This is a female of yet another scale insect (Coccoidea). We have discussed one recently.

I guess we can identify this one rather precisely as Ceroplastes sinensis or its close relative. Species of this group are of South American origin, but Ceroplastes sinensis has today an extremely broad distribution. So, if you found this plant ("Variegata" is a specific epithet, by the way: it would be of some help if you provided the generic name as well) in Europe or Asia it's likely sinensis itself.


What constitutes FDA's First in Class designation for New Molecular Entities?

"First-in-class drugs are ones that use a new and unique mechanism of action for treating a medical condition. These products are often referred to as innovative and cited as offering new treatment options for patients."
Lanthier, M. et al. (2013) "An improved approach to measuring drug innovation finds steady rates of first-in-class pharmaceuticals, 1987-2011." J.Health Aff. (Millwood) 32:1433-9;
Pharmaceutical Research and Manufacturers of America. 2015b. Innovative Oncology Medicines Have Led to Impressive Gains in Patient Survivorship. Retrieved August 26, 2015. <www.phrma.org/innovative-oncology-medicines-have-led-to-impressive-gains-in-survivorship>."
From: Lexchin, J. (2016) "How Safe and Innovative Are First-in-Class Drugs Approved by Health Canada: A Cohort Study" Healthc. Policy 12:65-7.


This is a wasp, (see that nice slim "wasp waist" it's got?), which means taxonomically that it is in the order Hymenoptera (which it shares with bees and ants).

Within Hymenoptera, wasps are diverse and often difficult to ID, but it's possible that this is a Braconid or Ichneumon (family Braconidae or Ichneumonidae). If you take a good closeup of its wing veins, chances are an expert (not me) could ID it.


What is the mechanism through which fractals arise in plants and animals?

because fractals are emergent structures created by simple rules, as are many biological structures. The same kind of simple recursive signals that lead to fractals are simple enough to be stumbled on by biological evolution and are effective ways to deal with the scaling problems created by the square cube law.
https://www.complexityexplorer.org/system/explore/model_series/pdf_files/000/000/008/original/Biological_Scaling_Series_.pdf?1554498961
https://www.jstor.org/stable/2898653?seq=1


Are bacterial RNA polymerases distributed evenly throughout the cell or localized?

In E. coli most RNA polymerase molecules are bound to DNA, and those that aren't are within easy reach of the DNA.

According to Larry Moran

  A typical E. coli cell contains about 5000 molecules of RNA polymerase. When the cells are growing rapidly, 2500 molecules will be bound to genes in transcription complexes. Another 1250 will be in initiation complexes of various sorts and most of the remaining RNA polymerase molecules (1200) will be bound to DNA non-specifically. Only a small number (~50) will be free in the cytoplasm.

The numbers that he quotes for number of molecules of polymerase and proportion that are engaged in transcription are in reasonable agreement with values available at Bionumbers. So it seems that most RNA polymerase molecules will be located in the nucleoid; any molecules that are free in the cytoplasm are within easy reach of finding a DNA binding site since a typical protein can diffuse across an entire E. coli cell in 10 ms. (Bionumbers)


Do we know a complete list of nutrients that humans must ingest to live?

For babies there is certainly a formula available for a complete menu for survival: formula*

Here are the nutrition facts from Nestlé's "Good Start":

Formula nutrition facts. source: Nestlé

Comparable lists are available for people that cannot eat normally (e.g. people in a comatose state) and are fed enteral or parenteral nutrition.

*. Remember though, breast is best :)


Why do mitochondria have a phospholipid bilayer?

I think the question is based on a false premise:

  Poster: Now, mitochondria are said to have been archaea, right?

  Me: Wrong, I’m afraid.

The closest bacterial relation of mitochondria is  Rickettsia, an alpha-Proteobacterium (see Lang et al. for a review). Rickettsia is a eubacterium, not an archaebacterium.

The confusion is probably due to misreading one of the two alternative theories of the origin of mitochondria. This is the theory that the host for the original mitochondrion was an archaebacterium (rather than a primitive nucleated eukaryote). In both theories this host aquired a eubacterium related to Rickettsia, which gave rise to the mitochondrion.


I was looking for the same thing and i found the answer in the anatomy of molluscs
you can clearly see that coelom is different from haemocoel and coelom is greatly reduced.
Haemocoel is a pseudocoelom it is a body cavity but not lined with mesoderm at all sides


What exactly is neuroplasticity, and can it be demonstrated with a simple experiment?

Your question is basically a matter of defining brain plasticity or more broader, neuroplasticity. According to a well-cited paper in Brain (Cramer et al., 2011) neuroplasticity is defined as:

  [...] the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections.

Hence, the term can be, and indeed is used very broadly. A more elaborate definition in the same article should answer you question as to whether learning and habituation can be considered to be associated with neuroplasticity:

  Neuroplasticity can be broadly defined as the ability of the nervous system to respond to intrinsic and extrinsic stimuli by reorganizing its structure, function and connections; can be described at many levels, from molecular to cellular to systems to behaviour; and can occur during development, in response to the environment, in support of learning, in response to disease, or in relation to therapy. Such plasticity can be viewed as adaptive when associated
  with a gain in function [...] or as maladaptive when associated with negative consequences [...]

Your vision example, however, is more appropriately referred to as adaptation. Although it strictly spoken falls under the above definition of plasticity (...reorganizing its... function,  color adaptation is (at least in my opinion) too short-lived (minutes) to be associated with plasticity.

Lastly, as to experiments - Although learning a chunk of material from a textbook as a homework assignment is definitely related to plasticity, it cannot be seen as proof; it is the result of neuroplasticity. Experiments showing plasticity can and have been done with imaging (most notably fMRI) or with electrophysiological approaches (patch clamp studies showing long-term potentiation reflecting learning). These techniques cannot be applied outside the laboratory, as they require advanced and pricey equipment, careful experimental design, and not least importantly ethical clearance.

Reference
 - Cramer et al., Brain 2011;134:1591–609

Further reading
 - Color adaptation: What is the science behind the   inaccurate perception of colors?


Does the human body metabolize what it smells, even in trace amounts?

Olfaction is the result of the neuronal impulse of ligand / receptor binding. To smell something requires 1) Specificity between the receptor and the ligand, 2) Concentration of the ligand molecule, and 3)The receptors that are on the surface of neurons in the olfactory bulb.

As for metabolize, then you need to be much more specific in defining what you are considering metabolism. Is the molecule broken down further; does it pass into the cells directly; does it need to be the unaltered molecule to qualify as metabolizing the molecule that you sensed as a smell.

The majority of our mucus in our airways is moved to the digestive tract as the result of ciliated epithelial cells "sweeping" the mucus and everything trapped in it to our esophagus, where it goes into the stomach and is digested. It is hard to say whether or not the molecules that you detect as smell are reactive, and if they are, whether or not they would chemically react with something else before it got to your stomach.

Also the volatile chemicals which you sense as an odor, aren't necessarily what would constitute the substance that they emanated from. So I would probably argue against your conjecture that someone who decides to be vegetarian or who has a peanut allergy is metabolizing something just because they inhaled it. It is likely the proteins in a peanut that cause an allergy, and that is not what you are inhaling, and as for the vegetarian, I think the justification is that it would be the protein that constitutes the consumption of a meat and not the molecules that come from the cooked or uncooked tissue.

If you want to broaden what you are calling metabolize, then you would only need to look at inhaled medicines such as corticosteroids or compounds to bronchodilate, to make a case for the fact that you are metabolizing what you inhale.


Why does freshly cut grass smell like a watermelon?

cis-3-hexenal is probably the main reason.  It is one of the main chemicals in fresh-cut grass smell (lots of references besides wiki if you google it).  This fairly comprehensive paper on watermelon odorants also says that they find a lot of cis-3-hexenal in fresh cut watermelon.  See tables 3.1, 3.2 and 3.3.


Finally I think I can answer my own question. Having spent the summer outside in full sun, the tree has produced flowers that helped us identify it.

It appears to be Cordia sebestena


Are there any disadvantages to HRP conjugated PRIMARY antibodies

You can compare directly coupled antibodies to the classical indirect primary-secondary systems:

Directly coupled antibodies

Advantages:

quicker workflow as only one antibody is used
eliminates the chance of a cross-reacting secondary antibody (possibly less background)
possibility to use differently labelled antibodies on the same blot

Disadvantages:

lower sensitivity because the signal is not amplified
only few labels are available
directly labelled primary antibodies tend to be expensive and you need relatively high amounts of them
the labelling can damage or reduce the immunoreactivity of the
antibody

Indirect Primary-Secondary Antibody systems

Advantages:

the secondary antibody amplifies the signal (which is especially
interesting for weakly expressed proteins)
differently labelled secondary antibodies can be used on the same
primary
primary antibodies from different species can be used simultaneously
one secondary antibody can be used with different primary antibodies
(for example for the protein of interest and the loading control)
the labelling reaction does not affect the primary antibody

Disadvantages:

cross-reactivity of the secondary antibody can lead to non-specific
bands
the method takes longer, as more steps in the process are necessary

For me the most important point is the higher sensitivity of the indirect method, for comparision see these images (from Life technologies):


How does membrane potential vary between intraceullar membranes and the cellular membrane?

Yes, various intracellular membranes do have potential differences, but as you can imagine they are more difficult to measure experimentally, so in general data on this is scarce.

Summary

Mitochondrial membrane: 150mV-180mV with negativity on the matrix side. Seth et al 2011
Endoplasmic reticulum membrane: 75-95mV with negativity in the ER. Qin et al 2011, Worley et al 1994
Golgi: No notable membrane potential. Schapiro & Grinstein 2000
Lysosomal: 20mV with more negativity on the cytosolic side. Koivusalo et al 2011

Discussion

The mitochondrial membrane potential is probably the best studied case. This is the potential difference over the inner mitochondrial membrane, between the mitochondrial matrix and the intermembrane space; it is about 150mV (more negative on the matrix side). There is also a potential difference between the mitochondrial cristae (folds of the inner membrane) and the matrix which is used to drive ATP synthesis; it is probably larger than 150mV, but this is still poorly understood I think. The outer membrane is permeable (has pores) so there should be no potential difference between the intermembrane space and the cytosol.

For the endoplasmic reticulum (ER), there is little data available I think, but there are some estimates based on measurements of ion transport, which gives a value of about 75 to 95 mV (more negative inside the ER). Probably this depends a lot on the situation, as the ER is involved in regulating ion homeostasis (notably Ca2+).

For the Golgi apparatus, this study found that no potential difference vs. the cytosol, based on the movements on H+ and counterions.

Lysosomal membrane potential has been measured directly, giving values of about 20mV (more positive inside).

For the nucleus I don't know of any data, but I would assume there is no potential difference here, given that the nuclear membrane has large pores.


Double stranded nucleic acids are more 'durable' than single stranded nucleic acids?

I'm interpreting "durability" as the DNA's resistance to physical stress, such as shearing. The Bustamante lab at UC Berkeley does a lot of very cool single-molecule biophysics looking at forces involved in protein-protein interactions and protein-DNA interactions. This Bustamante et al. review paper, Single-molecule studies of DNA mechanics includes a look at the force required to break ssDNA and dsDNA:

  Single molecules of dsDNA were broken
  with a receding water meniscus [26] at forces estimated
  to be 960 pN (correcting Young’s modulus doubles the
  published scission force of 480 pN). Short dsDNA molecules  pulled  with  an  AFM  tip  [27]  sustained  forces
  over 1700 pN.

pN = picoNewton
AFM = atomic force microscopy

dsDNA is more resistant to stretching/shearing forces because the double helix arrangement is "springy". I recommend giving the paper a read for more info. Very cool stuff.


Are there any primary structure sequences that strongly suggest b-sheet or alpha helix?

Yes, there are certain amino acid sequences that tend to form alpha-helices, and others that prefer to form beta-sheets. There is no perfect correspondence between sequence and structure, but there is a statistical relation where presence of certain amino acids in particular sequences makes one conformation or the other more likely. For example, alanine, glutamate, leucine and methionine tends to be present in alpha helices.

This topic has been studied for 50 years or so, and there are many methods available for predicting structural features from an amino acid sequence. See this list of available software, and this article about protein structure prediction in general.

See this table from another answer on this site which shows which individual amino acid prefers which secondary structure (higher value shows higher preference):


Calcium levels and nerve hyperexcitation

From Uptodate on Clinical Manifestations of Hypocalcemia:

  Acute hypocalcemia directly increases peripheral neuromuscular irritability [ 1 ]. As measured electromyographically, tetany consists of repetitive high-frequency discharges after a single stimulus. Hyperexcitability of peripheral neurons is probably the most important pathophysiologic effect of hypocalcemia, but hyperexcitability occurs at all levels of the nervous system, including motor end-plates, the spinal reflexes, and the central nervous system.

Guyton and Hall Textbook of Physiology:

  The concentration of
  calcium ions in the extracellular fluid also has a profound
  effect on the voltage level at which the sodium
  channels become activated. When there is a deficit of
  calcium ions, the sodium channels become activated
  (opened) by very little increase of the membrane potential
  from its normal, very negative level. Therefore, the
  nerve fiber becomes highly excitable, sometimes discharging
  repetitively without provocation rather than
  remaining in the resting state. In fact, the calcium ion
  concentration needs to fall only 50 per cent below
  normal before spontaneous discharge occurs in some
  peripheral nerves, often causing muscle “tetany.”This is
  sometimes lethal because of tetanic contraction of the
  respiratory muscles.

  The probable way in which calcium ions affect the
  sodium channels is as follows:These ions appear to bind
  to the exterior surfaces of the sodium channel protein
  molecule. The positive charges of these calcium ions
  in turn alter the electrical state of the channel protein
  itself, in this way altering the voltage level required to
  open the sodium gate.


Metabolism ≈ Anabolism + catabolism

Metabolism is the set of all chemical reactions happening inside a living body. These reactions can either breaks down big molecules and build up big molecules. The set of reactions the breaks down big molecules is called catabolism. The set of reactions that build up big molecules is called anabolism.

Energy

Generally speaking, anabolism cost energy and catabolism yield energy. The molecule that is directly used to transfer this energy is Adenosine triphosphate (ATP).

Any energy transfer is coupled with some loss of energy from the system (see Energy conversion efficiency).

Entropy

For any chemical reactions, there is always an overall increase of entropy. As a consequence, a living organism increases the entropy in its surrounding. In other words, it breaks more than it builds.

Your question

  does life make or break?

Life does both! But on average, it mainly breaks things up (just like any other chemical reaction).

Want to learn more?

The concepts of energy and entropy are studied in physics and chemistry but not so much in biology. I cannot really give you a good source of information.

Khan Academy offers a very good introductory course on metabolism (here), you should have a look!


qPCR: do both primers have to contain a GC-clamp in order to be effective?

You can have GC-clamps (3' terminal G/C) in both primers; this may overall improve the PCR efficiency. However you should take care not to put too many G/Cs. This may lead to stabilization of primer pairs, leading to formation of primer-dimers. Also see this post: When designing primers how important is the GC clamp?

GC-clamps are not always essential and you should look at other parameters too.


Why would glucocorticoids promote glycogenesis and not glycogenolysis?

Glucocorticoids have a number of physiologic effects on glucose metabolism, inflammation/stress response, bone metabolism, etc. In general they are called glucocorticoids because they were originally found to be associated with increased blood glucose concentrations. Simply put, glucocorticoids antagonize the actions of insulin and create a state of insulin resistance, as well as increasing the expression of enzymes involved in glucose metabolism. They have a number of effects on all sorts of tissues and biological processes.

With regard to your question specifically, it makes sense that glucocorticoids stimulate glycogen synthesis, because it will allow the body to store more glucose as glycogen and increase the body's capacity for liver glucose production (i.e. glycogenolysis). Remember, at the same time glycogen synthesis is being increased, the glucocorticoids are inducing a peripheral insulin resistance that antagonizes insulin action in skeletal muscle and fat that also leads to increasing glucose concentrations in the blood. Moreover, free fatty acid are released from adipose tissue to be carried via the circulation to the liver so they can be oxidized to produce ATP for gluconeogenesis.

There is an excellent chapter that describes the effects of glucocorticoids on glucose metabolism in the major metabolically-active tissues (e.g. liver, white adipose tissue, skeletal muscle) by Kuo et al from Vol 872 of Advances in Experimental Medicine and Biology (pages 99-126). The book is not open access so I can't paste a picture of any of the figures, but they essentially show what I describe above. Here is another link to a very nice review article in the Journal of Endocrinology that has some great figures showing fuel redistribution in response to glucocorticoids as well.


What is the advantage of the inverted image on the retina?

There may be no advantage of the inverted image on the retina. But there is an advantage with the lens that refractes the image inverted.

Our eye lens is of convex in nature. Now lets see what is the advantage of convex lens being our eye lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php

The light from the object, when reaches the convex lens it gets refracted and gets "converged" and is a "real image" and also "diminished" but the problem is it makes the light inverted.

Now let us see what happens if our eye lens is a concave lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php

In this case, when the light from the object from a distance reaches the lens, the lens "diverges" the light, also it "enlarges" the image, but it produces an "erect" image but the major problem is that the image is "virtual".

We know how evolution works, it selects more advantageous option generally.

Case - 1: If the lens is convex, the only problem the eye has to handle is that the image is inverted.
Case - 2: But if the lens is concave, it should converge the diverged light, it should diminish it and it should also make it real.

If we take both cases into consideration, case - 1 seems to be easily handled, that's why we have inverted image falling in the retina. There maybe no other specific advantage associated with it.


An older answer that referred to the physiological feats of ancient humans, and why modern humans are wimps made me look up a couple of papers on running speeds a while ago. One of the examples used to support the statement that modern humans are "wimps" is a study of ancient fossilized footprints from Australia, which claim that the individuals making the footprints were running close to Olympic record times. The footprint studies (Webb, 2007) basically attempts to describe the humans that have created the footprint paths, and also tries to calculate the speeds they were running at. For one of the individuals (T8), the estimated running speed is 37 km/h (i.e. 10.3 m/s). The interpretation by Peter McAllister in his book Manthropology seems to be (I haven't read the book) that these barefoot individuals running on mud could easily have outrun current day sprinters, especially with training and on a rubber track (also see this huffintonpost article on the book). If the estimates in Webb (2007) are close to accurate, it would seem that modern top-trained athletes might not have reached the edge of what is humanly possible when it comes to top speeds.

There is also a biomechanical study on potential human running speeds (Weyand et al., 2010) that you will probably find interesting. This paper looks at factors such as gait, stance, force application etc, and includes empirically estimated values from 10 subjects to discuss the limits to human speed. They conclude that (natural) human speeds are likely to be limited to ~50 km/h (as reference: Bolt's top speed during his 9.58 WR was ~44 km/h).

  Consequently, human running speeds in excess of 50 km/h are likely to be limited to the
  realms of science fiction and, not inconceivably, gene doping.

They also look at different scenarios and e.g. point out how important limb length is for top speed:

  Second, limbs lengthened through evolution or perhaps prosthetically could
  substantially increase the top running speed attained at the minimum period of foot-ground force application. For example, a relatively small increase in leg length of 10 cm would
  increase contact lengths by 9 cm and the top speeds of the subjects tested here from 9.1 to 9.8 m/s.

In general, important factors for maximum speed in animals are ground  reaction force and ground contact time. An earlier study by Weyand et al. (2002) also show how faster human runners in general have shorter ground contact times compared to slower runners. As a sidenote, this seems to be in contrast to cheetahs, which have longer ground contact times than greyhounds, while still being much faster (Hudson et al. 2012 and popular summary).

View these as a couple of interesting examples and a starting point. This is not my area, and I do not know the literature well.


What is the mechanism responsible for the periodicity of hiccups?

Check out Van Der Pol (chaotic) oscillator. It can be used to model heart rhythms. If a stimulus is applied to the oscillator, it will return to the curved envelope discussed in the article.

However, if "pushed just right", the oscillator's current state will be pushed towards the very center of the loop, and it will stop oscillating. This is the mechanism by which a sudden blow to the chest can stop the heart.

Reading up on hiccups, their "almost regular" interval sounds similar to a chaotic oscillator. The abrupt stop may represent pushing the oscillator towards the middle of the limit cycle, from which it cannot recover, effectively stopping hiccups


How broad are the conclusions that one can make from a heterologous expression experiment?

GSK3 is interesting because as a kinase, it is itself regulated by its phosphorylation status (particularly by Akt in neurons). Therefore, more protein does not necessarily mean more activity. For example from E13.5 to E15.5 GSK3 levels do not change but activity steadily increases. Hence if you increase GSK3 levels in neurons, it may not mean that downstream effects would change substantially, so I think although promising the in vivo effects may be hard to deduce from this experiment. If you see similar effects in in vitro neurons, you can be a bit more confident of potentially seeing similar effects with in utero electroporation in vivo


The rate of CO2 production is normally set by the rate of metabolism and breathing rate is determined by the level of CO2 in the blood.  What you are suggesting is known as hyperventilation. Because blood CO2 plays an important role in maintaining the pH of the blood, hyperventilation can lead to a dangerous increase in blood pH, referred to as respiratory alkalosis.

Apparently one response to respiratory alkalosis is an increase in metabolic rate as the body tries to compensate for the increased rate of loss of CO2. However, respiratory alkalosis is dangerous so I don't think hyperventilation is a viable strategy for losing weight.


Why is beta actin commonly used as a control in Western blots?

β-actin belongs to a class of genes called housekeeping genes. Their proteins typically perform functions that are required across essentially all cell types (for example, β-actin is part of the cytoskeleton's microfilaments), and are supposed * to be not affected by experimental conditions. In Western blotting, they are run as a "loading control" to show that very similar amounts of protein were loaded in each lane. This is absolutely essential in some experimental systems where it may not be possible to always collect the exact same number of cells for each sample, such as when working with primary cells, tissue samples, or systems where you may be altering protein synthesis, cell size/number, or apoptosis.

There are many different loading controls to choose from, and some may be dictated by the cell/tissue type you are examining — for example, when working with stem cells, you may want to show that your experimental conditions didn't induce differentiation in the cells, so a pluripotency marker like Oct-4A or Sox2 may be chosen. In other cases, you may be examining fractionated lysates (a membrane preparation, just the nuclei, mitochondria, only the soluble fraction, etc.) and so may choose Na/K ATPase, Histone H3, COX IV, or GAPDH, respectively.

The choice of loading control can also be influenced by the size(s) of the protein(s) you are analyzing, as investigators frequently either strip Western blots and reprobe them with the loading control, or run two different species and detect with different colored secondary antibodies when performing fluorescent Westerns. In either case, you want your loading control to be a different size than your original targets.

Finally, all of this is assuming that the researcher has already attempted to load equal amounts of total protein per lane by using any one of a variety of methods for quantitating protein concentration. These include Bradford, Lowry, and BCA type assays, which may or may not be detergent compatible, staining the membrane after transfer with dyes such as Ponceau S, SYPRO Ruby, or India ink, or staining the gel with Coomassie or other proprietary Western-compatible stains.

*In reality, some scientists are becoming more and more aware that many experiments actually do affect a number of "housekeeping" genes, but when most see variations by, for example, Western blot or qPCR, they often choose a different loading control to use.


How the conjunctivitis virus spread just by seeing a person's eye who is infected

You can't catch conjunctivitis by looking at someone, but you can spread it around by touching your eye and touching something else, which then can pass the virus to someone else (viral conjunctivitis can be highly contagious). There are no hard facts, but one estimate is that people touch their faces an average of 3.6 times per hour, more if your eyes are itchy. Wearing sunglasses can not only help the possibly increased sensitivity of eyes with conjunctivitis, but they may also cut down on the number of times you touch your eye (thus spreading the virus).

There is no evidence to support that our eye get watery when we see the eyes of an infected person.

Conjunctivitis (Pink Eye) - CDC
Stop Touching Yourself, Flu Researchers Say


What does it mean to have square brackets around a genus name?

The NCBI Taxonomy staff places square brackets around the genus for some species (examples: [Bacillus] aminovorans, [Candida] auris) to indicate that they are misclassified*, meaning placed incorrectly in a higher taxonomic rank.

References:

https://support.nlm.nih.gov/knowledgebase/article/KA-03379/en-us


Are nucleic acids found in cell membranes?

Nucleic acids are not structural components of cell membranes (ribosomes and nucleus are the main places where they are found).

However, being open system, cell exchanges chemicals with its surrounding and cellular membrane can transport nucleic acids as well. This is why these acids can potentially be detected in the cell membranes.

If you have the exact question expression it can help with more precise answer.


Why does it hurt when water touches cuts?

Water changes the local ionic concentrations and therefore induces an electric
signal at exposed neuron membranes.Oil is used to prevent entrance of water to the cut because it is hydrophobic i.e. repels water but attaches to the tissue.
Gravity plays no role here.


Synthesis of an additional DNA in Pachytene and Zygotene

About 0.3% of total DNA complement is synthesized during those 2 stages as a measure of replication repair mechanism.

Reference:

http://www.ncbi.nlm.nih.gov/pubmed/3731943

http://www.nature.com/nature/journal/v219/n5153/abs/219489a0.html


Do blood cells immediately die after leaving the body?

No. If they did, blood transfusions wouldn't be possible (or they would require some sort of direct body-to-body system).

Red cells collected can be stored under refrigeration for over a month. See for example the description of what happens to donated blood from the Red Cross. Platelets don't last quite as long, but they also survive for some time in the right conditions. Of course, some cells die during storage, but there is no instantaneous die-off once cells leave the body.


Why don't we see life form again and over again?

The first life was probably so fragile and simple we would likely not even recognise it if it did appear. We don't know exactly how, or where, life first appeared but nearly all theories suggest simple collections of enzymes in protected environments that slowly gather the mechanisms needed for free-living life over time.

This works in the ancient world because there is no competition so even the simplest and most inefficient replicator is able to reproduce, spread, and advance. Today, any new life would have to compete with existing life which has had billions of years to evolve into highly efficient forms. A new abiogenesis event would simply pass unnoticed, a brief flicker quickly snuffed out by modern life.


Do people need nitrogen from air for health?

No. This is well established!

Can people breath totally nitrogen-free atmosphere for a long time?

Yes. Also well established!

I know, nitrogen is essential for life, and in big quantities, but
maybe people can take it entirely from food, from proteins, etc?

As expounded on in the comments by AliceD, nitrogen gas (N2) is entirely taken in by humans from their diet, since atmospheric N2 is pretty inert. It is also not necessary for gas exchange to take place in the lungs.
Some extra questions as an addendum:

Can one substitute N2 in atmospheric air with another gas, and sustain human life?

Yes. All side effects would be attributable to the effects of the substituting gas (e.g. it may be heavier or lighter or equally or more reactive than N2).

Can 100% O2 sustain human life?

No, and such a case has never been recorded. Oxygen toxicity following hyperoxia is very dangerous. Ironically, too much oxygen damages lung tissue and epithelial membranes via oxidation and render the lungs unable to exchange gases correctly; and so death by suffocation follows in such extreme cases such as with 100% O2.


How do you see the stage of the second meiotic arrest in oogenesis in the given video?

I seem to understand the thing now.

The video is utterly simplified for animal cell meiosis I and II.
In oogenesis, you get after every anaphase one cell with very little cytoplasm, polar body, and another cell with much cytoplasm. In the video, the amount of cytoplasm is equal so the thing is idealized.

The video is better to explain male gametogenesis: spermatogenesis, since the amount of cytoplasm does not differ after each anaphase.

The video is too going too fast to teach you oogenesis, since in reality the things are arrested rather long time. The second meiotic arrest in oogenesis can lasts 12 - 50 years starting after puberty. The rupturing secondary oocytes lasts then again less in the second meiotic arrest of oogenesis, since they start to develop into ovum after the monthly release.


Why shouldn't there be any air between lungs and ribcage?

Pleural fluid is secreted by the pleural membrane and therefore it is not made up of living cells. Usually a trauma to the chest, such as a stab wound, would allow air to enter the thoracic cavity, called pneumothorax.

The problem caused by air building up in the thoracic cavity is due to the movement of the diaphragm and intercostal muscles cannot create a low pressure relative to that of within the lungs pressure, and air rushes into the thoracic cavity instead of the lung to equalizes the pressure. Note that oxygen that enters the thoracic cavity is not usable by the individual, and only the oxygen that enters the lung can. Also, air in the thoracic cavity is not connected to the nose or mouth, or else only little air would enter the lung when aspirating.


Difference between taking tissue of cancer from secondary place or primary place

I would disagree a bit with the previous answer. There are absolutely differences between the metastasis and the primary tumor. One result of this is that people very rarely die of primary tumors, but rather from the metastases of those tumors. The primary tumors will be quite heterogeneous and contain largely cells that have not undergone steps necessary for migration like epithelial to mesenchymal transition. After cells have metastasized they will be separate from the original primary tumor, and contain unique genomes. Because this is the more 'progressed' group of cancer cells, these are often the cells that need to be targeted. So, determination of the proper treatment strategy should be done on the metastasized cells.


What of Gould's contributions to evolutionary biology are still accepted in the mainstream?

His main contribution was making biologist consider that population size affects how fast selection changes a population, but he tended to imply this was some form of categorical difference and not a spectrum. But this was greatly overblown my media into some sort of insistence that they could not be the same. large population slow change and small population fast change are both points on the same spectrum. Nobody was right becasue both sides were not really saying the other could not occur they just emphasised their own area. Gould main problem was the idea of stasis in punctuated equilibrium that large populations somehow did not keep evolving this was a point he contested without ever really being able to provide evidence for. His own evidence often fit both interpretations. Since then it has been pretty thoroughly refuted by genetic studies, better resolution*, and modeling of stabilizing selection, all populations change, large ones just change slower, often with less direction. Gould himself later accepted this, but insisted on keeping the terms punctuated equilibrium and more oddly "stasis" for these periods of reduced change, this led to more misunderstanding especially with the public and media. Many scientist felt it was a sign of being unwilling to truly accept the evidence.

He also contributed a lot to our understanding of evolutionary development and how evolutionary baggage effects future adaptations. We often forget this but without his constant pushed of the importance of constraints and development both would probably be much more poorly understood. Panadaptationism was probably given more service by than many ever though it deserved, but Gould was right that that are far more aspects to selection than many considered. It just was not as popular an idea as his attention implied, but that is part of science harping on bad ideas is not really bad in science, it just starts to get old when the idea never had a lot of traction. It is however understandable considering Gould's own focus.

He has a serious problem(probably not unfounded) with sociobiology but probably pushed too far by implying searching evolutionary history for influence of our behavior was pointless. As much good as he did for understanding physical adaptations he seemed to have a blind spot when it came to behavioral adaptations. He mellowed about this in later years but still seemed to resist it. Sociobiology tended to be over applied, often without evidence, it was easily the worst offender with panadaptationism. Gould was right to push back against speculation but he often treated all behavioral science the same regardless of rigor.

Dennit who primarily researched evolutionary aspects of human behavior and publicly speculated a lot, of course ended up as a stanch opponent. But then as the more rigorous evolutionary psychology arose from sociobiology Gould seemed unable to see the difference which quickly led other to stand against him and probably did more than anything to produce his negative image. I know it is the thing that put me off his writing.

The other issue that I, as well as many other paleontologists, had with him was his resistance to the application cladistics and other computer based analysis. Both extremely important tools in understanding evolution, especially once to could be applied to genetic material. He always seemed to treat it as not real science, which always struck me as weird considering how much he emphasised rigorous investigation. He struck me a brilliant mind falling behind the technological curve and becoming disapproving of it. To myself as a young scientist he seemed to resist anything new regardless of rigor despite his own emphasis on rigor.

In short he was hard working scientist. He improved our knowledge in some areas while being unhelpful in others. He was a scientist who got a huge amount of media attention, which few scientist can do without sooner or later showing normal human flaws. Now take all this with a grain of salt, this is all my own personal impressions from observation of his work in paleontology along with reading his (and just about every other) book about evolution. I have not read many of his paper outside of paleontology. I say this becasue speculating on the beliefs and motivations of the dead has always struck me as dishonest especially without laying your cards on the table.

I wanted to give special mention to resolution and darwin finches, darwin finches undergo different selection every year depending on rainfall, large and small (specialized) beaks during wet years and medium (generalist) beaks during dry years, this changes every breading season with the amount of rainfall on any large scale this would appear to be no change as they tend ot average out, but with better resolution we can see many many small directional selection pressures adding up to no net change on a large scale.


Brain response frequencies while sleeping

Sleep as you may know is divided into 2 broad categories which are the REM (Rapid Eye movement) and NREM (non rapid eye movement). NREM is further divided into 3 stages (reference). You never know which stage of sleep you are in when you are subjected to a particular frequency of sound. Your response to different sounds differ in your different sleep cycles.

The present 3 stages in NREM sleep is an update by The American Academy of Sleep Medicine (AASM) in 2007 (reference).The original 4 stages in the Rechtschaffen and Kales (R&K) standardization of 1968 (reference) has been used to explain the effect of disturbances in different sleep cycles

  Stage 1 is still the phase of sleep from which it is easiest to wake
  someone up.

  People in Stage 2 sleep are unlikely to react to a light or a noise,
  unless it is extremely bright or loud.

  During Stage 3, the muscles still have some tonus, and sleepers show
  very little response to external stimuli unless they are very strong
  or have a special personal meaning (for example, when someone calls
  your name, or when a baby cries within earshot of its mother).

  Stage 4 is the stage of sleep that accomplishes most of the body’s
  repair work and from which it is most difficult to wake someone up (reference).

A study conducted to measure brain activity while sleeping subjects were subjected to varying degrees of sound found that some people did you wake up after being hit with 70db of sound while others woke up even at sounds between 40 - 50 db (reference). This could lead to new behavioral or drug therapies for people with sleep disorders.

A review on the affect of low frequency sound on sleep could not reach any significant conclusions warranting that more search needs to be conducted in the field.(reference).

You will be interested to know that different sounds have been found to wake up men and women. A list is available here. Differences between the sleep of men and women are listed in this article.


Why do we fall asleep when our eyes are closed?

You're confusing the cause with the effect. The effect is closing of the eyes (and maybe some component of relaxing.) The cause is sleepiness. In other words, when you're falling asleep, the eyes close, not the other way around. You can close your eyes for 24 hours straight, and you might sleep longer out of boredom, but you'll still spend most of the time awake. Closing your eyes doesn't cause sleep.

The reason our eyes close when we sleep is to protect the eyes from drying out and insuring the oxygenation of the corneas.

Take for example truck drivers. They need to keep their eyes open or bad things happen, like death and destruction. Yet, as they tire, try as they might, their eyes flutter closed and off to sleep they go.

Driver drowsiness detection with eyelid related parameters by Support Vector Machine


The progenitor cells of T-cells (they do not develop into T-cells and show their characteristics before reaching the thymus) are mobilized into the bloodstream and enter the thymus from it by crossing the endothelial barrier. The figure shows schematically the development of the precursor cells from hematopoietic stem cells (HSC) and the migration of the precursor cells (it is from the paper linked below):

See this review for the details (if you have problems accessing the article, let me know):

The long road to the thymus: the generation, mobilization, and
circulation of T-cell progenitors in mouse and man.


Question regarding 2 constructs of tobacco plant

Having a toxic product for the cell in an expression vector is a not uncommon problem when overexpressing proteins.

The other possibility is that the selection marker itself is the problem. Here you can have mutations either in the promoter of the gene as well as in the gene itself resulting in a protein which is not capable of protecting the cells from the selection. Both possibilities (no expression and mutated protein) leave to the death of the transfected cells, since there is no protection of them by the resistance protein.


How does pressure travel through the cochlea exactly?

Short answer
The pressure wave through the scala vestibuli drives the basilar membrane response (BM). Your option (1) is correct, (2) is not. The pressure not really permeates or penetrates Reissner's membrane though; it is the pressure differential across the scala vestibuli and scala tympani that is the driving force for the BM movement.
Background
The most accepted way of viewing acoustic activation of the auditory system is the traveling wave theory (Fig. 1) as posed by the famous experiments of Georg von Békésy in the 1960's. These experiments showed, basically, that the basal part of the basilar membrane (BM) starts vibrating first (near the cochlear 'entrance' at the round window) and as the wave travels through the scala vestibuli, more apical parts get activated (Fig 2). This phenomenon explains the cochlear delay that's seen, i.e., that low frequencies tend to activate hair cells later than high-pitched sounds do (He and Ren 2013).
Reissner's membrane separates the scala vestibuli from the scala media. The traveling wave generates a pressure difference between the scala vestibuli and scala tympani. As you rightfully say, this pressure difference is established across Reissner's membrane and across the BM (Fig. 3). It is the movement of the BM that ultimately results in the sensation of sound (source: Ento Key). In fact, the movement of Reissner's membrane is comparable to that of the BM (Reichenbach et al., 2012). However, Reissner's membrane is not tuned and contains no neural elements involved in hearing. The stereocilia of the hair cells are embedded in the tectorial membrane. The shearing forces between the BM and tectorial membrane eventually result in mechanotransduction (Fig. 3). See Fig. 12.5 on this web page from Neuroscience online textbook for an informative video on the BM movement relative to the tectotial membrane.
The traveling wave is basically confined from base  to apex. Because of the tuning of the basilar membrane, high frequencies resonate the basal part (because the BM is stiff and narrow) and low frequencies the apical part (because the BM is wide and floppy). Each time a resonant frequency is met, the BM starts vibrating maximally and basically the frequency cannot go further and its energy is dissipated. Thus, along the way, sound traveling through the scala vestibuli  to the helicotrema (the boundary of the scala vestibulu and tympani) more and more energy is used up from the pressure wave. Thus, the basilar membrane is set in motion primarily by the pressure differences occurring in the scala vestibuli and by the time the traveling wave reaches the helicotrema no appreciable energy is left as all auditory frequencies have been filtered out. Remaining energy containing frequencies outside the audible range (roughly 20 - 20,000 Hz) continue to travel to the scala tympani (think of static pressure during a deep dive) and therefore the round window is necessary to act as a buffer (Robles & Rugggero, 2001).
However, there are other theories, notably one from Hermann von Helmholtz, a brilliant scientist of the 1800's that has revolutionized sensory sciences. It is called the 'sympathetic resonance' theory. I am not at all familiar with this theory, as it has been largely abandoned, at least as far as I know. The theory from Von Békésy assumes that the basilar membrane is a place-to-frequency converter that acts like a Fourier transformer, known as the place coding theory. Basically, the traveling wave dissects complex acoustic stimuli into different acoustic frequencies by menas of frequency tuning of the BM (Fig. 2). By contrast, Helmholtz assumed there are tiny tuned elements positioned in the cochlea that basically perform the Fourier transform (not shown here). If you wish to read more of the latter theory, I happily refer you to Bell, 2004).

Fig. 1. Traveling wave. source: NY University

Fig. 2. Basilar membrane movement. source: NY University

Fig. 3. cross section through cochlear duct. source: Psychology Wiki
References
- Bell, Plos Biology (2004); 2(10):e337
- He & Ren, Scientific Reports (2013); 3: 1874
- Purves et al. (eds), Neuroscience (2001) 2nd ed. Sunderland (MA): Sinauer Associates
- Reichenbach et al., Cell Rep (2012); 1(4): 374–84
- Robles & Rugggero, Phys Rev (2001); 81(3): 1306-43


Well it turns out that when nucleotides are bonded together in a strand of DNA/RNA (nucleic acid) they ALWAYS HAVE only one phosphate group attached to their nucleoside (nucleoside = sugar + nitrogenous base (without phosphate)).

However, when they are by themselves, they are more often found with two or three phosphate groups as oppose to just the one. For this reason, the definition of a nucleotide is often misunderstood as it refers to containing one OR MORE phosphates, in reality, the official definition of a nucleotide states that only one phosphate group is present...

An example of a (so-called) "nucleotide" is ATP (adenosine triphosphate); it follows all of the rules that the misunderstood definition of a nucleotide states (these are; a nitrogenous base (adenine); a pentose sugar (ribose); and one "OR MORE" phosphate groups (triphosphate)). However, according to the official definition of a nucleotide, it is not, in fact, a nucleotide! It is instead considered a 'nucleoside triphosphate', since it is a nucleoside. with three phosphate groups (it is also a nucleotide with two additional phosphate groups, but I guess 'nucleotide-with-a-diphosphate' attachment doesn't roll off the tongue so well as nucleoside triphosphate).

Finally, as in nucleic acids and indeed anywhere else (according to the official definition of the nucleotide), there is only one phosphate group allowed to attached to each nucleoside (regular phosphate group) to form a nucleotide (officially). Therefore there is no variation allowed in the phosphate groups (since there's only one and they bond to other nucleotides, in the same way, every time (in nucleic acids)), furthermore in the pentose sugar the only variation allowed is whether it is a ribose (in RNA) or a deoxyribose (in DNA). So the phosphate-sugar backbone of the DNA strands and the RNA strands (nucleic acids) are consistent throughout the entire strand (and each strand of its type; differentiating only in the type of pentose sugar it consists of (ribose/deoxyribose)). Consequently, there is no phosphate-sugar backbone variation within DNA strands or RNA strands, for the phosphate or the pentose sugar to make any genetic difference to genetic material (those strands); only the nitrogenous bases and their sequences can make a difference to the genetic material...


Reasoning behind CO2 mouse euthanasia precharge prohibition

Quoting from guidelines to CARBON DIOXIDE EUTHANASIA OF RODENTS from University of Pennsylvania >>

  Do not “pre‐fill” the euthanasia chamber with CO2.  Start with room air then slowly fill the chamber with CO2 over several minutes
  (OLAW).  CO2 is heavier than room air, thus the chamber may need to be
  “purged” between groups of cages.

  “Because inspiration of high
  concentrations of CO2 is both aversive and painful, a recommended
  procedure is to place animals into a chamber that contains room air
  and then to gradually introduce CO2.” (ACLAM)
  CO2 first renders the animal anesthetized and then, with adequate exposure time, will result in death by CO2 narcosis.  Animals should
  be left for additional time within the euthanasia chamber, after
  spontaneous movements have ceased, with CO2 continuing to flow.

  “Animals should be left in the container until clinical death has been
  ensured.” (NIH)

Also, according to an article in The Scientist by Kerry Grens >>

It's been realized that at high concentrations, CO2 causes creatures torment. After reaching mucosal surfaces, it transforms into carbonic acid, which stings. Also, in people, even low fixations can be upsetting, bringing about shortness of breath.Therefore, explaining why high levels of CO2 is actually more painful for the rodents.


What are the "minimum requirements" for a single cell?

So, to make cells from scratch you would need: amphiphilic molecules to form a membrane, a decent mix of simple molecules (sugars, nucleic acids, peptides) that serve as reactant and building blocks for more complex things, some simple catalyzer (metals, minerals, pepetides, aptamers, etc..) to run the reactions, enough energy to maintain lots of reactions running and keep them far from the equilibrium. Of course, lots of time...

An even more minimalistic approach would use a single molecule to do the enzymatic job while storing evolvable informations. In this case RNA alone has been proposed as substitute for proteins and DNA in a very minimal cell. In theory also DNA alone could do the same. However the minimal tasks needed to be done: maintain the self (to be compartimentalized), to grow (to have a flux of molecule not in equilibrium), to divide, to maintain the information stably enough to be useful for the next generation and at the same time prone too mutability to evolve.

One more point. Life itself doesn't strictly require to be compartmentalized.
You can think of a network of chemical reactions that have the ability to grow, to replicate its components etc but without a cell membrane. However I think that a cell-like form of life is somewhat more likely to happen.


What's the percentage similarity between human individuals (and other primates) when comparing only exons?

One of the references to the chimpanzee genome paper linked by Maximillian is Inferring Nonneutral Evolution from Human-Chimp-Mouse Orthologous Gene Trios, where the authors seems to have focused on exons only:

  Here we apply evolutionary tests to identify genes and pathways from a new collection of more than 200,000 chimpanzee exonic sequences that show patterns of divergence consistent with natural selection along the human and chimpanzee lineages.

They conclude that:

  Perhaps the best way to understand the relation between DNA sequence divergence and the differences between human and chimpanzee physiology and morphology is to compare these differences to the variability among humans. Human-chimp DNA sequence divergence is roughly 10 times the divergence between random pairs of humans.

Unfortunately, they didn't compare this to the fold-difference of non-exonic DNA, so the comparative quantification between coding vs non-coding regions remains to be determined.

However, this does directly answer the question of how big the genomic differences are between individuals of the same species vs those of other species, when comparing only coding regions. I also found it useful to quantify the differences in these relative terms in addition to the previously stated percentages.


Ancient DNA of ancestors or existing species?

Assuming you mean by "modern descendants" "two different species that are also different from the ancient DNA", then to the best of my knowledge, no; the large vertebrates (bear, horse, humans, mammoths) that have been focused on for the most ancient DNA samples have common ancestors that are outside the range of ancient DNA isolation. I'm not very familiar with plant ancient DNA; maize DNA from a few thousand years ago is the oldest I'm aware of, but I might easily have missed some.

However, it's important to point out that the way this question is phrased makes it merely trivia, with no scientific significance.

Assuming (from the poster's other questions) that he believes this is somehow relevant to questions about speciation, I would point to modern genomes from ongoing speciation.  For example, Heliconius butterflies are speciating, and there's some work looking at the genomic components of that speciation:

Highly conserved gene order and numerous novel repetitive elements in genomic regions linked to wing pattern variation in Heliconius butterflies.
Genomic islands of divergence in hybridizing Heliconius butterflies identified by large-scale targeted sequencing.
Divergence with gene flow across a speciation continuum of Heliconius butterflies

Stickleback fish also show a number of examples of incipient evolution, and again genome studies have been done:

(Genomic landscape of early ecological speciation initiated by selection on nuptial colour.](http://onlinelibrary.wiley.com/doi/10.1111/mec.13774/abstract;jsessionid=DB86FB85259118805B95C1C52138D3EA.f03t03)
Genomics of Rapid Incipient Speciation in Sympatric Threespine Stickleback.

Since, as I say, the question as phrased is simply asking for scientifically unimportant trivia, I'll leave it that as far as guessing as to what the actual point is.


What is the proper format for genus and species names in latin?

The correct latin nomenclature is Sander vitreus, with the genus capitalized and the species name in lowercase.  This is known as binomial nomenclature.

  Carl Linnaeus chose to use a two-word naming system [...] binomial nomenclature scheme, using only the genus name and the specific name or epithet which together form the whole name of the species. For example, humans belong to genus Homo and their specific name is sapiens.  The first letter of the first name, the genus, is always capitalized, while that of the second is not, even when derived from a proper noun such as the name of a person or place.

Some scientific naming conventions:

Classification example (for Homo sapiens):


Identification of an insect found near Shirdi, Maharashtra

It's a household centipede whose scientific name is Scutigera coleoptrata.
It's venom doesn't do much harm to humans.

Sources:
Picture 1 and   Picture 2


What are some of the general characteristics of the DH5 alpha strain?

There are two possible sources: One is the article from the Bethesda Research Laboratories (reference 1), which names a few, the other is the book "DNA cloning: A practical approach" (see reference 2)., which sits here in my bookshelf.

Taking both together, the DH5 alpha strain is derived from the DH5 strain with the introduction of a few additional features. The naming DH are the initials of Douglas Hanahan which developed the strain. The strain is easy to transform with high efficency.

The new features of DH5 alpha are the recA and the endA1 mutations:

The endA1 mutation inactivates an intracellular endonuclease that
degrades plasmid DNA.
The recA mutation eliminates homologous recombination. This reduces the chance for deletions and plasmid multimerization.

The DH5 strain also has the following features:

The hsdR17 mutation eliminates the restriction endonuclease of the
EcoKI restriction-modification system, so DNA lacking the EcoKI
methylation will not be degraded. DNA prepared from hsdR strains that
are wt for hsdM will be methylated and can be used to transform wt E.
coli K-12 strains.
Δ(lacZ)M15 is the alpha acceptor allele needed for blue-white
screening with many lacZ based vectors.

Of special interest are the references 3 and 4, which gives you all the details you want to know.

References:

Bethesda Research Laboratories. 1986. BRL pUC host: E. coli DH5α
competent cells. Focus 8(2):9. The article is on page 13 in this paper.
DNA Cloning: A Practical Approach. Glover, D. M. (ed.), 1985, Vol. 1, p. 109, IRL Press, McLean, Virginia
Choosing a Competent E.coli Strain
E. coli genotypes


Is it true that it is mostly impossible, for any kind of antibiotic, to succeed in killing off every bacteria in a very rich environment?

Yes. It is down to mutations. DNA replication is not 100% accurate, there will be mistakes that are not corrected in the progeny produced.

Antibiotics works like a bit of gunk wedging itself into the machine of a bacteria cell but avoids jamming a human cell due to that very same shape. Gunk that wedges into both human and bacteria machines is just a really bad poison. So that gunk has a very special shape.

Resistance can be acquired by recognizing gunk of that particular shape and removing it (not something easy to evolve but very effective when it does) or just change the shape of the machine so the gunk cannot stick. Usually the altered machine doesn't work as efficiently as it can but in an environment polluted by fouling gunk, it works well enough.

And a rich environment means there are many bacteria.

So if your chances of mutating the right part of the bacteria machine to gain resistance is 1 in million, a rich environment with 10 million cells will have 10 such mutates.

Of course in reality we are talking about trillions (a million million) of bacteria cells per human (actually 39 trillion bacteria per human) and we are talking about billions of humans.  And we are not even counting the number of bacteria in the soil and in farm animals.  And it takes a few years for resistance to evolve.

When you look at the numbers involved , it is very difficult not to imagine resistances evolving. Even if the chances of that happening is 1 in hundred of trillions. It just takes a single bacteria cell to mutate and so gain resistance for it to spread and pass that resistance to other bacteria.


What specific mutations can cause an apoptosis mechanism to malfunction?

There are lots and lots of specific single mutations that cause problems with apoptosis.

Some of the most common are in P53, PTEN, MYC, APC, and KRAS. If you want a specific amino acid change, KRAS G12D is particularly potent. It works by disabling a regulatory domain and causing KRAS to be constitutively active.

These aren't "reversible" in a strict sense (except, I guess, for the struck-by-lightning-while-holding-a-winning-lottery-ticket level improbability of a second replication error in the same place back to the original base) but in many cases the cells will upregulate compensatory pathways or activate senescence pathways instead, rather than instantaneously becoming full-blown malignant.

As for mutations that don't cause disruptions to apoptosis,there are almost an infinite number, in that silent mutations or mutations to genes that aren't involved in apoptosis would count.

If you mean what kind of non-silent mutations can happen to genes that are important to apoptosis without causing problems, there are still a lot: swapping similar amino acids in non-active parts of proteins are unlikely to have huge effects.


Rate of Diffusion Through Cellulose Membrane

I think that your instructor was wrong.
For the type of experiment that you describe the dialysis tubing (cellulose acetate with pores) is acting as a semi-permeable membrane which can block the diffusion of a polymer (starch) but will allow the passage of a small molecule (glucose). The molecular weight cut-off of the tubing was probably 10 kilodaltons or greater, so glucose (180 daltons) would diffuse through the pores without hindrance, as would sucrose (342 daltons). But would the monosaccharide and the disaccharide move through the membrane at different rates?
This table gives values for the diffusion coefficient (D) of these two sugars as:

glucose 6.7 cm² s⁻¹ × 10⁻⁶
sucrose 5.2 cm² s⁻¹ × 10⁻⁶

The time τ to travel distance L by diffusive movement is given by
τ = L²/6D
Here all that matters is that τ is inversely proportional to D, so we can estimate that glucose 'diffuses' approximately 30% faster than sucrose.
Bulk diffusion is, of course, driven by a concentration gradient: if you were to start with, say, 0.1 M each of glucose and sucrose in a dialysis tube the glucose should reach equilibrium with the surrounding liquid faster than the sucrose.


Help me understand voltage patch clamping

I'll try to answer the sub questions 1-by-1

Does that mean that the change in membrane potential that I did resulted in changes in the conformational states of ion channels which in turn changed the membrane potential that I need to control ?

It's the other way around; your book is right - "When the membrane potential is suddenly increased by this voltage clamp from −90 millivolts to zero, the voltage-gated sodium and potassium channels open and sodium and potassium ions begin to pour through the channels". So the voltage step (depolarization) induced by the apparatus triggers voltage-operated channels to undergo conformational changes, this in turn results in additional current flowing through them. On the other hand, hyperpolarization of the potential from say -40 to -90 causes the neuron to close these channels, blocking current to flow. In other words; the patch clamp apparatus controls the membrane potential, the state of the ion channels has little to do with that, as the apparatus will automatically adjust the current injection.

Is this all still the step of setting the membrane potential to a certain specific value?

Yes.

"To achieve this level, the current injected must be equal to but of opposite polarity to the net current flow through the membrane channels."
I'm not sure I understand this.

To set a certain stable potential across the membrane, the flow of current needs to be stable, otherwise it will fluctuate; Ohm's law tells us U = IxR. The resistance R is set by the channels. Let's consider that R is stable for the moment. In that case, you will set the membrane potential U by tightly controlling the current I. If I fluctuates, i.e., when the apparatus doesn't balance the flow of current through the membrane channels exactly and oppositely, a net current will start flowing and u will change. You don't want that to happen.

do they make sure that the flow is only from sodium channels by setting the membrane potential to the equilibrium potential of other ions or a potential between the equilibrium potential of the other ions (so greater than it) and the equilibrium potential of Na (and also less than it )?

This part has nothing to do with equilibrium potentials. They substitute negative ions simply by ions that are not membrane permeable, and the only positive ion available in the test tube is Na+. In that case, only Na+ can flow and you are sure that it is Na+ that is flowing. At least, this is what I make up of this text.


Does our eyeball increase in size as we grow?

First of all, I should quote the sentence from the MOST reliable ophthalmology sourcing in the world - American Academy of Ophthalmology:

Section 11 - "Lens and Cataract"

"The equatorial diameter of the unfixed human lens measures 2 mm at 12 weeks and 6 mm at 35 weeks. Both the growth and the maturation of lenticular fibers continue throughout life." The antero-posterior dimensions of the lens enlarge from 3 mm at infancy to 6 and even more in adult years.

"The lens continues to grow throughout life (page 7 the same source)

Secondly, the growth of the eye continues after birth - at the beginning the growth is fast and later the growth is much slower but still - there is GROWTH of the eye after the birth.


What is the most reliable tumour suppressing gene for NSCLC?

The first resource I would look at would be the TCGA publication on NSCLC which can be found at this location. The first figure shows the most frequently mutated genes. TP53 rises to the top as most frequently mutated gene in the cohort studied, however, one also sees on the list KEAP1, NF1, ARID1A, SMARCA4, RB1, and CDKN2 as commonly altered tumor suppressors TSGs. You will want to take into account copy number data and mutation data in the frequency count in cohort also. Another issue to check in the data set is stage of the tumors in TCGA. You mentioned 'early stage' in your query, but if all the samples in TCGA are recurrent then it may not be appropriate for your question. The cBioPortal resource allows you to look and manipulate the data and I encourage you to look at that resource. It is very well done and shouldn't have too much of a learning curve. You will be able to put in TSGs and get back the freq of mutations. They may also have information on stage so might be possible to filter for only those samples. There are also a couple of text-mining resources that you can ask queries through pubmed to get back gene lists or to link gene lists. One tool is Glad4U (search this name in google) which allows you to type a query such as: "tumor suppressor AND early stage NSCLC" and it will return a ranked list of genes. Ranking is based on co-citation. However, one must check the returned list to make sure the genes returned are TSGs. A listing of putative TSGs can be found here. The second resource is CoCiter v2.0. On the Gene-Term search you can rank the lists of TSGs against search terms and it will return a ranking of the TSGs most associated with your search term. Hope this helps.


What are the pros and cons of eating earth (soil)?

The article (a PDF can be found here) suggests that this happens neither for feeding reasons (to get your belly filled, when anything else is available) nor that this is done for supplemental reasons.

They suggest that this happens more for protective reasons. In the abstract they write:

  Our results indicate that human geophagy is best explained as
  providing protection from dietary chemicals, parasites, and pathogens,
  whereas animal geophagy may involve both micronutrient acquisition and
  protection.

In the paper they give a few examples for this. First the earth eaten is usually digged up from deeper layers of the ground and sometimes even cooked. Then they bring in the example of people, which eat soil, when they have gastrointestinal problems as a kind of medicine to calm down the problems.

In my opinion there is not much nutritional value in eating soil. Organic compounds can usually not be metabolized (for example we don't have the possibility to break down cellulose). I am not sure, if we can get minerals from clay into our body, since a lot of them is present in soil as unsoluble minerals.


Why metacarpus is considered hand proper?

Proper in this instance means the main body of the hand, the part that has no other identifier. the fingers and wrist have other terms to identify them, the hand proper does not. If I say the the hand you are not sure whether I mean the hand as a whole or that part in particular so it is called the hand proper. Its an old usage of the word, but that is common in anatomy text.

From webster it is the 6th definition. Proper: strictly limited to a specified thing, place, or idea


Action of tetracycline on 30s ribosomal subunits

The crystal structure of tetracycline bound to the 30S ribosomal subunit of Thermus thermophilus has been determined by Pioletti et al. and the major binding site (Tet-1) interferes with the location where the A-site tRNA binds as shown in the stereo pair, below:

They write:

  “Thus tetracycline can physically prevent the binding of the tRNA to the A-site. This mode of interaction is consistent with the classical model of tetracycline as an inhibitor of A-site occupation, and hence offers a clear explanation of the bacteriostatic effects of tetracycline.”

So the proximal effect would appear to be the first alternative in the question, although the second may be an indirect consequence.


Ultimately, it seems that follicle-stimulating hormone (FSH), released from the pituitary gland, may be the direct signal for spermatocytes to enter meiosis [1]. It's worth noting, though, that these results come from in vitro studies, where spermatocytes were co-cultured with all cell types of seminiferous tubules in an artificial medium, which makes it a rather crude approximation of in vivo conditions: mimicking the complete spermatogenic cycle in vitro remains to be done [2].

It's a little bit more complicated with oocytes. They start meiosis during prenatal development, are arrested in diplotene stage of the first meiotic division, and then a surge of luteinizing hormone (LH), just before ovulation, makes them resume. But they are arrested again in the last phase, and only after conception do they finish meiosis. The pause occuring in prenatal development is thought to be induced by some kind of an "arrester" secreted by cells in the oocyte environment (specifically, mural granulosa cells) and sustained by high cAMP levels, that are produced in response to both intrinsic and extrinsic stimuli. [3]

Another matter, and quite interesting, is the issue of timing: meiosis starts in a distinct moment of a male mammal develompent, and then goes on continuously, but mammal oogenesis is a series of starts and stops. More on this can be found in [3] and [4].

[1] Tesarik, J., Guido, M., Mendoza, C. & Greco, E. Human spermatogenesis in vitro: respective effects of follicle-stimulating hormone and testosterone on meiosis, spermiogenesis, and Sertoli cell apoptosis. J. Clin. Endocrinol. Metab. 83, 4467–4473 (1998). PMID: 9851795. Free access.

[2] Sousa, M., Cremades, N., Alves, C., Silva, J. & Barros, A. Developmental potential of human spermatogenic cells co-cultured with Sertoli cells. Hum. Reprod. 17, 161–172 (2002). PMID: 11756382. Free access.

[3] Zhang, M. & Xia, G. Hormonal control of mammalian oocyte meiosis at diplotene stage. Cell. Mol. Life Sci. Epub ahead of print. (2011). PMID: 22045555.

[4] Albertini, D.F. & Carabatsos, M.J. Comparative aspects of meiotic cell cycle control in mammals. J. Mol. Med. 76, 795–799 (1998). PMID: 9846949.


Should be fine, but if I were you, I'd spare a few more minutes and carry on until ethanol precipitation (15 min of work at worst). Here's the protocol:
https://www.thermofisher.com/pl/en/home/references/protocols/nucleic-acid-purification-and-analysis/dna-extraction-protocols/phenol-chloroform-extraction.html

You can store it in -20 degrees for several days (extend the overnight incubation, that is the second step of ethanol precipitation) and you'll have the certainty that it will stay ok. In fact, freezing in most buffers, whether lysis buffers or extraction buffers shouldn't significantly hurt any nucleic acids. From my personal experience: I've frozen plant material in extraction buffer for RNA isolation (TRI-zol method) in -80 for a few days and got very high concentrations in most samples in the end. I was told freezing in -20 would impact quality but RNA is generally less stable than DNA.

If you had little to none material, you're better of doing the precipitation procedure and then freezing it. If those are minuscule amounts and/or you work with something sensitive like forensic evidence, following through with the procedure will be the most reasonable solution.


Difference of coverage between amplicons

Well, to plot the coverage I would use something like Python Matplotlib. Take a look at this example:

import matplotlib.pyplot as plt
import matplotlib

amplicons =  ('TTGCCAGTTAACGTCTTCCTTCTCTCTCTG',
      'CCCTTGTCTCTGTGTTCTTGTCCCCCCCA',
      'TGATCTGTCCCTCACAGCAGGGTCTTCTCT',
      'CACACTGACGTGCCTCTCCCTCCCTCCA')
countAmpl = (1635, 4734, 2156, 3085)

fig = plt.figure(figsize=(10,8.5))

subplt = fig.add_subplot(111)
subplt.set_ylabel('Count')
subplt.set_xlabel('Amplicons')
subplt.plot(amplicons, countAmpl,  linestyle='-', marker='o', color='blue')
for tl in subplt.get_yticklabels():
    tl.set_color('blue')

plt.savefig("amplicons.eps")

Check other types of charts in Matplotlib if you think you need something else.

You can also try to open and visualize the BAM in IGV from the Broad Institute.

Regarding the difference in coverage, I would say that some are from a repetitive region. Or the amplification depth of a region is greater than for the others. Or maybe the aligner found similar regions and decided that the amplicon aligns well in all those regions.


Are we capable to generate sounds of animals to the point that they mistakenly recognize it as members of their species?

The most clear and indisputable case of a human being generating a sound (using his own voice) that was mistakenly recognised by an animal as a sound made by a member of its own species is the case of Konrad Lorenz and the imprinting on birds.

Lorenz needs no introduction. However, in the case you don't know him, he is the father of modern ethology, together with Niko Tinbergen.

Among several other things, Lorenz studied and explained imprinting, specifically filial imprinting. According the Wikipedia link above:

  Lorenz demonstrated how incubator-hatched geese would imprint on the first suitable moving stimulus they saw within what he called a "critical period" between 13–16 hours shortly after hatching. For example, the goslings would imprint on Lorenz himself (to be more specific, on his wading boots), and he is often depicted being followed by a gaggle of geese who had imprinted on him.

For imprinting in an object (the mother), some species depend on movement that object makes, some depend on the sound it makes and some depend on a mix of movement and sound. From Brittanica:

  Lorenz demonstrated the phenomenon by appearing before newly hatched mallard ducklings and imitating a mother duck's quacking sounds, upon which the young birds regarded him as their mother and followed him accordingly. (emphasis mine)

During his life, Lorenz had several bird children, making several different youglings imprinting on him. As you can see in pictures like this one below, those animals will follow Lorenz (for the rest of their lives) as if Lorenz were their mother.

The funny thing is that, during some time after his early publications (but way before his Nobel Prize in 1973), some people had problems accepting Lorenz's discoveries, because they could not reproduce them.

It turned out that Lorenz was very effective in imprinting a lot of different bird species because of his uncanny ability of mimicking that bird species' sound, be it a goose, a chicken or a duck.

Of course, raising so many children has its problems:


Why bacteria and viruses are so much smaller than animal cells?

Cells/viruses vary in size mainly according to their function, components & requirements imposed by cell division/virus replication.

Bacterial cells are so small because they need a large surface area to cell volume to take in nutrients. Bacteria accumulate nutrients from the environment by diffusion alone, and so adopt certain sizes and shapes so they can import nutrients most efficiently. other evolutionary advantages are also existent in response to the demands of the environment and predators

Viruses function is pretty minimalistic. they pretty much consists of nucleic acid surrounded by a protective coat of protein called a capsid. this is the primitive virus, all it nedds is to infect cells and pass the information stored inside them.

The size of animal cells however depends partially on the type of cell and its function. Red blood cells are pretty small in comparison to other animal cells, they don't need to divide (so do not own a nucleus) and need a large surface area in order to diffuse Oxygen efficiently. Egg cells for example serve to store nutrients and don't need to carry out active metabolism, and so they are much bigger.

I took some of the examples from here, and for more technical information about the upper limits of cell size and plant cells click here.


This is in the discussion for quite a while. I have found no scientific studies which back the claims of kinesio tape. A review article (from which the quote below is taken) found no clinically important results which support the claims of the tape. The results about range-of-motion were inconsistant and it is not clear if the changes found were beneficial or not. They state:

  KT had some substantial effects on muscle activity, but it was unclear
  whether these changes were beneficial or harmful. In conclusion, there
  was little quality evidence to support the use of KT over other types
  of elastic taping in the management or prevention of sports injuries.
  KT may have a small beneficial role in improving strength, range of
  motion in certain injured cohorts and force sense error compared with
  other tapes, but further studies are needed to confirm these findings.

The study can be found here (links to the PDF):

Kinesio Taping in Treatment and Prevention of Sports Injuries

Other (also critical) studies are these:

A systematic review of the effectiveness of kinesio taping for
musculoskeletal injury.
The clinical effects of Kinesio® Tex taping: A systematic review.

The problem with these studies is that they are obviously not rigorous enough to make clear statements if KT is beneficial or not. Or (and this is also very possible) that the effect which is claimed to be there does not exist. Besides this, a placebo effect exists very well, since there is an intervention and also something present on the athlete.

There is now a new study avalaible which is blinded and placebo-controlled. This study finds no benefits for Kinesio Tape above a placebo. The study can be found here, there is also a summary available here.


How to get the file of a published phylogeny of a taxon

It is standard practice for authors to publish their trees on TreeBase for other people to use. They'll usually list the link in the supplementary material of the paper. Some journals made this a requirement for authors.


Ants do have eyes, though how well (and even whether) they see depends on the ant. They also have brains.

You aren't wrong to put quotes around "brain" since in many organisms the nervous system isn't as centralized as in vertebrates, and when they do have concentrations of neurons in various places ("ganglia") it isn't always in the head, and the one in the head isn't always significantly larger than the other ones, so it's often hard to call that having a brain. This can be true of many insects:

http://cronodon.com/BioTech/insect_nervous_systems.html

Having said that ants do have a centralized nervous system, with the neurons in the head making a larger percentage of their body than most other insects, i.e. they have brains. It appears social insects tend to have larger brains for their body size, which includes bees and ants.

http://guides.library.harvard.edu/fas/Brains/ants

Ants also have eyes; they're just often too small to see clearly, especially when the ant itself is small and the eyes are the same color as the ant's head. Ants descended from wasp-like ancestors that probably had quite good eyes, like modern wasps and bees do. But ants mostly live on and underground and don't need eyes as much as flying, pollinating insects do, and how well ants can see varies a lot between the species.

Or I'll just quote Wikipedia:

  Like most insects, ants have compound eyes made from numerous tiny lenses attached together. Ant eyes are good for acute movement detection, but do not offer a high resolution image. They also have three small ocelli (simple eyes) on the top of the head that detect light levels and polarization. Compared to vertebrates, most ants have poor-to-mediocre eyesight and a few subterranean species are completely blind. However, some ants, such as Australia's bulldog ant, have excellent vision and are capable of discriminating the distance and size of objects moving nearly a metre away.

And the cite for that latter example:
ATTACK  BEHAVIOUR  AND  DISTANCE  PERCEPTION
IN THE  AUSTRALIAN  BULLDOG  ANT
  MYRMECIA
NIGRICEPS

Those same ants even have color vision it seems. Conversely, African army ants appear to be blind, although even that depends on the caste. From Sociobiology of the hypogaeic army ant Dorylus:

On workers:

  Eyes are either reduced or absent.

On males:

  Army ant males do indeed resemble wasps, having large and robust bodies and well developed eyes and wings

So it's very possible the ants you ran into could see your fingers.


Can anyone identify this small shrub? Has white flowers

Looks like the common olive, Olea europea.  Cut into one of the fruits and see if there is a stone/pit, which will confirm.  You can search online for images to compare (use the Latin name as your search term).


Many black people I've met have bigger lips than white people, why?

Regard this one as a comment

I prefer to cite some text form this website instead of providing the link only (as it could be removed).

  In general, this pattern can be observed across the planet with the
  size of lips and nose decreasing as we move away from the equator
  towards the poles. So what could the reason be?

  For someone living in hot climatic conditions, cooling down the body
  is critical for their survival. Our body has many cooling mechanisms
  and one of them is simply disseminating heat when it comes in contact
  with colder air (simple thermodynamics). This however requires larger
  surface area so that more heat can be disseminated.

  Given that a significant portion of breathing also happens through the
  mouth (especially when exposed to heat), lips are pretty much like the
  gateway for colder air being inhaled and exhaled. So, the larger the
  lips, the more heat that can be disseminated. Thus, people living in
  hotter climatic conditions gradually evolved to have bigger lips.

  The opposite is true for people in colder climates. They get a
  survival advantage if they are able to retain as much heat as possible
  and so they gradually evolved to have smaller lips thus limiting the
  amount of heat that can escape when cold air brushes past their lips
  while inhaling and exhaling.

Notably, there was no scientific source provided for this claim, however intuitively this could make sense.


That is a beautiful Pink Quill, or Tillandsia cyanea. I have included two websites below about this plant, both of which include care tips.

http://home-and-gardening.info/2009/09/18/a-guide-on-growing-tillandsia/
http://houseplants.about.com/od/bromeliads/a/Bromeliads.htm


What do "reduced antipredator defense" and "reduced antipredator vigilance" mean?

When groups of prey use certain mechanisms to defend against predators, those mechanisms are known as antipredator defenses. For example, groups of tuna and starlings flock together to confuse predators. A reduction in this defense would be 'reduced antipredator defense'.

Groups of prey also exhibit shared antipredator vigilance, as in certain members of a group will look out for predators to protect the group. This is seen most predominantly in meerkats. A reduction is said vigilance would be a 'reduced antipredator vigilance'.

With reference to the Allee effect, which is what you appear to be reading about, this reduced antipredator defense and vigilance can significantly effect the population and the population growth.

Some related links:

On the ecological mechanism of the Allee effect.
Vigilance, predation risk, and the Allee effect in desert Bighorn sheep, a recent research paper.


Short answer: yes.  It also includes unspecific leakage without the aid of uncoupling proteins, since the mitochondrial inner membrane is not entirely impermeable to protons. For example, protons might fall backward through the proton-pumping complexes, through other solute carriers, or through other openings or irregularities in the membrane.


Which sex is homogametic in side-blotched lizards?

Lizards of the genus Uta are apparently male heterogametic (XY) (Pennock et al. 1969). The XY system seems to be the most common mode of sex determination in iguanid lizards (Kasahara et al. 1983).

Kasahara, Y et al. 1983. Chromosome mechanisms of sex determination, G- and C-band patterns and nucleolus organizer regions in Tropidurus torquatus (Sauria, Iguanidae).  Genetica 60: 151-156.
Pennock, L.A. et al. 1969. Minute Y chromosome in the lizard genus Uta (Family Iguanidae). Cytogenetics and Genome Research 8: 9-19.


Is there a difference between "cell line" and "cell strain"?

"Strain", in general, is usually used for whole organisms (whether they are unicellular or multicellular). For example, there are mouse strains.

"Cell line", on the other hand, is a very specific term that is used to refer cultured cells obtained from a multicellular organism. They need not be necessarily aneuploid.

  Is a cell line always aneuploid and capable of indefinite growth, as
  opposed to being euploid and incapable of indefinite growth?

Aneuploidy does not have any causative relationship with indefinite growth. Most cancerous cells evade the cell cycle checkpoints, which allows them to grow out of control. Some of these checkpoints also ensure proper segregation of chromosomes. Bypassing them leads to aneuploidy.

  Are cell lines essentially immortal?

Usually primary cell cultures are not referred to as "cell lines" these days. However, originally, any cultured cell that grows in vitro is called cell line. From Freshney (Basic Principles of Cell Culture):

  When cells are isolated from donor tissue, they may be maintained in
  a number of different ways. A simple small fragment of tissue that
  adheres to the growth surface, either spontaneously or aided by
  mechanical means, a plasma clot, or an extracellular matrix
  constituent, such as collagen, will usually give rise to an outgrowth
  of cells. This type of culture is known as a primary explant, and the
  cells migrating out are known as the outgrowth (Figs. 1.1, 1.2, See
  Color Plate 1). Cells in the outgrowth are selected, in the first
  instance, by their ability to migrate from the explant and
  subsequently, if subcultured, by their ability to proliferate. When a tissue sample is disaggregated, either mechanically or enzymatically
  (See Fig. 1.1), the suspension of cells and small aggregates that is
  generated will contain a proportion of cells capable of attachment
  to a solid substrate, forming a monolayer. Those cells within the monolayer that are capable of proliferation will then be selected at
  the first subculture and, as with the outgrowth from a primary
  explant, may give rise to a cell line.

Elsewhere, a cell strain is defined as positively selected subpopulation of cells:

  A cell strain is a subpopulation of a cell line that has been positively selected from the culture, by cloning or some other method.  A cell strain will often have undergone additional genetic changes since the initiation of the parent line. Individual cell strains may, for example, have become more or less tumorigenic than the established line, or they may be designated as a separate strain following transfection procedures.

This definition does not say anything about what kind of selection was used. You can select for cell that express GFP, for instance. So that strain would be simply designated as GFP+.


Is there any way to differentiate between a contractile and a non contractile vacuole by observation alone in any given organism

Contractile vacoules are usually surrounded by distinguishing structures

  The contractile vacuole has several structures attached to it in most cells, such as membrane folds, tubules, water tracts and small vesicles. These structures have been termed the spongiome; the contractile vacuole together with the spongiome is sometimes called the "contractile vacuole complex (CVC). The spongiome serves several functions in water transport into the contractile vacuole and in localization and docking of the contractile vacuole within the cell.

This type of arrangement is not common in non-contractile vacuoles like gas, sap or food vacuoles.


Will genetically modified food affect our health?

It's a popular public sentiment that - GM foods like tomatoes (flavr
  savr) will affect our health.. Is there any logical scientific
  explanation behind this?

GM organisms can have different genes and gene expression than natural ones, so they can create more protein or different proteins. Proteins can be toxic, can cause allergy and can catalyze reactions which can lead to toxic products.

To create a GM plant you need dollar millions, so it is not a cheap business. The GMO food regulations are very strict (at least in the EU), so it is unlikely that you will eat a GMO which contains toxic compounds.

  Whereas food safety organizations find nothing inherently unsafe in
  the process of genetic engineering, they note that new plant
  characteristics developed in the next wave of agricultural
  biotechnology could present new risks. At the same time, future
  generations of biotechnology may well provide food products with
  higher vitamin or protein content and lower allergenicity, yielding
  benefits to food consumers.

2014 - Agricultural Biotechnology: The Promise and Prospects of Genetically Modified Crops

Despite all the effort to make GMO foods safe, there are issues:

  Pesticides associated to genetically modified foods (PAGMF), are
  engineered to tolerate herbicides such as glyphosate (GLYP) and
  gluphosinate (GLUF) or insecticides such as the bacterial toxin
  bacillus thuringiensis (Bt). The aim of this study was to evaluate the
  correlation between maternal and fetal exposure, and to determine
  exposure levels of GLYP and its metabolite aminomethyl phosphoric acid
  (AMPA), GLUF and its metabolite 3-methylphosphinicopropionic acid
  (3-MPPA) and Cry1Ab protein (a Bt toxin) in Eastern Townships of
  Quebec, Canada. Blood of thirty pregnant women (PW) and thirty-nine
  nonpregnant women (NPW) were studied. Serum GLYP and GLUF were
  detected in NPW and not detected in PW. Serum 3-MPPA and CryAb1 toxin
  were detected in PW, their fetuses and NPW. This is the first study to
  reveal the presence of circulating PAGMF in women with and without
  pregnancy, paving the way for a new field in reproductive toxicology
  including nutrition and utero-placental toxicities.

2011 - Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada

  The study of combined effects of pesticides represents a challenge for
  toxicology. In the case of the new growing generation of genetically
  modified (GM) plants with stacked traits, glyphosate-based herbicides
  (like Roundup) residues are present in the Roundup-tolerant edible
  plants (especially corns) and mixed with modified Bt insecticidal
  toxins that are produced by the GM plants themselves. The potential
  side effects of these combined pesticides on human cells are
  investigated in this work. Here we have tested for the very first time
  Cry1Ab and Cry1Ac Bt toxins (10?ppb to 100?ppm) on the human embryonic
  kidney cell line 293, as well as their combined actions with Roundup,
  within 24?h, on three biomarkers of cell death: measurements of
  mitochondrial succinate dehydrogenase, adenylate kinase release by
  membrane alterations and caspase 3/7 inductions. Cry1Ab caused cell
  death from 100?ppm. For Cry1Ac, under such conditions, no effects were
  detected. The Roundup tested alone from 1 to 20 000?ppm is necrotic
  and apoptotic from 50?ppm, far below agricultural dilutions (50%
  lethal concentration 57.5?ppm). The only measured significant combined
  effect was that Cry1Ab and Cry1Ac reduced caspases 3/7 activations
  induced by Roundup; this could delay the activation of apoptosis.
  There was the same tendency for the other markers. In these results,
  we argue that modified Bt toxins are not inert on nontarget human
  cells, and that they can present combined side-effects with other
  residues of pesticides specific to GM plants.

2012 - Cytotoxicity on human cells of Cry1Ab and Cry1Ac Bt insecticidal toxins alone or with a glyphosate-based herbicide

  Though GM crops promises to meet the world's food need and eliminate
  the world hunger and starvation, the potent harmful effects cannot be
  overlooked and these need to be taken seriously. The long term impact
  on the society cannot be overruled as it includes the health risk of
  all the people involved be it producers (farmers) or the consumers
  along with the scientists who are working in the laboratory. Hence, it
  is the need of the hour to reach and try for sustainable development
  that meets the needs of humans and the balance of nature maintained.

2013 - Cry1Ab Treatment Has No Effects on Viability of Cultured Porcine Intestinal Cells, but Triggers Hsp70 Expression

I think it is the same story as by food, pharma and plastic industry. The billion dollar profit can be more important than the consequences. Btw. if you check a regular food, which you can buy in the shop, you will find a lot of unhealthy components e.g. trans fatty acids, omega-6 fatty acids, fungicide remnants, etc... which can affect your health as well.

My conclusion is that in most of the cases it is safe, however in rare cases it might have a mild harmful effect. To filter out those cases and their causes we need further studies and better regulation.


What, if any, diseases do larder beetles carry?

I have never heard of larder beetles carrying any serious diseases and chances are slim that it could have laid any eggs, so you probably have nothing to worry about. If you want you can spray the area down with a cleaner, but as I said earlier, it's probably fine.


How does the human ear guess the direction of the source?

The ear doesn't actually find the source, it's how the sound is perceived across both ears.

A sound coming from the side is the most obvious case where you get blasted on 1 ear and a relative muffled identical sound on the other ear.

A sound coming from the front is balanced across both ears. Same as behind, except that the forward-biased shape of the ears will distort the acoustics, leaving a distinct distortion signature that tells you the sound is coming from behind you. (For reference, modern 3D video game engines mimic this distortion so you can tell when something is happening behind your character or the camera if you are wearing headphones).

Sound from above or below you will have slightly different distortion signatures due to how the shape of the ears is different from above versus below.