in definition may be the emphasis on the end-product of the fermentation — ethanol fermentation, lactic acid fermentation etc. However, it seems clear to me that the fermentation is the whole chain of metabolic events from sugar (or whatever) to alcohol (or whatever); and if glycolysis is part of that process (which it is in this example) then glycolysis is part of the fermentation. (Of course, glycolysis can occur in other circumstances where the product, pyruvate, is oxidised in the tricarboxylic acid cycle, which is not a fermentation process.)

Footnote

The extent to which one can tie oneself in knots with trying to define fermentation is illustrated in the best-selling and well-respected text book, originally written by Lubert Streyer and subsequently maintained by Berg et al. I mention this text both because an older edition is available on-line, and because a book of such value to the publishers is carefully vetted by referees. In the chapter on Glycolysis there is an attempt to define Fermentation:

  Fermentation: An ATP-generating process in which organic compounds act as both donors and acceptors of electrons. Fermentation can take place in the absence of O2. Discovered by Louis Pasteur, who described fermentation as “la vie sans l’air” (“life without air”).

So the biochemical lawyers have produced a definition that very few readers will be able to take in at first sight. What is this business about electron donors and acceptors? Well what it means in relation to the fermentation process in which lactic acid is produced (note my legalistic choice of words) is that one organic compound is reduced (glyceraldehyde 3-phosphate) — by NAD+ — and one organic compound is oxidized (pyruvate) — by NADH. And as the production of ATP is included in the definition this means that Berg et al. include glycolysis in this definition of fermentation.

…except that on the same page there is the following statement:

  pyruvate is converted, or fermented, into lactic acid in lactic acid fermentation or into ethanol in alcoholic fermentation

So here it seems that the word is being used for the conversion of pyruvate to lactate or ethanol, i.e. it excludes glycolysis.

Pasteur managed to talk about fermentation without being aware of glycolysis or ATP, and it is clear to me that you can write whatever carefully phrased definitions you like, but people are going to continue to use venerable terms like fermentation in whatever way seems natual to them.


There is Milton’s Law of resource availability and allocation.

It states that branches act as if they were different individuals, and they grow relative to the availability of their own resources.

The cells that grow are called meristems, there are different kinds of meristems, cambium ones that grow the trink, apical meristems that grow at the top,

Apical dominance is phenomenon where one meristem prevents or inhibits the growth of other meristems. As a result, the plant will have one clearly defined main trunk. For example, in trees, the tip of the main trunk bears the dominant meristem. Therefore, the tip of the trunk grows rapidly and is not shadowed by branches.

If the dominant meristem is cut off, one or more branch tips will assume dominance. The branch will start growing faster and the new growth will be vertical.

Over the years, the branch may begin to look more and more like an extension of the main trunk. Often several branches will exhibit this behaviour after the removal of apical meristem, leading to a bushy growth.

The mechanism of apical dominance is based on the plant hormone auxin. It is produced in the apical meristem and transported towards the roots in the cambium.

If apical dominance is complete, it prevents any branches from forming as long as the apical meristem is active. If the dominance is incomplete, side branches will develop.


What are cells not affected by hormones called?

How about non-target cells? I found several examples of that usage including:

A book section titled: 9.3 How are steroid hormone target cells differentiated from non-target cells?1
Containing the following line:

  Thus, estrogen will stimulate mRNA and protein synthesis in a target cell, but not in a non-target cell.

A book chapter titled: Target or non-target: Hormonal signal perception and response in the determination of cell performance2

References

1: Brown, R., Brown, R. E., & Brown, R. E. (1994). An introduction to neuroendocrinology. Cambridge University Press., p. 149.
2: Osborne, D. J., & Thompson, D. S. (1992). Target or non-target: hormonal signal perception and response in the determination of cell performance. In Progress in Plant Growth Regulation (pp. 237-247). Springer, Dordrecht.


Genotoxic agent and their metabolic pathway

In terms of DNA mutations, it's usually just pure chemistry.  The mutagens article gives a brief rundown of some of the usual suspects, but to pick a few of the ones I'm familiar with:

UV light can cause pyrimidine dimers, which clearly is a dimerization of Cytosines or Thymines, which can cause replication issues.
Deaminases, which remove amine groups, is probably the coolest example.  Deamination can occur naturally, turning Cytosine into Uracil, but is often done deliberately as part of bisulfite sequencing to determine methylation status.
Alkylation can occur, in particular of Guanine, which can lead to a preference in binding for Thymine; subsequent replication will result in an Guanine to Adenine conversion.

Similarly, there are many base analogs that will fill in for a given nitrogenous base.  These analogs often prefer to bind to an "incorrect" base as above (and in the figure below with 5-bromouracil) which will lead to specific errors.

On a more intentional basis, biotechnological tools such as zinc finger nucleases, TALENs, and the (oh-so-sexy) CRISPR system can be used to specifically alter genome sequences of choice.  ZFNs are in particular being used as a gene therapy tool for just that reason.

Otherwise, viruses (and transposons) that insert into the genome can cause specific mutations or errors if they do so non-randomly.  Figuring that out, though, can be tricky; most oncoviruses cause mutations through specific genes that allow uncontrolled growth and tumorigenesis, not in a site-directed manner.  There is, however, a growing hypothesis that certain retroviruses which tend not to cause cancer, in particular HIV, may be inserting into sites with certain characterizations, such as chromatin level.  That is far from known, though.

If you're looking for random causes, that's easy.  Anything that disrupts DNA repair mechanisms such as p53 or Rb will do that.  For chemicals, intercalators such as ethidium bromide and thalidomide insert in between DNA bases and prevent proper DNA repair.


Do the recent findings of an ape-like creature in Europe with human-like teeth change the Out of Africa narrative?

Does this change the narrative of the Out of Africa theory?

Not at all since the Out-Of-Africa hypothesis is about the African origin of all modern humans (Homo sapiens), i.e. that the species originated in Africa and then spread over the rest of the world. It is not about where possible, early ancestors may have originated. The ape from the article, Graecopithecus freybergi is claimed to be one of the oldest Homininesa, but that does not change the claim of the Out-Of-Africa hypothesis.

Reference

a Fuss, Jochen, et al. "Potential hominin affinities of Graecopithecus from the Late Miocene of Europe." PloS one 12.5 (2017): e0177127. https://dx.doi.org/10.1371/journal.pone.0177127


Welcome to BiologyBeta.SE!

On stackExchange sites, an OP should always limit his/her post to one question and should make his/her question is not too broad. But before you split up your question I invite you to have a look to some other post that will give you some answers. For this reason your question will very likely get closed as too broad. But I am giving some indices below. Also your post is a bit poorly written. This also lead people to close posts. Please come back with better posts, show some efforts in seeking for some information and it will be my pleasure to help you!

  Origin of life

There are already a bunch of posts on the origin of life for example. Note that the origin of life is not a field that is part of evolutionary biology as evolutionary biology only explain the evolution of life and not its origin. As a mathematician you may prefer saying something like the domain of definition of evolutionary biology does not include the origin of life just like the shannon's theory of information says nothing about the euclidian geometry.

  What i understand till now is that the "improvement" of the dna is a purely random development and the Selection criteria if the improvement was not negative is by surviving

Hum… that's sounds very weird. If I didn't know I would hardly recognize that you talk about evolution. You should have a look to some introduction to the field. Also, you should not confound the concepts of evolution, natural selection and mutations that I guess you confuse. A good, extremely simplistic view of evolution is that mutations occurs and create variance in the population. This traits are heritable. The variants that replicate the best increase in frequency in the population while the other variants will decrease in frequency up to the point to disappear. This is called natural selection.

  Consider a pre-bird without wings, to get wings it has to have interstage with some useless pre-wings and then it has to learn how to flight

You also seem to ask a question about how some traits may come to exist while what seem to be necessary intermediate would not be beneficial. This question has been answered probably a thousands of time as it is a common creationist argument.

Because your questions really sounds like creationist arguments I am a bit afraid that you are not trying to understand evolution but you wondering whether evolution does occur or not.

Note also that evolutionary biology is a very big field. You cannot expect to have a more or less good understanding of the whole science of evolutionary biology in less than a year. But if you are trying to just understand the very basic, sufficiently to persuade you that evolution does occur, then few weeks will probably be enough if you show some effort
Please don't forget the questions you may have. Seek by yourself for more knowledge and if you can't find something, then you're really welcome to come back to this site with an accurate question.

EDIT

Have a look to the definition of scientific theory. Also, please read @Chris comment below.

You misunderstand the meaning of "direct observation" that canadianer used. Observations we do in evolutionary biology are just as valid as those that has been made to confirm the theory of gravity. The only point concerns the easiness of understand these observations for non-literate in the field.

Yes, you are totally right. Just like the theory of gravity, the theory of evolution does not explain everything. It only applies to a subset of the phenomenons existing on earth. The theory of evolution is true, we know for a fact that evolution occurs but our theory is not global enough to explain things like the big bang or the surface tension and will never do so. The theory of evolution will never prove or disprove the existence of God as well (supposing you're concerned about that) because again it is not within its scope and will never be. However, the sociological impact of this theory tells much about the human behavior and our difficulties to accept something we know to be true if it contradicts some pre-establish believes even when these pre-established believes are not based on any logical developments.

Your question has been closed because it is too broad. The issue also is that your questions concern much more than evolutionary biology and biology. It also concerns the very nature of science and this is a common reason why creationist missundestand evolution. They don't (only) missunderstand evolution but they missunderstand what science is.


How do I read an RNA expression pattern?

This image shows the expression of a gene (in your case Lamin A/C) in various tissues. A picture with a higher resultion for mouse looks like this (from here):

You can see the median expression (calculated from all samples) and can also see, in which tissues this gene is highly expressed and in which there is less or no expression.

This is important if you want to analyze the function of a gene. The tissue specific expression pattern can vary strongly between different tissues (as you can see in the figure) which can give information about the function of the gene. The same is true if you look on the time distribution of gene expression, you can identify genes which are important for different steps of differentiation.


How do animals perform detailed active camouflage?

Some of it is voluntary and some involuntary and is detailed in this book. Chameleons have chromatophores (pigment containing light reflecting organelles in cells) which help in their colour change and many factors like age, health, etc does affect it. And no, they do not form a picture on their head and print it on their bodies.


Why do mushrooms grow in rings (sometimes called "Fairy Rings")?

When spores germinate, they do not generate mushrooms directly, but haploid mycelium starts to grow. Only when the mycelium from spores with the other mating type is met, cells fuse and generate diploid mycelium, from which mushrooms can grow.

Fairy rings are caused by a radial outgrowth pattern of the diploid mycelium, followed by resource depletion in the oldest part (middle).

This page seems to have good additional information about hyphal growth.


It's more than just sperm count that matters for a pregnancy if you are considering normal methods of insemination such as intercourse or assisted methods such as artificial/intrauterine insemination or in vitro fertilization. For couples having trouble getting pregnant, most OB-GYNs and/or Reproductive Endocrinologists/Infertility physicians do a semen analysis. This involves checking several things:

Ejaculate Volume (>1.5mL)
Sperm Concentration (>15million/mL)
Motility (>40%)
Morphology (>4%)

(and a host of other factors including rapid progressive motility, pH, etc). Why? Because there is no point of there being high numbers of sperm, if their motility is poor, because they won't be able to reach the oocyte. There's no point if they can reach an oocyte, if they are poorly shaped and cannot penetrate it. There's also no point in there being a high concentration of sperm, if the ejaculate volume is so low that it thins out before reaching the cervix. All these factors matter.

Total Motile Sperm Count (TMSC) is the most common way that physicians determine what route is best to increase chances for getting their patients pregnant.

TMSC = Concentration x Ejaculate Volume x % Motile (in decimals). Thus if, the value is:

greater than 10 million = normal male factor; check anatomy, check female causes
less than 10 million = low male factor; consider intrauterine insemination (IUI)
less than 5 million = severe male factor; consider in vitro fertilization (IVF) with intracytoplasmic sperm injection (ICSI)

Sources:

Paper 1
Advanced Fertility


Is DNA sequencing coverage a function of sample purity?

So factors which go into coverage in short-read sequencing (and Sanger sequencing).

Depth is the obvious one. All else being equal you get a bang-on Poisson distribution of coverage over a genome, which is why more sequencing = more coverage.
The human genome and transcriptome is not all equal. Illumina sequencing is ultimately (most protocols) dependent on PCR amplification which means that any factors which influence PCR-amplification ability will also effect sequencing depth. The two obvious ones in this respect are: 1) Regions of extreme GC content and 2) Regions containing secondary structures (RNA mainly).
Alignment is the next major source of error for regions being 'dropped off' depending on how your aligner deals with multi-mapping reads. Some genomes have very young transposable elements which are highly similar to one another and very abundant. For most aligners that means that you can get either huge coverage or really small coverage depending on how the genome is assembled.
For low-input sequencing techniques you get major sources of DNA/RNA contamination from the enzymes, reagents and preparation of the samples. This can largely be minimized by having 'clean' samples and using large amounts of input DNA/RNA.

Depending on the sequences you're studying read-depth can be the only factor you consider or if you have difficult regions or specific questions you can deal with a whole swath of problems.

So in answer to your question: yes DNA quality will directly effect coverage. Sometimes you can 'just sequence more' to get over this problem, sometimes you need to go back to the drawing board.


Your headline question:

How can we know which alleles are together on a chromosome?

is not quite the same as the question at the bottom of the body of your post:

how we can get any information as to whether genes are on the same chromosome or not from this crossing

These questions are different in two ways that matter: (1) the second question is asking about a single crossing, the one shown in the diagram, and (2) the second question asks about knowing if the genes are on the same chromosome or not, whereas the first asks if the genes (I presume, it says "alleles") are "together on a chromosome" (depending on how you take that phrase).
On difference (1): the single crossing in the diagram does not give information about distinguishing gene locations, but the Khan Academy page you got this from goes on to describe further crossings using the flies created in the first crossing, and those crossings can show information about gene locations.
On difference (2): I would take the genes being "together on a chromosome" to mean "linked to each other", that is close enough to each other on a single type of chromosome to tend to stay together during recombination events.  Maybe you meant "on the same chromosome", but that is, importantly, a different thing.  Recombination testing cannot tell you if genes are on the same or different chromosomes; it can only tell you if they are on the same chromosomes and are close enough together that recombination will not sort them randomly, but rather tend to sort them together.  If they are far apart, the genes will stay together or be separated by recombination with equal probability, which is the result that also happens when genes are on different chromosomes.
So, the full procedure that is described on the Khan Academy page will show how much recombination you get in the fly grand-offspring.  If you get few recombinant forms compared to the number of parental forms, then the genes are close together on the same chromosome.  If you get equal numbers of recombinant and parental forms, it indicates that is not the case, and therefore the genes are either on separate chromosomes or so far away on one chromosome that recombination has full effect and randomly separates them.


Is the chemical composition of urine detrimental or beneficial for a tree?

Here is a book about dry-matter production of urine treated plants. If we consider that trees are large plants, it's fair to apply the study to trees too:

The findings of the study suggested that urine and urine products are equally as effective as mineral fertilizer especially in sandy soil and that splitting the application is a useful strategy to manage urine and urine products for optimum dry matter production.

Some plants do live in harsh environments with chalky pH and other specifics, and they may weakened by it. It's safe to say most trees are unaffected or improved by some urine, although the biggest trees are because of rain and steady underground streams (groundwater).


Identify arthropod with many legs in Mumbai

I'm pretty sure It's a millipede from the Julida order, that includes 750 species distributed in the northern hemisphere.
https://en.m.wikipedia.org/wiki/Julida


Generally the coating is of poly D-Lysine. Proteases act only on L-amino acids. So, I guess nothing should happen to the usual coated flasks. I have reused the flask even after 2 rounds of trypsinization, and the cells seemed to be fine.

In your case, the matrix is made of proteins isolated from animal sources. They are susceptible to proteolysis. You are right to assume that these flasks should not be reused. If you have a shortage of flasks then you can buy uncoated petriplates (which are cheaper) and coat them yourself.


I presume it is an Indian bark Mantis , Humbertiella ceylonica.

  This mantis can be kept at between 21 and 28 degrees comfortably and does not need a drop in temperature at night.

References: bugzuk.com and Google


Why ml scale blood retrieval is required to run a blood test?

It might be better to consider the sampling technology, economic and logistical issues with this question as well as the tech behind the tests.

First, some tests still will want a few milliliters of blood - e.g. cell counts for specific cell types.  Then there is the need to create and stock many different kinds of sample collection devices and train the collection centers to use them effectively- the industry won't be wanting to completely retool whenever the volume requirement for the assays changes.

Mainly, since the expense of collecting and shipping a few milliliters of blood is pretty much identical to doing so with a few microliters of blood, what has happened is that the tubes are used to do multiple assays with excess included in case an assay has to be redone.

Probably all this blood currently collected is not necessary at all.   I expect that the cost of changing all the blood collection systems and protocols is not worth the cost of collecting the exact minimum amount of blood needed.  The benefit to the patient or the lab between collecting 3-5 ml of blood and collecting 50 microliters of blood to be shipped off for lab analysis is probably close to zero.

Having more blood than you need does not hurt the lab either should they need to repeat the assay or when you need to use the sample for more than one different test.


Is ATP produced in a different manner during glycolysis from that generated by the Krebs Tricarboxylic Acid Cycle?

The ATP in glycolysis is produced directly in certain reactions of the type:

  X-PO32– + ADP → Y + ATP

in a process is called substrate-level phosphorylation.

A key preceding reaction in the pathway is the one catalysed by glyceraldehyde 3-phosphate dehydrogenase, in which free orthophosphate is incorporated into a sugar phosphate in a reaction of the type:

  Z + PO43– → X-PO32–

(I have used X, Y and Z because other changes occur in the structures.)

This is totally different from the oxidative phosphorylation that occurs in the mitochondrion. In both cases the (free) energy driving the generation of ATP comes from oxidation of sugars involving cofactors such as NAD+ to NADH. In oxidative phosphorylation the reoxidation of NADH in the membrane (ultimately by molecular oxygen) is used to set up a proton gradient, which can then be used to drive the ATP-synthase. In substrate-level phosphorylation the chemistry of the intermediates is manipulated so that particular reactions involve sufficient free energy change to drive the conversion of ADP to ATP directly. (The anaerobic reoxidation of the NADH does not produce ATP in this latter case.)

You should read a text-book of biochemistry for the details, which are too extensive to present here. Berg et al. Section 16.1 covers this well, and is available on-line.


Why does dehydration lead to low blood pressure

The blood pressure is the  exertion of force upon the blood vessels by the blood fluids. Thus having less fluids will results in decreased pressure.


Is it harmful for someone to consume things full of bacteria if they don't get physically sick from the bacteria at all?

It really depends on what you consume, how much of it you consume, and the state of your immune system. Let me give you some examples. Yogourt is full of bacteria, and yet we can eat it without issue. The bacteria likely don't survive digestion, but if they do, they will quite happily live in our intestines contributing to the already existing population of good bacteria.

Streptococcus is a genus of bacteria that contains some species that live all over us. They are on our skin, in our upper respiratory tract and intestine. If the species, S. pneumoniae makes it into our lungs, this can cause a bacterial pneumonia. There are likely few bacteria making it into our lungs on a regular basis, and normally our immune system can fight this off without concern. If we some how become immune depressed or compromised (for a number of medical reasons) then that's when we become symptomatic and ill.

On a more extreme side, if we have a bacteremia it is called a bacteremia. There are benign cases of this every time your brush your teeth and bacteria are able to enter tiny cuts in your gums from the brushing action. A healthy person fights this off. If a bacteremia is left unchecked, because of a lack of immune response or trauma, this can develop into a sepetcemia, a toxic infection of the blood. This can be very life threatening and is quite serious.

In general, we always have bacteria all over our hands which we likely transmit to our food or otherwise ingest. This is normally not a problem, but there is an appreciable risk of getting some kinds of viral or bacterial infection (eg, strep throat or a cold). Washing with soap (and to a lesser degree, using hand sanitizers) minimizes this risk.


Why do large neurotransmitters travel faster down the axon?

I presume you are referring to fast versus slow axoplasmic transport.

I presume by "small neurotransmitters," you are referring to "small molecule" neurotransmitters like GABA, glutamate, acetylcholine, and the catecholamines like dopamine.

For the "large" neurotransmitters, I assume you are referring to peptides.

(for a quick reference on these two categories you can see this book blurb)

Although local protein synthesis is possible outside the soma, particularly in dendrites, and there is even evidence for protein synthesis in axons, including neurotransmitter peptides, most protein synthesis still seems to occur in the vicinity of the nucleus, at the soma. Synthesis anywhere else means you need to transport the mRNAs and translation machinery instead, since the mRNA needs to be made at the nucleus. Even the "large" neurotransmitters, which are peptides, need to be synthesized just like bigger proteins.

Back to axoplasmic transport... There are two main mechanisms for moving things down the axon. The faster version of this transport is really for the transport of vesicles. To transport a neurotransmitter peptide in this fashion, you fill a vesicle full of the peptide and send it on its way along the microtubules via kinesin and dynein motors.

Larger, non-membrane bound proteins, however, are often not transported in vesicles, but by the slower transport mechanism. Note that this transport is still pretty fast, way faster than simple diffusion, it just isn't as fast as the "fast" transport. The exact mechanisms of slow transport are still an active area of research and not fully understood.

To get back to your question, "is there a specific reason?" The reason isn't so much about the speed, but about the mechanism of transport. Small peptides and membrane-bound proteins move in vesicles via fast transport. Large proteins not bound in membranes move via slow transport. The enzymes that synthesize the small neurotransmitters fall into this latter category. Importantly, although the neurotransmitters may be small, the enzymes themselves can be big, at least certainly bigger than the small peptides that are equivalent to the "large" neurotransmitters.


How can sequence analysis establish whether a genomic sequence is a functional gene or a pseudogene?

There is no good single answer genes which long have been though to be pseudogenes may have function in a very narrow set of cells.

That being said, some of the best indicators are; destruction of the ORF, accumulation of C->T and G->A mutations (methylation/deamination in mammals).

Expression is probably not a good indicator, because once you start including long non-coding RNA, pseudogenes may be transcribed, but may not have a protein-encoding function (if any).

You can also measure loss of introns and a poly-A tail in the DNA sequence which is consistent with a retro-pseudogene, but that doesn't mean that the 'pseudogene' doesn't have it's own function.

Overall, evolutionary conservation is the fastest and most reliable indicator, but ultimately genetic knock-out would be required.

If you have more information about the pseudogene, there may be other useful information which could help distinguish the two.


You are quite right: it's Loranthus europaeus. Vienna was the prime example in our botany lectures where to see that plant without a fuzz.

c/p from the Flora of Vienna:
"Auf Eichen, vorzüglich auf Quercus pedunculata und Qu. sessiliflora, selten. Im Eichenwalde von Schönbrunn, auf dem Gallizin, hinter Neuwaldeck, hin und wieder; viel häufiger auf dem Bisamberge {A}. ... auf den grössern Donau-Inseln z. B. ... in der Lobau {C}."

"Häufigkeit des Vorkommens: häufig bis sehr häufig"

(Confused about the contradicting "rare" and "frequent to very frequent" statements, but anyway.)

Here are some more pictures.


How do ion channels transport only specific ions?

I am restricting the answer to only $Na^+$ and $K^+$ channels, assuming similar mechanism for other channels. In these 2 channels, such high level of specificity is achieved because of two main differences between $Na^+$ and $K^+$:

difference in size of $Na^+$ and $K^+$ ions.
difference in chemical properties of $Na^+$ and $K^+$ ions.

Lets discuss these points one-by-one:

Difference in ionic size: the ionic size of $Na^+$ ion is 0.96$\overset{\circ}{A}$ while that of $K^+$ ion is 1.33$\overset{\circ}{A}$. How this size difference of 0.38$\overset {\circ}{A} $ is exploited by channels will be discussed in later section.

source

Difference in chemical properties: the property we are concerned here with is hydration enthalpy. $Na^+$ ion has hydration enthalpy than $K^+$ ion, meaning $Na^+$ has higher tendency to remain bounded by water molecules than $K^+$. How this enthalpy difference is exploited by channels will be discussed in next section.

source

I will discuss different methods used by these channels one at a time.

$Na^+$ channels: $Na^+$ channels are less studied than $K^+$ channels, but some of the mechanisms used are known and explained below:

$Na^+$ ions pass through channels in partially hydrated form1, and these channels have 2 rings of selection filters2 in mammals.
The first (outer) ring contains amino acids EEDD (or EEMD)3 while second (inner) ring contains amino acids DEKA4. How these amino acids bind to specifically $Na^+$ ions is not completely known yet, but it is hypothesized that the inner ring, being more conserved, is more important as a filter than the outer ring. Also, it has been shown that by changing the amino acid K in DEKA makes the channel more permeable to $K^+$ and $Ca^{2+}$ ions, and by changing sequence from DEKA to EEEE makes the channel more selective towards $Ca^{2+}$ ions5.
$K^+$ ion, in hydrated form, cannot pass through inner filter due to larger size and presence of negatively charged D and E of DEKA, whereas $Na^+$ easily passes through due to smaller size and higher hydration enthalpy6.

Negative charge in channel is such that it mimics the hydration shell (regular octahedron) of $Na^+$ from side

source (1)           source (2)

$K^+$ channels: $K^+$ channels have been studied more intensively, so their mechanism is much more understood. The main points to ponder are:

The filter of $K^+$ channel contains amino acids TVGYG 7 and is present in the narrowest region of the channel.
To pass this channel, $K^+$ ion needs to be completely dehydrated i.e. without any water molecule bound to it. The amino acids in the filter replace water molecules with polar oxygen atoms. On the other hand, $Na^+$ cannot get rid of water molecules so easily and hence, its passage through the channel is thermodynamically unfavorable8, partly also because dehydrated $Na^+$ is so small that it cannot even bind with all of the polar oxygen atoms of amino acids.
Here nature shows some clever techniques. The amino acids, TVGYG, having their electronegative carbonyl oxygen atoms aligned toward the center of the filter pore, form a square anti-prism similar to a water-solvating shell around each potassium binding site. The distance between the carbonyl oxygens and potassium ions in the binding sites of the selectivity filter is the same as between water oxygens in the first hydration shell and a potassium ion in water solution, providing an energetically-favorable route for de-solvation of the ions9.

This is how the passage of a $K^+$ ion through $K^+$ channel looks like:
source

The carbonyl oxygens mimic this configuration as this is how a $K^+$ looks in hydrated form (square antiprism):source

P.S. as more deep studies are made, more mechanisms may be revealed. Also, above mentioned points are just theories and not conclusive proofs.

References:

Hille, B. The permeability of the sodium channel to organic cations in myelinated nerve. J. Gen. Physiol. 58, 599–619 (1971).
Guy HR, Seetharamulu P. Molecular-Model of the Action-Potential Sodium-Channel. Proc Natl Acad Sci USA. 1986;83:508–512.
McNulty, M. M., Edgerton, G. B., Shah, R. D., Hanck, D. A., Fozzard, H. A. and Lipkind, G. M. (2007), Charge at the lidocaine binding site residue Phe-1759 affects permeation in human cardiac voltage-gated sodium channels. The Journal of Physiology, 581: 741–755. doi:10.1113/jphysiol.2007.130161
Favre I., Moczydlowski E. & Schild L. On the structural basis for ionic selectivity among Na+, K+, and Ca2+ in the voltage-gated sodium channel. Biophys J 71, 3110–3125 (1996).
Calcium channel characteristics conferred on the sodium channel by single mutations.
Heinemann SH, Terlau H, Stühmer W, Imoto K, Numa S 1992 Apr 2;356(6368):441-3.
Mechanism of Ion Permeation and Selectivity in a Voltage Gated Sodium Channel. Ben Corry and Michael Thomas
Chemistry of ion coordination and hydration revealed by a $K^+$ channel–Fab complex at 2.0 Å resolution, Yufeng Zhou, João H. Morais-Cabral, Amelia Kaufman & Roderick MacKinnon
Mechanism of potassium channel selectivity revealed by $Na^+$ and $Li^+$ binding sites within the KcsA pore.
Ameer N. Thompson, Ilsoo Kim, Timothy D. Panosian, Tina M. Iverson, Toby W. Allen, and Crina M. Nimigean
A comparison between two prokaryotic potassium channels (KirBac1.1 and KcsA) in a molecular dynamics (MD) simulation study; Mikko Hellgrena, Lars Sandberg, Olle Edholm, 1 March 2006