What are the various types of plugs found in a bee house and how do they help us with identification?

Not an expert on bees, but there 39 known genera of solitary bees in eastern Canada1.  That reference contains a key, so at very least you can start to identify your tenants when they emerge next year.

The clay plugs are due to one of the genera of "mason bees", but that doesn't really appear to narrow things down much.

Your area does have "leafcutter bees" in the genus Megachile that use cut leaves to line and separate the chambers of their nests1,2, so that probably explains the holes containing crushed leaves.

There are also "resin bees", but the only species in your area (Paranthidium jugatorium) I've read about that fits that description is supposed to nest in the ground.1

Finally, bees in the genus Hylaeus and Colletes are known to use a membrane rather than a plug.2

1: Packer, L., Genaro, J. A., & Sheffield, C. S. (2007). The bee genera of eastern Canada. Canadian Journal of Arthropod Identification, 3(3), 1-32.

2: Michener, C. D. (2000). The bees of the world (Vol. 1). JHU press.

ETA: A guides to wasps in your region from the Canadian Journal of Arthropod Identification may also be of help.


This question makes a number of incorrect assumptions and I don't have time to correct them. The short answer is that the virus has mutated probably hundreds of times since it entered humans in late 2019.

The lower figure on the NextStrain.org ncov page, "Diversity", shows the known mutations that have been identified so far. As I look at it now, there are maybe 100-200 shown there, but that will change daily and I can't be bothered to count them.

Is it possible the virus has mutated twice in a period of time of months? Of course it is. That's what we expect from coronaviruses. It would be shocking if it did not.

The default assumption (based on a vast amount of experience with coronaviruses and many other viruses) is that these mutations are neutral and do not affect the virus in terms of fitness, virulence, or transmissibility in any way; they are occasionally useful in tracking sources, but unless you have spent a lot of time looking at virus phylogenetic trees for several years, your interpretations of these mutations are almost certainly wrong.

An example of people making claims based on unfamiliarity with virus evolution is the "two different types of the virus" claim. That claim is addressed by MacLean and colleagues in their Response to “On the origin and continuing evolution of SARS-CoV-2”. Summary:

  Two of the key claims made by this paper appear to have been reached by misunderstanding and over-interpretation of the SARS-CoV-2 data, with an additional analysis suffering from methodological limitations


What is the mechanism of transgene integration (from expression vector to the host genome)?

What is your host in this case? For integration into the genome of a bacterium, you would need to use an "integration" vector. Most commercial vectors (such as pUC18) will be maintained without integrating into the host genome.

Here is a description of an integration vector from the Bacillus Genetic Stock Center to give you an idea of how foreign DNA would be integrated into a Bacillus genome:

  Integration vectors are plasmids that feature conditional replication
  coupled with a selectable marker. If the plasmid is transformed into
  an appropriate host under conditions that select for the plasmid’s
  presence but restrict its replication, all transformants will have
  integrated the plasmid into their chromosome (or some other resident
  DNA capable of replicating under the selective conditions). In
  practice, the selectable marker usually specifies antibiotic
  resistance. Conditional replication usually means that the plasmid has
  replication functions that work in E. coli but not in gram-positive
  bacteria, such as B. subtilis. Sometimes a temperature-sensitive
  replication phenotype is employed instead. Integration is targeted to
  a particular locus on the chromosome by including identical sequences
  on the plasmid. If there is a single homologous sequence, a single
  crossover will integrate the entire chromosome into the target locus
  by a Campbell-type mechanism. If there are two homologous sequences,
  and they are relatively close together on the chromosome, then a
  double crossover will result in a cassette integrating between the
  chromosomal targets. (source)

For most routine molecular biology labwork, there is no need to integrate genes into the E. coli genome. Integration is usually used to generate "knockout" cell lines to study gene function in the bacteria of interest.


About embryonic and genetic evidence of evolution?

Question 1 asks whether ontogeny recapitulates phylogeny. It is striking that the when observing e.g. human embryo development, the embryo seems to go through stages that its ancestral species would go through, but where those 'lower' species would terminate at a specific stage. In other words, embryonic development seems to recapitulate a species' evolutionary lineage.

This is the recapitulation theory, which is outdated and incorrect, but a great example from the history of science. The most prominent of these was Ernst Haeckel's biogenetic law and the Meckel-Serres Conception. There were many problems with this, especially because they focused on noting similarities rather than differences, and several exceptions exist to the rule. They were not very scientific. It also incorrectly presumes that complex organisms have more predecessors. However, it is a compelling piece of evidence to elegantly show that evolution acts incrementally on existing embryological processes.

Question 2 asks whether there is evidence of ancestral DNA in our genome. The answer is yes. Where to begin? We share almost all of our genes with close relatives (e.g. chimpanzees and bonobos) and progressively fewer with more distant relatives. 50% of a banana’s genes (and indeed most other plants') can be found in the human genome. But remember, logically, that doesn't necessarily mean that 50% of human genes are found in bananas, though, because of the way divergence works. The human genome also contains a record of many viruses that have inserted themselves over tens of millions of years. Though they are not ancestors, they have been added 'horizontally' as opposed to the 'vertically' that ancestor DNA is modified over a species lineage.

It's very possible to answer your questions from many, many different angles, and present countless pieces of evidence in favor, but I think this should suffice.


It's a female Eastern Hercules beetle (Dynastes tityus). Unlike the male, the female doesn't have 'horns' as it doesn't need to fight in order to find a mating partner. It's the largest and heaviest beetle in North America. It belongs in Scarabaeidae or scarab beetles.

Source from BugGuide.com


What is the mIU unit as used in hCG hormone levels?

IU stands for "International Units" and it is an arbitrarily chosen unit of measure used mostly to quantify hormones, vitamins or various substances found in the blood.

The idea is well explained by the Wikipedia article on international units)

  Many biological agents exist in different forms or preparations (e.g. vitamin A in the form of retinol or beta-carotene). The goal of the IU is to be able to compare these, so that different forms or preparations with the same biological effect will contain the same number of IUs. To do so, the WHO Expert Committee on Biological Standardization provides a reference preparation of the agent, arbitrarily sets the number of IUs contained in that preparation, and specifies a biological procedure to compare other preparations of the same agent to the reference preparation. Since the number of IUs contained in a new substance is arbitrarily set, there is no equivalence between IU measurements of different biological agents. For instance, one IU of vitamin E cannot be equated with one IU of vitamin A in any way, including mass or efficacy.

For hCG, in the 55th report for of the WHO Expert Commitee on Biological Standardization, you could find:

  The Expert Committee on Biological Standardization, after consideration of this issue (11), concluded that the choice of unit should be made on a case-by-case basis and reflect, and be based on, the biological and medical as well as the physicochemical information available.
  Many biologicals exist in both active and inactive states, and the clinically relevant form of the analyte may depend on the diagnostic aim. For example, the active state of the placental hormone chorionic gonadotrophin (hCG) is the relevant molecule to measure in the diagnosis of pregnancy, whereas the biologically inactive free beta subunit (hCG-beta) is measured to diagnose choriocarcinoma. Generally, a measurement of biological activity is expressed in IU, whereas measurement of the amount of a protein or of a specific protein structure is expressed in SI. In this case there would be a compelling reason to relate the measurement of hCG to a unit of biological activity, and the measurement of hCG-beta to an SI unit of quantity. Accordingly WHO has established a reference preparation for hCG (currently the fourth International Standard, with an assigned content of 650 IU/ampoule) (7) and a reference preparation for hCG-beta (currently the first WHO Reference Reagent for immunoassay of hCG beta subunit, with an assigned content of 0.88nmol/ampoule) (18). The former preparation was assigned a value based on bioassay, whereas the latter preparation had been extensively characterized by physicochemical and
  immunological methods and calibrated in nanomol by amino acid analysis. Applying these considerations of the properties of biological analytes, and their measurement in the clinical situation allowed the WHO biological reference standard for hepatitis B surface antigen, assigned a value in arbitrary IU rather than in SI units, to be adopted by the medical devices sector of the European Commission as the standard required for the fulfilment of the so-called Common Technical Specifications (CTS) for in vitro diagnostic devices. The Common Technical Specification document supporting the European (IVD) Medical Devices Directive 98/79 EC is a legally binding document within the 25 countries of the European Union.
  Where it is appropriate for a WHO biological reference standard to be calibrated in SI units, the principles outlined in ISO 17511 (8) should be followed. This will necessitate the existence and use of an appropriate single reference method and an assignment of uncertainty, derived from calibration data. Such a reference method should not be a biological assay because the factors that affect the results of such assays are not fully understood. Where they are used, SI units assigned to biological reference standards should be derived from, and traceable to, physicochemical procedures.

Note that IU are not the same as enzyme units (U) which is a measure of enzymatic activity


It is the sap; you can see the composition of the sap (of Indian mangoes) in this article. Some plants also produce latex from injury sites. The mango sap is not supposed to be eaten as it can irritate the skin; a condition referred to as Mango Dermatitis.


The closest example I can think of is Lystrosaurus, which was one of the most common animals in the early Triassic period. It was distributed across many modern continents, and was roughly the size of a pig or cow, depending on the species. Lystrosaurus was not a dinosaur, despite its name.

Excerpt from the Wikipedia page (emphasis mine):

  Lystrosaurus is notable for dominating southern Pangaea during the Early Triassic for millions of years. At least one unidentified species of this genus survived the end-Permian mass extinction and, in the absence of predators and of herbivorous competitors, went on to thrive and re-radiate into a number of species within the genus, becoming the most common group of terrestrial vertebrates during the Early Triassic; for a while 95% of land vertebrates were Lystrosaurus. This is the only time that a single species or genus of land animal dominated the Earth to such a degree


It comes from a Y nondisjunction in the father. Anaphase nondisjunction of the Y yields a YY, which goes with one X from the mother to give XYY.


Can humans live without their right atrium?

This is an interesting theoretical question, but several things would need to be clarified:

Does removing the R atrium relocate the SA node to the R ventricle or remove it completely from the picture?
Does the remaining R ventricle have a tricuspid valve?

Technically, the R atrium is the home of the sino-atrial node, which provides natural pacing of the human heart between 60-80 beats/min. Without this natural pacing, our hearts would rely on back-up pacer systems such as atrioventricular node, His-Purkinje systems or the intrinsic but ectopic pacing of individual atrial or ventricular cells.

1

It is possible for humans to survive without the SA node because of these back-up systems. However, our heart rates would be lower, or bradycardic. Although there are many individuals who survive with bradycardia ranging from top athletes to the elderly, this condition could lead to negative symptoms including fatigue, dizziness, lightheadedness, syncope, and even cardiac arrest [2]. Ideally, the SA node would be located at or near the area of blood entry into a chamber (or, put another way, opposite from the side where blood exits the chamber), so that blood is pushed synchronously out of the chamber rather than against a wall or the entry, causing turbulence.

The R atrium also provides a chamber through which venous blood can sit before it is pumped into the R ventricle to be pumped again into the pulmonary vasculature to be oxygenated. This function allows blood to enter the pumping ventricle quickly, a physiologic benefit [3]. In a heart without a R atrium, if the R ventricle still had valves to be able to keep blood from backing up into the vena cava system, then this function of filling and pumping would still be preserved, although it would not be as efficient as if there was a preceding atrium.

In nature, there are three-chamber hearts found in certain amphibians and reptiles. However, usually it is made of 2 atria and one ventricle, rather than 1 atrium and 2 ventricles. In this model, deoxygenated blood and oxygenated blood are mixed (to different degrees, based on the animal), which is not ideal. However, these animals usually have other modes of oxygenation such as through the skin.

In summary, the short answer is- yes, probably, humans can survive without the R atria but it would not be without serious consequences in quality of life.


What kind of fish is this, caught in Cape Coral, Florida?

It looks like the spotfin jawfish, Opistognathus robinsi. The larger ocellated spot on the foredorsal fin is a key identifier for this species. They are not so common in Florida, but do inhabit sandy bottoms, such as canals. Are you sure about the length? It looks about 5 inches from the photo provided, when compared with the the size of the hole on the dock. This species grows to about 5 to 6 inches.

See here for more info.


Why does an complete molar pregnancy not result in a clone?

"However if the sperm has X chromosome the embryo will survive to have the 46 XX karyotype and will start to grow as molar pregnancy."

Complete molar pregnancy is diploid, and there is no fetal tissue identifiable. It is a disease of the placenta, a uterine tumor (cancerous in some cases, non-cancerous in others); fetuses do not develop from such pregnancies, not haploid or diploid (though they are usually 46, XX). A male haploid 23,X replicates, but only trophoblastic (what should be the placenta) tissue results.

Partial molar pregnancies are triploid, and a fetus can sometimes be identified. However, it is non-viable, as polyploidy is non-viable in humans. Even if it were, the abnormal placenta could not support it.

Molar Pregnancy
p57KIP2 immunohistochemistry in early molar pregnancies: emphasis on its complementary role in the differential diagnosis of hydropic abortuses


In chromatin, what are the differences among states, interactions, and structures?

Chromatin state refers to the marks (i.e. methylated DNA, histone modifications, euchromatin v. heterochromatin) found at specific loci and is often referred to as open (readily bound by DNA binding proteins, like transcription factors) or closed (inaccessible to most factors).

Chromatin interactions can include the binding of transcription factors and other DNA binding proteins, but is usually used to describe local and long distance functional contacts between two or more regions of chromatin. These interactions are generated actively through protein-dependent chromatin organization and passively via polymer physics and the nuclear environment.

Chromatin structures can refer to the actual molecular shape and composition of the DNA or to the molecular modifications found at specific regions of chromatin (e.g. heterochromatin, DNA methylation). It can also refer to the ordered compaction of mitotic/meiotic chromosomes.

Chromatin loops are structures that may act in promoting regulatory interactions. Conversely, chromatin interactions may induce looping.

Cavalli and Misteli, Functional Implications of Genome Topology, Nature Structural and Molecular Biology 2013


First there is one major difference between HIV and TB: As long as the TB bacteria are still susceptible to treatment (which is developing into a major problem in some regions of the world) there is a effective treatment which can eradicate the infection. For HIV this is not possible. Here we can only lower the viral load (sometimes under the detection limit), but when the treatment is stopped, the virus will return.

Then it seems that patients under treatment of a drug susceptible TB are infectious for a longer time than previously thought. Until now they have been isolated at the beginning of the treatment (typically around the first two weeks) until three consecutive sputum samples had been negative. Then they were released from isolation and thought to be non-infectious. At this point they are not cured, the treatment has to go on for several weeks.

Now there is newer research indicating that patients can still be infectious although they are under treatment and have negative sputum samples. It seems here that the currently used detection method is not sensitive enough. See these references for more information:

How Many Sputum Culture Results Do We Need To Monitor
Multidrug-Resistant-Tuberculosis (MDR-TB) Patients during Treatment?
High incidence of tuberculosis, low sensitivity of current diagnostic
scheme and prolonged culture positivity in four colombian prisons. A
cohort study.
Prolonged infectiousness of tuberculosis patients in a directly
observed therapy short-course program with standardized therapy.


Where can I find the pZ189vector plasmid vector sequence?

Turns out the sequence is not actually written down anywhere. I asked one of the original authors of the plasmid (not the paper above) and he said that nobody ever did it because at the time when the plasmid was used it would have been a laborious task with little utility. Bummer :(

He also said that plasmid pSP189 is sort of the same but much more efficient and what it does, and is also more studied, with the sequence freely available around the internet.


Short answer
Given your comments you are referring to the cause of fainting after being triggered by certain stressors. The reason is a sudden drop in blood pressure due to parasympathetic nervous system activation (vagus nerve activity). This leads to reduced blood flow to your brain, which results in a brief loss of consciousness (Mayo Clinic).

Background
There are various types of fainting (syncope) with various causes. The type you are referring to is neurally mediated syncope (Arthur & kaye, 2000). It is evoked by emotional activation due to stressors (pain, fear etc.) Stress responses are accompanied by the release of stress hormonses, most notably Adrenaline (epinephrine). Epinephrine release results in sympathetic nervous system arousal, resulting in increased blood pressure, increased pulse and sweating. It also increases amounts of blood being funneled to peripheral organs. These mechanisms aids in the fight,fright and flight response, as more blood in the periphery allows more glucose to be transported to the muscles (Agarwal, 2007). The funneling of blood in the periphery (venous pooling), however, can reach a point in which venous return of blood to the heart falls too sharply. This in turn can lead to a substantial increase in the muscle activity in the ventricles, as they are likely struggling to pump the small available amounts of venous blood into the heart chambers. The increased muscular activity in the ventricles is believed to activate mechanoreceptors that would normally fire only during stretch.

Stretch of heart muscle is normally associated with a high blood pressure. The warning message of a high blood pressure by the mechanoreceptors is sent to the medulla in the brainstem, which in turn leads to parasympathetic nervous arousal. As a part of the parasympathetic response, the vagus nerve is stimulated which reduces heart activity to reduce blood pressure.

However, when the mechanoreceptors are stimulated due to the overt contractility of the ventricles due to a low blood volume, they sent the same neural input to the medulla which normally signals hypertension, thus causing vagus nerve stimulation and hence a paradoxic parasympathetic arousal that results in low blood pressure (hypotension), low heart rate (bradycardia), and ultimately fainting (syncope) (Grubb, 2005).

References
Agarwal et al., Postgrad Med J 2007;83:478–80
Arthus & Kaye, Postgrad Med J 2000;76:750-75
Grubb, Circulation 2005;111:2997-3006


Firstly excess amino acids are deaminated to form keto acids and not urea.
Urea is formed utilising the ammonium released as a consequence of deamination via Ornithine-Arginine cycle

Secondly the released ammonium is toxic because of two reasons:

1)pH changes in the tissues (as mentioned in the question)

2)disturbs the balance of K+-Na+ gradient between the intra and extracellular fluids.

  ammonium ions compete with potassium ions for inward transport, over the cytoplasmic membrane, via potassium transport proteins like the Na+/K(+)-ATPase and the Na+K+2Cl(-)-cotransporter.

This causes increased demand for maintenance energy, caused by the need to maintain ion gradients over the cytoplasmic membrane.That is why converting the ammonium to urea is neccessary.

why amino acids are deaminated:
to form glucose via gluconeogenesis or to form anaplerotic compounds

why acidic group of keto acids fail to neutralise the basicity of ammonia:
because they keep getting utilised for the energy expenditure that increases in the tissues as mentioned above.


What does reflected onto means in the text below?

"Reflected" here describes the relationship between the continuous, but differently named parts of the pleura. The parietal pleura lines the chest wall and mediastinum (costal, cervical, mediastinal, and diaphragmatic areas marked in the image below). The visceral pleura covers the surface of the lungs (orange area below). There is a transition point at the root of the lung where the parietal pleura and visceral pleura meet. This transition is referred to typically as a reflection.

I think that the terminology is used to emphasize that the layers are continuous, but it is as if the parietal pleura bounces back off the body wall as visceral pleura.


In molecular docking, what is the difference between ligand and cofactor?

Ligand is an umbrella term for non-covalently bound anything. A cofactor, substrate, or allosteric regulator could be a ligand. This is a biochemical definition ligand, don't confuse it with a formal chemistry definition of ligand.

What's generally important about cofactors is they're not protein, but they're essential to the protein's biological activity. They could be a metal ion, organic complex, a vitamin, etc. Organic complexes that act as cofactors are also known as coenzymes. Cofactors that bind tightly or become covalently bound are called prosthetic groups. The protein without the required cofactors is called an apoenzyme, and with it's cofactors is called the holoenzyme.

Keep in mind to be on-topic for this site you need to do some research ahead of time and produce a focused, studied question. Wikipedia regularly provides the same answer verbatim!


Are human eyes equally sensitive to AC, and DC lamps?

Let's not confuse the type of power of a light emitting device with the type of light it produces.
This question is not about AC or DC current. It is about flicker frequency, light wavelength and their biological effects.
Flicker frequency
The term "ache in the eye sockets" probably refers to asthenopia.
Human eye cannot detect flicker with a frequeny above 75 Hz. But many computer displays have a refresh rate of 60 Hz [1]. Out of focus and  low refresh rate monitors are known to cause eye strain and asthenopia [2], favored by existing hypermetropia (and other vision issues).

Visual discomfort has been related to 1) the presence of flicker; the possibility to regulate, 2) brightness, 3) height; and 4) inclination of monitor. Asthenopia has resulted statistically correlated to the presence of flicker and to the impossibility of regulating height and inclination of monitor for both sexes. The possibility to regulate monitor brightness has not determined a reduction of visual discomfort either in men or in women [3].

Wavelength
Eye sensitivity is different (see spectral sensitivity):
"Cones SMJ2 E" by Vanessaezekowitz at en.wikipedia / Later version uploaded by BenRG. - Based on Dicklyon's PNG version, itself based on data from Stockman, MacLeod & Johnson (1993) Journal of the Optical Society of America A, 10, 2491-2521d http://psy.ucsd.edu/~dmacleod/publications/61StockmanMacLeodJohnson1993.pdf (log E human cone response, via http://www.cvrl.org/database/text/cones/smj2.htm)
Transferred from en.wikipedia to Commons by User:Richard001 using CommonsHelper.. Licensed under CC BY-SA 3.0 via Wikimedia Commons.
Light color and color contrast matter:

The study results showed that both visual acuity and the subjective visual fatigue were significantly affected by the color of light [4].
Images with excessive energy at medium spatial frequencies (Fernandez and Wilkins, 2008 Perception 37 1098-1113), or that have high color contrast and little or no luminance contrast (Wilkins et al, 2008 Perception 37 Supplement, 144-145) appear uncomfortable or aversive and can induce headaches in hypersensitive observers. Such stimuli are uncharacteristic of natural images [...] [5].

Blue light can also reduce melatonin levels and affect sleep and mood (the studies don't have a strong conclusion though):

Melatonin concentrations after exposure to the blue-light goggle experimental condition were significantly reduced compared to the dark control and to the computer monitor only conditions. Although not statistically significant, the mean melatonin concentration after exposure to the computer monitor only was reduced slightly relative to the dark control condition [6].
All light is not equal: blue wavelengths are the most potent portion of the visible electromagnetic spectrum for circadian regulation. [...] evening use of amber lenses to block blue light might affect sleep quality. Mood is also affected by light and sleep; [...] At the end of the study, the amber lens group experienced significant (p < .001) improvement in sleep quality relative to the control group and positive affect (p = .005). Mood also improved significantly relative to controls [7].

References:

Wikipedia contributors, "Flicker fusion threshold," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Flicker_fusion_threshold&oldid=615159751 (accessed July 29, 2014).
Wikipedia contributors, "Asthenopia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Asthenopia&oldid=617227613 (accessed July 29, 2014).
Rechichi C, Scullica L. [Asthenopia and monitor characteristics]. J Fr Ophtalmol. 1991;13(8-9):456-60. PubMed PMID: 2081858.
Lin CJ, Feng WY, Chao CJ, Tseng FY. Effects of VDT workstation lighting conditions on operator visual workload. Ind Health. 2008 Apr;46(2):105-11. PubMed PMID: 18413962.
Juricevic I, Land L, Wilkins A, Webster MA. Visual discomfort and natural image statistics. Perception. 2010;39(7):884-99. PubMed PMID: 20842966.
Figueiro MG, Wood B, Plitnick B, Rea MS. The impact of light from computer monitors on melatonin levels in college students. Neuro Endocrinol. Lett. 2011;32(2):158-63. PubMed PMID: 21552190.
Burkhart K, Phelps JR. Amber lenses to block blue light and improve sleep: a randomized trial. Chronobiol. Int. 2009 Dec;26(8):1602-12. doi: 10.3109/07420520903523719. PubMed PMID: 20030543.


Is 'disorientation event' a common term among biologists?

As sort of a "teach to fish" answer, let's approach how to answer a question like this:

Google Scholar is a pretty good index of scientific literature: good enough for this purpose. If you search:

"disorientation event" -turtle

you will return all results that use the specific phrase "disorientation event" except those that mention turtles.

You can also do the search:

"disorientation event" turtle

to find the turtle papers. As of today, "disorientation event" returns 57 results; 14 also include the word "turtle", 43 do not.

Among the 43, it looks like the majority of papers are discussing human disorientation, particularly in the context of human pilots but also in the context of cognitively impaired individuals or simply lost pedestrians. There is one paper that uses the term referring to rats in a maze-like task.

Overall, these results lead me to conclude that "disorientation event" is not a common general term used by biologists to refer to non-turtle species losing their way, although I would also say that I would expect a biologist to understand the meaning of the term given sufficient context.


can recessive alleles produce codominance?

An allele is not dominant or recessive by itself. It is dominant or recessive compared to another allele. Therefore, if you consider one locus (position on a sequence) that has two alleles (bi-allelic locus), you cannot have two dominant or two recessive alleles. It is like saying that two things are darker. In reality you can either say that one is darker than the other one or that the color is as dark as the other one. So either one allele is dominant (or partially dominant) and the other is necessarily recessive (or partially recessive) or the two alleles are codominant.

Think of a gene that influence a phenotypic trait such as tail length for example. This locus is bi-allelic (two different alleles (=variant of a gene) exist (=segregate) at this locus). We'll call the two alleles $A$ and $B$. An individual that homozygous $AA$ has trait value $M_{AA}$. The homozygotes $AB$ have trait value $M_{AB}$ and individuals $BB$ have trait values $M_{BB}$. Viewing this in a table it gives:

$$
\begin{array}{c|lcr}
\text{Genotype} & \text{Tail length} \\
\hline
\text{AA} & M_{AA}\\
\text{AB} & M_{AB}\\
\text{BB} & M_{BB}\\
\end{array}
$$

The following table gives the tail length of the different genotypes under the different types of interactions (dominance, partial dominance and co-dominance).

$$
\begin{array}{c|lcr}
\text{Interaction} & \text{AA} & \text{AB} & \text{BB} \\
\hline
\text{A is dominant and B is recessive} & M_{AA} & M_{AA} = M_{AB} & M_{BB} \\
\\
\\ & & M_{AA} > M_{AB} > M_{BB}\\
\text{Partial Dominance} & M_{AA} & \text{or} & M_{BB}
\\ & & M_{AA} < M_{AB} < M_{BB} \\
\\
\text{Codominance} & M_{AA} & M_{AB} = \frac{M_{AA} + M_{BB}}{2} & M_{BB} \\
\end{array}
$$

Because, in the codominance case $M_{AB}$ is necessarily between the values of $M_{AA}$ and $M_{BB}$ ($M_{AA} > M_{AB} > M_{BB}$ or $M_{AA} < M_{AB} < M_{BB}$), one can consider codominance as being a special case of partial dominance where neither $A$ or $B$ dominates because they both contribute as much to the determination of the tail length.

Various definitions may exist for such concepts as well as for overdominance (also sometimes called heterozygous advantage) or stabilizing selection for examples. Those definitions differ in the sense that they sometimes apply to the value of the quantitative trait, to the fitness value (which is another quantitative trait) or to genetic polymorphism.


How does one confirm the discovery of a new species of plant/animal

Basically, you have to examine as much of the relevant 'material' (preserved museum specimens) of the proposed new species and its closest relatives, and compare the diagnostic characters of your proposed new species versus those of its presumed closest relatives to confirm it is actually distinct. For example, with snakes (my field), we use counts of head and body scales, relative distances between features, relative length of tail, hemipene morphology, and even colouration, to determine species.

When combined with genetic evidence of monophyly of the new species and adequate divergence from closest relatives, it becomes a very robust species description.
Finally, names can be accepted or rejected by the ICZN based on existing names for proposed species, though it's a very confusing mess for most groups. I'd recommend checking out their website for more in-depth guidelines


Given the number of individuals who have a recessive disorder, how can one calculate the probability that the disorder was inherited?

Assuming...

The parents are the real biological parents (no cheating allowed!)
There is a purely dominance/recessivity relationship between the alleles and no individual can express the disorder without being homozygous for the disease causes allele
De novo mutations for the disorder are rare enough to be ignored in the calculation of this probability
Trisomy and monosomy is not involved

, then the two parents must necessarily be carrier (both of them) as long as at least one of their children express the disease.

Note, by the way that some of the above assumptions are too strict and could be partially released.

This question does not require any complicated bayesian statistics (or any statistics at all) or any use of Hardy-Weinberg rule. If a children expresses a purely recessive disease, then (s)he is necessarily aa, where a is the recessive allele and A is the dominant allele(s). It means that both parents must have at least one a. Because, no parents express the disease, both parents are necessarily Aa (or aA)


On which part of the DNA will the new DNA nucleotide connect?

The numbers come from the numbering of the carbon atom of the ribose in the backbone of the DNA. The ribose is numbered as shown in the figure below:

In the nucleotides the phosphate groups are attached to the 5' carbon atom and new nucleotide will be added at the 3' carbon atom. See the image below:

First you have a OH-group at the 3' position which is then "replaced" by the new nucleotide.


How do you biologists draw a protein when you write a paper?

As mentioned in the comments, diagrams like these are generated by software. The one I use is Chimera, it is free. The structure of the protein is recorded as a list of atoms and their 3D coordinates, as well as bonds, helices, sheets, etc. When a structure file is loaded, the software generates a 3D model based on the data. The user can rotate the model, move it, zoom in, change the color, an many other options, then export a 2D image when they are satisfied. If you want to use structure data files other researchers have generated, the Protein Data Bank is probably the best resource. Research articles that involve new structural data will list the PDB numbers of their structures near the end. In the article you link, the authors include pdb accession numbers for the structures they used for their figures. For the image you use as an example, here is the caption:

  Fig. 56 PEGylation of four solvent-accessible Tyr residues of chymotrypsinogen (pdb: 1EX3) reported by Francis et al.


Really interesting question.
I am not sure, if the mutation rate is something "actively done" by the virus. I think its more a byproduct of vast replication after taking over the host cell. Mutations with a negative effect are deleted, those with neutral effects will be there, and those with positive mutations will be selected for. This paper looks interesting in this context: "Viral Mutation Rates". Looking for related publications on the site, I found this two:

Rates of evolutionary change in viruses: patterns and determinants.
A short introduction to the origin and molecular evolution of
viruses.

The whole list is here.

Answering your second question: There is obviously no connection between the mutation rate of the virus and the host. I have found this paper ("Rates of Spontaneous Mutation") which gives some pretty interesting numbers. In short: The rate of mutation for DNA viruses is much higher than for eukaryotic cells and for RNA viruses 2-4 orders of magnitude higher than for DNA viruses.

At least RNA viruses encode for some own polymerases, the reverse transcriptase. Depending on which these have a proof-reading (exonuclease) function they induce more or less errors.


Summarising ChIP-seq and controls needed

Good experiment! ChIP-seq is good for a whole genome look at transcription factor binding. KEY POINT:  The data generated are only as good as the antibody. Considerable effort needs to taken to prove antibody is specific for only the protein of interest.  It is for this reason, that some TFs still haven't been characterized by ChIP-seq.

As far as controls for your experiment:

The breaking of DNA from sonication isn't uniform from experiment to experiment, and sonication will preferentially break at some regions of open chromatin more often.
Controls for this:

Isolate DNA from cells that have been x-linked and fragmented under same conditions but don't use antibodies to IP.  This is "Input" DNA.
You can conduct a "mock" ChIP using a control AB that reacts with some non important non-nuclear protein, such as IgG.

Then sequence these samples to same depth as the Immunoprecipitated DNA.

Here is a good paper that is a little dated, but still relevent: Go to Control Sample Section

Here is a link to the guidelines for ChIP-seq for ENCODE PDF

Last but not least, if you are working on a much smaller scale, don't forget about things like DNA footprinting and EMSA to identify the ACTUAL binding site.


Can a person survive on blood in place of water?

Blood is not a good source of water.
1 liter of blood contains about 800 mL of water, 170 grams of protein and 2 grams of sodium (calculated from the composition of lamb blood).
When metabolized, 170 grams of protein yields the amount of urea that requires 1,360 mL of water to be excreted in urine (calculated from here); 2 grams of sodium requires about 140 mL of water to be excreted (from here).
This means that drinking 1 liter of blood, which contains 800 mL of water, will result in 1,500 mL of water loss through the kidneys, which will leave you with 700 mL of negative water balance.
Fish blood can contain less protein, for example, trout (check Table 1) contains about 120 g of protein (plasma protein + hemoglobin) per liter of blood. Using the same calculation as above (1 g protein results in the excretion of 8 mL of urine), drinking of 1 liter of trout blood, which contains about 880 mL of water, will result in 960 mL of urine, so in 80 mL of negative water balance.
Turtle blood can contain about 80 g of protein (plasma protein + hemoglobin) and 3.4 g of sodium per liter. Drinking 1 liter of turtle blood, which contains about 920 mL of water, will result in 80 x 8 mL = 640 mL loss of urine due to protein, and ~240 mL due to sodium, which is 880 mL of urine in total. This leaves you with 40 mL of positive water balance (to get 2 liters of water per day you would need to drink 50 liters of turtle blood, which isn't realistic.
In various stories (The Atlantic, The Diplomat, The Telegraph), according to which people have survived by drinking turtle blood, they have also drunk rainwater, so we can't conclude it was turtle blood that helped them. I'm not aware of any story that would provide a convincing evidence that the blood of turtle or any other animal is hydrating.


I think you're confounding two separate things.

The Lipid Hypothesis is about the creation of atherosclerosis (only atherosclerosis) and was proposed as an explanation for why plaques of cholesterol, fatty acids, and somatic cells form in arteries. It does not try to explain adipocyte behavior, which would result in weight gain.

For the Lipid Hypothesis, after the glycerol has been removed from fatty acids, they are free to diffuse into the blood and can start plaques.

Weight Gain/Loss due to adipocyte behavior is significantly more complicated. One of the weight-related regulatory hormones present in adipose tissue is Leptin: http://en.wikipedia.org/wiki/Leptin

And a more scholarly article from 1995 discussing Leptin:

http://www.nature.com/nature/journal/v395/n6704/abs/395763a0.html

Leptin helps inhibit appetite, along with Ghrelin and a host of other molecules that control hunger and keep track of nutrient levels. However, as the wiki article states, Leptin and Insulin based activities are the primary functions of adipocytes, so a high-fat diet would conceivably deal with either or both of those molecules.

One of the quirks of Leptin is that fad dieting or starvation techniques have a very undesirable affect on Leptin levels (for years after a starvation diet, sometimes) that cause adipocytes to accumulate lipids that they normally would not have.

Obesity can also cause Leptin resistance (which might be aggravated by Fructose intake: http://www.ncbi.nlm.nih.gov/pubmed/11723062 ), much the same way that a diet rich in simple sugars can cause Type II Diabetes: http://www.ncbi.nlm.nih.gov/pubmed/8532024  The Leptin levels are at the expected concentrations in obese individuals, but the proper neuro-receptor activity isn't taking place.

Come to think of it, this may be what you're after. High fat diets will result in more Leptin and thus quicker/more Leptin resistance. Once Leptin resistance occurs, the mechanisms for controlling hunger are no longer as effective as they once were, resulting in more food intake and more weight gain.

However, the actual satiatory signal of Leptin is still debated. Some researchers have proposed that it's more of a "starvation" signal than a "satiation" signal, and thus Leptin resistance might be a normal condition when energy-dense foods are widely available: http://www.ncbi.nlm.nih.gov/pubmed/19644451


Are there more true codes found in biology besides the central dogma?

DNA is a code that occurs via stepwise polymerization, like all major macromolecules. In respects to DNA, it is Nucleic Acid sequences that polymerize to create the DNA. In eukaryotic cells this happens at multiple replicons (regions of replication). So you can look DNA as code for itself. You also have rRNA, mRNA, and tRNA. All of these code for and do specific things. rRNA facilitates the creation and movement of the ribosome, where mRNA and tRNA "code" for the final protein. tRNA serves as the principle code strand for the correct Amino Acids. This is read as a series of three N.A's (codons) One codon for a respective Amino Acid. mRNA actually guides the synthesis of these polypeptide chains. You also have something called operons. These are groups of genes with related functions that are clustered together. This allows for rapid initiation and termination of gene expression. Im sure there are a few others but these are those that come off the top of my head. The term "code" and molecular bio are very much intertwined.


What are the highest and lowest possible pH, paCO2 and HCO3 in the blood of living human?

As discussed in the comments, there are theoretical and practical problems with arriving at such data. There have been controlled experiments using canines, but you have specifically stated your interest in humans. I offer a summary of a few observational studies that may be helpful.

In this study, 117 patients in intensive care units (who are likely to have the most abnormal blood gas parameters among the living) were monitored with continuous optode-based blood gas analysis system. Of the 1,341 measurements, the ranges were:1,2

pH: 7.14 to 7.64
PaCO2: 19 torr  - 98 torr
PaO2: 38 torr – 413 torr3

Another study included a total of 487 samples were obtained in ICU patients with severe respiratory failure and found the following ranges:

pH 7.23 – 7.55
PaCO2: 19 torr – 83 torr
PaO2 30 torr – 522 torr3

These are reasonable ranges for pseudo-stable ICU patients.
Contrast that with normal ranges (+/- 2 standard deviations):

pH: 7.35 – 7.45
PaCO2: 35 torr – 45 torr

On the other hand, you’re interested in the most extreme recorded values, which are likely going to occur during cardiac arrest. According to this case report and literature review, the lowest published arterial pH of an adult who survived cardiac arrest with neurologic recovery is 6.33. The caveat here is that this was a near-drowning victim, and the associated hypothermia provides neurologic protection. The authors go on to report several others including their own patient with pH in the range of 6.5 - 6.6 with neurologic recovery in the absence of hypothermia.

Notes

1. Bicarbonate measurements on whole blood are calculated rather than measured and so not included in such studies. The more accurate test for this measurement is serum chemistry. The bounds are usually defined by the assay. It’s possible for a living human to have HCO3 less than assay (5 mmol/L in most labs by serum chemistry) or greater than assay (~50 mmol/L by most labs).

2. All data provided are arterial. Venous blood gases are of little clinical utility except as a cop-out for obtaining an arterial blood gas.

3. These upper values are intubated patients breathing 100% FiO2. (The lower values are those about to be intubated breathing 100% FiO2....) The theoretical maximum PaO2 on room air is derived from the alveolar gas equation, ~100 torr.


Effect of steroid hormone on specific cells?

The quick answer is that only certain cell types express the required steroid hormone receptors that are necessary to induce signaling and gene regulation when bound to their target steroid hormones, like estrogen, testosterone, cortisol, etc. If no receptor is present, the steroid doesn't effect any change.

The second part of the answer involves the particular signaling pathways induced by the ligation of certain receptors by certain classes of hormones. Testosterone, for example, has numerous effects across the body, from promoting the growth of hair to building muscle mass to effects on mental well-being. Testosterone and its primary metabolite 5α-dihydrotestosterone bind primarily to the cytoplasmic androgen receptor, which then translocates to the nucleus, binds DNA at hormone response elements, and alters the transcriptional activity of genes (either increasing or decreasing, depending on the gene and the cell type). Testosterone can also be metabolized to estradiol and bind estrogen receptors, which function similarly to the androgen receptor (although it can have DNA-independent effects as well).

So, depending on the cell type, receptor expression levels, other DNA regulatory elements, the presence or absence of various testosterone-metabolizing enzymes, and other factors like age, gender, etc., a single steroid hormone can have a multitude of effects throughout the body.


How C. Elegans is used for siliencing genes

From the way that you have described your experiment, feeding C.elegans bacteria that are expressing a plasmid that will induce gene silencing, then both @Kendall and I think that you are likely performing an RNAi (interference) experiment.
As @Kendall writes:

If it's what I'm thinking of, you probably have GFP+ worms that end up getting fed some
DH5-α E. coli that were transformed using CaCl2. The outcome is your control worms should nicely fluoresce, and the experimental worms will be a noticeably weaker color. The RNAi process is explained nicely in that link provided by AMR. –  Kendall

The bacteria will transcribe RNA molecules encoded by the DNA plasmid. These RNAs will have complimentary sequences to sequences from your gene of interest.
When the nematode eats the bacteria, they RNA molecules that the bacteria has produced will be taken up by the cells of the worm.
The Dicer enzyme then cleaves the dsRNA into small fragments. These fragments are then able to hybridize with the mRNAs transcribed from the gene of interest. This will either cause the ribosomes not to bind properly or will start translation out of frame or without key amino acids or will terminate translation early.
The net effect is that the cells will either not produce the protein encoded by the gene of interest or will produce a non-functional protein. If, as @Kendall said, the gene of interest is a reporter gene such as GFP, then the result of the interference experiment will be C.elegans that do not fluoresce. If the gene of interest is a structural protein such as actin, then you will see the effects of knocking out the actin gene on the cells of the worm.
This online video protocol from JoVE.com gives a detailed overview of the RNAi in C.elegans experiment and also demonstrates how the protocol is carried out.


Neurons with thousands of connections: where are the extra connections coming from?

As you say, a neuron can have thousands of inputs via its thousands of dendrites.  Each of those dendrites can have a synaptic connection to the (axonic) output of a different neuron.  So the neuron can take inputs from thousands of different neurons, not just from one other neuron.

At the other end of the neuron, the output of the axon can form synaptic connections with many distinct neurons; that's what the branching at the end of the axon is for.

Also, it's misleading to say neurons don't "decide to initiate signals".  Neurons in the brain do "decide" when to initiate an output.  The decision is a complicated function of the arrival of pulses at dendrites from different neurons.  Only some combinations of incoming pulses will cause the neuron to fire a pulse on its output axon while other combinations will not.  The specific combinations can change over time; this forms the basis of learning.

So a brain neuron is in the middle of a very complicated network of synaptic connections from many neurons to many other neurons.


Could the growth rates of Vibrio vulnificus be affected by an oil spill?

I found these article, which show exponential increase in population of Vibrio in BP oil spill region (published in 2011 supported in 2013).$^{1,2}$
There is evidence that Vibrio representatives can metabolize oil-derived compounds $^{3,4}$. There is a sizable amount, more than 31%, where found in the Deepwater Horizon Spill.$^5$. Though the reason is still to be proved $in\ vitro$, but studies shows they can persist in the presence of oil.$^6$
Source:
[1]:
High Numbers of Vibrio vulniﬁcus in Tar Balls Collected from Oiled Areas of the North-Central Gulf of Mexico Following the 2010 BP Deepwater Horizon Oil Spill
[2]:
Associations and dynamics of Vibrionaceae in the environment, from the genus to the population level
[3]: West 1984, Numerical taxonomy of phenanthrene-degrading bacteria isolated from the Chesapeake Bay.
[4]: Moxley K., Schmidt S. (2010). Preliminary characterization of an estuarine, benzoate-utilizing Vibrio sp. isolated from Durban Harbour, South Africa. Curr. Res. Technol. Educ. Top. Appl. Microbiol. Microb. Biotechnol. 1249–1254
[5]: Hamdan L. J., Fulmer P. A. (2011). Effects of COREXIT® EC9500A on bacteria from a beach oiled by the Deepwater Horizon spill. Aquat. Microb. Ecol. 63, 101 10.3354/ame01482
[6]: In situ and in vitro impacts of the Deepwater Horizon oil spill on Vibrio parahaemolyticus.


Are there dog breeds that are so far apart genetically that they can't produce viable offspring?

I actually found some sort of reference for this.  Apparently in the case of a beagle and irish setter pairing, they had a lot of difficulty in producing pups, but as breeds have a lot of genetic quirks, this might be due to a genetic accident; this is probably a case of mutual infertility rather than speciation.  There are probably mutations in their genomes which are causing non viability in the pups the way that it does with some human parents who have difficulty having children - an immunological incompatibility or traits which cause most offspring non-viable.

In fact the discussion points out that the species designation does not always mean they cannot produce offspring, but simply do not.  Coyotes and wolves will produce offspring too if they are encouraged to do so, but are competing and antagonistic in the wild and so never do mate in practice.

So the answer is probably no. (the beagle/setter pups did show up, but with a much smaller litter than usual with just 2 pups).


Non Coding DNA and its effect on evolution

Richard Dawkins discusses this in his book The Greatest Show on Earth: The Evidence for Evolution

Bacteria and other microorganisms, specifically Archaea, are able to exchange in a sort of 'copy and paste' genetic exchange that differs wildly from sexual reproduction.  They can even exchange genes with other distantly related species.  This, coupled with their short (compared to Humans) lifecycle, accounts for much of the difference in evolutionary rates.  Often, it makes sense to speak in terms of evolution in terms of specific genes themselves (in the case of bacteria), as opposed to evolution of the species as a whole, due to the 'copy and paste' exchange that can take place.  For Bacteria, there is something to be said for compiling a 'true' family tree for each gene separately, regardless of which kind of bacteria in which it resides.

Dawkins remarks, "The philosopher Dan Dennett has put it, 'Where the tree of life for animals is a majestically spreading oak, that for bacteria is more like a banyan.'"

Also, evolution by Natural Selection and random mutation does act on 'non-coding' DNA, just to be clear.


This is to a large extent a question of how reliable the data in the database needs to be. Reliability (and spatial scale) will differ between datasets and between species groups within datasets, and it is difficult to give a general recommendation. I doubt that you will find a single database with good coverage over all taxonomic groups, even if it is in the form of country checklists. For the most reliable information, curated country checklists for specific taxonomic groups will probably be best, but these have to be searched for individually for each taxonomic group of interest.

As a starting point, you might want to look at the occurence data that can be found in gbif.org (The Global Biodiversity Facility). The data found there is certainly not complete, and it will be misleading for many species. However, for the current distribution of relatively well-known groups of species it will give you a good idea of their distribution. This has to be evaluated on a case-by-case basis though. You can access the data in gbif using external tools, for instance using R through rgbif (there is also tools for python or other languages). At the blog recology.info you can find a tutorial on how to get a species list for a particular country using rgbif (more specifically the function density_spplist).


How do special NK cells get to the uterus?

They are attracted via chemokines, which are molecules that NK cells sense and move towards the increased chemical gradient.


What is the number of synaptic vesicles in an axon terminal?

Short answer
Several to thousands of vesicles per synapse. In the cortex, 0-1 are released per typical synapse. At neuromuscular junctions or specialized CNS synapses there can be more.
Longer answer
It doesn't make much sense to talk about an "average", since there are different types of synapses with very different properties, but we can talk about some examples from synapses used as models. In Rosenmund & Stevens, 1996 they estimate about 10 readily releasable vesicles at one synapse in hippocampus. Rizzoli & Betz, 2004 count hundreds at a frog neuromuscular junction.
In hippocampus and neocortex, for a typical synapse there are from 0-1 vesicles released per spike. Higher release probabilities to activation of single cells are achieved by making multiple synaptic contacts; in a typical cortical synapse, there's really just one active site so a max of one vesicle released (Silver et al 2003; Auger & Marty 2000 and Abbott & Regehr, 2004 also discuss this a bit).
Short-term plasticity can strongly influence release probability (Abbott and Regehr 2004 is a good reference to thinking about synaptic computations like this). Multiple action potentials occurring quickly can cause a sustained increase in calcium concentration in the presynaptic cell, increasing release probability at otherwise low-probability synapses (short-term facilitation). Alternatively, many spikes over a longer time period or at higher probability synapses can exhaust the pool (short-term depression). Rosenmund & Stevens used this to estimate the readily releasable pool size of about 10: they triggered a ton of rapid-fire spikes and counted release events, finding only 10. Rizzoli & Betz mention that 10 seconds of 30 Hz stimulation (300 pulses) depleted the available vesicle pool.

Abbott, L. F., & Regehr, W. G. (2004). Synaptic computation. Nature, 431(7010), 796-803.
Auger, C., & Marty, A. (2000). Quantal currents at single‐site central synapses. The Journal of physiology, 526(1), 3-11.
Reyes, A., Lujan, R., Rozov, A., Burnashev, N., Somogyi, P., & Sakmann, B. (1998). Target-cell-specific facilitation and depression in neocortical circuits. Nature neuroscience, 1(4), 279-285.
Rizzoli, S. O., & Betz, W. J. (2004). The structural organization of the readily releasable pool of synaptic vesicles. Science, 303(5666), 2037-2039.
Rosenmund, C., & Stevens, C. F. (1996). Definition of the readily releasable pool of vesicles at hippocampal synapses. Neuron, 16(6), 1197-1207.
Silver, R. A., Lübke, J., Sakmann, B., & Feldmeyer, D. (2003). High-probability uniquantal transmission at excitatory synapses in barrel cortex. Science, 302(5652), 1981-1984.


they might be embryoid bodies:

https://en.m.wikipedia.org/wiki/Embryoid_body


Flower identification (England, late May)

MY guess would be Centranthus ruber coccineus, also known as red valerian. See this picture (from here):


The bird in Picture-1 is  Purple-rumped sunbird (Leptocoma zeylonica) according to this decription from wikipedia:

  The males have a dark maroon upperside with a blue-green crown that glistens at some angles, bright green shoulder patch and violet/purple rump patch which is generally hidden under the wings. The underparts are whitish with dark throat, maroon breast band and purple/violet patch in the throat which is visible in some angles.

The birds in Pictures 2-5 is a single species, non-breeding male of purple sunbird (Cinnyris asiaticus) according to this description:

  The male is glossy metallic purplish black on the upper parts with the wings appearing dark brown. The breeding male has the underparts also of the same purplish black, but non-breeding males may show a central streak of black on yellow underparts.

References:

Wikipedia
r/whatsthisbird


What are the sites of nutrient digestion and absorption in the human GI tract?

The saliva from your mouth will slowly start to digest starches.

Then the stomach specializes in digesting protein with enzymes and its highly acidic content.

The small intestine will digest proteins, starchs and carbs (with the help of the enzymes traveling from the stomach).

The liver and pancreas secretions will join in the small intestine will help break down fats and complete digestion.

The small intestin is responsible of absorbing the vast majority of digested nutrients and the water is then mostly absorbed by the colon.

Source: Your Digestive System and How It Works


In the first image, flowering occurs in the stage labeled "Pollination", which is when the male releases pollen and the female accepts pollen.  It give the time as 56-63 days after emergence, but note the asterisk ("*"); the footnote for it says their given times vary by "growth class" (such as "early" or "late"), indicating that these numbers are just a guide and actual times will vary by the cultivar (breeding strain) selected.


How are chromatids correctly segregated during mitosis?

It's a spatial constraint.  As the DNA is replicated, the two resulting chromatids are kept stuck together by cohesin proteins.  The DNA sequence that corresponds to the centromere then coalesces the kinetochore.  It seems that the DNA-protein interactions at the centromeres creates a particular structure along the chromosome.  Since the two chromatids have their kinetochores pointing in opposite directions, when a spindle microtubule attaches to the kinetochore, it is nearly impossible for another microtubule from the same spindle to attach to the opposing kinetochore.


Where are interneurons in Autonomic Nervous System?

It sort of depends on your definition of interneuron. Many school-level textbooks suggest that any neuron that has neurons both pre and post synaptically are interneurons. Therefore both the preganglionic neuron and the spinal sympathetic interneurons could be considered interneurons. This means that all neurons in the brain are interneurons and vastly oversimplifies the CNS.

I would argue that it's probably more helpful to think of the preganglionic neurons as "projecting" neurons, as they come down the spinal cord. The post-ganglionic neuron is more like a motor neuron.

Edit: I answered a similar question in more detail here: Is the bipolar neuron of the retina considered a sensory neuron?


I kind of hate using Wikipedia as a reference, but this article offers a general overview of spider evolution...
https://en.wikipedia.org/wiki/Evolution_of_spiders

And this article mentions fungus gnats (and perhaps other species) as examples of convergent evolution...
http://www.mapoflife.org/topics/topic_267_Silk-production-and-use-in-arthropods/

I can't remember with certainty, but I believe some jellyfish (and/or perhaps other marine invertebrates) have sticky tentacles that function somewhat similar to spider webs. In fact, some carnivorous plants have sticky structures that trap prey.


How do birds deal with their eyes drying out at high speeds?

Birds have a body part known as the nicitating membrane otherwise known as the "third eyelid". This part has become vestigial in humans, where it remains as the plica semilunaris.

This image of a masked lapwing clearly shows its nicitating membrane in action, where it covers the eye in a horizontal motion. This is analogous to blinking in humans, and the membrane moisturises the eye and removes debris while the bird is in flight.

This paper explains in detail how the peregrine falcon (the world's fastest bird) clears and moisturises its eyes when diving at speeds of over 300km/h.


What are embryophytes? And how are they characterized?

The name derives from their innovative characteristic of nurturing the young embryo sporophyte during the early stages of its multicellular development within the tissues of the parent gametophyte.

source
https://www.revolvy.com/main/index.php?s=Embryophytes&item_type=topic

Similar definitions are in the New World Encyclopedia and Merriam Webster Dictionary.


What species of butterfly is this? Picture taken on 9-18-2018, near Helena, Mt

That is a California Tortoiseshell google[https://www.butterfliesandmoths.org/species/Nymphalis-californica]


Can we identify an individual from their palm lines

It was tricky searching for this through the morass of palmistry sites.  But, in the field of biometrics, I found the article "Palm Print Recognition", which states that (bolding mine):

  Because fingerprints and palms have both uniqueness and permanence..

it has been used for identification the same as fingerprints. The only reason it is not as widespread as fingerprints is largely due to logistics such as computer processing.


Why a brain's hemisphere controls the opposite side of the body?

"How" is easy to answer (signals from the right side of the body cross the midline and end up in the left cerebral hemisphere; answered well in a previous question). This pattern of wiring appears to have existed since bilateral symmetry first evolved.

"Why" is not a well-defined question; the possible evolutionary advantage gained by having cross-wiring is unclear.

To answer your explicit question: there is no "opposition" in any meaningful sense between the location of a sensory nerve on the body and the location at which the information is processed in the brain. There are a raft of visual areas in the neocortex, spanning from the back but extending forward. The areas that control eye movement are much more frontal ("frontal eye fields"). Before arriving in the neocortex, signals from the eyes pass through the dLGN, a nucleus in the thalamus which is a subcortical structure closer to the middle of the brain than the rear. This flow of visual information is similar across many (most? all?) mammals.


Why do (some) cats chase their own tail?

I will try to answer this. First of all we have to make a claim. This behavior can be found in many animals behaviors but it is much more common in dogs.

In cats there is a few reason for that:

Born hunter

Feline predators have a genetic desire to chase anything what is moving. So the chasing tail behavior can be just game for practising hunting skills.

OCD

But if this behavior doesn't stop after the cat grew up it might be a serious problem.  Just like any compulsion behavior in general it might indicate that your lovely cat has obsessive compulsive disorder. If this is the case, your pet can become much more aggressive, hyperactive.

Source

Perfect Paws: Predatory Behavior of Cats

Psychology Today: It's Alive! Why Cats Love Laser Pointers

Pet Place: Feline Hyperesthesia (FHS)


Why can't we use plasmids to add genes to ourselves?

First, plasmids do not usually integrate into the chromosomes of human cells. In the laboratory, plasmids can be introduced into the cytosol of cells, and plasmid DNA will then be "read" by the host cell and used to make new proteins, for example. But plasmids usually remain separate from the cell's own DNA, and in that sense they are not effective for gene therapy.

Second, our cells are quite good at detecting and destroying plasmids, as well as other foreign DNA. This is a self-defense mechanism, evolved to get rid of viruses and other nasty parasites that might be trying to hijack the cell. In the lab, where we are working with isolated cells in a culture dish, with no immune system, plasmids are typically tolerated. But in a human being, immune cells that have specialized in detecting intruders are very competent at detecting such manipulations, and they will quickly sound the alarm and wreak havoc ... So if injected into the body, plasmids are quickly detected and destroyed.

Research in gene therapy aims to find more efficient ways of "editing" the DNA of human cells, ultimately in a way that can be safely applied in the body. Such a technique does not exist yet. The latest CRISPR-Cas9 gene editing system is a phenomenal tool, and is very efficient at getting into the DNA of human cells; but the CRISPR-Cas9 proteins must themselves be delivered into the cell, for which a virus is typically needed, and this would again cause immune reactions if attempted in a human body.


How are electrons entering the electron transport chain in cellular respiration energised (excited)?

It may be useful to start with a quotation from the Introduction to Ch. 9 of Berg et al. Biochemistry (6e) that addresses the question, more or less as asked. I can’t find a link to the pages in the 5e online so I will transcribe it from my text:

  “A principal difference between oxidative phosphorylation and
  photophosphorylation is the source of the high energy electrons. In
  oxidative phosphorylation these electrons come from the oxidation of
  carbon fuels to carbon dioxide. In photosynthesis these electrons are
  excited to a higher energy level by the energy from photons.”

It is important to think about one of the ways in which the excited electrons are used in photosynthesis. To quote from earlier in the Introduction:

  “In essence, light is used to create reducing potential.”

What this means chemically is that in photosynthesis the electrons have sufficient energy to reduce NAD+ to NADPH. In the biosynthetic (dark) reactions of photosynthesis the NADPH can be used to reduce carbon dioxide to sugars from which glucose can be produced.

So glucose is a reduced compound and can be thought of as ‘embodying’ the excited electrons, as its oxidation to carbon dioxide generates NADH (from NAD+). Hence:

There is no need for any additional excitation of electrons — that was done originally in photosynthesis.


Why does agrose gel runs horizontally, and SDS-PAGE gel runs vertically?

When you stand general agarose gel vertically, the gel is slippery coming out from the bottom; although, some run vertically.

To polymerize acrylamide, it is good idea to avoid air because oxygen inhibits polymerization of acrylamide. You would get an air tight condition, pouring acrylamide between glass plates, but how could you run gel made between glass plates. When you set such gel plates horizontally, how do you load samples? Then, it is easier to set gel plates vertically.


ID this insect please. SE Brazil Oct 2017

This is, for sure, a robber fly (Diptera, Asilidae). My guess is that this one belongs to the Genus Promachus.

Here is a photo of Promachus rufipes (from North America) for comparison:

Coincidentally, even the prey (a wasp) is in the same position of the one in your photo!

This Genus has 9 species. If this is in fact Promachus, you'll have to find out which are found in South America.


If cells regularly renew, why do we have scars?

Scar tissue formation is part of the normal healing process in which fibrous material braces and pulls the wound together, in other organisms (and young mammals) this process is mild and just serves to temporarily reinforce the damaged tissue as new cells migrate in to begin replacing the missing tissue, sometimes to the point of replacing missing limbs in lizards and amphibians. However in adult mammals and birds the process of fibrous tissue is far more exaggerated, creating longer lasting or even permanent scars, Here the wound keeps filling in with more and more fibrous tissue instead of moving on to regenerating what was there originally. This dense fibrous tissue often prevents new cells from easily migrate into the tissue, essentially stalling the healing process. It seals the wound much faster than the more mild deposition of other animals but can often prevents replacement of the fibrous tissue which would otherwise happen as the missing tissues is regenerated. This mass of fibrous tissue is what we call a Hypertrophic scar. this is why scars can also fade, as cells often can migrate in and slowly replace the the matrix but this is severely limited by the dense packing.

Note there is a second rarer form of scar tissue that can form, called keloid scarring. This form of scar spreads beyond the original wound area and seems to be caused by some form of runaway extracellular matrix deposition. It should also be noted adult mammals sometimes do regenerate decent portions of tissue, albeit not well, possibly because some of the controlling cellular signalling machinery has be lost or reappropriated. All the factors that affect this are not understood and are a main focus researched. We do know it varies quite a bit from tissue to tissue and is not terribly consistent.

It is believed that mammals and birds develop this stronger matrix deposition which leads to permanent scar tissue becasue healing fast is more important for them than healing completely since their metabolism runs so much higher. They can't wait around for it to heal they need to get moving as soon as possible or risk starvation,additionally a stable body temp makes for a more inviting environment for bacteria so sealing the wound is paramount. Thus sealing and mechanically reinforcing the wound is more important than regeneration. As you can imagine the worse the injury the more important it is to plug it fast which is why minor injuries are less likely to scar. This is also why lizards and amphibians end up with less permanent scars they can take the time to better regenerate the tissue. Of course this is difficult hypothesis to test, however there has been some success in getting mammalian tissue to regenerate more by removing scar tissue as it forms or just preventing collagen production.

Evolution is one lang story of "good enough" and scar tissue is good enough functionally that the speed at which it can seal a wound favors it over slower regeneration.


How does natural selection favour large body mass and size (or so it seems)

Well first of all I don't know if natural selection favors larger animals - most of the living things in the world are single celled.

Still there are advantages to being larger.  I don't know if I can list them all!  In no particular order:

1) Living things that are large are more metabolically efficient. The amount of food required goes as a 3/4 power of the size of the animal.  Thus a cat 100 times the mass of a mouse requires only 31 times more food.  I don't believe that it is not known how this works.

2) r vs K selection: larger animals have greater individual "value".  Smaller animals tend to live by r-selection - they are cheap and reproduce in large amounts, then lead short and highly competitive lives where most offspring die without reproducing.  Larger animal tend to live longer and reproduce offspring with a greater chance of life. In the extreme case you can compare a cockaroach to an elephant here.  This is not a hard and fas rule, but cheap offspring do tend to be small.

I seem to remember that there are lots of other surveys done and body size correlates to life span and any number of other attributes, which I will try to add after I get some sleep unless someone slips in and lists them all.

3) Cope's rule - an observation as much as a rule that size must convey some advantge because most animals become larger the longer they are around.  Not always true, but there is a trend that the longer evolution works, the more likely a large animal will show up.  This might be because as niches for smaller animals are filled, niches for larger animals become more accessible?


What is the distinction between deoxyribonucleases and restriction enzymes?

This paragraph from Lehninger's Principles of Biochemistry (in my opinion the best textbook on biochemistry) is very didactic:

   DNA Is Degraded by Nucleases

  To explain the enzymology of DNA replication, we first introduce the enzymes that degrade DNA rather than synthesize it. These enzymes are known as nucleases, or DNases if they are specific for DNA rather than RNA. Every cell contains several different nucleases, belonging to two broad classes: exonucleases and endonucleases. Exonucleases degrade nucleic acids from one end of the molecule. Many operate in only the 5'→3' or the 3'→5' direction, removing nucleotides only from the 5' or the 3' end, respectively, of one strand of a double stranded nucleic acid or of a single-stranded DNA. Endonucleases can begin to degrade at specific internal sites in a nucleic acid strand or molecule, reducing it to smaller and smaller fragments. A few exonucleases and endonucleases degrade only single-stranded DNA. There are a few important classes of endonucleases that cleave only at specific nucleotide sequences (such as the restriction endonucleases that are so important in biotechnology; see Chapter 9, Fig. 9–3).

We can conclude that restriction endonucleases (or restriction enzymes) are a type of endonuclease, and that endonucleases are a type of DNAse. So, all restriction enzymes are DNAses, but not all DNAses are restriction enzymes.

Besides that, we can conclude that your initial statement ("Both deoxyribonucleases (DNases) and restriction enzymes are endonucleases") is wrong.

For a more complete table have a look at Molecular Biology of Nucleases, page 18.

Sources:

Lehninger, A., Nelson, D. and Cox, M. (2000). Principles of biochemistry. New York: Worth Publishers.
Mishra, N. (1995). Molecular biology of nucleases. Boca Raton [u.a.]: CRC Press.


Yes they can. The viruses that cause a cold include rhinoviruses (up to 80%), coronaviruses and influenza (together accounting for much of the remaining 20%) and a small percentage of adenoviruses. When discussing cross species transfer, influenza is the most important to discuss as it is a fairly common cause of the "common cold".

Influenza A has humans, pigs, bird and horses as its host. Different influenza strains have different hosts. Influenza can recombine if two strains infect the same host (antigenic shift) and also mutate (antigenic drift). With a combination of these influenza can and has numerous times crossed the species barrier which has caused the major flu pandemics as well as swine and avian flu. It's this reservoir that makes these viruses so hard to eradicate. When we are the only host such as in polio virus, it is a lot easier. Pigs don't adhere to national flu guidelines.

Comparing recovery times, all mammals are roughly similar although due to our slightly more evolved immune system as well as social factors of knowing what to do when we are ill we recovery very slightly earlier.


Does animal blood, esp. human, really have similar salinity as ocean water, and does that prove anything about evolution?

Short answer
Early sea water had a very different osmolality than blood plasma.

Background
The reference range of serum osmolality is 275–295 mosm/kg (mmol/kg) (MedScape). The osmolarity of sea water is about 1000 mOsm/l (Wikipedia), but it can vary substantially between different seas, namely between 642 and 1,480 mOsm/kg (Ninawe & Banik, 1998). Nonetheless, the range of osmolalities are substantially higher than that of serum. That's why we cannot consume sea water, without losing more water than gaining it (NOAA). According to Astro Biology Magazine, the salinity of early oceans 3.5 billion years ago, when life first developed, was even higher. So popular accounts that they are the same and that this has important evolutionary consequences are likely far-fetched.

Reference
- Ninawe & Banik, J. Mar. Biol. Ass. India (1998); 53(2): 230-36


How do GPCRs transmit a signal across the plasma membrane?

The G-coupled protein receptors (GPCR) transmit signals from outside of the cell into the cell and activate downstream signalling pathways. These change for example the expression of certain genes.

The whole process is a coorperation between the receptor, a G-protein, GTP as a co-factor and the ligand of the receptor (which starts the whole process). An extensive description (including much more images) is available in the Wikipedia, but in short, it looks like the images below (from the Wikipedia article on GPCR):

To answer how this signal is tranferred from the outside to the inside look at the first image: Upon ligand binding the conformation of the receptor changes its conformation and brings some of it transmembrane helices together so the G$\alpha$ subunit can bind here and activate downstream signalling.

The whole process happens in a few steps:

In the resting state the receptor has a trimeric G-protein (consisting of the subunits $\alpha, \beta$ and $\gamma$ bound on its cytosolic site. The G-protein also has a GDP molecule bound to it $\alpha$ subunit.
Upon binding of the ligand, the receptor changes its conformation, and G$\alpha$ exchanges the GD against GTP, which activates the complex.
The G-protein dissociates into the active G$\alpha$ the G$\beta\gamma$ subunits, which signal to downstream signal transduction pathways like the MAP-Kinase pathway.
Binding of RGS (regulator of G-protein signalling) to the g$\alpha$ subunit activates the intrinsic GTPase function of the subunit and hydrolyses GTP into GDP and P. The GDP stays bound to the G$\alpha$ subunit, which changes its conformation and forms the G-protein trimer at the receptor. At the receptor itself this induces also a change in conformation which makes the ligand dissociate from the receptor.

At the end of the fourth step the receptor has returned into its inactive form and stays there until the next ligand binding.


Do patella bones form in people born with the inability to walk?

In mice, patella would form, but not separate from femur.
On the development of the patella:

Previous studies have suggested a central role for mechanical load in
the initiation of sesamoid development.
Our finding that the patella initially forms as part of the femur and
is later separated by joint formation led us to revisit the issue of
mechanical contribution to patella development. To achieve this, we
studied patella development in mutant embryos devoid of contracting
muscles, as a result of the naturally occurring autosomal recessive
mutation muscular dysgenesis (mdg; Cacna1s). These mice lack
excitation-contraction coupling and, consequently, their skeletal
muscles lack contractility.
Histological analysis of sagittal sections of hindlimbs identified at
E13.5, in both mutant and control littermates, the existence of
patella progenitors, which were part of the femur. However, at E14.5,
whereas in the control we observed joint formation between the patella
and the femur, in mdg mutants this process was not detected.
Consequently, at E16.5 the mutant patella was still part of the femur.
These results suggest that, although muscle contraction does not
affect patella initiation, it plays a crucial role later during the
separation phase.

I know, you asked for human, but it is the only relevant information I found. However, while sources mention a role of physical stress in the calcification of sesamoid bones, the preceding formation of cartilage seems unaffected. Now, given the information that ossification occurs in mice without physical stress, I personally would conclude that the human patella would also calcify in paralyzed persons. Strictly, the question whether the patella forms, should be answered, if a non-detached patella counts.


Again, the full answer is too complex to answer here. The CDC has a broad explanation (Selecting Viruses for the Seasonal Influenza Vaccine) and the WHO has a presentation summarizing the process (The WHO Vaccine Strain Selection Process: Review of the Evidence).

The major factor for choosing a new vaccine virus is based on surveillance from the preceding season and from the opposite hemisphere's season. The surveillance data shows which virus groups are expanding or shrinking. Antigenic variation (high or low HI titers) is also a part of the decision, but every season has a number of viruses that have low HI titers to the current vaccine and the real question is whether those occasional outliers are just sporadic, or whether they're showing signs of becoming increasingly common.

Interpreting whether particular virus families are increasing or not requires a lot of familiarity with influenza behavior, genetics, and antigenicity. You can look at some of the data used in strain selection on the WHO site, e.g. Recommended composition of influenza virus vaccines for use in the 2018- 2019 northern hemisphere influenza season.


Your question does not have a single answer, and depends on several factors: the type of photosynthesis (C3, C4 or CAM), the species of the plant, temperature, amount of ground water, relative humidity, luminosity etc.

However, as a good guess, I used to say to my students that around 1% of the absorbed water is used in photosynthesis, the remainder (99%) being either lost by transpiration or used for cell growth. Once more, have in mind that this is a rough estimate, the real number varies.

Now let's have a look at more precise figures, from Bieleski et al. (1999):

As you can see, we have here three kinds of plants (C3, C4 and CAM) here. The column you want is TR ratio (which stands for Transpiration/Photosynthesis ratio). If we consider a C3 plant, the number goes from 450 to 600.

Let's take 600 as an extreme example. A TR ratio of 600 means that the plant loses 600g of H2O to fix 1g of CO2, using approx. 0.4g of water (You'll have to do some math here, using photosynthesis equation), but that tell us that the amount of water used for photosynthesis is less than 0.1% of the transpired water.

Source: Bieleski, R., Farquhar, G., Eamus, D., Atwell, B., Turnbull, C. and Kriedemann, P. (1999). Plants in action. 1st ed. South Yarra: Macmillan Education Australia.


It's probably the larval state of a tortoise beetle, or a closely related beetle. They are known to build a "faecal shield" at the end of their tail, sometimes including shed exoskeleton and any debris that sticks to it. They hold this shield over their bodies for defensive purposes that aren't fully  understood.
Lacewing larva look somewhat similar and also cover themselves with debris, but their legs are longer and their head and mandibles look quite different.
Here's an image of a thistle tortoise beetle larva:


How does a blunt force stimulate histamine to develop early stages of inflammation?

An brunt force (trauma) may destroy cells and tissues by mechanical action. It simply squashes them.

Cells contain different kinds of chemical substances in specific cellular organelles. The most important in this context are enzymes from lysozyme.

Once enzymes are released (by squashing the cell) they induce irritating reactions to other cells and activate specific receptors found on immunitary system cells. This is how non-infectious inflammation occurs.

Cell components act as inflammatory mediators responsible for the clinical signs of inflammation. Here are some examples  [Wikipedia]:

Lysosome granules from destroyed cells
NO (Nitric oxide) from endothelial cells and some neurons

Other inflammatory mediators are produced by macrophages, neutrophiles and plasma cells, thus leading to a chain reaction, in which immunitary system cells activate one by another.

Macrophages have enough to 'swallow': all the destroyed cells which must be removed from the tissue.

Antibodies are produced because altered cell structures are considered non-self and gain antigen properties.

Source: Wikipedia, Inflammation


What do the signs +/+ +/- mean in this image?

Diploid organisms, such as we are, generally have two copies of each gene (excepting the sex chromosomes in males).  In order to display the genotype for each, geneticists use shorthand.  When referring to a gene, + means the wildtype, which is the "normal" version, and - means that the gene is missing, often a knockout.  So a typical individual's genome for a particular gene will be +/+, a hemizygote (one copy deleted) is +/-, and a complete knockout is -/-.

The image is talking about peroxisomes, claiming that they are required for life, specifically the gene Pex5.  You can look at the graph at see that compared to the wildtype (open circles), the -/- individuals (open squares) don't make it to a normal birth weight; their lifespan is less than three days.  The +/- hemizygotes (filled circles) match the +/+ wildtype, indicating that this locus displays haplosufficiency, which means that only one functioning copy is needed for a typical phenotype.


How does noradrenaline result in rise of systolic blood pressure even when the cardiac output is decreasing?

Your question involves comparing an observed response to administration of noradrenaline/norepinephrine, which causes vasoconstriction thereby increasing the BP (during both systole & diastole,) to the hemodynamic/pharmacodynamic response of the cardiovascular system as a whole, which is decreased cardiac output & decreased cardiac work.  This is similar to asking why opening a finite water tank eventually slows down even though the pressure increases when you turn on the faucet.


Cloned animals, at least in the first generation, are often subfertile and have lower viability than their progenitors. The reasons for this are complicated but often are related to epigenetic changes that lead to altered gene regulation.

Further reading:

  Although the technology of SCNT has been applied successfully by many research teams, some SCNT animals have abnormal or lethal phenotypes, including facial abnormalities, pulmonary hypertension [3], contracted tendons [9], low birth weight [10, 11], as well as distinct depigmentation of the skin and hair ... Based on previous studies, insufficient epigenetic reprogramming of somatic donor cells may result in phenotypic abnormalities in the offspring ...

--Dysregulation of genome-wide gene expression and DNA methylation in abnormal cloned piglets

  The epigenetic state of the ES cell genome was found to be extremely unstable. Similarly, variation in imprinted gene expression was observed in most cloned mice, even in those derived from ES cells of the same subclone. Many of the animals survived to adulthood despite widespread gene dysregulation, indicating that mammalian development may be rather tolerant to epigenetic aberrations of the genome.

--Epigenetic instability in ES cells and cloned mice.

  Because few clones survive to birth, the question remains whether survivors are normal or merely the least severely affected animals, making it to adulthood despite harboring subtle abnormalities originating from inadequate nuclear reprogramming ...  Our results suggest that many expression abnormalities are common to the NT procedure whereas some reflect the particular donor nucleus. These results further emphasize the severity of placental dysfunction and illustrate abnormalities in clones surviving to birth.

--Abnormal gene expression in cloned mice derived from embryonic stem cell and cumulus cell nuclei

  Although clone D had a poorer libido and entered puberty later than those of the other cloned male cats, he produced gonadal hormones within the average range. Four of the cloned male cats had normal fertility.

--Reproductive fertility of cloned male cats derived from adult somatic cell nuclear transfer.

(Note that this paper concluded that the cloned male cats had "normal fertility", but one of four (25%) had reproductive abnormalities (reduced libido and delayed puberty); the numbers are too small for anything definite but I would say this is evidence for abnormal fertility, not the reverse)

Some early papers do claim normal fertility of cloned mice, but those are simply based on the fact that the cloned mice could have offspring (i.e. were not completely infertile) and didn't actually compare fertility of cloned vs. "normal" laboratory mice.

Wakayama, T., Perry, A.C.F., Zuccotti, M., Johnson, K.R. & Yanagimachi, R. Full-term development of mice from enucleated oocytes injected with cumulus cell nuclei. Nature 394, 369–374 (1998).
Wakayama, T. & Yanagimachi, R. Cloning of male mice from adult tail-tip cells. Nature Genet. 22, 127–128 (1999).


How to predict the top microRNAs that bind to 3`UTR of a specific gene

You'll find TargetScan quite useful. You can pick from a number of species and simply enter a gene name. It will then get the 3' UTR, show its conservation across species (binding sites in a conserved area are more likely to be active), find miRNAs that can bind to the 3'UTR, and then split those up by whether they bind to highly or poorly conserved regions. It also categorizes the hits according to various properties, like proximity to the open reading frame, in case you want to perform any sort of filtering by that.

Edit: BTW, you may want to take the target miRNAs and look at their expression in your tissue of interest. That's a good way to further narrow down their relevance.


Could humans theoretically see infrared better than regular light?

No, retina doesn't have or has too few infrared receptors.

Practical example: most remote controls use IR LEDs (infra red light emitting diodes) to send commands to a receiver device. So take a remote control, keep pressing a button and look at its front. Do you see any flashing light? Now take a camera (phone camera, photo camera or video camcorder) and look with it at the remote while pressing a button. Now you see it producing white light. The camera sensor detects IR. That is how night vision in cameras work.

What you read in that article is about how light is reflected by the eye (the pupil). There is nothing to do with the retina which is on the 'back wall' of the eye ball.


What distinguishes Mendelian Inheritance from Non-Mendelian Inheritance?

You can discuss multiple genes within the framework of Mendelian inheritance; what you're probably thinking of, though, is the fact that Mendelian inheritance doesn't recognize the idea of multiple genes that contribute to a single trait.

For example, if there is a gene that controls petal color (blue vs. white, with blue = dominant) and a gene that controls height (short vs. tall, with tall = dominant), then Mendelian inheritance predicts that two short plants with white flowers will only produce short plants with white flowers.

But if there are multiple genes that interact to determine height in a complex way, that's outside the scope of Mendelian inheritance.


Identify bee in photo (found in Utah, USA)

Yes, this looks like Apis mellifera, which is also one of the most common bees you'll run into. If you have other pictures, you could check the identification tips at the bugguide page for the species.

As a side note, in general to really confirm an identification a specialist would need to see a collected specimen (that is, a live or pinned bee) as the distinctive characters (things like size, wing veins, or in this case, long hairs on the eye) may not be visible in photographs.


Confusion about how to compute probabilities for linked genes

0.000625 looks right to me.  On one chromosome, you have a 50% chance of a.  Then you have a 40% chance of b (if and only if a crossover occurs).  These multiply out to 20%.  You multiply that by 50% for three unlinked genes to get 2.5% abdef.
Your approach was correct overall, but you used a 60% chance of b, so your final answer was too high by (60%/40%)^2.  Don't let capital and small letters trick you - ab comes from a recombined chromosome.


Beetle (?) on Acacia (Senegalia) greggii?

Looks to me like the Longhorn beetle (Schizax senex), possibly a female, but it is hard to judge the length of the antennae. This beetle has long antennae (hence the longhorn name), with the male having antennae that are nearly twice as long as the female. S. senex is the only species of the genus.
They are hirsute with a pale margin to the wing cases. The species was described in 1873 by LeConte, with the description being rather wonderful (in my opinion):

Niger opacicus, pube breve minus subtili cinerea vestitus, prothorace fortus, elytrus subtilius punctatus, his marginae suturali laterali apicali et scutello fulvo-pubescentibus

My very rough translation - better Latin scholars please fix:

Black opaque, hair short with subtle grey arrangement, prothorax strong, wing cases with subtle dots, and the join margins and edges pointed and scutes fawn-coloured and very hairy.

Note that I found this with a very quick google of "beetles arizona" and scanning through the linked arizonensis beetles page, which was at the top of the links provided by google. I am not from the USA or in the USA, so please anyone with a better identification, feel free to chime in.


This is a kind of trunkfish. (They have different names, this could be a smooth or spotted trunkfish.). It's really a lovely and comical little fish when observed alive in coral reefs. It has the ability to change its coloration depending on whether it's excited or calm, or to minimize its contrast to the background. It is related to puffer fish.

It has a boxy, triangular body shape, and propels itself with relatively tiny, delicate fins. Like pufferfish, they are toxin producers.

In death, the body shape and coloration are different, of course. Never saw a dead one before; sad. The juveniles are adorable:

  Members of this family occur in a variety of different colors, and are notable for the hexagonal or "honeycomb" patterns on their skin. - Wikipedia


In what ways can mechanisms of apoptosis be damaged?

Lot's of ways. Apoptosis is complex, but falls under two pathways ending up at caspase 3. Anywhere in the pathway may there be a problem but also in things that trigger the pathway. For example in cancer there is loss of tumour suppressors which ensure a damaged cell undergoes apoptosis or prevents replication and oncogenes which allow controlled replication. Damage to these genes allows a cell to divide in the absence of signals to divide and also forget to check that it's DNA isn't damaged before replicating. This is then passed on to the daughter cancer cells. As each check is removed the cell permits more and more mutations meaning more and more likelihood for the next mutation to occur. Cancer is caused literally by one cell having defects and every daughter cell also possess the defects. Those that have defects which accidentally kill the cell are selected out.