Why ketoacidosis is less common in patients of Noninsulin Dependent Diabetes Mellitus?

This is a good and important question. The answer is not obvious, or necessarily well understood. Hyperglycemic crises occur in both Type 1 and Type 2 diabetes. In type 1 diabetes, the crisis is more likely to be diabetic ketoacidosis (DKA). In type 2 diabetes, it's more likely to be something called hyperosmolar hyperglycemic state (HHS), though type 2 diabetics can develop DKA, especially later in the course of the disease. Both can be brought on by similar precipitating events (for example, infection) in an individual who has had diabetes for a very long time (and this is where we often see these patients now -- pneumonia or the flu in an older diabetic). With type 1 diabetes, though, it can be how diabetes is discovered in a young, otherwise healthy individual.
The key difference between type 1 and type 2 diabetes is that type 1 is an absolute loss of insulin production, typically due to autoimmune destruction of the cells of the pancreas that produce insulin. Type 2, on the other hand, starts as insulin resistance. In fact, insulin levels may be high early in the course, but the tissues do not respond appropriately.
Insulin actions in glucose and fatty acid metabolism
Broadly, a key role of insulin is to respond to increases in blood glucose by shifting energy metabolism from fatty acids to glucose.
In a healthy individual, insulin is secreted as blood glucose rises, and causes peripheral tissues, especially fat and muscle, to take up and use glucose. It also causes the liver to release less glucose into the bloodstream from glycogen stores and gluconeogensis, and instead to store it (in glycogen).
At the same time, since there is plenty of glucose available, insulin diverts fatty acids to fat cells, promoting their storage in and inhibiting their release. Insulin indirectly prevents fatty acid catabolism in the liver by promoting its storage in fat cells, but also directly inhibits liver ketogenesis, a process by which byproducts of fatty acid and protein catabolism are converted to ketone bodies that can be used by, among other tissues, the brain.
Impaired insulin signaling
In both DKA and HHS, despite high levels of blood glucose, the muscles, fat cells, and liver act as if the organism is starving. In response to this state, counter-regulatory hormones (catecholamines, cortisol, glucagon, and growth hormone) are released. The liver releases glucose from glycogen stores and generates even more glucose from other metabolites through gluconeogenesis.
The difference between DKA and HHS is how lipid metabolism is regulated. It is unclear why, exactly, in HHS insulin fails to regulate glucose metabolism but seems to succeed in suppressing lipolysis and ketosis, but that is the current hypothesis. In DKA, fatty acids are released from adipose tissue and delivered to the liver, where massive unregulated lipid catabolism and ketogenesis occurs. In HHS, the existing insulin seems to be effective at suppressing lipolysis and ketogenesis.
You can read more about the pathophysiology of both these diabetic hyperglycemic crises in this excellent review.


Is Asteraceae and Compositae the same family?

They are either treated or even declared to be synonyms in all the texts using both of the terms that I have ever read.

Just one reference: the nearest Flora on my desk, G. Marconi, F. Corbetta, Flora della Pianura Padana e dell'Appennino Settentrionale, uses the notation Compositae = Asteraceae.

It is worth to note that Compositae, 'composite ones' in Latin, refers to the their typical capitulum inflorescence, while Asteraceae comes from Aster, a genus belonging to the family, meaning 'star' in Latin, which represents an allusion to the shape of the inflorescence of Aster, and of many other species, which is supposed to look like a star whose rays are represented by the ligules of the ligulate tiny flowers of the capitulum. Nevertheless, there also are species of the family having no ligulate flowers, for ex. Tanacetum vulgare.


Why do people say that smallpox has been eradicated?

The viruses that caused smallpox (Variola major and Variola minor) are generally not stable in the environment (<24 hours as an aerosol), though they may persist for more than a decade within scabs Reviewed: Sinclair et. al., 2008 OSHA.

UV light is an excellent disinfectant, so typically any virus exposed to sunlight will lose rapidly infectiousness.

You may also find this answer to a related question of interest:
https://biology.stackexchange.com/a/59165/46609


Why isn't there a standard unit of promoter strength?

Transcription rates are very context dependent. This shouldn't surprise you, since the same genes aren't expressed in your lungs and your eyes. They're also very environment dependent, this shouldn't surprise you either, since it's pretty obvious every organism is going to respond to temperature, their current nutritional state and so on.

So, in order to define promoter strength, you'd first need to define the exact conditions under which you're measuring it, including the exact strain you're measuring it in. Because if you get any of those even slightly different you're going to get a different answer. Doing this might get you a consistent number but you're abstracting away the most important parts of differences in transcription anyway: how it varies between cells and contexts.

Moreover, even if got past these hurdles you'd not have a particularly useful answer anyway since the rate of transcription is only a small part of the whole process. Why not consider mRNA durability, or rates of translation, or protein durability? What matters very much depends on what you're considering.


Cleanliness of cast iron never cleaned between meals

Soap or detergent does nothing to kill organisms. Instead each detergent molecule has two ends, one being hydrophobic (meaning it's repelled by water) and the other end is hydrophilic  (attaching the end to water). When anything is washed with soap or detergent, the oils and dirt on the object - whether it's a dish or your hands - can combine with water as an emulsion and be rinsed away.

Dishes and utensils are only susceptible to bacterial growth if there's traces of food on them. Washing is meant to remove traces of food and oil so bacteria can't multiple on them. The conditions must be right for bacteria to multiple. If traces of food were to be completely dry and hardened on a dish and someone ate off it, the likelihood of any bacteria present on it is close to nil. They need moisture to grow. If dishes had no oily food on them, washing and rinsing with very warm water would be sufficient. I've seen people from other cultures wash dishes with traces of food that are soluble in water. They come out perfectly clean. (As an aside, using a tea towel can often spread bacteria when they're not used properly.) Towels top kitchen contamination hazards list

Bacteria can't multiple in oil. For example, ordinary cooking oil doesn't need to be refrigerated although it can go rancid. A cast iron frying pan is properly meant for frying foods only. No watery sauces should be cooked in them. Even "scraping it clean" shouldn't be done with a sharp metal object as it can remove some of the polymerized hardened oil layer.

I have several cast iron pans that I don't wash. I wipe them out after each use, then I add a little oil nd roughly a teaspoon of salt. With a paper towel, I rub at any bits of stuck on food. If done within a few hours of being used, it effectively removes any food traces, leaving a smooth surface. I usually rinse off the salt in warm water, dry it and then apply a very thin film of oil. I've been cooking in cast iron pans for decades and have never gotten sick or had mild food poisoning (what many people call a 'stomach flu').

Cast iron pans with a layer of proper seasoning and treated like this will definitely not cause sickness. It can't support bacterial growth and as @jeanquilt mentions, the pan gets very hot - enough to blister your skin if you touch them with a bare hand.


Vitamin and mineral contents of common fruits

I know two databases for such information: The "National Nutrient Database for Standard Reference" (reference 1) from the United States Department of Agriculture (which you list yourself) and the "Nutrition Data" (reference 2) Database. Both allow searching for specific foods and give the values back. I like the second more, since it gives you the complete output it has and you don't have to choose three single nutrients like for the USDA database.

References:

USDA National Nutrient Database for Standard Reference
Nutrition Data


I can't think of a more succinct way to phrase it than the explanation in your post.

"...the genotype frequencies of the next generation depend only on the
allele frequencies of the current generation..."

The genotype frequencies still do depend on the initial generation, they just depend on the allele frequencies of the previous generation, not the genotype frequencies. For example, an initial generation consisting of only (XX) and (xx) genotypes will produce F1 offspring with (XX), (Xx), and (xx) genotypes through random mating. Since the (Xx) genotype frequency was 0% in the initial generation, and >0% in the subsequent generations, it can't be equal that of the initial generation. But it will still be a function of the relative frequencies of the two alleles in the population, (X) and (x).


Are MHC Proteins the Most Polymorphic Human Proteins Known?

Yes.  There are many MHC (MHC in humans is called HLA) genes.  The classical loci — Class I A, B, and C, and Class II DP, DQ, and DR — are the most polymorphic.

Here's a table from a 2002 article which clearly shows the number of polymorphisms.  It's no contest.

It's worth me pointing out that those numbers are wildly out of date.  The IPD-IMGT/HLA can provide full lists of known HLA alleles, but the exact numbers are in the tens of thousands:

The person you spoke with was probably referring to sequences called microsatellites.  These are small regions that are polymorphic and quite variable between individuals, and using a number of these together can be useful for genetic fingerprinting, but each individual microsatellite will not be as polymorphic as HLA class I A, for example.


What is the name of the bond between phosphate and the sugar in a nucleotide?

Phosophoester is a valid term. There are at least a 1000 peer-reviewed articles that use this term. IUPAC Goldbook defines nucleotides as:

  Compounds formally obtained by esterification of the 3 or 5 hydroxy group of nucleosides with phosphoric acid. They are the monomers of nucleic acids and are formed from them by hydrolytic cleavage."

Phosphoester or phosphoric ester means an ester of phosphoric acid.


What is the name of cell structures that have an adaptation to increase their surface area?

The small intestine requires a high surface area in order to increase the rate of absorption of digested food.


Virus cannot survive on surface after certain time period, but why and how?

Many important viruses are coated with a lipid envelope and rely on this to enter the host cell. This envelope is fragile - it's similar to a soap bubble - and it can be disrupted in many ways. Lipids will oxidize in air over time and this will degrade their ability to maintain an envelope. Surfactants such as soap or solvents such as alcohol will disrupt an envelope quickly. Even if the genome inside survives, if the envelope is disrupted the virus won't be able to infect cells.
The exact mechanism of inactivation likely varies a lot from virus to virus, and hasn't been studied extensively.
This paper found that Hepatitis C virus RNA survived alcohol treatment, but lost infectivity, presumably due to envelope disruption. In contrast, heat treatment (80°C) destroyed both the envelope and the RNA.
Another paper found enveloped viruses survived being dried out a shorter time than non-enveloped viruses. (5 days vs. weeks)

Speaking generally, the environment outside a body is hostile! If you were taken out of your home and dropped somewhere in the wilderness, there's many different ways you could die, and it's more remarkable if you survive. A similar situation arises for viruses.


Current Trend in Evolution of Human Intelligence

There appears to be some - note that this, of course, is highly controversial - evidence pointing at the direction that intelligence declined in the US and UK during the last century. There is a relatively new review by Michael Lynch (2016) in which he suggests that modern humans are accumulating slightly deleterious mutations with increasing rate due to relaxed purifying selection (a consequence of technology, medicine, ...), resulting in a 'future genetic load'. Let me just sum up some of the major points he makes that are relevant to assess current evolution of human intelligence:

Heritable mutations that lead to a reduction in fitness of 1% take about 100 generations to be eliminated by selection. Many of these mutations have a direct or indirect effect on the mutation rate (mostly increasing) and relaxed purifying selection on them might cause a positive feedback loop that causes even more mutations. Additionally, parental age increases the number of mutations passed on to the offspring. Most mutations will be slightly deleterious (keep in mind that the majority of new mutations is neutral, the majority of the remainder is deleterious and only very few mutations are beneficial. Therefore the really deleterious ones will still be selected against, but the slightly deleterious ones will not be removed by purifying selection). Accordingly, relaxed purifying selection increases the amount of slightly deleterious selection and decreases the efficiency of getting rid of them.
Lynch argues that the brain might be particularly sensitive to mutations as brain function depends on the finely tuned expression of thousands of genes which for him leads to the proposition that the effect of germline mutation rate on psychological disorders could be higher than expected by chance. In support, he cites Iossifov et al. (2015) who have suggested that autism spectrum disorders might be caused by de novo mutations in at least 30% of the cases and also looked at mutations interfering with IQ measurements.
Finally, he cites two papers that are of interest here as they deal with the change of intellectual abilities of humans over time (Crabtree (2013) and Woodley (2015)). The latter is a meta-analytic study based in the US and UK and Lynch already points out that there there are the usual issues with entangling genetic and environmental factors. However, in that study a slow decline of general intelligence of about 0.39 points per decade due to selection and about 0.84 points per decade due to mutational load is suggested. Interestingly, Woodley points out that there are two major hypothesis for this decline: (i) Since the industrial revolution people with lower general intelligence have higher average number of offspring (that might be the 'differential procreation' you have been hinting at). (ii) Mutation accumulation due to relaxed purifying selection against deleterious variants. Woodley concludes that the decline is a combination of both.

Of course, these points are strongly debatable. One of the major conceptual criticisms on Lynch's view is that slightly deleterious mutations (that Lynch claim to be accumulated as a consequence of relaxed purifying selection) are not slightly deleterious but totally neutral if they do not have a fitness effect. In terms of evolution it does not make a difference if an allele is neutral or negative selection is not acting on it because of technological interference. Another objection - more relevant to your question - is that measuring intelligence in general, or the IQ in particular, is a controversial thing to do and not at all easy to standardize which causes great difficulty in obtaining comparable data. Moreover, tracking down underlying genetics, estimating heritability of intelligence (a trait we even have difficulties to properly define and that is known to be strongly influenced by the environment), and consequently putting together a comprehensive assessment of the evolution of intelligence in humans is really tricky, set aside the ethical problems that may arise which we have not even touched yet.

A last note: In your edit you write:

  [...] a summary of fecundity and IQ would potentially answer my question but only if it accounted for the current selection process we see going on in modern technophile societies.

This is problematic as to date it is really difficult, if not impossible, to detect recent selection. This is mainly due to the fact that most methods depend on detecting changes in allele frequencies over time and this needs a considerable number of generations to integrate over.

There have been some efforts to develop more accurate methods, but looking at selection in the last 100 years (which you would need to be able to when looking at the technologically modern populations) is not possible so far. The best attempt I am aware of so far is Field et al. (2016, preprint) who looked, based on genome-wide association study data, at recent selection in the last 2000 years. However, they do not mention intelligence.

Update: This paper was a pre-print. It is now published in Science: Field et al. (2016).


How to safely sterilize urea-containing growth medium?

Autoclaving is the best way for sterilization. If your growth medium is large, how much chemical disinfectant do you think you would need to bring up to its working concentration?

Add some acid to your waste medium (so that it's only weakly acidic), not as disinfectant, but to suppress ammonia formation. Urea will still break down during autoclave, but ammonium ion (pKa~9) will generally stay in solution.


How does a veggie-less diet affect the human body?

There is a list of several implications of not eating vegetables (references 1, 2, 3):

Weight gain (by eating fat-rich products);
Malnutrition (not reveiving enough vitamin A, C, D, K, etc);
Digestive problems (low fiber intake leads to digestion disorders, which could lead to health problems);
High risk of heart disease;
High risk of certain cancers.

I also pulled up the nutrition fact sheets for vegetables, fruits, and seafood created by the US Food and Drug Administration.

In order to obtain all the necessary vitamins, one can substitute vegetables for fruits. For example, to obtain 100% of the daily value of vitamin A, one should eat as little as one carrot a day. In order to get the same amount of vitamin A from fruits, one should eat 134g of cantaloupe, or 462g of grapefruit, or 50 large apples a day. Although this could be difficult but possible, the sugar content of the above-mentioned fruits should be taken into account.

Something else which needs to be considered is that vegetables are richer in minerals (iron, potassium, calcium), compared to fruits.

All this in mind, perhaps all minerals and vitamins could be acquired from a source other than vegetables.


What is the cause of the spots on this leaf?

This is a "Tar Spot" disease usually found in Europe and North America. It mostly affects the Maple tree leaves. Tar spot is caused by 'Rhytisma acerinum' a plant pathogen fungus. This pathogen does not seem harm to tree but disturbs the leaves as it finds a suitable condition in summer with bit of wetness. It enters the leaves through stoma and then creates yellow lesions of various sizes over the leaf area which later gradually turns into brown-black tar colored spot. It reduces the photosynthesis process of leaves and thus creating more wide dark spots on the leaves. After sometime the leaves will fall.

Entire detail is available in the Wikipedia link with the detail of the pathogen. (Add some more info if you find this detail not enough)


Why do mosquitoes not collect blood after platelets activate?

Blood from a cut or a wound is tainted with bacteria from the surrounding environment. To a mosquito from an evolutionary perspective it would be like eating off the floor. The blood which flows through your veins is clean(er) due to your immune system and so evolution selected a pathway based on insertion into the skin in order to obtain the meal.


Was Raymond Gosling supervised by Rosalind Franklin?

Well, according to this editorial in Nature:

  Next week marks the 60th anniversary of the publication of the famous Watson and Crick paper — and that of two other papers on DNA that appeared in the same issue. Neither was so high profile, but each was essential to the structure’s discovery. Both were written by scientists at King’s College London: one by Maurice Wilkins and his colleagues Alec Stokes and Herbert Wilson, and the other by Gosling and his PhD supervisor, Rosalind Franklin. (emphasis mine)

There is also a podcast, an interview with Gosling himself (at the age of 86)! The full podcast can be found here: http://www.nature.com/nature/podcast/index-pastcast-2013-04-18.html

Source: Nature 496, 270 (18 April 2013) doi:10.1038/496270a


What's the (or some of the) minimum(s) amount of atmospheric carbon dioxide needed by plants?

The values provided in the other answer are actually related to the minimum values experienced by land plants in the past, not the theoretical minimum possible concentration of CO2 capable of maintaining plant life.

According to Gerhart and Ward (2010):

  During the Last Glacial Maximum (LGM; 18 000–20 000 yr ago) and previous
  glacial periods, atmospheric [CO2] dropped to 180–190 ppm, which is among the
  lowest concentrations that occurred during the evolution of land plants.

Thus, what is the theoretical minimum possible concentration of CO2 capable of maintaining plant life?

According to the same paper (Gerhart and Ward, 2010), there has been several experimental studies focusing in low concentration of CO2:

  In the mid-1990s, a later phase of technology was introduced at the Grassland, Soil, and Water Research Laboratory (USDA-Agricultural Research Service) that involves an outdoor tunnel system, whereby plants are grown across a continuum of modern to low [CO2] (Mayeux et al., 1993; Fig. 3b,c). During the day, air of known [CO2] is pumped into one end of the tunnel where plants experience relatively high [CO2]. Plants near the end of the tunnel, on the other hand, experience low [CO2] (similar to glacial values) as a result of photosynthetic removal of CO2 from air as it moves progressively through the tunnel. At night, airflow is reversed while plants are solely respiring, and this serves to equalize [CO2] throughout the tunnel.

Despite those studies not focusing explicitly on what's the minimum possible concentration, we can still draw some conclusions based on them. For instance, in Fig.4 (ibidem):

As you can see, those vertical lines represent the minimum concentration experienced in the past. However, we still observe CO2 assimilation (photosynthesis) below those values. Unfortunately we cannot simply get the value where the line touches the x axis, because those values are intracellular CO2 concentration.

That being said, the answer depends on other concept: CO2 compensation point. For a C3 plant, carbon dioxide compensation point is around 50ppm (Tolbert, Benker and Beck, 1995).

Thus, we can say that, as a rough estimate, the value you want lies between 50ppm and 170ppm (probably closer to 170ppm than to 50ppm).

Of course, that minimum possible value depends on several factors, as the species of the plant, the type of photosynthesis (C3, C4, CAM), temperature, humidity etc.

Sources:

Gerhart, L. and Ward, J. (2010). Plant responses to low [CO2] of the past. New Phytologist, 188(3), pp.674-695.
Tolbert, N., Benker, C. and Beck, E. (1995). The oxygen and carbon dioxide compensation points of C3 plants: possible role in regulating atmospheric oxygen. Proceedings of the National Academy of Sciences, 92(24), pp.11230-11233.


Why does one combine PCR and cloning as ways for amplification of sequences?

There are several reasons to clone a PCR product but the main reasons include expressing the product and maintaining the library inexpensively.

In the study you mentioned, the cloning and transformation is apparently done for obtaining single clones (from single colonies).

  Clones were picked randomly and colony PCR was then performed using
  vector primers T7 and SP6 to amplify the cloned inserts. Cycle
  sequencing was performed using BigDye version 1.1 (Applied Biosystems)
  and an automated capillary DNA sequencer Genetic Analyzer 3100
  (Applied Biosystems).

Since the original PCR would have a mix of different sequences, cloning is done to separate them out for the ease of studying them by sequencing. If they don't separate the sequences, they would have to use NGS (or more expensive methods like PacBio for longer reads). They have used Sanger sequencing. This article was published in 2007. At that time NGS was not as cheap as it is today and was hence not used by everyone. Also, the NGS machines of that time had even smaller read lengths (~40 for Solexa/Illumina GA and ~75 for GA-II). Considering these, Sanger sequencing may have been preferable to the authors of this paper. However, as I mentioned before, Sanger's method cannot be used for sequencing pooled samples; you need pure templates or else there will be mixed signals and base calling would be inaccurate.

(See the example chromatogram below: look at the position with the Y which has mixed T and C signals. It is not from a pooled sample, though).

Therefore cloning, transformation and colony picking was necessary.

Moreover, in many cases picking individual clones would be necessary for performing functional assays to associate phenotype with genotype.


Why don't we feel hungry after waking up?

I will try to keep the answer as simple as possible, but feel free to point out if I make this too simple.

Well, you are not alone with this observation. This is quite a common, but rather complex, phenomenon which controls our apetite and causes us to not feel hungry after waking up.

The feeling of being hungry is under constant regulation by two antagonistic (having opposite effects) hormones:

leptin, released from adipose tissue, decreases our apetite and suppresses our hunger
ghrelin, released from stomach, does just the opoosite i.e. increases our hunger.

And guess what, these hormones are controlled through the circadian cycle. When you sleep, your body produces more leptin and stops the production of ghrelin. Why? The answer is quite obvious: because you're sleeping. While sleeping, your metabolism is lowered because your body needs to repair the damaged cells and tissues. To control metabolism, we need to control our apetite, and to control our apetite, we need to suppress our hunger. So...? When you wake up, you still have a hangover of this effect. In other words, it takes some time to change the secretion rates of leptin and ghrelin and the resulting effects.

Lets get into some analytical details now. According to Sharma et al, 2010, metabolic rate and brain temperature are lowered during non-REM sleep to deal with the damages that may have occured during time of wakefulness. In their study, the subjects were deprived of sleep for 2 nights (4 hours per night) and then allowed to sleep for next 2 nights (10 hours per night). The result? Leptin levels decreased by 18% and ghrelin levels increased by 28%. The subjects also craved for more carbs. Also, craving for salty foods increased by 45%. Overall hunger increased by 23% due to reduction in leptin levels. They also showed that people who sleep less than 5 hours have increased Body Mass Index (BMI). All this points to the fact that sleep does cause reduction in apetite and hunger. In short, don't think of missing your breakfast.

References:

Sharma, Sunil; Kavuru, Mani (2 August 2010). "Sleep and Metabolism: Overview". International Journal of Endocrinology. 2010: 1–12. doi:10.1155/2010/270832.
Wikipedia contributors. "Sleep and metabolism." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 8 Feb. 2017. Web. 26 May. 2017.


computing relative synonymous codon usage from a coding sequence alignment while accounting for phylogenetic inertia?

It looks like you want to test a very specific hypothesis. Wether a sequence accumulates more non-synonymous changes than expected given its phylogenetic backgroun. The programme CODEML, included in the package PAML was designed specifically for this:

http://evomics.org/learning/phylogenetics/paml/


For reference: a normal P QRS from an EKG

from https://www.healio.com/cardiology/learn-the-heart/ecg-review/ecg-interpretation-tutorial/qrs-complex

The question and the different looking beat: one cannot say it is ectopic because the strip represents some sort of atrial arrhythmia.  Atrial fibrillation is the most common of these.  The beats are not regularly spaced and there is no sign of a P wave (the one produced by the atrium).

From link

  Atrial Fibrillation occurs when multiple electrical impulses occur
  within within the atria. This chaotic electrical activity results in a
  chaotic wave form between the QRS complexes. P waves are absent. They
  are replaced by lower case "f" waves. No P waves means there is no PR
  interval measurement. This rapid electrical activity overwhelms the AV
  node causing impulses to enter the ventricular conduction system at
  irregular points. This results in irregular R to R intervals.

"Ectopic" beat suggests there is a regular beat going on and some rogue beat elbows its way in.  In A fib they are all rogue beats - "multiple electrical impulses".  The one you see is not in structure different from the rest - there is a T for every QRS and so they are all coming from the atrium.  It is just that with that beat the S wave is deeper.  Maybe because it is so close to the T?   I bet if you ran that strip a while you would see others comparably deep.

I am betting this is homework.  What exactly is the question?


You're correct that tonicity needs two solutions to define.

Osmolarity (or osmotic concentration) is the measure of solute concentration, defined as the number of osmoles of solute per litre (L) of solution (Osm/L).

Tonicity, on the other hand, refers to the relative concentration of two solutions separated by a semipermeable membrane.

The difference is based what is considered for osmosis and tonicity. In case of osmosis, it is the water (or solvent) which moves across the membrane, while tonicity depends on the solutes which cannot move across the membrane. From Wikipedia:

  ... osmolarity takes into account the total concentration of penetrating solutes and non-penetrating solutes, whereas tonicity takes into account the total concentration of only non-penetrating solutes.


What causes the development of antibiotic-resistant strains of bacteria?

Bacteria usually gain resistance mechanisms through horizontal gene transfer (such as conjugation and phage infection). The four main mechanisms in which bacteria elude antibiotics are:

Drug Inactivation: For example, E. coli can produce beta-lactamase that inactivate many lactam based antibiotics such as penicillin.
Alteration of Target Site: Mutations in genes encoding for target sites can reduce drug binding affinity. Example: Random mutations in DNA gyrase and topoisomerase IV reduces binding affinity to fluoroquinolone.
Alteration of Metabolic Pathways: Many drugs target certain parts of metabolic pathways by inactivating enzymes or sequestering substrates. Bacteria can use alternative metabolic pathways or find ways to uptake the necessary nutrients from the environment.
Reduced drug accumulation: Caused by reduced drug permeability or the ability of the bacteria to transport drugs out of the cell (for example, tetA encodes for a tetracycline efflux transporter). They can gain these abilities through conjugation, phage infection (transduction), or uptake of environmental DNA (transformation).

Wikipedia has a pretty extensive and comprehensive article on antibiotic resistance. There's also a good list of references. http://en.wikipedia.org/wiki/Antibiotic_resistance


As @canadianer mentions in his comment, Protein G is more than likely named after the human group G strain of Streptococci, G148.

  Protein G, a bacterial cell wall protein with affinity for immunoglobulin G (IgG), has been isolated from a human group G streptococcal strain (G148).

Purification and some properties of streptococcal protein G, a novel IgG-binding reagent. - Björck et.al.

Protein G is a  Streptococcus protein that can bind the the Fc portion of the Immunoglobulin G protein. While it is similar to protein A, it was found to have better binding affinities to the different varieties of heavy chain constant regions of IgG molecules.

The G comes from Lancefield grouping. Lancefield grouping was a method that used to be used to classify bacterium. Group G Streptococci could be identified using Lancefield serum type G and that is how they received their classification.


Looks like a termite; male; after loss of wings.


It is, as stated by @rg255 a seed (or actually a fruit, see below). The seed itself is the small brownish thing. The white hairs are attached to make the seed fly with the wind. Looking at the seed and the hairs, I think the seed belongs to the daisy and dandelion familie asteracae/compositae. Altough there are other possibilities, see comments.

EDIT:
@AlwaysConfused is right if he states that in case of daisy family, it should be called a fruit, that containes one single seed. To be more precise, it is an Achene/Cypsula. In many species, what is often referred to as the "seed" is actually a fruit containing the seed. The seed-like appearance is owed to the hardening of the wall of the seed-vessel, which encloses the solitary seed so closely as to seem like an outer coat. Info derived from here on fruits and seeds and more specifically on Achenes/Cypsela here


What is the beneficial function of IgE antibody?

No, they are of course not there to cause allergies.
It is thought (although not directly proven in human) that IgE is important to fight parasites and worms. They bind to antigens from the parasites, which leads to the secretion of histamines. This causes a local immune reaction (which also is a problem in allergies) which is helpful to fight the parasites.

See these papers for example:

IgE, allergies and helminth parasites: a new perspective on an old
conundrum.
IgE Enhances Parasite Clearance and Regulates Mast Cell Responses in
Mice Infected with Trichinella spiralis
Immunology of Parasitic Helminth Infections

There is also some evidence, that IgE is involved in the immunological response to cancers:

Activity of human monocytes in IgE antibody-dependent surveillance
and killing of ovarian tumor cells.
Animal models for IgE-meditated cancer immunotherapy


How do you consider an organism to be a new species?

There are various hypotheses and concepts proposed to define a species, but no definitive answer. Mostly a combination of these concepts are used because each hypothesis has exceptions. Classification is constantly being debated, reevaluated, and changed as we learn more. Some of the most notable definitions are:

The is the biological species concept in which Ernst Mayr defines a species as actually or potentially interbreeding populations that are reproductive isolated from other groups and produce viable, fertile offspring. But this doesn't by definition exclude hybridization between species, but often hybridization does not produce viable or fertile offspring. (This definition doesn't work with parthenogenesis. Also, hybridization is accepted as a mechanism that can lead to speciation, most notably seen in plants, where the hybrid offspring can interbreed with other hybrids, but are not able to reproduce with their parental species.)

There is also the morphological species concept which uses morphology and body features to classify organisms, which is more useful when there is little population information available, such as for fossils. But this can result in one sexually dimorphic species being classified as two. (The eclectus parrot was initially classified as two species because the males are green, while females are red.)

In the phylogenetic species concept Willi Hennig defines a species as the smallest group of individuals sharing one common ancestor and a set of fixed heritable differences to make up one phylogenetic branch. Genomics is often used to define this. There is debate that this method creates "taxonomic inflation" and creates more species than necessary because different populations may be able to interbreed, are not reproductively isolated, but are genetically differentiated enough due to local adaptation.

The ecological species concept defines species by their environmental niche--organisms that look, act, and share similar life history patterns. This definition includes parthenogenic species as a separate species from its non-parthenogenic relatives.

(It becomes much more complicated when trying to classify prokaryotes and viruses because mutation occurs at a much higher rate and many of the above definitions cannot be effective applied.)

Ultimately, yes, there are various accepted species that reproduce only by parthenogenesis (like the mentioned New Mexico whiptail lizard), and parthenogenesis can be a defining factor which separates them from a sexually reproducing counterpart species that is similar in morphology, niche, and evolutionary history.

Information comes from courses and textbooks from my Ecology & Evolutionary Biology major within the last year.


I am not sure I'm answering your question but I hope this will help.

There are two main models of genetic drift in biology: Moran model and Wright-Fisher model.

The Wright-Fisher model implies picking $N$ beads (where $N$ is the population size) with replacement in order to form the new population. Therefore, the change in allele frequency (due to genetic drift) follows a Poisson distribution.

$$\frac{2N!\cdot p^kq^{2N-k}}{k!(2N-k)!}$$

The Moran model consists of the following: At each time step you draw two beads. One disappear from the population and the other replicate in order to keep a stable population size.

The two models yield to similar results. Moran model runs twice as fast as Wright-Fisher model.

I don't fully understand your model. You say that in your model you pick one bead at a time. What do you do with this bead? How do you construct your population at the next time step? Do you allow changes in population size? Can you please try to develop how you defined your model. If it is a computer simulation you might paste the important part of your code, that might help.

Haldane and Kimura both worked a lot on these models of genetic drift. For example, they provide different ways of calculating the mean time to fixation of a given allele given their selection coefficient $s$ starting from a given initial frequency $p_0$. Also some work has been done on genetic drift in population where the population size changes over time. Some work have been performed considering more or less complex probability density function for the number of offspring per individual. This kind of literature is very interesting but sometimes ask for quite good knowledge in mathematics (especially for Kimura's articles).

I once asked this question concerning the different models of genetic drift and their assumptions but I didn't get an answer yet.


Why can CO₂ be transported dissolved in plasma?

The bulk of CO2 is transported as bicarbonate/carbonic acid.  The conversion between CO2 and carbonic acid is catalyzed by carbonic anhydrase in red blood cells, otherwise the conversion would be very slow. The bicarbonate is then shuttled out of the RBCs and into the blood plasma. The CO2 (gas) in blood plasma accounts for <10% of CO2 transport, and the solubility isn't that much different from that in water.

Source: Guyton and Hall Textbook on Medical Physiology


Why the "cfr." in 'Cirrhipathes cfr. anguina' and not "cf."?

It's the same as cf. Both abbreviate confer-- meaning the specimen has most of the defining features of the species indicated, and the ID would likely be confirmed with comparison to reference material.

Ref: Sigovini, M. et al. 2016. Open nomenclature in the biodiversity era. Methods Ecol Evol. 7: 1217-1225. http://onlinelibrary.wiley.com/doi/10.1111/2041-210X.12594/abstract


What does cell-to-cell variability means?

I won't ask a question that's related to an article before reading it completely! The answer was in the first paragraph.

  Cell-to-cell variability defined as when genetically identical cells in an identical environment behave differently, leading to significant consequences in many biological processes from bacterial decision-making to mammalian development.


What's the mixture of carbon and haemoglobin called

I'm going to agree with the comment left by @anongoodnurse and assume you are looking for the terms that define CO2 + hemoglobin and CO + hemoglobin.

CO2 + hemoglobin = Carbaminohemoglobin

CO + hemoglobin = Carboxyhemoglobin


What evolutionary mechanism caused felines to develop purring?

It makes sense that the ability to express your emotions improves the quality of the interaction you have with those around you. If a cat purrs those around it know it's feeling good, which can be useful information for future interaction.

I'm sure there have been cats who had a worse life because they didn't bond as well because they didn't purr, and consequently had a slightly lesser tendency to have their DNA end up in the next generation.

This argument goes for every ability to express emotions.


How would i describe a Cladogram as paragraph?

I provided some edits in my comment -- hope the following clarifies things for you a little bit.

  To construct a cladogram, two characters are defined.

You may be confusing character and character state. It's valid to have a cladogram with a single character (e.g. the single character, "warm-blooded"), but you will need at least two character states to infer a non-trivial cladogram. The states for the character warm-blooded would be Yes or No.

A molecular example would be a cladogram inferred from a column of a sequence alignment. That column is the character, and for, say, DNA, the character states are the set {A,C,G,T}.

  Then the outgroup of various species are identified based on the sequencing or closeness of the derived characters in the clades.

The outgroup is specified by you, the investigator. It's typically a hypothesis (viz. model parameter), which is either a guess or is based on some external evidence.

In short, the analysis starts from character-state data for some number of taxa ("species" in your paragraph). From this data you are selecting (constructing) a tree-topology that best fits this data.

E.g. for four taxa, labeled A,B,C,D, with D the outgroup, the process is like:

 start  --> cladogram
 ABC(D)     A  B C (D)
             \/ / /
              \/ /
               \/

There are many different methods to construct the cladogram. One popular method is  maximum parsimony, but the assumptions of that model are severe. However, any method is effectively selecting a tree topology out of all the finitely-many possible tree topologies over N leaves, where N is the number of taxa (species) in your investigation.

  In making a cladogram, ______ assume that groups that _____ more derived characters have a more close common ancestor.

In this sentence, you seem to be expressing a relationship between the number of shared derived characters (synapomorphies) for a given clade, and the common ancestor of that clade.

This can be very confusing, maybe an example will help. Let me annotate the above tree with a binary character, having states + and -.

            +   +  -   -
            A   B  C  (D)
             \ /  /   /
              +  /   /
               \/   /
                -  /
                 \/
                  -

The idea is that the ancestral state for the entire group is -, as was the state for the ancestor of {A,B,C}. However, the + state was derived after the ancestor of {A,B,C} but before (or "in") the ancestor of {A,B}. Then it was passed to the terminal units, A and B. (Note: typically you don't have this ancestral-state information, only the information at the tips of the tree. You're actually inferring the ancestral states and topology from the data at the tips.)

I would claim that, in general, taxa that share more derived character (states) have a more recent common ancestor than taxa that do not. Although, this can be confounded by homoplasy.


It's a bit early yet, but it looks very much like a weed known in my area as "cleavers" or "clingweed" (Galium aparine) because of it's tiny stiff hairs which make it catch and cling to clothing. The picture below is for a fully mature plant, which is stiffer and stickier than when they first sprout. Note the whorl arrangement of (usually six) leaves, with each leaf having a "point" protruding from the tip, the distrubution of hooked hairs along stem and leaf, and the initially prostrate habit (they grow along the ground initially). The mature stem will be squarish and easily crushed.

Though your plant's leaves are broader, there are ~650 species of Galium, and I believe yours will be either Galium aparine or Galium mollugo. But you'll be able to tell what it truly is when it flowers.


How do eukaryotes terminate transcription? (clarification on Campbell Biology)

According to Lewin's Genes XI - Krebs et. al on Eukaryotic Transcription, RNA Splicing, and Processing

  It is not clear whether RNA polymerase II actually engages in a termination event at a specific site. It is possible that its termination is only loosely specified. In some transcription units, termination occurs more than 1000 bp downstream of the site, corresponding to the mature 3' end of the mRNA (which is generated by cleavage at a specific sequence) Instead of using specific terminator sequences, the enzyme ceases RNA synthesis within multiple sites located in rather long "terminator regions." The nature of the individual termination sites is largely unknown.

It does go on to say,

  The site of cleavage/polyadenylation in most pre-mRNAs is flanked by two cis-acting signals: an upstream AAUAAA motif, which is located 11 to 30 nucleotides from the site, and a downstream U-rich or GU-rich element. The AAUAAA is needed for cleavage and polyadenylation because deletion or mutation of the AAUAAA hexamer prevents generation of the polyadenylated 3' end (though in plants and fungi there can be considerable variation from the AAUAAA motif).

I should add that the significance of 11 to 30, or as you said 10 to 35 nucleotides is that it is telling you the approximate size of the protein complex that is sitting on the RNA and where the active site of the protein is. The domain that recognizes the termination sequence is about 10 to 35 bases wide. It is likely that the variation is due to the RNA sequence following the termination sequence ability to form a stem loop structure.

Campbell takes a necessarily basic and less nuanced approach to the information that they provide on molecular biology. The approach is to provide some details and show the evolutionary commonalities between a diverse range of biological systems. The approach is okay as it gets you into the frame of mind of thinking about the interconnectedness of biological systems.

As you progress in your studies you will see that the reality and specifics are far more complex and exception based than was presented in introductory courses. But the more advanced courses spend an entire semester focused on what Campbell covers in one chapter. Campbell is accurate but incomplete out of necessity.


Are mitochondrial genes decoded in the same way as nuclear genes?

Answer Summary

  Translation in the mitochondria of mammals differs markedly from that
  in the cytoplasm. Although it has more similarity to translation in
  prokaryotes, it also shows significant changes from the latter. A smaller
  repertoire of tRNAs is able to translate a ‘simplified’ genetic code
  through structural alterations and base modifications that allow their anticodons
  to decode groups of synonymous codons, not possible according to the standard wobble ‘rules’.

Relationship to the eubacterial translation system

One of the pieces of evidence for the endosymbiotic theory of the origin of mitochondria was the fact that their translation machinery was more similar to that of prokaryotes than to that in the eukaryotic cytoplasm. The similarities to prokaryotes included the (smaller) size of their ribosomes, the susceptibility of their ribosomes to antibiotics specific for bacterial ribosomes, and the formylation of their initiator tRNA — fmet-tRNA.

Although in no way rebutting the endosymbiotic theory (which is widely accepted), mitochondrial translation shows several differences from that in prokaryotes. These include there being a single tRNA to decode methionine in both initiation and elongation (discussed below), the lack of leader sequences preceding the initiation codon, hence precluding a Shine & Dalgarno type of recognition by the ribosome, and additional ribosomal proteins which are thought to “provide a specialized platform for the synthesis and membrane insertion of the highly hydrophobic protein components of the respiratory chain”.

Decoding with 22 mitochondrial tRNAs

General Review: Suzuki et al. (2011) Annual Review of Genetics 45, 299–329

As the question states, mammalian mitochondria encode 22 mitochondrial tRNAs, which would be insufficient to decode mRNAs using the standard genetic code and the wobble ‘rules’ that apply to translation in the eukaryotic cytoplasm and in prokaryotes.

One way out of the dilemma would be if some of the tRNAs were encoded in the nucleus and imported into the mitochondrion in a similar manner to that of nuclear-encoded mitochondrial proteins. Although this turns out to be true for certain organisms (although the import system is different from that for proteins), and important in some cases, this is not the answer for mammalian mitochondria. Thus, as reviewed in Current Genetics (2009), the mitochondrial tRNAs encoded in the nuclear genome of H.sapiens only duplicate the 22 mitochondrial tRNAs and their anticodons. (The one exception is an extra Gln(anticodon CUG) in addition to the Gln(anticodon UUG).)

Let us look more carefully at the problem. Although there are 61 codons specifying amino acids, because of wobble, fewer than this number of tRNAs are required to decode them. The left-hand frame of the figure below shows the standard genetic code, and the minimum number of tRNAs needed to decode it using the wobble ‘rules’ shown beneath, indicated by the colour-coded rectangles.

For those not familiar with the actual pattern of wobble (summarized in my answer to another question), in elongator tRNAs the 5′-position of the anticodon has some flexibility such that a G in that position can form base pairs with U or C in the 3′-position of the codon, an inosine (I) can pair with U,C or A, but an anticodon C can only pair with a codon G. The unmodified bases A and U are rarely found in anticodons, but a variety of different chemically modified Us are found (U* in the figure) which only pair with A. Thus, the minimum number of elongator tRNAs needed would be the number of coloured rectangles — 36 — and, as there are separate species of tRNAmet for initiation and elongation, the minimum number of tRNA species is 37.

When the human mitochondrial genome was sequenced, two anomalies stood together: the limited number of tRNA genes already mentioned and (more sensationally) changes from the standard genetic code (indicated in red on the right-hand side of the figure). It was immediately realized that these changes served to rationalize the code so that all synonymous codons were in groups of four or two. If it were assumed that the decoding specificity or wobble of mitochondrial tRNAs were different, then 22 tRNAs would be sufficient using the ‘wobble’ shown beneath the right-hand frame of the figure for groups of four amino acids (dark blue) and groups of two amino acids with codons ending in A or G (red).

One further requirement was that a single tRNAmet be involved in both elongation and initiation, a requirement the fulfilment of which has already been mentioned.

What features of the tRNAs could change the wobble ‘rules’ that have been conserved between prokaryotes and eukaryotic cytoplasm? There turn out to be two types of changes. The first, and most obvious, is the fact that certain (but not all) mitochondrial tRNAs have non-canonical cloverleaf structures, the most extreme being tRNAser in which the whole D-loop is missing. The second is the post-transcriptional modification of bases in the anticodon — just as is the case for tRNAs in the cytoplasm, this can markedly affect decoding specificity.

It is not yet possible to describe the codon–anticodon interaction in mitochondrial translation in the way that this has been done in for the cytoplasm or for prokaryotes. The problem would appear to be the difficulty of obtaining sufficient pure tRNAs. Whereas it is easy enough to clone and transcribe the tRNA genes, this is insufficient without the secondary chemical modifications of the bases which is key to the structure and function of the tRNAs.


Why don’t humans have eyes at the back of their heads?

Vertebrates have ears which sense 360 degrees for a range of many meters, and they have social eyes, where they group many eyes and ears into one social group, it's easier to listen and live in groups, than grow eyes in the back of the head.

2 eyes exists in nearly all bilateral animals, arthropods, flatworms, sea-slugs, crabs, crickets, squids, flies. Arthropods have compound eyes and it would be easier for them to have 4 eyes, and only spiders and horseshoe crabs have more than 2.

It would be easier for a vertebrates to develop 4 nostrils and ears than 4 eyes because they are simpler than the orbs of the eye.

Same reason as 5 fingers has been the optimal numbers for all vertebrates since early lizards. in short, it's very easy to lose extra organs and to modify old ones, but it's very difficult to evolve new organs, and to relocate ones around the nerves and veins... centrally connected organs travel around the body and the circulation moves in front of them, i.e. if you did get 4 eyes and two of them moved to the back and sides, the nerves for your face expressions that are next to your ear would have to go in front, around, and through the moving eye pathways.

To simplify, we stopped evolving our symmetrical archetypes when we were related to starfish, ammonites and ediacaran fauna, and the fastest most versatile animals all had 2 sided symmetries, with entirely symmetrical nervous systems, and forwards moving at that point in time, using binocular compound vision, which did have 180, and that binocular compound vision afterwards became our 2 eyes. We share the kingdom Animalia with starfish, our common ancestor experimented with shape during the Ediacaran era.

To understand the difficulty of adding new eyes later, you should learn why nearly all vertebrates have 5 fingers, except some frogs which have 4. it

google: why do animals all have two eyes?


What is this brown spider with black and white stripes? (Atlanta, Georgia)

It resembles Dolomedes tenebrosus, commonly called the Dark Fishing Spider, and it belongs to the family Pisauridae.

Image Source: Bug Guide

Males are generally thinner in profile than the females, which is well depicted below.

Image Source: Spiders.Us

Based on the pictures provided, you seem to have captured a male Dolomedes tenebrosus.


Does body mass have a bearing on reflex speed?

I went into this with the same assumptions that jello did, but I found two studies that had some interesting results.

Isojärvi (2010) found that in obese and under-exercised adults, physical fitness level predicted, among other things, a significant proportion of the variance of nerve conduction velocity and F-wave latency.  So, these individuals may theoretically have a slower response to noxious stimuli.

While Type II diabetes is not always a result of obesity, there is often a high correlation between the two.  Oltman (2005) found that, in "Zucker diabetic fatty" rats (an animal model of Type II diabetes), motor nerve conduction velocity in the sciatic was significantly slowed.  This effect, too, would affect the rate with which an individual could withdraw a limb from a noxious stimuli.

So, I don't think that anatomical changes in the bodies of individuals who are obese would have any effect, but clearly there are physiological changes in the neurons of these individuals.

References:

Isojärvi H, Keinänen-Kiukaanniemi S, Kallio M, Kaikkonen K, Jämsä T, Korpelainen J, Korpelainen R. (2010). Exercise and fitness are related to peripheral nervous system function in overweight adults. Med Sci Sports Exerc. 42(7):1241-5.

Oltman CL, Coppey LJ, Gellett JS, Davidson EP, Lund DD, Yorek MA. (2005).  Progression of vascular and neural dysfunction in sciatic nerves of Zucker diabetic fatty and Zucker rats. Am J Physiol Endocrinol Metab. 289(1):E113-22.


Why did the process of sleep evolve in many animals? What is its evolutionary advantage?

This good non-scholarly article covers some of the usual advantages (rest/regeneration).

One of the research papers they mentioned (they linked to press release) was Conservation of Sleep: Insights from Non-Mammalian Model Systems by John E. Zimmerman, Ph.D.; Trends Neurosci. 2008 July; 31(7): 371–376. Published online 2008 June 5. doi:  10.1016/j.tins.2008.05.001; NIHMSID: NIHMS230885. To quote from the press release:

  Because the time of lethargus coincides with a time in the round worms’ life cycle when synaptic changes occur in the nervous system, they propose that sleep is a state required for nervous system plasticity. In other words, in order for the nervous system to grow and change, there must be down time of active behavior. Other researchers at Penn have shown that, in mammals, synaptic changes occur during sleep and that deprivation of sleep results in a disruption of these synaptic changes.


The linearity of a Lineweaver–Burk plot assumes that your system follows standard Michaelis–Menton kinetics.

Not every enzyme system follows Michaelis–Menton kinetics with all the assumptions made in its derivation. There are a number of reasons for non-linear behavior, including cooperativity, substrate inhibition, substrate activation, limiting cofactors, isoenzymes, and non-steady-state kinetics.

Further reasons for a non-linear plot involve experimental issues. Depending on your experimental setup, you may not have accurately measured the initial rates of some of the faster conditions, which can lead to non-linearity of your Lineweaver–Burk plot. If you're operating under conditions which may lead to product inhibition, you might also see non-linear behavior.


Mapping a mutation to known SNP, 3' UTR, miR

In order:

Unfortunately, there's no easy way to batch query with only location. You could look up SNPs within genes here.  (You could find the gene a SNP is located in by searching an annotated human genome file for the position.)
You can figure out whether it's in 3'UTR by comparing to a list of human 3' UTRs. The UCSC genome browser page here will help: change the region to "genome", output format to "BED", click "get output", and then filter for 3' UTRs.
You can figure out if it's in a miRNA by comparing chr/start positions to the database available here.
You could use the chromosomal locations and compare to the human genome sequence.  There is probably a better way to do this, but the FASTA for each chromosome is available here.
You could use the SNP IDs to map to Genbank accessions, as per the instructions here.

You don't need BioPython for the first three steps, since it's just parsing each line and comparing values. BioPython is useful for working with FASTA files (so part 4).  All in all, this is mostly reduced to a programming question with all of these resources (basically, you need split each string to get the appropriate numbers/IDs and then compare).


Do all chromosomes in one human body contains same genome?

Yes, all cells contains the same genome. This is because, for a given individual, all of its cells comes from the zygote, a singular cell formed after fecondation of the maternal ovum and paternal spermatozoa, through repeated cell division (mitosis). This is a process which replicates quite exactly the genome that will be passed to the newly formed cells.

There are some exceptions however, such as :

Red blood cells, and platelets : these cells lack a nucleus, and don't contain DNA at all.
Cells bearing mutation(s) : even though the replication machinery try to make an exact copy of the DNA, error(s) may happens.
Gametes : ovum and spermatozoa are produced through meiosis, a specific replication mechanism that keeps only half the genome, and may produce new sequences through recombination.
Lymphocytes undergo V(D)J recombination and somatic hypermutation which alters their DNA, a process that is necessary to the working of our immune system.


What causes the tonotopic organization of the inner ear?

The frequency tuning in the cochlea is due to a number of factors.

The primary factors of cochlear frequency tuning are generally ascribed to the passive physical characteristics of the basilar membrane (BM), which OP already identified in the question - The BM is wider and more flexible at the apical end (low-frequency region) and narrower and stiffer at the basal end (high-frequency region). Like the strings on a guitar, stiff and thin cords produce high-pitched sounds, while loose and thick cords produce low-frequency sounds. The stiffness of the BM gradually decreases from base to apex, while its width gradually increases along that length, thereby creating the gradient of characteristic frequencies of the basilar membrane (Purves et al., 2001) (Fig. 1).
Another factor that may play a role is the length of the stereocilia. Stereocilia are the mechanotransductive hairs that give the hair cells their name. In the inner hair cells (IHCs) the stereocilia are mechanically deflected when a sound wave eneters the cochlea. That in turn leads to neurotransmitter release from the IHC and that in turn stimulates the auditory nerve. The stereocilia increase in length towards the base of the cochlea. Longer stereocilia respond most optimally to longer wavelengths (lower frequencies). Hence, stereocilia length also provides another mechanical gradient that facilitates frequency decomposition in the cochlea (Snow & Wyckam, 2009).
A last factor is more physiological in nature; the frequency tuning of the cochlea is much sharper than can be explained on the basis of the passive membrane properties of the BM. For example, studies in dead cochleas show a shallow tuning of the BM, while the tuning in alive cochleas is much sharper. Hence, it is thought that an active mechanism has to be at play. Generally, the outer hair cells (OHCs) are attributed this function. OHCs start to increase and decrease in length when the BM moves in response to sound. They are thought to amplify the BM response to sound. If these OHCs only amplify a very narrow set of frequencies and not others, they may indeed be capable of sharpening the tuning curve of the associated nerve fibers, but the exact mechanism behind this is unknown (Purves et al., 2001).

Fig. 1. Frequency tuning along the basilar membrane. source: Purves et al., 2001

References
- Purves et al. (eds.) Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates (2001)
- Snow & Wyckam, Ballenger's Otorhinolaryngology: Head and Neck Surgery, John Jacob Ballenger (2009)


Because all available ATP will likely be quickly spent by various cellular machinery.
If there was 20-30mM of ATP, what would stop muscle from contraction and how could you keep ATP level constant at rest, be ready for rapid movement? By blocking all myosin? This creates enormous regulatory problems for the cell.

Phosphocreatine buffers energy for a period of time when it will be actually needed. Having buffer allows for more robust control of energy spending, for example via regulation creatine kinases and other enzymes. Just by activating single enzyme you then start rapid conversion of ADT into ATP via phosphocreatine.


Why is venom more common in fish and snakes than other vertebrates?

This write up by Carl Zimmer basically covers anything I could have said.  He links to a number of resources, in particular Casewell et. al. 2013, which at a cursory glance looks utterly fascinating and very well done.  Zimmer recapitulates figure 1, which sums it all up, or to quote Carl:

"Each lineage of venomous animals became deadly on its own, independent of all the others. And yet, in the end, their venoms echo each other... These results show that there are a limited number of ways to kill your victim quickly. No matter what genes you borrow for the evolution of venom, they will end up very similar to other venoms."

Another Zimmer piece specifically points out research purporting to show that snake venom genes are much older than snakes, maybe 200 million years old.  That gets around but doesn't quite answer your question.  An older review tried to coalesce things (as best as he could in '92), spending time focusing on insectivora and dealing with mammals.  The theory is that while venom is an excellent advantage, it requires a significant investment and is often slow-working.  In a world with sharp teeth capable of tearing, venom may not be necessary.  Mammals, for example, might evolve to not use venom, as it may not be suitable for their high daily energy demands.  The pdf linked above briefly touches on the concept of "reverse recruitment," where venom genes may be usefully re-purposed for other biological processes.
Reference:
Nicholas R. Casewell, Wolfgang Wüster, Freek J. Vonk, Robert A. Harrison, Bryan G. Fry. Complex cocktails: the evolutionary novelty of venoms. Trends in Ecology & Evolution
Volume 28, Issue 4, April 2013, Pages 219-229


This is a passionfruit. It comes from a plant whose scientific name is Passiflora edulis.

It's indeed a climber, as you can see:

Finally, a curiosity about the name passion fruit. The fruit is called passion fruit because the flower is called passion flower. This is the flower:

But why it is called passion flower? Passion here has nothing to do with sexual love or desire, the common meaning of "passion", but with the suffering of Jesus.

Some say that it's because the flower resembles (?) the crown of thorns placed in Jesus' head. Other say that it symbolises Jesus' wounds. In fact, in portuguese we call it "flor das cinco chagas", or flower of the five wounds.

EDIT: thanks to @AlanBoyd's comment, you can see that its connections with Christianity are way more complex: https://en.wikipedia.org/wiki/Passiflora#Etymology_and_names

Post Scriptum (not related to the question): this plant is native to Brazil, and I had a couple of specimens in my yard. One of the most interesting things about passionfruits in Brazil is that it attracts an insect that we call "percevejo do maracujá", or passionfruit bug in a very free translation. Its scientific name is Diactor bilineatus, and it's one of the most beautiful insects to me. I loved to see them feeding on my passionfruits. This is the adult on a passionfruit (where you normally find them), and the nymph is even more colourful:


A neutralization reaction occurs between Brönsted acids and bases to form a salt.

In this case, you have to add a Brönsted base to neutralize your acid. If the final pH is important, you should work out the exact quantity of base to add. Otherwise, just use litmus paper to check the pH of your solution, and add base until it's neutral.

EDIT

In view of the other answer proposed, I want to stress the following:

Do NOT dispose of your solution in the sink/sewer. Leave it in its plastic bin until a lab technician takes it to the furnace.

If the base you use is sodium bicarbonate (NaHCO3), there will be bubbling, caused by the decomposition of carbonic acid (H2CO3) into water (H2O) and carbon dioxide (CO2). You've successfully neutralized the TCA once there's no bubbling upon addition of NaHCO3.

It is indeed best to proceed slowly while adding your base.


What happens to the holes in the skull where teeth were developing?

Bone growth continues in the human body for quite awhile after permanent teeth come in. Generally, the complete closure of all growth plates doesn't occur until the mid 20s.

As the top and bottom primary teeth come in, the empty space left behind is gradually filled by growth of the maxilla and mandible, respectively. During the time period when teeth are actively coming in, teeth can displace into the empty space left by other permanent teeth that are no longer there, resulting in crooked teeth.


Are there any situations in which phenylephrine is preferred to pseudoephedrine?

Yes, in all clinical situations where you need pure vasoconstriction without heart rate acceleration (mostly valid for iv administration route).

The classical example would be in the operative setting. If the patient is in a hypotensive state due to hypnotic drugs, opiates, etc. and has atherosclerosis, you will prefer a drug that will reverse the hypotension without an increase in heart rate, i.e phenylephrine. The reason is that an increase in heart rate will shorten the duration of diastole, which will therefore shorten the time interval where the coronary arteries are perfused. Moreover, an increase in heart rate also means an increase in heart oxygen consumption. The end result will be an imbalance between oxygen input and requirement, i.e ischemia and potential heart infarction.

Conversely, if you have a patient with aortic valve insufficiency (regurgitation), you will prefer ephedrine (or any drug with beta 1 activity), because you will be aiming at shortening the available time for regurgitation to occur.


How long could Earth's oxygen supply last if no new oxygen were produced?

Disclaimer:

This is going to be a very mathematical answer. Before answering it, I assume that you are only asking about humans, assuming that all other organisms don't require $O_2$ to survive (as it will complicate the answer many many times).

List of variables:

V     = total volume of air on earth (in l)
V'    = total volume of oxygen on earth (in l)
V(1)  = volume of oxygen used by 1 person in whole lifetime (in l)
V(a)  = volume of oxygen used by whole mankind (one generation) in whole lifetime (in l)
V(p)  = percentage of total oxygen used by whole mankind (one generation) in whole lifetime

Method used:

$ \%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation = \underline{\hspace{3mm}Volume\hspace{5mm}of\hspace{5mm}O_2\hspace{5mm}in\hspace{5mm}air\hspace{3mm}}\times\hspace{1mm}100$
$\hspace{83mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}by\hspace{1mm}humans$

$Number\hspace{1mm}of\hspace{1mm}years = \underline{\hspace{2mm}Number\hspace{1mm}of\hspace{1mm}years\hspace{1mm}in\hspace{1mm}1\hspace{1mm}generation\hspace{2mm}}$
$\hspace{42mm}\%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation$

Procedure:

Lets first find out the total amount of air on earth.

From this:

  The air sphere measures 1999 kilometres across and weighs 5140 trillion tonnes.

From here:

  At sea level and at 15 °C air has a density of approximately 1.225 kg/m3

Total volume of air:

$volume = mass \hspace{1mm} / \hspace{1mm} density$

$V = 5140 \times 10^{12} \hspace{1mm} tonnes \hspace{1mm} / \hspace{1mm} 1.225 \hspace{1mm} kg.m^{-3}$

$V = 4195.9 \times 10^3 \times 10^{12} \hspace{1mm} m^3$

$V = 4195.9 \times 10^3 \times 10^{12} \times 10^3 \hspace{1mm} l$

$V = 4195.9 \times 10^{18} \hspace{1mm} l$

Now, from this, 20.95% of this is $O_2$ i.e.

$V' = 4195.9 \times 10^{18} \times 20.95 / 100$

$V' = 87904.489 \times 10^{16}$

$V' = 879.04 \times 10^{18} \hspace{1mm} l$

Moving on to next part, from this:

  a human being uses about 550 liters of pure oxygen per day.

From this:

  71 years was the average life expectancy at birth of the global population in 2013.

$V_1 = 550 \hspace{1mm} l.day^{-1}.person^{-1} \times 25915 \hspace{1mm} days$

$V_1= 142.53 \times 10^5 \hspace{1mm} l.person^{-1}$

From this:

  The world population (the total number of living humans on Earth) was 7.349 billion as of July 1, 2015.

So

$V_{a} = 142.53 \times 10^5 \hspace{1mm} l.person^{-1} \times 7.349 \times 10^9 people$

$V_{a} = 1047.452 \times 10^{14} \hspace{1mm} l$

Finally

$V_p = V_a / V' \times 100$

$V_p = (1047.452 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$

$V_p = 1.191 \times 10^{-2}$

$V_p = 0.0191 \hspace{1mm} \% $

This gives the percentage of total $O_2$ in air used by one human generation. From this, we can find the number of years for which $O_2$ will last, as I have done below:

$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$

$71 \hspace{1mm} years = 0.0191 \hspace{1mm} \%$

$1 \hspace{1mm} \% = 71 / 0.0191 \hspace{1mm} years$

$100 \hspace{1mm} \% = 3717.277 \times 100 \hspace{1mm} years$

$\hspace{13mm} = 371,727.748 \hspace{1mm} years$

Conclusion:

So, yes at least humans can live for a very long time without plants doing any photosynthesis (ideally). 371,727 years seems too large a period of time, but it is just based on ideal assumptions, this number would come down (maybe into your specified range) when more variables are added.

For example:

To show extent of deviation by addition of factors, I add a very general, but complex factor in the expression: air pollution.

How much $CO_2$ is released per year can be estimated from this:

  In 2011, utility coal plants in the United States emitted a total of 1.7 billion tons of CO2

And with the contribution of countries like China, India, Europe, etc. that number should rise up to at least 2.5 million tonnes (its just that I couldn't find the worldwide data on it).

Now:

$1 \hspace{1mm} C + 1 \hspace{1mm} O_2 \rightarrow 1 \hspace{1mm} CO_2$

$2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} CO_2 \Rightarrow 2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} O_2$

So, 2.5 million tonnes more $O_2$ is being used each year from the environment. But, there is another twist in this. From this:

  WHO reports that in 2012 around 7 million people died - one in eight of total global deaths – as a result of air pollution exposure.

It means that 7 million people less will consume $O_2$ each year i.e.

$Net \hspace{1mm} population = 7349 \times 10^6 - 7 \times 10^6$

$\hspace{32mm} = 7.342 \times 10^9$

$V_{a} = 142.53 \times 10^5 \times 7.342 \times 10^9$

$V_{a} = 1046.455 \times 10^{14} \hspace{1mm} l$

$V_p = V_a / V' \times 100$

$V_p = (1046.455 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$

$V_p = 1.1904 \times 10^{-2}$

$V_p = 0.01904 \hspace{1mm} \% $

$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$

$71 \hspace{1mm} years = 0.01904 \hspace{1mm} \%$

$1 \hspace{1mm} \% = 71 / 0.01904 \hspace{1mm} years$

$100 \hspace{1mm} \% = 3728.991 \times 100 \hspace{1mm} years$

$\hspace{13mm} = 372,899.159 \hspace{1mm} years$

So, overall number increases instead of decreasing. This example was just to show how adding more factors to the equation would deviate the overall answer, and how large that deviation can be.


Ramifications and possibility of a diet consuming exclusively of human semen

No, you cannot live off of semen.

A source from Columbia.edu:

  A typical ejaculation fills up about one teaspoon; the actual amount is determined by a man's age (younger men usually make more semen), when he last ejaculated, and how long he's aroused before ejaculating, among other factors. Contrary to what you've heard, semen is not loaded with calories. Each teaspoon of ejaculate has about 5 - 7 calories and some 200 - 500 million sperm. Since sperm make up only about 1 percent of semen, what accounts for the other 99 percent? Well, its other ingredients include:

  Fructose sugar
  Water
  Ascorbic acid (a.k.a., vitamin C)
  Citric acid
  Enzymes
  Protein
  Phosphate and bicarbonate buffers (bases)
  Zinc

  Can swallowing semen enrich a protein poor diet? Unless you're gulping gallons of it each day, it's no substitute for real nutritious cuisine!

From a non-academic, but apparently well-informed source, semen contains:

  Semen contains only 15 calories and boy does it have a lot of stuff in it. So let's have a look. Ejaculate contains ascorbic acid, blood-group antigens, calcium, chlorine, cholesterol, choline, citric acid, creatine, deoxyribonucleic acid (DNA), fructose, glutathione, hyaluronidase, inositol, lactic acid, magnesium, nitrogen, phosphorous, potassium, purine, pyrimidine, pyruvic acid, sodium, sorbitol, spermidine, spermine, urea, uric acid, vitamin B12, and zinc.

I've highlighted the nutritionally-relevant ingredients. You'll notice that there is some overlap - with the Columbia source. What you won't notice, though, are the rest of the Essential Vitamins and Minerals:

Vitamin A (retinol)
Vitamin B1 (thiamin)
Vitamin B2 (riboflavin, vitamin G)
Vitamin B3 (niacin, vitamin P, vitamin PP)
Vitamin B5 (pantothenic acid)
Vitamin B6 (pyridoxine, pyridoxamine, or pyridoxal)
Vitamin B7 (biotin, vitamin H)
Vitamin B9 (folic acid, folate, vitamin M)
Vitamin D (ergocalciferol, or cholecalciferol)
Vitamin E (tocopherol)
Vitamin K (naphthoquinoids)
Chloride (Cl−)
Chromium (Cr)[4]
Cobalt (Co) (as part of Vitamin B12)
Copper (Cu)
Iodine (I)
Iron (Fe)
Manganese (Mn)
Molybdenum (Mo)
Nickel (Ni)
Selenium (Se)
Sulfur (S) numerous roles[5]

I should also mention that the specific amounts of each ingredient will vary from person to person, as diet can play a major role in flavor resulting from the changed nutritional content (i.e. - higher fructose levels).

As perhaps the most reliable source I could find, there is a Wikipedia article with references concerning the makeup of human seminal fluid and has this information:

  amino acids, citrate, enzymes, flavins, fructose (2–5 mg per mL semen,3 the main energy source of sperm cells, which rely entirely on sugars from the seminal plasma for energy), phosphorylcholine, prostaglandins (involved in suppressing an immune response by the female against the foreign semen), proteins, vitamin C

  acid phosphatase, citric acid, fibrinolysin, prostate specific antigen, proteolytic enzymes, zinc

It echoes the other sources closely, and still yields insufficient evidence that a person could live off of semen exclusively.

As for how long you can live? From a Scientific American article concerning starvation there have been confirmed instances of hungers strikes lasting up to 40 days. Assuming you could consume enough semen to sustain your body's daily Caloric requirements, you would die of malnutrition eventually. Scurvy - the inadequate intake of Vitamin C (Ascorbic Acid) - would probably be the culprit, as deficiency becomes clinical in 1 to 3 months with the later stages of Scurvy being: "...more severe and life threatening; common manifestations include generalized edema, severe jaundice, hemolysis, acute spontaneous bleeding, neuropathy, fever, convulsions, and death."

Assuming that there is enough Vitamin C in semen, you would die of other deficiencies. Since Vitamin B1 (Thiamine) is water-soluble (is not stored in your fatty tissues), not found in semen at all, and the body only reserves about a month's worth, after 30 days you would start to experience Beriberi - which is only slightly less fun than Scurvy.


it looks like medlar. Medlar is a fruit sized about 4cm (1 1/2 inch). it must be common medlar.

You can find out more about this interesting fruit here at Wikipedia.

  The medlar was already being cultivated about three thousand years ago in the Caspian Sea region of northern Iran and Azerbaijan. It was introduced to Greece around 700 BC, and to Rome about 200 BC. It was an important fruit plant during Roman and medieval times. By the 17th and 18th centuries, however, it had been superseded by other fruits, and is little cultivated today.


Is there a way to know how many sodium channels are active (conducting) at a given time in the brain?

Unfortunately, there is no way to know how many sodium channels are active (or even present) in one person's brain due to the extremely high variability of channel and neuron density in a population and the lack of methodology around quantifying total number of healthy active synapses (1). Diseases like epilepsy can occur due various points of the sodium signaling process going wrong. It could be sodium channels are deformed and not accepting the proper signal, it could a low density of channel proteins, or it could be damage to the neuron themselves (2-4). No one has examined the "normal/healthy range" of sodium channels in the brain. When categorizing sodium channel deficiency scientists will often compare the number of sodium channels in a healthy brain vs. a disease brain using bioluminescence imaging or some other visualization technique. Bioluminescence specially quantifies the number of active sodium channels by binding causing healthy sodium channels light up and then quantifies density by the brightness of the synapse. This is not a direct quantification of the number of proteins, but I can not think of any technique that allows you to count the number of proteins on a cell without damaging the cell. I'm sorry this isn't technically an answer to your question, but hopefully it provides some helpful references to understand molecular brain protein imaging.

Principles of Neuroscience
Low Sodium Channel Density and    Epilepsy
Sodium Channel Mutations and Epilepsy/ Other Nervous    System Disorders
Neuropathy and Sodium Channel Related    Diseases


Biological meaning of taking zero as coefficient of the Laplacian in mathematical models of cell motility

Just so we're on the same page..

$u(x,t)$ is a concentration/density function that describes the number of particulate species (bacteria, gas molecules, etc.) at point-in-space $x$ and time $t$. And although it may be an obvious statement to make.. with $u$ having the parameters $(x,t)$, this indicates that particulate concentration values are dependent upon both position and time.

$\delta$ is the diffusion coefficient of the particulate concentration, defined as a proportionality constant between particulate diffusion and the overall particulate concentration gradient. Particulate diffusion can be regarded as local behavior, whereas the overall particulate concentration gradient describes the behavior of distribution for the entire particulate concentration, and of which may be affected by forces other than the particulate's response to an attractant/repellant gradient, including temperature, pressure, and/or other environmental variables. An in depth understanding of this coefficient can be obtained by reading sections 2.1 & 2.2.

Your questions

Biologically, what is the meaning of a situation where $\delta = 0$?

Well, if you did in fact read the recommended sections, you may already have realized that it's just not possible for $\delta = 0$, unless you're considering concentrations of mass that simply can't diffuse throughout one another, but even then $\delta$ would be considered as $DNE$.
To reference a portion of 2.1 & 2.2:

Molecular diffusion, strictly speaking, cannot occur under conditions in which both the net flux and the [concentration gradient] are simultaneously zero. If the [concentration gradient] is uniform, then in general fluxes are different for different species, and the net flux is not zero. If the net flux is zero, a small [concentration] gradient must exist in order to counter the tendency for the different species fluxes to be different.

That being said, the diffusion coefficient can be an extremely small value - of which is based on the nature of the particulate(s) undergoing diffusion, and the medium for which they travel throughout - but it's never zero. See here for a series of tables that contain diffusion coefficients for common substances at standard conditions.
And as for the biological meaning to $\delta = DNE$.. the only conclusion that could be made is that the mass concentrations under consideration can't diffuse with one another, for whatever reason. Whether or not there's meaning beyond this, I believe that would be dependent upon what's specifically being studied.

.. that is, where there is not Fickian diffusion governed by the Laplacian term?

This statement however, does have biological meaning to it. When $\delta \Delta u(t,x) = 0$, this means there is a zero net flux occurring at point-in-space $x$ at time $t$. Which is to say that - the number of particulates of a given species entering a given region of space over a given time interval is the exact same as the number of particulates of the same species leaving that exact same region of space over the exact same time interval. When this is true for all regions of space within the [biological] system, it means that the system is in a steady-state, and/or has reached equilibrium.
Note: Equilibrium and steady-state systems are not the same, however, the differences involved aren't relevant to the scope of this discussion, and so nothing further will be said about this.
When a biological system is in a steady-state, and/or is in equilibrium, that can carry significant implications. Perhaps the most ubiquitous example that also first comes to mind are the steady-states of ion channels, with the effects of cell activation/non-activation being the implications. Another example could be pretty much any chemical reaction that reaches equilibrium.

Is there any interest in studying such situations? Can you point out some references on this topic?

Yes, there are many occurrences where these states are studied, of which you may already be aware of. Regardless, here are a few that seem worthy enough for me to provide in this response:

Steady-state Distribution of Bacteria Chemotactic Toward Oxygen

Equilibrium of Two Populations Subjected to Chemotaxis

The Hodgkin-Huxley Model

In summary
The biological meaning of $\delta \Delta u(t,x) = 0$ usually deals with scenarios where the region(s) in space experiences a flow of mass that has equal incoming & outgoing rates for a given particulate species. Most of the time, this is indicative of a steady-state, and/or equilibrium, and this can be confined to local regions, or globally throughout the system.
And I'd also like to offer a slightly different perspective. Normally, the diffusion coefficient is a temperature & pressure dependent function. However, if you're considering situations with STP/NTP, the diffusion coefficient can truly be treated as a constant. When this is the case, the Laplacian term is analogous to the heat equation. By taking this perspective, the Laplacian term [being zero] is stating that there is no loss or gain in heat (species-specific particulate motion) when considering a region of space over a defined time interval, and the overall model would describe the change(s) in motion (heat) for the entire system. From there, biology could explain as to why the "heat" behaves the way it does, of which would involve the mechanisms & behaviors of an organism with respect to its reaction(s) to an attractant/repellent.
And lastly, for the sake of inclusivity, the other terms in these models generally represent behaviors that are external to local interactions, and each may carry differing effects, such as birth/death rates in population dynamics, or particulate concentration movement that's perpendicular to the axis to which the concentration gradient moves upon, as is the case with the second term in the chemotaxis model. So then, when the Laplacian term is not contributing to any change, i.e., when there is a zero net flux, these other terms will then be the only candidate contributors to any potential changes in the system, whatever those changes may be.

References

A Mathematical Model For Chemotaxis
Keller-Segel Models for Chemotaxis
Gaseous Diffusion Coefficients
Fick's Second Law


What you are seeing is a cocoon for a moth pupa.

Here is a link to a YouTube video of one hatching that is normal found in the soil.


Could an animal with an open circulatory system survive in a near-zero gravity environment?

I believe that fruit flies have been taken aboard the Space Shuttle for experiments. They survived and the adults have an open circulatory system.


What species is this burrow-digging insect?

That is clearly a type of wasp.  Some digging leads me to think it could be something in the genus Ammophila (a type of "thread-waisted wasp") for example Ammophila sabulosa:

However, 6 cm is huge for a wasp and twice the size of Ammophila sabulosa — are you sure about that length?


No.  Certainly not.  There is only a very limited number of cells in the body of any creature which pass on genetic material to the offspring generation; these are referred to as gametes.  Mutations to these cells, however, do not affect the parent in the least, as their sole function is to produce offspring.

One gamete from the father & one gamete from the mother fuse to produce a child with a combination of genetic code, which means that mutations in those gametes (which did not affect the parent) will be present in every cell of the child's body, and affect the child.

Furthermore, do remember that most mutations are not "enhancements"; rather the vast majority of mutations are harmful.

After birth (and really, long before birth) mutations acquired in the organism are unable to be passed on to the offspring, unless they happen in the gametes, in which case they do not affect the parent carrying those mutations.


Do babies conceived naturally or artificially have any differences in long-term health?

A review paper on children born by the advent of assisted reproductive technologies (ART) and frozen sperm (Lansac & Royere, 2001) concludes that ART children, as compared to the general population:

Have normal weight;
Do not suffer increased occurrence of premature births;
Do not have increased rates in stillbirths;
Have equivalent sex ratios;
Show no increased occurence of birth defects and no chromosomal abnormalities;
Have normal overall health.
Have normal psychosocial development, at least up to 8-9 years of age, but the available data is scant in this area.
However, the rate of multiple pregnancies was higher in the ART group. This may be caused by excessive hormonal treatments during artificial insemination therapy, or by ovulation induction treatments and embryo transfer policies (multiple embryos implanted) that may increase the rate of multiple pregnancies.

The authors do conclude that larger and longer studies are needed to support these findings more conclusively, given that their review paper was based on just two studies. It deserves note, however, that both of these studies were prospective in design and included a large population of subjects.

Reference
- Lansac & Royere, Hum Reprod Update (2001); 7(1): 33-7


Is it possible to transfer acquired hemophilia with breast milk?

Acquired Hemophilia is an AutoImmune Disease, hence it is possible to transfer it from mother to child through breastfeeding milk. The antibodies subjected to autoimmune disease also passes into the infant or baby from breastmilk in addition to the healthy antibodies. These abnormal antibodies will act as an inhibitor to the enzyme responsible for production of Factor VIII , a blot clotting protein. Less number of factor VIII protein results in increased amount of internal bleeding.


Why does azithromycin not affect human mitochondria?

There are two general points that should be appreciated in relation to this question:

Your statement that mitochondria “have prokaryotic ribosomes” is a misleading simplification. Although mitochondria and plastids are thought to be derived from eubacteria — and their ribosomes have some similarities  in antibiotic sensitivity — the structures of their large rRNAs differ (as indeed do those of their small rRNAs and their ribosomal proteins). This is important because the large rRNA (the equivalent of 23S rRNA in E.coli) is the target of many antibiotics, including the macrolide antibiotics, of which azithromycin is a member.
Experiments in vitro have shown that human mitochondrial ribosomes are not sensitive to some of the macrolide antibiotics that inhibit eubacterial ribosomes, whereas those of some lower eukaryotes are.

Therefore it should not be particularly surprising that macrolide antibiotics do not affect human mitochondria, or that they do affect Toxiplasma etc., the ribosomes in the apicoplasts of which are sensitive to these antibiotics in vitro — presumably because of their rRNA structure in the specific target region.

An answer to the question in your title would seem to require an explanation of the molecular basis of these different sensitivities. It is thought (although not, I gather, definitely proved) that this is the identity of the base at the position equivalent to 2058 of E.coli 23S rRNA: those ribosomes that are sensitive to the antibiotics have the base A in that position, whereas those that are resistant have the base G.

References

Böttger, E.C. et al.(2001) EMBO Reports vol 21, pp. 318–323. Structural basis for selectivity and toxicity of ribosomal antibiotics.

Greber, B.J. et al.(2014) Nature vol 515, pp. 283–286. The complete structure of the large subunit of the mammalian mitochondrial ribosome.


What value type would a chromosome position be in a database or form?

Since it sounds like you are the one designing the database, you can make this a number of ways. The simplest is probably to reduce it to two variables, likely two decimals.

See this hemoglobin example for a chromosomal locus example.

There are N chromosomes (23 for humans, if you like, sex chromosomes can be treated as a pair).
There are 2 chromatids per chromosome.
The part of the chromatid is either p or q (short or long arm).
Then there is the location on the portion of the chromatid (eg, 15.5).

Chromatid can be easily represented as a decimal, where the integer portion is the chromosome number, and the decimal portion corresponds to the chromatid and arm.

The chromosomal locus can be another decimal, such as 15.5 for the example above.

This is of course one way, and there are many other ways you could do this.


The reason is simple: Chocolate contains cocoa which contains Theobromine. The darker the chocolate is (meaning the more cocoa it contains) the more theobromine it contains. This is a bitter alkaloid which is toxic to dogs (and also cats), but can be tolerated by humans.

The reason for this is the much slower metabolization of theobromine in the animals (there are reports for poisonings of dogs, cats, birds, rabbits and even bear cubs) so that the toxic effect can happen. Depending on the size of the dog, something between 50 and 400g of milk chocolate can be fatal. As mentioned by @anongoodnurse the cocoa content in milk chocolate is the lowest and much higher the darker the chocolate gets.

The poisoning comes from the Theobromine itself, which has different mechanisms of action:

First it is an unselective antagonist of the adenosine receptor, which is a subclass of G-protein coupled receptors on the cell surface which usually bind adenosine as a ligand. This influences cellular signalling.

Then it is a competitive nonselective phosphodiesterase inhibitor, which prevents the breakdown of cyclic AMP in the cell. cAMP is an important second messenger in the cell playing an important role in the mediation of signals from the outside of the cells via receptors to a reaction of a cell to changing conditions. The levels of cAMP are tightly controlled and the half-life of the molecule is generally short. Elevated levels lead to an activation of the protein kinase A , an inhibition TNF-alpha and leukotriene synthesis and reduces inflammation and innate immunity. For references see here.

The LD50 for theobromine is very different among species (table from here), with LD50 as the lethal dose killing 50% of the individuals and TDlo the lowest published toxic dose:

The LD50 also differs between different breeds of dogs, so there are online calculators available to make an estimation, if there is a problem or not. You can find them for example here and here. The selective toxicity makes it even an interesting poison for pest control of coyotes, see reference 4 for some details.

References:

Chocolate - Veterinary Manual
Chocolate intoxication
The Poisonous Chemistry of Chocolate
Evaluation of cocoa- and coffee-derived methylxanthines as toxicants
for the control of pest coyotes.