Why is the thalamic reticular nucleus called a nucleus?

The thalamic reticular nucleus (TRN) is a thin layer of GABAergic cells adjacent to the thalamus (Fig. 1).  Because of its strategic location between the thalamus and cortex, the TRN is often suggested to be important to attention and regulation of information flow between the thalamus and cortex (Lam & Sherman, 2011).

A nucleus is defined as a

  [p]ortion of tissue that are compact accumulations of neurons having roughly similar connections and functions

Reticular is defined as

  A fine network or net-like structure.

So reticular nucleus translates itself as a net-like accumulation of neurons.

In contrast to the wikipedia meaning, therefore, I interpret nucleus as more of a cluster of functional organizational units rather than a morphological characteristic of that cluster per se.

Fig. 1. Thalamic reticular nucleus. source: Dana Foundation

Reference
- Lam & Sherman, J Neurosci (2011); 31(18): 6791-9


Which of the following demonstrates the pattern of development in Greylag Geese?

Your logic seems fine to me..

Option B: The hatching at an advanced stage is critical for imprinting.

This is wrong because Konrad Lorenz (who rediscovered imprinting)

  demonstrated how incubator-hatched geese would imprint on the first
  suitable moving stimulus they saw within what he called a "critical
  period" between 13–16 hours shortly after hatching (reference).

So saying that the hatchling should be at an advanced stage is incorrect.

Option C: The capacity to recognize an adult of its own species is necessarily inherited.

Again this is incorrect because Lorenz has also stated that

  The human-imprinted gosling will unequivocally refuse to follow a
  goose instead of a human, but it will not differentiate between a
  petite, slender young girl and a big old man with a beard (Lorenz,
  1965) (reference).

Also in this article it is implied that starlings that are imprinted to humans do not relate to its own kind.

Option D: Rearing by humans does not alter the object of the behavioral routine.

From the earlier findings, this is obviously false. Moreover a duck keeper has explained imprinting thus:

  An imprinted duck--a duck that was raised from the moment of hatching
  by a human and so views the human caretaker as a parent or equal--may
  become accustomed to riding in the car. Imprinted ducks might go
  camping with you (although you must keep them beside you at all times
  or in a crate) or go on play dates to a friend's house (you will not
  want to take them to a farm or a public pond where they may contract
  diseases). If your duck is in a diaper, you will need to change the
  diaper every hour or so (reference).

This shows clear behaviour changes.

Option A:  Geese reared by humans cannot be taught to respond to its own species.

It is mostly accepted that it is not with Lorenz himself stating that

  imprinting is irreversible. It is essential in learning that what has
  been learned can be either forgotten or modified (reference).

However there are claims to the contrary nowadays with it now firmly established that filial and sexual preferences are reversible (reference). Another interesting article by the American Psychological Association with a few links you might want to check out.

In conclusion, Option A could also have its problems with some response to its species possible, but overall it is the most and best plausible answer.

Dr Lorenz with his imprinted geese. Also a very interesting read (reference)


What is the change in ratio of histone to protamine in men with infertility called?

It is termed "abnormal packing".

Source: "Sperm Chromatin: Biological and Clinical Applications in Male Infertility and Assisted Reproduction" by Armand Zini & Ashok Agarwal (2011), p 172.


You can calculate the energy consumption using basic physics formulas.

Work = Force x Distance

and the unit of work is the Joule. Therefore if force is a function of change in length then substituting this function in for force in the above calculation we have that work is a function of length.

If you want to talk about energy consumed in terms of calories rather than joules,

1 calorie = 4.184 joules


What is the mechanism of regulation of PER /CRY genes?

Wikipedia gives a very good explanation of this, on the page for the suprachiasmatic nucleus.

  For example, in the fruitfly Drosophila, the cellular circadian rhythm
  in neurons is controlled by two interlocked feedback loops.

  In the first loop, the bHLH transcription factors clock (CLK) and
  cycle (CYC) drive the transcription of their own repressors period
  (PER) and timeless (TIM). PER and TIM proteins then accumulate in the
  cytoplasm, translocate into the nucleus at night, and turn off their
  own transcription, thereby setting up a 24-hour oscillation of
  transcription and translation. In the second loop, the transcription
  factors vrille (VRI) and Pdp1 are initiated by CLK/CYC. PDP1 acts
  positively on CLK transcription and negatively on VRI. These genes
  encode various transcription factors that trigger expression of other
  proteins. The products of clock and cycle, called CLK and CYC, belong
  to the PAS-containing subfamily of the basic helix-loop-helix (bHLH)
  family of transcription factors, and form a heterodimer. This
  heterodimer (CLK-CYC) initiates the transcription of PER and TIM,
  whose protein products dimerize and then inhibit their own expression
  by disrupting CLK-CYC-mediated transcription. This negative feedback
  mechanism gives a 24-hour rhythm in the expression of the clock genes.
  Many genes are suspected to be linked to circadian control by "E-box
  elements" in their promoters, as CLK-CYC and its homologs bind to
  these elements.

  The 24-hr rhythm could be reset by light via the protein cryptochrome
  (CRY), which is involved in the circadian photoreception in
  Drosophila. CRY associates with TIM in a light-dependent manner that
  leads to the destruction of TIM. Without the presence of TIM for
  stabilization, PER is eventually destroyed during the day. As a
  result, the repression of CLK-CYC is reduced and the whole cycle
  reinitiates again. (http://en.wikipedia.org/wiki/Suprachiasmatic_nucleus#Fruitfly)

The suprachiasmatic nucleus (SCN) is a tiny part of our brain residing in the center. It maintains a biological clock through a gene expression cycle in the individual neurons. The mechanism for humans is very similar to the mechanism for fruit flies, as explained above, but to rehash a bit...

In the fruit fly model there are five players: CLK, CYC, PER, TIM, CRY.

CLK and CYC are transcription factors for PER and TIM, and bind to their promoters in order to activate the expression of PER and TIM.

When the expression level of PER and TIM gets very high, the PER and TIM proteins return to the nucleus, and inhibit their own transcription factors (CLK and CYC) through molecular interactions.

The CRY protein is light-sensitive, and so daylight (or artificial light) will cause CRY to destroy the TIM proteins. Without TIM, we no longer get the PER-TIM dimers that inhibit the CLK-CYC transcription factors.

In humans and other mammals it's the same concept, but with slightly different players (e.g., homologous genes).

What's important here is that we have a biological clock on the cellular level. We haven't gone into how this clock is used yet... But, it's my understanding that the SCN uses the information to tell the pineal gland when to produce melatonin.

The melatonin causes us to be drowsy, lowers our body temperatures, and causes us to fall asleep.

You can see another cycle at work here - our body temperature, which rises with wakefulness, and declines with sleep.

This gives a more general answer to how circadian rhythms are used to influence our sleep cycle. Your question was how the genes involved in circadian rhythms regulate each other. The answer is the transcription-translation negative feedback loop described above.

Hope this helps...


Humans are believed to be mostly serial monogamists with a noticeable components of secret cheating. Serial monogamy means most will have a single partner at a time but  will likely have several partners throughout their life, there is however an under current (~15%) of hidden cheating in most studied populations. Also I say mostly becasue human behavior is plastic and nearly every possible combination exists, albeit in small numbers.  Males do have a stronger tendency to seek multiple partners at the same time, which makes biological sense.
 like many social species you really have several mating strategies coexisting, often in the same head. Our large brains allow for more flexible approach to strategies.

In other animals exclusive (one mate forever) monogamy is exceptionally, almost breathtakingly rare, (not counting animals that only ever mate once). The Azara's night monkey is one of the few that has been backed by genetic research. Almost every monogamous species ever studied either has some rate of cheating, or is serial monogamous.


Is the tomato a very very close relative of the pepper?

There are different unrelated plants called "pepper" in English. Black pepper (species of the Piper genus), as indicated by Chris, is not related to tomato and doesn't "look alike".

I guess the OP meant actually a different plant (Capsicum genus), to which the common bell pepper (Capsicum annuum) belongs. This one is similar to tomato and they both belong to Solanaceae, the same subfamily Solanoideae, but different tribes: tomato is classified in Solaneae and Capsicum in Capsiceae.

In this study you can see, how distant phylogenetically the two genera are. Currently accepted classification generally reflects phylogeny, and there are three more tribes that are closer to Capsiceae, to which Solaneae is nevertheless a close relative.

The most striking morphological difference between Capsicum and Solanum is that the first one is characterized by hollow fruits, while tomato and other Solanum species have fleshy berry-like fruits.

EDIT: It's actually not a difficult task for one's imagination to see that the two types of fruit are structurally very similar. In reality a pepper-structured tomato cultivar is known, and even quantitative trait loci underlying this morphological trait were already found.


How does the tRNA recognise the first methionine during translation?

There are different processes for recognising the initiator site in prokaryotes and eukaryotes.

In prokaryotes the process relies upon the Shine-Dalgarno sequence, this is a well conserved sequence throughout prokaryotes found upstream of the start codon. It interacts with the 16s ribosomal RNA to place the initiator codon in the A site of the ribosome.

In eukaryotes the process is somewhat more complex and relies upon a large protein complex which assembles on the 5' cap of mRNAs. This complex mediates an interaction between the mRNA and the ribosome, the ribosome then scans (using GTP for energy) 5' to 3' to detect the start codon.

One final process which is unusual but does occur is cap independent initiation mediated by internal ribosome entry sites (IRES). These are sequences which form structured loops which can mimic the interactions usually formed by the cap complex. These sequences appear in viral mRNAs allowing viruses to bipass anitviral mechanisms in cells.

You will need to do some reasonably extensive reading if you want to uderstand fully these processes and how they may be manipulated by cells to alter expression.


How to write a stoichiometric matrix for a part of the Pentose phosphate pathway

This is not a particularly well written homework question. I'll try to give some hints based on how I interpret it.

1) The stoichiometric matrix. You have exactly the right idea. I would write the reactions as enzyme names or gene names instead of the EC numbers (e.g. G6PD or G6P dehydrogenase instead of 1.1.1.49). For the reversible reactions, there's no a priori reason to write them in one direction or another, but convention would be to make glucose consumption the positive direction. I would not include "glycolysis" as a separate reaction. I would also consider including cofactors and byproducts in the molecules affected by the reaction (e.g. CO2, NADP+, NADPH, (maybe ADP, ATP, NAD+, NADH also if those come up)).

2) Yes, it's basically what you already have. It's not a particularly great diagram, so you could draw it in a clearer way.

3) I have no idea what this means, but perhaps the next point will help.

4) Primary metabolite is not a super well-defined term, but I think in this context, I would say that the way they're intending the question, they're looking for a "total pathway reaction" that describes the net inputs and outputs of the pathway.

Something like this:

$$
X_1 G6P + X_2 NADP+ \implies X_3 GAP + X_4 FBP + X_5 CO_2 + X_6 NADPH
$$
(G6P=Glucose-6-phosphate, GAP=Glyceraldehyde-3-phosphate, FBP=Fructose-bis-phosphate)

I'll leave it to you to figure out what the X's are or whether I left anything out (since it's a homework assignment after all.)


Is "tonic activity" common for neurons firing in the brain?

Most neurons that have been studied have spontaneous activity. Tonic firing is common in sensory neurons as well as cortical neurons. However, this could be very biased since it is difficult to study neurons that are silent in vivo. In vivo studies are blind, meaning that we usually do not see which neurons we are recording from. This is known as the "dark matter" problem (ref 1).

Also, it is known that there are homeostatic mechanism for maintaining average firing rate. Basically, if a neuron doesn't fire much, then the input sensitivity of the neuron increases to produce more activity (ref 2). But we don't know how widely this can be applied.

References:

Shy Shoham, Daniel O’Connor, Ronen Segev. How silent is the brain: is there a "dark matter" problem in neuroscience? Journal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology, Vol. 192, No. 8. (1 August 2006), pp. 777-784  doi:10.1007/s00359-006-0117-6
Gina G. Turrigiano. Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same. Trends in Neurosciences, Vol. 22, No. 5. (1 May 1999), pp. 221-227, doi:10.1016/S0166-2236 (98)01341-1


What is the justification of Chargaff's second parity rule?

This is an excellent question, which was the cause of some confusion in the field over the years:

"The validity of the second Chargaff rule was unexpected. Obviously it should be regarded as a global rule, i.e. applicable to large sections of chromosomes. Nonetheless, not being derived from a compelling principle, such as the one underlying the first rule, it remains a mystery. This is even more so, when one studies extended versions of Chargaff’s second rule." (paper)

There are a few things to note here:

Chargaff's rules were purely observational; they pre-existed the double helix (see your same Wikipedia ref), and thus pre-existed the double helix model (which was in fact famously a rendering of the first rule in a 3-D model, as Watson wrote about in his book "The Double Helix"). There is thus no logical or mechanistic justification for the rules; they were simply what Chargaff et al. observed for dsDNA and ssDNA. Perhaps I have misinterpreted, but I felt the question implied a belief that there must be some logical requirement for this.
Note that the first rule uses "=" and the second rule uses "~" ("approximately"). That is, if we believe that all bases in a genome are paired, then it follows as a mechanistic/logical requirement that Watson strand and Crick strand must match up compositionally. This is obviously not the case with ssDNA, as I think you indicate in the Q. However, it is nonetheless true that genomes have overall compositional biases; they tend to have consistent (G+C)/(A+T) ratios across the molecule (on average). More recently, it has become clear that this is true not only for single nucleotides, but also for $k$-mers, or short DNA sequences of length $k$ (paper). Indeed, these patterns have been used to match up different pieces from the same genomes (paper). These biases exist on both strands, therefore each strand of a genome is subject to these biases. (The reasons why these biases exist are often argued over, but may have something to do with mutational biases). Therefore, both ssDNA strands of a dsDNA genome have the same compositional biases, and they must complement each other's similar biases, so even within a strand the statistical expectation is Chargaff's second rule. Chargaff, again, probably didn't know many of these things when he came up with the rules. This explanation for Chargaff's second rule has been explicitly discussed in the literature, in the first paper cited.

Notably, the second rule only holds reliably for long sequences, because in short sequences sampling error may lead to a failure to match the biases of forward and reverse strands. This is more or less what everyone means when they call it a "global" rule.


That is a Priapulid worm, also known as a "penis worm". In its own phylum, Priapulida. https://en.wikipedia.org/wiki/Priapulida


Michaelis-Menten equation type - how it is derived?

These kind of equations (the Michaelis-Menten [MM] like term) denote  saturation kinetics. The basic mechanistic assumption behind saturation kinetics is this:

A rate (of lets say product formation) is dependent on the concentration of a molecule such that the rate increases linearly with increase in the concentration of the molecule.

Example 1: Substrate in an enzyme catalysed reaction
Example 2: Transcription factor in a transcriptional activation

However at a certain point increasing the concentration of the molecule will have no effect on the rate of reaction. For the above examples this point will arrive when (respectively):

Active sites in all the enzyme molecules are bound and there is no more space to accommodate a new substrate molecule.
All the binding sites in the DNA are occupied by the existing TF molecules and no more can bind.

In other words, the reaction kinetics changes from first order to zeroth order.

We can provide mechanistic explanations for some cases but in many we do not know how exactly the saturation happens. In modelling we just use a function that will mimic this kind of behaviour.

  Why functions of the form $\dfrac{X}{K+X}$ ?

In deterministic modelling using differential equations, it would be preferred to use a continuous function (instead of using a piecewise linear function) because:

Numerical integration is better in case of continuous functions
In biochemical systems, operations are always continuous. There is no digital logic.

The MM function can actually be derived using an equilibrium or a quasi-steady state approximation (See the wikipedia page for the explanation).

In the MM function, when $X \gg K$ then the function is almost 1. This multiplied by the maximum rate constant will give you the max catalytic rate. At $X=0$ the rate will also be equal to zero. Note that in this model the catalytic rate will not indefinitely increase with $X$.

There are several functions that have values between 0 and 1 for increasing concentration of the substrate. Hill function and logistic function are common examples. However MM is a simpler model. You can always revise your modelling approach when you have better information of the biological system.

Now back to your question:

In this model $C$ denotes alcohol concentration $\alpha$ denotes maximum clearance rate and $\beta$ denotes half saturation concentration (concentration of alcohol at which the rate of clearance is half the maximum rate). Intuitively you can think about the mechanism like this: rate of clearance of alcohol depends on the level of alcohol i.e. if you have a lot of alcohol the amount of it removed per unit time will be higher. Think of it as water that is pumped through a pipe; more water in the tank will result in higher flow rate. However when the kidney (or pipe) is overloaded or "clogged" with an already excess of alcohol then clearance rate would remain the same (the maximum that the kidneys can excrete).

  the amount of alcohol that is introduced in the body, equals the amount of the alcohol that leave the body

That is called mass balance which can be summarized as follows:

Accumulation = Input + Production - (Output + Degradation)


Garlic may affect testosterone metabolism. Its beneficial effect on prostate cancer is not attributed to this, but it is attributed to the direct effect on prostate cancer cells.

What is garlic's connection to DHT?

Cytochrome P450 enzymes. Diallylsulfide, a constituent of garlic, suppresses oxidative demethylation by competitively inhibiting cytochrome P450 2E1, an enzyme that activates carcinogens. Since testosterone metabolism occurs through the mixed function oxidase cytochrome P450 system, garlic may affect the rates of metabolism of testosterone and dihydrotestosterone. The metabolism of testosterone is catalized by inducible P450 1A1, 1A2, 3A3, 3A4 and 3A5 enzymes. These mixed function oxidases can be modulated by a wide variety of environmental facts and dietary constituents. Little is known about the potential for modifying testosterone risk or its treatment modality by administration of garlic constituents [1].

S-allylcysteine (SAC), a potent compound derived from garlic, suppressed the proliferation of PC-3 cells and led to cell cycle arrest at the G0/G1 phases, as well as induced cell apoptosis, which was accompanied by the decreased expression of Bcl-2 and increased expression of Bax and caspase 8. This demonstrates the chemopreventive activity of SAC in vitro, and that SAC may be a promising candidate for prostate cancer treatment [2, 4].
Diallyl disulfide (DADS) is another major component of an oil-soluble allyl sulfide garlic (Allium sativum) derivative. Inhibitory effects of DADS on prostate carcinoma LNCaP cells motility and invasiveness were found to be associated with increased tightness of the tight junctions (TJ), which was demonstrated by an increase in transepithelial electrical resistance (TER) [3, 4].

References:

Paul A. LaChance. Nutraceuticals: Designer Foods III: Garlic, Soy and Licorice. John Wiley & Sons, 2008. Pages 177-180.

Liu Z, Li M, Chen K, Yang J, Chen R, Wang T, Liu J, Yang W, Ye Z. S-allylcysteine induces cell cycle arrest and apoptosis in androgen-independent human prostate cancer cells. Mol Med Rep. 2012 Feb;5(2):439-43. doi: 10.3892/mmr.2011.658. PubMed PMID: 22052207.

Shin DY, Kim GY, Kim JI, Yoon MK, Kwon TK, Lee SJ, Choi YW, Kang HS, Yoo YH, Choi YH. Anti-invasive activity of diallyl disulfide through tightening of tight junctions and inhibition of matrix metalloproteinase activities in LNCaP prostate cancer cells. Toxicol In Vitro. 2010 Sep;24(6):1569-76. doi: 10.1016/j.tiv.2010.06.014. PubMed PMID: 20600798.

Bhandari P. Dietary botanicals for chemoprevention of prostate cancer. J Tradit Complement Med. 2014 Apr;4(2):75-6. doi: 10.4103/2225-4110.130371. PubMed PMID: 24860728.


Are vertebrate wings and fins considered vertebrate limbs?

There is no alternative definition of "limb" in evolutionary biology. Legs, arms, wings and fins are all limbs. Note that a prehensile tail can also be called a limb. From wikipedia > limb

  A limb (from the Old English lim), or extremity, is a jointed, or prehensile (as octopus arms or new world monkey tails), appendage of the human or other animal body.

You can have a look at Cohn et al. (1997), where the term limb is used to refer to legs, arms, wings and fins.

Apparently some authors (as OP has shown examples in the comments) use the term differently. I think it is always made clear so as to not yield to any possible confusion. If you've ever been confused, you might want to let us know which article got you confused.


What is the difference between contig- and read-based sequence alignment?

I have never heard the term “contig based alignment”, and your question is the only Google hit of this exact query (apart from a 2012 patent application).

That said, and without knowing the exact context, I am assuming that you are essentially right: contig-based alignment probably refers to the de novo assembly of reads into contigs, which are then aligned into a scaffold by use of a reference.


Glass petri dish to replace plastic petri dish?

Glass labware is usually made of borosilicate glass which is resistant to temperature changes, so putting a glass petri dish in a -20°C freezer should not be problematic, at least with respect to glass cracking because of temperature changes. I think the warning on your freezer is probably meant to warn against closed glass containers filled with liquid; as water freezes it expands and may mechanically break the glass, but for a petri dish is should not be an issue.

I would be more cautious about heat shocks with a -80°C freezer, though; in my experience at that temperature there is still a risk if the glass is not of good quality.

On a side note, depending on what you use the petri dish for, the surface chemistry  may be different from the polystyrene of plastic petri dishes, and if you are growing cells directly in contact with the surface, switching to glass may change their behavior.


What are the requirements for a spectrometer to be used in biological research?

For all the common uses of a spectrophotometer in biology, any commercial one should be sufficient. For all the routine stuff, the quality of the spectrophotometer is usually of negligible importance.

There are no general rules on what errors and resolution are acceptable, that always depends on what you're measuring. The error should be significantly smaller than size of the effect you're looking at, otherwise you get no useable data.

There are many sources of error with biological systems, the spectrophotometer is really one of the last ones you would think of. Simply the error of pipetting is likely far larger than the error of the spectrophotometer, and differences in the preparation of your biological samples might introduce an even larger error. Unless you're doing something beyond the routine uses of UV/Vis spectrometry, you probably don't need to worry about this.


I think parallel evolution is likely due to the cost to produce the pigments in plants.
Xanthophylls and carotenes are made from only carbon, oxygen and hydrogen. This provides most of the yellow colours without using up nutrients.
Anthocyanins and betalains also need nitrogen, which can be a limiting nutrient for plants.
Wikipedia has a section on plant pigments at:
http://en.wikipedia.org/wiki/Biological_pigment


What are the physiological roles of Hydrogen sulfide?

$H_2S$ is the end product of sulfur related respirations (like sulfate respiration, sulfur respiration, etc...).

By aerob (oxygen) respiration the oxygen in $O_2$ has 0 oxidation number, by $CO_2$ the oxygen has -2 oxidation number, so it was reduced while the carbon was oxidized.

By the thiosulfate respiration of Salmonella enterica the following reaction happens by the reduction of thiosulfate: $S_2O_3^{2-} +2H^+ + 2e^- \to HS^- + HSO_3^{-}$. In this case the sulfur in $S_2O_3^{2-}$ has +2 oxidation number while the sulfur in $HS^-$ has -2 oxidation number, so the sulfur was reduced, it was an electron acceptor, just like oxygen by aerob respiration.

So in the case of Salmonella enterica $H_2S$ production is a byproduct of anaerob respiration. It makes growth faster.

  Sulfate-reducing bacteria are those bacteria that can obtain energy by
  oxidizing organic compounds or molecular hydrogen (H2) while reducing
  sulfate (SO2- 4) to hydrogen sulfide (H2S).1 In a sense, these
  organisms "breathe" sulfate rather than oxygen in a form of anaerobic
  respiration.

wikipedia - Sulfate-reducing bacteria

  Salmonella typhimurium produces H2S from thiosulfate or sulfite.

1987 - The phs gene and hydrogen sulfide production by Salmonella typhimurium.
2011 - Thiosulfate Reduction in Salmonella enterica Is Driven by the Proton Motive Force

S. enterica uses gut inflammation to enhance its sulfur related respiration to outgrow the resident microbes in the intestinal lumen (microbiota). The inflammation creates tetrathionate $S_4O_6^{2-}$ in which the sulfur has an average oxidation number of +2.5. This tetrathionate is reduced by the tetrathionate reductase into thiosulfate with sulfur having +2 oxidation number. So sulfur related respiration helps to make growth faster in order to colonize the gut.

  Here we show that reactive oxygen species generated during
  inflammation react with endogenous, luminal sulphur compounds
  (thiosulphate) to form a new respiratory electron acceptor,
  tetrathionate. The genes conferring the ability to use tetrathionate
  as an electron acceptor produce a growth advantage for S. Typhimurium
  over the competing microbiota in the lumen of the inflamed gut. We
  conclude that S. Typhimurium virulence factors induce host-driven
  production of a new electron acceptor that allows the pathogen to use
  respiration to compete with fermenting gut microbes. Thus the ability
  to trigger intestinal inflammation is crucial for the biology of this
  diarrhoeal pathogen.

2010 - Gut inflammation provides a respiratory electron acceptor for Salmonella
2001 - The Alternative Electron Acceptor Tetrathionate Supports B12-Dependent Anaerobic Growth of Salmonella enterica Serovar Typhimurium on Ethanolamine or 1,2-Propanediol

Since $H_2S$ is a gasotransmitter in the human body, there can be other mechanisms which help S. enterica.

in small amounts $H_2S$ has anti-inflammatory and anti-apoptotic effects
in large amounts $H_2S$ has pro-inflammatory and pro-apoptotic effects

So S. enterica can probably cause inflammation due to killing cells with a fast release of $H_2S$ or prevent inflammation and keep infected cells alive with a slow release of $H_2S$. I found many evidence of the pro-inflammatory theory. By the anti-apoptotic theory I wasn't so lucky, I found only a single review about anti-apoptotic strategies of intracellular pathogens, but it did not mention $H_2S$ production as a possible mechanism. So it might not be true, further studies needed...

  In the digestive system, H2S exerts potent anti-inflammatory actions,
  regulates blood flow and smooth muscle tone, modulates epithelial
  secretion and promotes healing of ulcers [4, 5].

2012 - Hydrogen Sulfide: A Rescue Molecule for Mucosal Defence and Repair

  Hydrogen sulfide (H2S) is the most recent endogenous gasotransmitter
  that has been reported to serve many physiological and pathological
  functions in different tissues. Studies over the past decade have
  revealed that H2S can be synthesized through numerous pathways and its
  bioavailability regulated through its conversion into different
  biochemical forms. H2S exerts its biological effects in various
  manners including redox regulation of protein and small molecular
  weight thiols, polysulfides, thiosulfate/sulfite, iron-sulfur cluster
  proteins, and anti-oxidant properties that affect multiple cellular
  and molecular responses.

  Understanding precise pathophysiological signaling mechanisms and the
  metabolism of H2S is a topic of active research. Unraveling H2S
  interactions within different tissues, with other biochemical
  molecules and various signaling mediators is becoming ever more
  complex.

  These results demonstrate that H2S donors can down-regulate adhesion
  molecule and proinflammatory cytokine expression, therefore
  identifying H2S, its synthesis enzymes, and molecular targets (e.g.,
  KATP channels) as potential targets for novel anti-inflammatory
  therapies.

  Thus, all of the above findings demonstrate that H2S induces
  cytoprotection by an anti-apoptotic pathway.

2013 - Hydrogen sulfide chemical biology: Pathophysiological roles and detection

  A short course of H2S infusion was associated with reduction of lung
  and kidney injury. Prolonged infusion did not enhance protection.
  Systemically, infusion of H2S increased both the pro-inflammatory
  response during endotoxemia, as demonstrated by increased TNF-α
  levels, as well as the anti-inflammatory response, as demonstrated by
  increased IL-10 levels. In LPS-stimulated whole blood of healthy
  volunteers, co-incubation with H2S had solely anti-inflammatory
  effects, resulting in decreased TNF-α levels and increased IL-10
  levels. Co-incubation with a neutralizing IL-10 antibody partly
  abrogated the decrease in TNF-α levels. In conclusion, a short course
  of H2S infusion reduced organ injury during endotoxemia, at least in
  part via upregulation of IL-10.

2012 - A short course of infusion of a hydrogen sulfide-donor attenuates endotoxemia induced organ injury via stimulation of anti-inflammatory pathways, with no additional protection from prolonged infusion

  H2S causes apoptosis in HPSCs by activating the mitochondrial pathway.
  It is suggested that H2S might be one of the factors modifying the
  pathogenesis of pulpitis by causing loss of viability of HPSCs through
  apoptosis.

2011 - Hydrogen Sulfide Causes Apoptosis in Human Pulp Stem Cells

  The level ofendogenous H2S was increasing along with the infection
  occurrence and the gradient of infection aggravate. We can presume
  that endogenous H2S participated in inflammatory reaction of abdominal
  infection and could be one of the serology index which concerned with
  the gradient of infection.

2012 - P53 The level changes and clinical significance of endogenous hydrogen sulfide of patients with acute abdominal infection

  The evidences showed that H2S has an obvious effect on colon smooth
  muscle contraction, and can increase the intestinal movements in slow
  transmit constipation. Our experiment states that H2S has
  anti-inflammation effect in prophase of acute peritoneal cavity
  infection.

2014 - P48 Regulation of hydrogen sulfide in digestive stystem
2010 - Hydrogen Sulfide Improves Neutrophil Migration and Survival in Sepsis via K+ATP Channel Activation
2012 - Hydrogen sulfide and resolution of acute inflammation: A comparative study utilizing a novel fluorescent probe
2008 - Staying alive: bacterial inhibition of apoptosis during infection

  H2S is believed to have two contradicting roles in inflammation. It
  acts as both pro- and anti-inflammatory molecule(9). Li et al.
  reported that the physiological concentration of H2S has
  anti-inflammatory effects, while higher concentrations of H2S can
  produce pro-inflammatory effects(10). The H2S inflammatory role was
  also studied in different systems. In the gastrointestinal tract, the
  H2S regulating role functions by activating KATP channels in order to
  promote the inflammation response(57). The similar H2S function was
  observed in pancreas(7), but the actual mechanisms are largely
  unknown. In conclusion, H2S pathway is a possible route for targeting
  the inflammation treatment. However, much work needs to be done for
  understanding the mechanisms of the contradictory roles of H2S in
  inflammation.

2012 - The Crosstalk between H2S and NO Signaling Pathways
2013 - Gasotransmitters, poisons, and antimicrobials: it’s a gas, gas, gas!

  Developing evidence suggests that dysbiosis (abnormal microbial
  composition or function) can contribute to if not cause chronic
  intestinal inflammation. 5,7 This inflammation can be caused either by
  an abnormal composition of entericbacteria with an elevated ratio of
  aggressive vs protective species, defective production of short-chain
  fatty acids and other protective microbial products, or enhanced
  production of hydrogen sulfide and nitrates that block butyrate
  metabolism and disrupt the mucosal barrier.

2010 - Inflammation and Nutrition in Chronic Disease
2013 - Potential Role of Hydrogen Sulfide in the Pathogenesis of Vascular Dysfunction in Septic Shock

  These results showed that physiological concentrations of H2S can
  induce apoptosis of PDL cells and HGFs in periodontitis, suggesting
  that H2S may play an important role in periodontal tissue damage in
  periodontal diseases.

2009 - Hydrogen sulfide induces apoptosis in human periodontium cells
2010 - Bacteria-derived hydrogen sulfide promotes IL-8 production from epithelial cells

  We have shown that inactivation of H2S producing enzymes
  (cystathionine beta-synthase, cystathionine gamma lyase, or
  3-mercaptopyruvate sulfurtransferase) and NO-synthase in several Gram
  (+) and Gram (−) bacteria render them highly sensitive to different
  classes of antibiotics (Gusarov et al., Science 325 (2009) 1380–1384;
  Shatalin et al. Science 334 (2011) 986–990). We also presented
  evidence that Bacillus anthracis-derived NO is critical at the early
  stage of infection (Shatalin et al. PNAS 105 (2008) 1009–1013). Here
  we show that: (1) cbs/cse and nos mutations change Bacilli global gene
  transcription profile; (2) apore formation process in cbs/cse and nos
  mutants of B. anthracis is affected; (3) virulence of cbs/cse and nos
  mutants of B. anthracis is diminished. These results demonstrate that
  bacterial H2S and NO are an important virulence factors, and that
  enzymes generated these gases may serve as an attractive target for
  antimicrobial therapy.

2014 - S7-6 Role of H2S and NO in Bacillus anthracis spore formation and virulence

Btw. there is non-hydrogen sulfide producing S. enterica too, which can probably (no study about this yet) cause salmonellosis. So using thiosulfate as electron acceptor and producing $H_2S$ might not be essential by the infection. (There are other non-sulfur electron acceptors e.g. nitrate, fumarate, etc... for the case of anaerob metabolism.)

2013 - Genetic Analysis of Non-Hydrogen Sulfide-Producing Salmonella enterica Serovar Typhimurium and S. enterica Serovar Infantis Isolates in Japan
2011 - Salmonella enterica Serovar Typhimurium Colonizing the Lumen of the Chicken Intestine Grows Slowly and Upregulates a Unique Set of Virulence and Metabolism Genes
2013 - Salmonella Uses Energy Taxis to Benefit from Intestinal Inflammation
2006 - Role of Gluconeogenesis and the Tricarboxylic Acid Cycle in the Virulence of Salmonella enterica Serovar Typhimurium in BALB/c Mice
1981 - Aerotaxis in Salmonella typhimurium: role of electron transport.
2010 - IDENTIFICATION OF NOVEL VIRULENCE GENES OF SALMONELLA ENTERICA
2014 - Increasing prevalence of hydrogen sulfide negative Salmonella in retail meats

Overall hydrogen-sulfide and other gasotransmitters are important virulence factors of many pathogens.


Why can Toll-like receptors be found either inside and outside the cell?

TLRs are used to identify features that are typical of pathogens. Different TLRs tend to identify different features, so that a wide range of pathogens can be identified. Some of these pathogens may be extracellular (such as some kinds of bacteria that are recognized by TLR4, which is extracellular) and some are intracellular, like viruses (some of which may be identified by TLR7, which is intracellular).

The fact that innate immune cells have these is a little bit of a red herring, because they aren't limited to innate immune cells -- they're widespread among many cell types, and are effective at protecting the specific cell, not just activating innate immune cells.


What are the floating translucent little objects called in the field of view?

I think you are talking about floaters (a.k.a. eye floaters or flying flies). You may want to have a look at this english.SE post in case you were not talking about floaters.

  Floaters are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent.

You can read the wikipedia article to better understand the causes. These floaters are typically not microorganisms unlike you seem to think. Their scientific name is 'Muscae volitantes' and they are mostly caused due to degenerative changes in vitreous humour due to aging.


Judging by the stripes, it's most likely a wolf spider.

If they didn't have a web I would say they're almost certainly wolf spiders, since they don't build webs. Like most spiders in North America, they are harmless to humans.


What is a good multiple alignment of large genome sequences when working with limited hardware?

First of all, do not, I repeat not, use ClustalW. That is horribly out of date and was never very good to begin with1. It was just the first to become common. At least use ClustalΩ. Anyway, while I haven't done much aligning in the past few years, back when I did, I got the best speed/quality ratio from MAFFT.

MAFFT has been used in various sequencing projects and can deal with whole genomes easily. Whether or not it will run correctly on your machine depends on the specs of your machine, of course. However, it should be considerably more efficient than clustalW, although not necessarily more than muscle.

Before doing any of this though, are you sure you need to align whole genomes? Could this be an XY problem? You might want to consider posting a new question here and explaining what your final objective is. Also, if these are published genomes, you might be able to find an existing alignment.

If you really do need to run a whole genome alignment and your machine can't use MAFFT or muscle or any of the other modern aligners, you need a new machine. No matter how efficient your aligning algorithm, a genome is a lot of data and you need a strong machine with serious RAM for it. If you are on a *nix machine, you could ask about how to create a swapfile to increase your memory on Unix & Linux.

1Don't get me wrong, it was state of the art and everything back in the day, but the state of the art wasn't very good, that's all.


Two subunits connected by only one disulfide bridge: quaternary structure?

I don't know of any examples of this but I would say no doubt, that's quarternary structure. Quarternary isn't so much defined by the kind of interaction but much more the fact that it's between different polypeptides; all lower-level structures are within one polypeptide. (Wikipedia agrees.)


Do animals' facial expressions have similar meanings to humans'?

I would say no, facial expressions in humans do not generally relate to facial expressions in other animals. Even though there are some cases (as described in the comments an previous answers) that refer to domesticated animals, I do not know of any convincing evidence that the facial expressions of humans are faithfully interpreted, or even mimicked, by other animals - at least outside the group of great apes. Further, the cases arguing that (domesticated) animals can do it are often anecdotal (I am not saying wrong!). Taking an evolutionary perspective, I would not even expect it to be happening (or rather by very close relatives only, i.e. other great apes) because facial expressions as behavioural signals are part of communication and therefore often rather species-specific.

But not only that ... there is emerging evidence that facial expressions are not even interpreted uniformly in all human populations: in this article by Crivelli et al. (2016) in Front. Psychol. the authors argue to include anthropological data to cognitive studies. According to their findings, not including a human evolutionary perspective might result in strong biases. They strengthen their point by giving an example of differential interpretation of facial expressions in a Melanesian society which is described in more biological terms in PNAS [Crivelli et al. (2016)]. What they found is that adolescents of this society interpret a facial expression (gasping face) that in other societies conveys fear as a threatening and angry expression.

Generalising this means that if there is divergence in signaling by facial expressions even among human populations, I would consider it unlikely that there is a general homologous system of facial expressions among mammals. There might, however, be a trend in domesticated animals to understand human expressions and adapt behaviour according to them. It still is an extraordinary claim to infer from this that they can actually mimic these expressions, and I have not yet seen convincing evidence for that.


Do strictly anaerobic organisms use metabolic reactions requiring oxygen?

Strict anaerobes do not use molecular oxygen for oxidation reactions.

The oxidation of ferrous iron to ferric iron (viz. the example given by Septimus G) can be done anaerobically by anaerobic purple bacteria [eq. 2 in Ehrenreich & Widdel (1994) Appl Environ Microbiol 60: 4517-4526]:

4 FeCO3 + 10 H20 --> 4 Fe(OH)3 + (CH20) + 3 HCO3- + 3 H+

https://www.ncbi.nlm.nih.gov/pubmed/7811087


Is bootstrapping an acceptable way to determine standard error for binding constants?

My understanding of bootstrapping is that you may estimate variance (and thus standard error of the population mean) iff your measurements are independent and have the same population distribution, in which case a number of sampling-with-replacement calculations can be done. I suspect that this method of estimation would be less desirable with small n values because of the effect that outliers or large standard deviations may have on the calculation. If you have a large dataset then it shouldn't be an issue.


Reliability comes from the fact that in Sanger sequencing (AFAIK) the synthesis of the new strand to the template and the actual reading of the sequence is separated. As you may know Sanger seq uses capillary gel elfo. thus separating the newly produced DNA fragments on a single nucleotide difference, and the reading is done by fluorescence detectors (then base calling etc.) Now compared to this the other sequencing methods like Illumina and 454 detect each nucleotide incorporation that may produce less reliable signals. For eg. in Illumina colonies may overlap on the plate, or in 454 incorporation of multiple nucleotides at homopolymer regions cause a hard time deciding how many nucleotides have actually incorporated. Also it must be noted that quality of the singals / reads is not constant through out Sanger sequencing. The beginning and the end of the reads tend to have noisy and low quality signals, thus actually only the 100-500(-600)bp segment of the whole fragment can be read reliably. Also ABI's SOLID uses a 2 color color-space and each base is read twice and is extremely reliable (99.96% is said by the inventors). Also clever base calling and error correction algorithms may improve accuracy.

It is noteworthy to say that next gen sequencers also achieve high accuracy by taking advantage of their immerse throughput / output - due to clonal amplification of template sequences each original fragment is sequenced multiple times and errors in a single read can be corrected by the use of others.


Loss of allelic variation per generation of full-sib mating

A classical result from the Wright-Fisher model of genetic drift is that at each generation the heterozygosity ($2x(1-x)$) is expected to decrease by $\frac{1}{2N}$ due to genetic drift. ($x$ is the frequency of one of the two alleles). In your example the expected loss of heterozygosity is $¼$. This same result has been derived from coalescent theory and a similar result is derived from the birth-death Moran model. The issue is that this model assume bi-allelic loci only.

Let's think of 1 tetra-alellic (4 alleles) locus and let's assume that the 4 alleles in our two original parents are all different. We can draw the 16 possible pairs of offsprings and see the probability to lose 0, 1 or 2 alleles in the next generation

lose 0 allele: ¼
lose 1 allele: ½
lose 2 alleles: ¼
lose more than 2 alleles: 0
Therefore, the expected number of lost alleles is $1$!

We can then do the same (calculate the probability mass function) for two parents with 3 alleles and then 2 alleles (with various frequencies). It is not very complicated. But it would be much better to have a general model to describe the loss of heterozygosity through time for more than 2 alleles. This paper probably gives this solution but I haven't read it yet. I will probably read it once and I will improve my answer then!


The gases NO, H₂S, CO even have a function in the human body!

Nitric oxide is produced in endothel and neurons as messenger, and in macrophages as cause of nitrosative stress for imprisoned bacteria. Hydrogen sulfide is produced in cysteine catabolism and functions as messenger (only recently discovered). Carbon monoxide appears to act as messenger, too.

http://en.wikipedia.org/wiki/Biological_functions_of_nitric_oxide

http://en.wikipedia.org/wiki/Hydrogen_sulfide#Function_in_the_body

Wu, L; Wang, R (December 2005). "Carbon Monoxide: Endogenous Production, Physiological Functions, and Pharmacological Applications". Pharmacol Rev 57 (4): 585–630. doi:10.1124/pr.57.4.3. PMID 16382109


Is it biologically possible for an adult's eye color to change?

Short answer: The genes that encode eye color do not change, but the pigments in the eye can change due to external factors like diseases of medication.

Long answer: Yes, it is possible that the eye color of adults can change, and it can also only happen to one eye. It is then called Heterochromia. There are two possibilities for different colored eyes, either congenitial (genetic) or acquired. Since you ask only for eye color changes in adults, we can skip here the genetic reasons, as these show up in kids already. If you are interested in them, have a look into the Wikipedia article on Heterochromia.

The basis for our eye color is genetically determined, changes can later occur due to diseases (so if one experiences a change in eye color, it is always a good idea to consult a doctor) and also due to medications.

The eye undergoing a change in pigmentation can either lighten up or darken.

Fuchs’ Heterochromic iridocyclitis: (also known as Fuchs’ Heterochromic uveitis) The change is caused by an eye infection with different microorganisms like Toxoplasma gondii, Herpes simplex virus or Rubella (an probably others) but it can also have an autoimmune pathology. See reference 1 and 2 for more details.

Horner's Syndrome: This is a syndrome which mostly occurs in kids after damages to some nerves. This can lead to insufficient signals towards the pigment production and heterochromia. Rarely this can occur also in adults, where this is called acquired Horner's syndrome, see reference 3 for details.

Pigmentary Glaucoma: In this disease (also known as Pigment dispersion syndrome) pigment cells from the back of the iris float are seperated from the original place and float through the aqueous humor of the eye where they can produce pigment which over time changes the appearance of the eye. See reference 4 for more details.

Medications: Some of the medications against glaucoma (the prostaglandins latanoprost and bimatoprost) can cause a deeper pigmentation which will not always diminish after the end of the treatment. See reference 5 for more details.

Cancers: Some cancers as melanoma can also cause heterochromia, either when they are darker pigmented that the eye or when they are not pigmented. In both cases they influence the eye color. See reference 6 for more details.

References:

Fuchs' heterochromic cyclitis: review of the literature on the
pathogenetic mechanisms.
Associations of Fuchs heterochromic iridocyclitis in a South Indian
patient population
Acquired Heterochromia with Horner's Syndrome in Two Adults
Pigment dispersion syndrome and pigmentary glaucoma – a major review
Incidence of iris colour change in latanoprost treated eyes
Diffuse iris melanoma: Report of a case with review of the
literature


What Is This Tactic Called? (Banishing Adolescent Females)

The reason the dominant female doesn't want her daughter to breed is that she would prefer her own children survive, rather than her grandchildren (the children of her daughter).
I wouldn't call this population control - the dominant female isn't thinking to control the group size, rather, to monopolise the group composition.
The difference with bees is that the genetic relationship between the individuals is more complex (haplodiploid), so the female bees are more closely related to their sisters than to their own offspring!
The general term for the fact that only some animals are taking part in breeding is "reproductive skew".


Fatty acids originating from  chylomicron  triacylglycerol  are delivered mainly  to  adipose  tissue,  heart, and muscle (80%), while ~20% goes to  the liver. - source: Harper's illustrated biochemistry.

Lipoprotein lipase which is present in wall of blood capillaries anchored to endothelium by negatively charged proteoglycan chains of heparin sulfate requires phospholipids and apoC2 for its activity to take place.

Hydrolysis takes place while the lipoproteins are attached to  the enzyme on  the endothelium. Triacylglycerol  is hydrolyzed progressively through a diacylglycerol  to  a monoacylglycerol  and finally to  FFA plus glycerol with the help of lipoprotein lipase.  Some of the released free fatty acid return to general circulation bound to albumin but the bulk is transferred to peripheral tissues like adipose tissue, muscles of heart etc.

Fate of chylomicron
The lipase activity results in loss of 70%-90% of triacylglycerols and apoC2.(source: Harper's illustrated biochemistry) The remnant chylomicron is then taken up by liver by receptor mediated endocytosis. Here cholesteryl esters (present in concentrated form after loss of most of triacylglycerol) and remaining triacylglycerols are hydrolysed and metabolised.


how can a pseudo coelomate like ascaris lay 200k eggs in a single day

First of all, the statement that "pseudo coelomates have very minute width of their body cavity and rest of the body cavity is filled with mesoglea" is not correct at least for (large) nematodes and priapulids: they have quiet voluminous body cavity and no mesoglea. In small nematodes (to which Ascaris doesn't belong) the body cavity is indeed vestigial, but the "space" between the organs is filled with extracellular matrix.

Another point is that the eggs in nematodes develop not in the body cavity directly, but in the ovaries and uteri (as correctly shown in the picture you provided), which indeed occupy very large part of the body.

Now to the question about the counts: individual capacity of a single female 29 cm long was once (see also) estimated to be ca. 27 mln eggs contained in its ovaries and uteri, which is impressive, but reasonable given the extremely small size of the eggs and extremely large size of the worm.

If we very coarsely approximate the volume occupied by a single egg with a cube 70x70x70 µm3, we get ca. 9 ml for 27 mln of them, and not much imagination is required to see, how a female ascarid can find room for this volume of relatively loosely packed eggs in its genital system.

EDIT:
To check my statement about "quiet voluminous body cavity and no mesoglea" one can open any modern textbook on invertebrates (or attend a practical course of invertebrate zoology). This is how the nemotode body cavity is described in the monograph "Nematoda" by Vladimir Malakhov (the original I cite is in Russian, but there is also a translation of the book):

"The presence of a spacious body cavity is considered to be the most characteristic property of the whole class of nematodes".
"Schizocoel [= primary body cavity] doesn't have its own walls made of cellular material and is represented by spaces between organs filled with liquid".
"Nevertheless, it should be stressed, that the opinion of the schizocoel being a voluminous body cavity, appeared as a result of investigations on large parasitic nematodes."


Can anyone identify this tall vine that has volunteered in our back yard?

I believe it is in the genus Dioscorea which is a wild yam.  There are several species native to the Eastern US.  A common species is Dioscorea villosa but you will have to look up details and compare to your specimen.


Examples of virus originated from a living system

Prion diseases are still very poorly understood, but one of the dominant theories is that they are misfolded proteins that cause disease by catalyzing the misfolding of more proteins of the same type.  If that is the case, then they arise from the organism that they affect simply by protein misfolding.  In the case of bovine spongiform encephalopathy (mad cow disease) being transmitted to humans and resulting in new variant Creutzfeldt-Jakob disease, it seems like it might be transmissible between species, but it probably needs to infect a closely related species so that the protein has a homolog it can act upon.

Can't say I know of any examples where people have shown the de novo creation of a virus from a living organism.  There are definitely virus protein homologs in the genomes of organisms, but directionality is hard to argue since its common for viruses to pick up host genes, or leave behind viruses genes.


Why do bees fly inside the gaps between the decoration on the exterior wall of a building and the wall?

They just want to escape from.the heat. If there are no trees near your area, the bees can make a hive to live in. The bees don't constantly fly around; they only do so to gather food (or looking for a partner to mate).
Regarding the particular side of window, I'm not sure, may be that part is a little dry or (damp). What I mean is that the microenvironment of that crack may be more likeable to the bees, though that is just my wild guess.
Hope you found your answer. Thanks for reading.


Is HSV-vector-mediated miRNA expression in dorsal root ganglia stable?

The vector used in this study is based on the herpes simplex virus genome (HSV).

Wildtype HSV mainly infects sensory neurons. After infection, it resides in a latent state in the nervous systems of the host for a lifetime. The viral genome persists in the cell, without integrating into the host genome (Marconi et al., 2000).

The article cited is devoid of background on the vector and its characteristics and I understand your issues. I think that the expression of the RNAi is quite stable in your linked article, because the authors infected neurons in the dorsal root ganglia. The dorsal root ganglia contains sensory neurons. It is an immuno-privileged region, because the blood-brain-barrier (BBB) limits the access of immune cells. Indeed, protein expression through HSV-transfection in the brain is stable, at least up to a year (Suzuki et al., 2008) and possibly longer. Peripherally, outside the BBB, the expression of HSV-plasmids may be compromised within weeks through cellular immunological responses targeting the expressing cells (Suzuki et al., 2008).

Regarding regeneration - The DRG contain mature neurons and is part of the peripheral nervous system. These neurons are known to regenerate readily after injuries, but these injuries are mostly investigated through physical damage (Muratori et al., 2015). Latent HSV infection does not kill neurons, and even an active infection seems to leave neurons relatively unscathed (Rautema, 2002).

References
- Marconi et al., In: Madame Curie Bioscience Database. Austin (TX): Landes Bioscience (2000)
- Muratori et al., (2015); 2015, 860546
- Rautemaa et al., Immunology (2002); 106(3): 404–11
- Suzuki et al., Molecular Therapy (2008); 16(10): 1727–36)


Definitely some sort of fly (order Diptera). Specifically, you found the legless larva, or maggot, of a fly that then developed into a pupa.

 Source: Univ of Florida IFAS
The above picture represents the life-cycle stages of the common house fly (Musca domestica).

M. domestica is one of the most common and widespread flies in the world:

This common fly originated on the steppes of central Asia, but now occurs on all inhabited continents, in all climates from tropical to temperate, and in a variety of environments ranging from rural to urban. Source

According to Wikipedia, M domestic larvae take 2-5 days to metamorphose into a pupa.

Although the OP mentions that a housefly emerged from the pupa, I'll caution the OP that many flies look like house flies to the untrained eye. Houseflies typically deposit their eggs in fecal matter or dead flesh, so finding a maggot deposited into the body of a living millipede seems unlikely behavior from the common house fly. (Edit: Though I see now that the OP said the millipede was dead, so this is not an unlikely candidate).
IF the larva was deposited when the millipede was still alive, then other genera would be more likely.
One example would be a Sarcophagid (or flesh fly; family Sarcophagidae), which some species being known to be internal parasites.
As for proper ID, according to Wikipedia:

Generally, only males of this family can reliably be identified to species, and then only by examination of dissected genitalia. The literature is incomplete or scattered for all regions

Here are some images for a fairly widespread species, Sarcophaga crassipalpis (which is very unlikely to be your species, but demonstrates general appearance of this family):

 Source: Univ of Florida IFAS
Your specimen might still belong to another group of flies, the tachinids (family Tachninidae), which very often parasitize other arthropods.
It'd be very difficult to differentiate most of these taxa without up-close examinations of specimens.


Are there any effects of elevated Cysteine levels on cognitive function?

Your shown homocysteine pathway is way too simple. Especially the production of the neuromodulator H2S from excess sulfur amino acids is not shown. In the last years many more enzymes and reactions have been discovered. I have summarized human sulfur amino acid metabolism in reactome.org, so please use this link to discover all the details and new papers. I'll also append some of the relevant papers below.

Brosnan, JT, Brosnan, ME The sulfur-containing amino acids: an overview 2006 J Nutr PMID 16702333

Remethylation of homocysteine to methionine can also happen using betaine as a methyl donor. This reaction is also part of choline catabolism.

Li, F, Feng, Q, Lee, C, Wang, S, Pelleymounter, LL, Moon, I, Eckloff, BW, Wieben, ED, Schaid, DJ, Yee, V, Weinshilboum, RM Human betaine-homocysteine methyltransferase (BHMT) and BHMT2: common gene sequence variation and functional characterization 2008 Mol Genet Metab PMID 18457970

Bearden, SE, Beard RS, Jr, Pfau, JC Extracellular transsulfuration generates hydrogen sulfide from homocysteine and protects endothelium from redox stress 2010 Am J Physiol Heart Circ Physiol PMID 20817827

Dominy, JE, Stipanuk, MH New roles for cysteine and transsulfuration enzymes: production of H2S, a neuromodulator and smooth muscle relaxant 2004 Nutr Rev PMID 15497768

Stipanuk, MH, Ueki, I Dealing with methionine/homocysteine sulfur: cysteine metabolism to taurine and inorganic sulfur 2011 J Inherit Metab Dis PMID 20162368

Chiku, T, Padovani, D, Zhu, W, Singh, S, Vitvitsky, V, Banerjee, R H2S biogenesis by human cystathionine gamma-lyase leads to the novel sulfur metabolites lanthionine and homolanthionine and is responsive to the grade of hyperhomocysteinemia 2009 J Biol Chem PMID 19261609


Is studying complete mitochondrial genome need biological lab work?

All papers you mentioned have involved biological lab work. They all have sequences specific mitochondrial genome and then have analyzed it with the help of bioinformatics. Sequencing genome requires lot of bench work (wet work or "biological lab work"). Even one of them have mentioned it in abstract itself.

  The complete mitochondrial genome of Himalayan bee Apis laboriosa, from Mizoram, India, has been sequenced using Illumina NextSeq500 platform and analysed.


Can mexican salamander regenerate any organ?

I'm going to assume you meant Ambystoma mexicanum also known as the axolotl. There are other kinds of salamanders that live in Mexico, but the axolotl is widely-studied and sometimes called the 'mexican salamander'.

The axolotl has exceptional regenerative powers, and although I suspect this ability is shared among salamander larvae(even if not the adults) there's not much research into phylogenetic distribution of regenerative capability. So in the absence of a more refined answer I'm going to hope axolotl results generalize to other salamanders.

Axolotls, as long as they don't die, can regenerate nearly any part of their brain. As a rule, as long as they don't die they can regenerate from any injury. There are a couple exceptions(it's very hard to keep an axolotl alive without a heart, so that hasn't been tested) like the eye but in general they can grow back nearly anything.

The Hox gene research I've found was done explicitly on worms and frogs, but I would feel safe concluding that axolotl regeneration relied on a similar mechanism, and that therefore they have Hox genes for internal organs. I mean, they had to grow them the first time, right?


The concepts you raise in your question are not founded in neurobiology. We do not know what the biological correlates of a "unit of memory" are in the central nervous system.

Although oscillations are widespread in the brain, the relationship between oscillations and memory storage and recall is a subject of active research. The way you state this process in your question is not justified by any experimental evidence that I am aware of.

Memories do not have a "root neuron" — as I wrote above, we do not know how memories relate to neurons. Inhibitory neurons simply provide inhibitory input currents to their post-synaptic targets. Any relationship with "resonance" or oscillations relies on explicit assumptions about emergent network properties, and these are currently unfounded.


Genetic carrier Pedigree of Recessive Traits

Let's take Question A:

Both fathers have siblings with red ears, and red ears are an autosomal recessive trait. The grandparents did not have red ears, we know then that they were carriers of the recessive allele. Each grandparent was Nr (for Normal and red alleles respectively).

The fathers have normal ears, so they could be NN (probability 0.33) or Nr (probability 0.67).

The answer then is that each father independently has a 2/3 chance (0.67 probability) of carrying the red ears gene.

The male's mother, being RR, makes the male a carrier only if the male's father is himself a carrier. To put it mathematically, he has a 1/2 chance of being a carrier with 2/3 probability that he was a carrier to begin with. (2/3)*(1/2) = 1/3.

Therefore the male can be carrier with 1/3 chance.

Now Question B:

Short answer:

Since the male and female have symmetrical pedigrees, and we just solved the chance of the male being a carrier with 1/3 chance, then the chance of them having a child with red ears is (1/3)*(1/3) = 1/9.

Long answer:

The male's and female's fathers may each be heterozygous or homozygous normal, given the information, with both mothers being homozygous normal (NN).

If Father A is NN (crossed with Mother A, also NN), there is a 0 probability of passing on the red ears allele.

If Father A is Nr, then Person A has a 0.5 probability of carrying the red ear allele.

Person A can now be NN (with 0.25 probability) or Nr (with 0.5 probability).

Likewise with Person B.

Now lets consider all 4 combinations of genotypes that Person A and B can have when they have a child. I will write a table with one Person on each side of the table, with the probability of their genotype written in brackets beside. Each intersection will represent the frequency of carrying the red ears allele.

                Person B
             (1/3)     (2/3)
Person A      NN        Nr
(1/3) NN      0/4       2/4
(2/3) Nr      2/4       2/4

Carrying the red ear gene: (A more interesting example)
There are a total of 6 outcomes in which the child carries the red ears allele, but these must be weighted by the probability that each parent has the associated genotype.

Probability of carrying 'r' = [ (1/3)(1/3)(0/4) + (1/3)(2/3)(2/4) + (2/3)(1/3)(2/4) + (2/3)(2/3)(2/4) ] / [ (1/3)(1/3) + (1/3)(2/3) + (2/3)(1/3) + (2/3)(2/3) ]
 = 0.25

Having a child with red ears:
Probability of having red ears = [ (1/3)(1/3)(0/4) + (1/3)(2/3)(0/4) + (2/3)(1/3)(0/4) + (2/3)(2/3)(1/4) ] / [ (1/3)(1/3) + (1/3)(2/3) + (2/3)(1/3) + (2/3)(2/3) ]
 = 1/9 or about 0.11

It's left as an exercise to the student to derive the remaining probabilites.
Nr 4/9
NN 4/9
rr 1/9


Is there a GPS super tiny for passerine birds?

The technology is not there (yet) for deployments on 10 gram birds. The limits for GPS technology are around the 50 g range, for birds. Also bear in mind that the smallest loggers are generally not capable of transmitting, so you would need to recapture the animals to retrieve your data.

As your question implies, there is a strong trade-off between device weight and battery life. There are GPS devices weighing as little as 1 g, but their lifespan is very limited (10 fixes for the 1 g device; 50 for a 1.1 g device).

As a side note: your question implies that small passerines can carry 20 - 50 % of their body mass in tracker without their flight being affected. The ethics boards I am familiar with generally limit trackers to ~ 5 % of the mass of the animal.


First of all, though bone marrow is not considered a part of lymphatic system because it is not connected to lymph vessels, yet it is the site of production of both B- and T-lymphocytes and is thus considered as primary lymphoid organ1. So, it is closely related to lymphatic system.

On doing some research, I can conclude that bone marrow itself actually does not perform the role of a valve. It is the lymph vessels itself which perform the valve-like function. See this2:

  As lymph capillaries carry lymph away from the tissue spaces, they merge to form larger and larger vessels. These larger lymph vessels resemble veins, but their walls are thinner and they have more one-way valves to prevent lymph from flowing backward. Whereas the cardiovascular system has a pump (the heart) to move fluid (blood) through the system, the lymphatic system does not. It relies on the contraction of muscles to move lymph throughout the body. The larger lymph vessels have a layer of smooth muscle in their walls that contracts rhythmically to "pump" lymph along. The contraction of skeletal muscles, brought about by simple body movement, and the mechanics of breathing also help to move lymph on its way.

So, I'd consider that paragraph as one of the few places where Wikipedia has given incorrect fact.


What happens if we continuously stimulate a mimosa plant?

Mimosa leaves have mechanoreceptor cells which sense the mechanical stress through proteins called mechanoreceptors (they are similar to the ones responsible for sense of touch in animals). When stimulated the mechanoreceptors cause ion channels to open leading to depolarization. This generates an action potential (AP; like neurons) which in turn activates the motor cell (Visnovitz et al., 2007). Motor cells cause leaf movements by change in their interior turgor pressure (similar to opening and closing of stomata).

Repolarization (like in neuronal AP) takes time and Mimosa would not respond to stimuli that are too frequent. The time required for the turgor pressure to relax would be an additional factor.

I am no plant biologist but if I compare this situation with that in neurons, I can speculate that long term non-responsiveness similar to LTD may happen because of down-regulation of mechanoreceptors. It has actually been shown that Mimosa does actually become insensitive to a persistent stimulus such as a continual water drop and moreover exhibits a long-term "memory" of this non-responsiveness (Gagliano et al., 2014). However, the exact molecular mechanism has not been elucidated. Again, there would be thresholds (on amplitude and frequency) for the signal to elicit these kind of changes.

References

Visnovitz T, Világi I, Varró P, Kristóf Z. Mechanoreceptor Cells on the Tertiary Pulvini of Mimosa pudica L. Plant Signaling & Behavior. 2007;2(6):462-466.
Gagliano, Monica, et al. "Experience teaches plants to learn faster and forget slower in environments where it matters." Oecologia 175.1 (2014): 63-72.


Species that have evolved to be near identical?

Simple answer: yes, an uncounted number of them.  You need to read up on two topics: convergent evolution and mimicry.
Convergent evolution is when environmental factors cause different creatures to evolve similar appearance and lifestyle.  Perhaps the classic example of this are the dolphins and ichthyosaurs.  Despite being of different groups - mammals vs reptiles - they both evolved from land-dwelling creatures that adopted a marine lifestyle, and as a consequence a similiar appearance.
Mimicry is when one creature evolves to appear similar to another because that gives them some advantage.  Here the classic example is the viceroy butterfly, which supposedly evolved a similar appearance to the monarch because the latter tastes bad, so that birds avoid eating it.


Yes; It is possible to inhibit cell death.

There are several possibilities, of which many - as correctly recognized by you - involve changes in the activity of the cell death pathway (or related ones);

For a long (but still incomplete) list of commercially available drugs that inhibit cell death, please see: https://www.sigmaaldrich.com/life-science/cell-biology/cell-biology-products.html?TablePage=9559839

P.S.: Note that selectively inhibiting a pathway (note: not only cell-death) in only one cell type (or tissue - as you hinted at) usually requires a lot of tests and experimentation and isn't trivial.


How do we feel sensations from a tooth surface that is made up of enamel?

How do we feel the tactile sensations when we touch our teeth

The same way you feel tactile sensations when you tap a bicycle helmet on you head: the motion (or vibration) is transferred through the material to your head & the nerve endings in your scalp the same as tapping a tooth sends vibrations to the nerves in & at the base of the tooth.


What were the mammal ancestors like 65 million years ago?

Many of them looked like little rodents. However, several distinct mammalian lineages were already present, including Monotremes, marsupials and placental mammals. Throughout the whole Mesozoic era, mammals were already quite diversified! Also, even though most of the mammals that survived the K/T boundary were rather small, there were already some larger mammals around in the Cretaceous.
Here is a nice picture of a symmetrodont:

See a nice page on early mammals.


How are new chromosomes replicated into the next generation via sexual reproduction?

You are right that a person with an abnormal number of chromosomes will be unlikely to find an "equal" partner to mate with. This does not prevent a chromosome aberration from spreading though, and it is not necessary that the mutation is initially beneficial for it to spread. While it is true that many chromosomal aberrations may be detrimental and cause various syndromes, a chromosome split or multiplication may also be netural except for the matter of reproduction. A change in chromsome number will not be inherited deterministically, but can give rise to various new permutations in the offspring due to the mechanics of chromosome segregation during meiosis.

You can find a good explanation at Scienceblogs.com: http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/ :

  The net result [of a chromosome split] is that although this
  individual is fine and healthy, a significant number of his or her
  gametes may carry serious chromosomal errors, which means they may
  have reduced fertility. They aren’t sterile, though; some of their
  gametes will have the full complement of genes, and can similarly
  produce new healthy individuals who will probably have fertility
  problems. (...)
  So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant. Which leads to another misconception in
  the question: something doesn’t have to provide a benefit to spread
  through a population! Chance alone can do it. We don’t have to argue
  for a benefit of chromosome fission at all in order for it to happen.


Are erythrocytes lysed during alpha hemolysis?

Alphahemolysis simply oxidizes hemoglobin to methemoglobin and causes a color change on blood-agar. The RBC membrane is left in tact as far as I know. If you look at a picture of the 3 types of hemolysis, you will see that there is no zone of clearing in the alphahemolysis plate. Compare that to the obvious zone of clearance observed on the betahemolysis plate, in which complete lysis occurs. Here is a nice picture


What are the differences between white and brown adipose tissue?

Not sure what you are asking, except to add to the list?

Its worth mentioning that brown adipose tissue is the only organ in the human body whose primary purpose is to generate heat.  We are warm blooded, but the body temperature is regulated by other organs generating heat while they do work (like muscles or I suppose the stomach, kidney, etc).

Brown Tissue is supposed to not a juvenile attribute - doesn't show up in adults to the same extent (usually being limited to neck and upper chest.

Brown Tissue is thought to be present in only critical areas of the body - even in infants.  Its found in the inner body cavity around vital organs.

The color comes from the large number of mitochondria in the cells, which is where the heat is generated via uncoupling protein 1 (UCP1).

White adipose tissue is what we more commonly call fat tissue - its primary function is to store energy in the chemical form of long chain fats.  Fat tissue as it grows can inhibit the function of insulin in the body, increasing insulin resistance.

You could almost call them 'good fat' and 'bad fat'


Why are there "Old World" and "New World" families?

Yes, I think this is exactly right in the three cases you mention, convergent evolution noticed by the humans who were doing the naming. There are other cases (Remi.b mentions simians) where the "Old World" and "New World" versions are sister clades that became geographically isolated from each other.


What is the pH of cytosol? And plastids?

The optimum cytoplasmic pH for performing physiological activities in
plant cells is a neutral pH of around 7.2 to 7.4.
The pH of apoplastic space outside plasma membrane and vacuolar pH is
acidic ranging between 5 to 7.
The thylakoid lumen is more fluctuating which varies during light /
dark cycles and is highly acidic.
The mitochondrial compartment and chloroplast maintains a basic
conditions of about pH 8 for optimization of biochemical reactions
occurring in these two particular compartments.

(Via: https://www.frontiersin.org/articles/10.3389/fpls.2017.02079/full#:~:text=Plastid%20stromal%20pH%20could%20only,cytosolic%20pH%20(around%207.3).


Defining dominance and selection in these formulae

Fry (2010) borrowed his variables from Kidwell et al. (1977).  Kidwell defines the fitness of each genotype as,

$w_{m1}$, $w_{f1}$ = male and female fitness of the A$_1$A$_1$ genotype.

$w_{m2}$, $w_{f2}$ = male and female fitness of the A$_1$A$_2$ genotype.

$w_{m3}$, $w_{f3}$ = male and female fitness of the A$_2$A$_2$ genotype.

Kidwell then establishes the following parameters for each fitness variable for opposing additive selection,

$w_{m1} = w_{f3} = 1$,

$w_{m2} = 1-.5s_m$,

$w_{f2} = 1-.5s_f$,

$w_{m3} = 1-s_m$, and

$w_{f1} = 1-s_f$.

Therefore,

$s_m = 1-w_{m3}$, and

$s_f = 1-w_{f1}$.

$s_m$ and $s_f$ are the relative fitness differences between the two homozygous genotypes of each gender. The heterozygotes are assumed to have half of that differential. This is what Fry refers to on page 2 (page 1511 of the publication):

  In Kidwell et al.’s notation ... the most fit genotype in a given sex has a relative fitness of 1, and $s_m$ and $s_f$ are the selection coefficients against the less-fit homozygote (or hemizygote) in males and females, respectively.

For opposing selection with arbitrary dominance, Kidwell parameterizes the heterozygous fitness components as

$w_{m2} = 1-h_ms_m$, and

$w_{f2} = 1-h_fs_f$.

Notice that $h$ is modifying the fitness difference $s$ in the heterozygotes. This is due to incomplete dominance of one allele over the other. If both alleles in a heterozygote contribute equally to the phenotype, then $h = 0.5$, and you have the additive fitness described above ($w = 1-.5s$).

If one allele is incompletely dominant over the other, the selective difference $s$ will be modified by some amount, $h$. If A$_1$ is only slightly dominant over A$_2$, (say, $h=0.6$), the effect on $w$ won't be much different than if $h=0.5$. Both alleles will affect fitness but the more dominant allele will have a slightly greater affect on fitness than the other allele. If one allele is much more dominant, then $h$ becomes larger and the more dominant allele contributes more to the overall fitness than the other allele.

Finally, if $h=1$ then one allele is completely dominant so the other allele will not contribute at all to fitness. When $h=1$, the equations reduce to $w = 1 - s$ (for the respective genders), remembering that $h$ is based on the dominance of the allele with maximum fitness in the other gender.

Consider a female. Her maximum fitness is the A$_2$A$_2$ genotype.  If A$_1$ is completely dominant over A$_2$, then a heterozygous female would have fitness equal to the A$_1$A$_1$ genotype which, for females is defined as $w = 1-s_f$. On the other hand, if A$_1$ is not completely dominant over A$_2$, then the heterozygote will have some reduction in fitness but not as much as for complete dominance.

To answer your final question about your figure, given the following values for A$_1$A$_1$, A$_1$A$_2$, and $_2$A$_2$, respectively:

$w_m = 1, 0.9, 0.2$, and

$w_f = 0.3, 0.7, 1$, then

$s_m = 1 - 0.2 = 0.8$, and

$s_f = 1 - 0.7 = 0.7$.

For the heterozygosity effect ($h$), given that

$w = 1 - hs$, then

$h = \frac{1-w}{s}$, therefore

$h_{m2} = \frac{1 - 0.9}{0.8} = 0.125$.

A$_1$ is nearly completely dominant over A$_2$ in males, so the presence of A$_2$ is the male is not reducing his fitness by very much. For females,

$h_{f2} = \frac{1-0.7}{0.7} = 0.429$.

The presence of the dominant A$_1$ allele in females has stronger heterozygous effect so her fitness is reduced more, compared to heterozygous males.

Citations

Fry, J.D. 2010. The genomic location of sexually antagonistic variation: some cautionary comments. Evolution 64: 1510-1516.

Kidwell, J.F. et al. 1977. Regions of stable equilibria for models of differential selection in the two sexes under random mating. Genetics 85: 171-183.


In German we call it "Kindchenschema" which is unfortunately translated only to the more unspecific "Cuteness", but sometimes also to "baby schema". This seems to be applying to most (care taking) mammals, also over species borders. The specific looks release hormones in the adult triggering care taking behaviour. This is to ensure the babies safety. That it not only works with the own parents helps ensuring the baby is cared for even if the parents cannot do it themselves.
Interestingly, the head and eye shape seems to trigger this hormone release. And it is the same for many animals. Like always, evolution uses the same winning scheme over and over again. This is why you can get a dog to care for abandoned kittens, and why you will find those puppies ever so cute.


There are many good papers by Karl J. Niklas where he models tree growth. I'm not sure if he used L-systems in particular, but I'm sure his work can inform you about the 'rules'. You can find out more here and here.


What exactly does 'reverse use-dependence' mean?

Reverse use dependence is the reduction of a drug's efficacy with the repeated use of the target. This contrasts with ordinary use dependence, for instance with $\mathrm{Na}^+$ blocking local anaesthetics, where they exert more block after tissue use. Reverse use dependence is particularly (but not exclusively) seen with channel blockers such as quinidine.

Quinidine is a $\mathrm{Na}^+/\mathrm{K}^+$ blocker that can slow heart rates, and does so more effectively when the heart rate is already slow. Increased use of the tissue, with a raised heart rate, reduces the effectiveness of the drug. So, strangely, quinidine exerts less block when the target is in use. This is shown in figure 4 from (Breithardt et al., 1995). As the tissue is used less (cardiac cycle length increases), the effect of the drug becomes stronger (action potential duration prolongation increases).

The reverse use dependence of quinidine can be demonstrated on a molecular level with application of quinidine to a voltage-clamped channel with an $\mathrm{i}_\mathrm{Ks}$ current. We see better block when short electrical pulses are given than when longer ones are. The mechanism behind use- and reverse use dependence is by state-dependent affinities, e.g. the drug can bind more easily to the channel in open/closed state. For example, a channel blocker whose binding site becomes occluded when the channel is opened could exhibit use dependent block.

But be warned: reverse use dependent drugs may also exhibit normal use dependence. Quinidine is not just reverse use dependent, but also use dependent
as a $\mathrm{Na}^+$ blocker. The type of tissue and its state change the effect of the drug and must be taken into account.

See (Breithardt et al., 1995) for a review of the topic:

  In 1990 Hondeghem and Snyders introduced the concept of reverse use dependence as being a drug effect which is less marked with increased use. Specifically
  quinidine, N-acetyl-procainamide and sotalol lengthened action potential
  duration markedly at slow heart rates but much less or not at all at fast heart rates
  (Fig. 4 [27)). Frequently, reverse use dependence has become equated with reverse
  use-dependent block of ion channels. Although reverse use-dependent block of ion
  channels can lead to a reverse use-dependent drug effect, this does not need to be
  the case. Worse, reverse use-dependent drug effect does not require reverse use dependent block of channels.

References:

Breithardt, G., Borggrefe, M., Camm, A., Shenasa, M., Haverkamp, W. and Hindricks, G. (1995). Antiarrhythmic Drugs. pp.97-98.


No. No other group found in the fossil record after the K-T boundary (the extinction "event") descends from dinosaurs.

It is likely that the extinction event was not itself instantaneous so if you wanted to be extremely picky you could argue that small numbers of individuals survived the K-T boundary but, apart from birds, none of these survivors went on to form long lasting lineages.

Non-avian dinosaurs that survived the extinction event are referred to as "palaeocene dinosaurs", there are some links on Wikipedia that might interest you.

You can see a diagram linking vertebrate groups here, similar diagrams can be found in most evolution texts.


The classic application is analysis of graph data. For example, protein-protein interaction networks or gene regulatory networks and the like. There are various types of data that can be presented in the form of a network and network analysis is an integral part of Systems Biology.

Another example is determining the similarity of functional annotations from the Gene Ontology. One of the ways of doing so is finding the shortest path between two nodes in the GO graph.

Or, for a more concrete example, I recently published a paper where I examined various features of a particular group of proteins. One of the pieces of information I used was how central these proteins were to the network and, for this, I measured how often they served as a node in the shortest path between two others.

The simplest way for you to find more example is to go to PubMed and search for "shortest path":

https://www.ncbi.nlm.nih.gov/pubmed/?term=shortest+path


I think it's indeed a young, and possibly worn, specimen of Orgyia antiqua (also Rusty Tussock Moth or Vapourer, see also UKmoths). This species is relatively common in large parts of Sweden. However, the tufts and "tail" are usually more pronounced, but there is probably intra-species variation, and old, worn individuals can have sparser tufts. As you say, they are usually longer than 1.5cm but there is large variation, sexual dimorphism and younger larvae (early instars) are natually smaller.

(picture from wikipedia)

Swedish specimen:

( from http://krypinaturen.se/fjarilar-lepidoptera/nattfjarilar/tofsspinnare-lymantriidae/orgyia_antiqua_1878_20130626/)

Lymantria dispar is rather rare in Sweden and is only found in certain localities in the south (Blekinge, Småland coast) along with Öland and Gotland.


You are correct. Anything within the universe is part of the closed system of the universe. Therefore, they must also increase the entropy of the universe. You are correct, they do release a lot of heat. Plus, while making ATP, the major source of cellular energy, they convert a complex molecule, glucose, to simpler molecules, H2O and CO2, increasing entropy as they release these chemicals.

Also, the key fact is that to lower entropy in their body, organisms must use up energy. Energy is required to avoid the entropy from increasing (which actually means they actually expend energy to prevent equilibrium; high entropy means reaching equilibrium). So they would follow the 2nd law of thermodynamics. Which reminds me of a joke!

Old chenists never die, they just reach equilibrium!


What is the easiest way to measure a human body surface area?

How cost efficient does it has to be? Do you want these data to be comparable to another study?
Fundamental issues
What do you call surface area?
The interior of the guts (interior of the mouth, stomach, intestins, ...) are typically considered as exterior to the body. I would assume you don't want to consider these things in your measurements, right?
Coastline paradox
By aware of the coastline paradox

The coastline paradox is the counterintuitive observation that the coastline of a landmass does not have a well-defined length. This results from the fractal-like properties of coastlines.

Similarly, for the surface of the human body, the results will be drastically different depending upon the scale of measurement you want to consider. If you want to measure the small bumps of each atom or if you're happy to consider the the skin is a perfectly flat surface, the answer will vary a lot (numerous order of magnitudes)!
So, if you want to make your results comparable to those of another study, then you should definitely copy their methodology. If all that matters is that you can compare the different individual you measure, then you can pick a methodology that works well for you.
Methods
Those are in no way an exhaustive list.
3D scanner
3D scanner is probably the way to go for accuracy.
Approximation of body shape into cylinder and spheres
If you want cheap and inaccurate, you can assume each body part is a cylinder. Consider for example reducing the human body to 4 limbs (which you could further split in two separated by the knee and the elbow), a torso and a head. Just measure the perimeter of each body part and and approximate the surface area.
It might sound like a silly technic but it might well be good enough for your purpose (esp. if you're not comparing your results with another study).
Polyethylene film
Following Walsberg & King (1978) (thanks to @bshane for pointing this paper out), you can wrap people in a polyethylene film and then measure the area of the film. When measuring the area of the polyethylene film, you are going to have to make some approximation into some simplified (or series of simplified) shapes just like I suggested above. Walsberg & King (1978), when measuring birds, assumed the overall shaped was a prolate spheroid with a hemispherical head. You're going to have to try to find what simplified shape ressembles most to the polyethylene film.
Of cours, you might want to eventually consider other fabrics than polyethylene film and you might want to consider different number of fabrics.
You could prepare pre-measured rectangles and triangles of a given fabrics with colors matching a known size. Then you can just stick those fabrics on the individual body and simply add up the size of the shape you add on the body. This sounds like a difficult solution as you will have a hard time to correctly place the fabrics to avoid wrinkles, overlaps and gaps.
Test reliability of your measure
Reliability of your measure
Do not forget to repeat measurement on a few individuals to measure the accuracy of your measure.
inter-raters reliability
If several people are going to work on this project, you should also make sure to test the inter-raters reliability


Difference between NCBI's /genomes and /1000genomes

The simplest difference is the scale and range. The aim of 1000 genome project was to provide comprehensive library of human genetic variation. DNA of individuals coming from different ethnic groups, geographic locations were sequenced and the results of the study were published here.

Genomes from NCBI come from different organisms and the number of sequenced individuals differ between species (including human). This database is constantly growing. Detailed description can be found here.


Are insects capable of gliding on the air with their wings spread, similar to birds?

It's worth mentioning that insects' flight is somehow different from birds' one, mainly because of the Reynolds number.

However, there is evidence of (some) insects gliding. For instance, Walkeling and Ellington (1997) have filmed gliding in dragonflies and damselflies:

  The free gliding flight of the dragonfly Sympetrum sanguineum was filmed in a large flight enclosure. Reconstruction of the glide paths showed the flights to involve accelerations. Where the acceleration could be considered constant, the lift and drag forces acting on the dragonfly were calculated. The maximum lift coefficient (CL) recorded from these glides was 0.93; however, this is not necessarily the maximum possible from the wings. Lift and drag forces were additionally measured from isolated wings and bodies of S. sanguineum and the damselfly Calopteryx splendens in a steady air flow at Reynolds numbers of 700-2400 for the wings and 2500-15 000 for the bodies. The maximum lift coefficients (CL,max) were 1.07 for S. sanguineum and 1.15 for C. splendens, which are greater than those recorded for all other insects except the locust. The drag coefficient at zero angle of attack ranged between 0.07 and 0.14, being little more than the Blassius value predicted for flat plates. Dragonfly wings thus show exceptional steady-state aerodynamic properties in comparison with the wings of other insects. A resolved-flow model was tested on the body drag data. The parasite drag is significantly affected by viscous forces normal to the longitudinal body axis. The linear dependence of drag on velocity must thus be included in models to predict the parasite drag on dragonflies at non-zero body angles. (emphasis mine)

Source:

JM Wakeling, CP Ellington, Dragonfly flight. I. Gliding flight and steady-state aerodynamic forces. Journal of Experimental Biology 1997 200: 543-556.


Has the concept of allostasis been adopted in biology, in place of homeostasis?

Allostasis is more than changing set points. The theory of allostasis attempts to unify the theories of stress and homeostasis. And, although Peter Sterling and Joseph Eyer were the first to coin the term "allostasis", the concept is today proposed by a plethora of researchers.

Allostatic responses ensure „stability through change“ in situations of strain and stress. If in allostatic mode a feedback control system is able to change both its set point and its parameters to approach a state vector that is more suitable for survival. An allostatic response involves the activation of actuator variables that is referred to as allostatic state. Although allostasis is basically beneficial for viability it also exposes the organism to some kind of strain, referred to as allostatic load. If ongoing or being excessive, allostatic load may be life-threatening on its own terms. In this situation, it is referred to as allostatic overload.

Figure taken from Chatzitomaris et al. 2017.

The idea of allostasis might have been omitted in your biology class due to didactical reasons. For an introductory course it may be beneficial to begin with the simpler theory of homeostasis.

Today, the concept of allostasis is of increasing importance for psychology and medicine. As of today, a PubMed search for the term "allostasis" results in 730 papers and a search for "allostatic load" delivers 1123 publications (with growing tendency).

The theory of allostasis helped to improve our understanding of a broad range of diseases and non-pathological bio-psycho-social situations. Typical examples include starvation, obesity, exercise, fever, type 2 diabetes, hypertension, thyroid disorders, post-traumatic stress disorder (PTSD) and psychosomatic diseases. Additionally, the recent development of panels for allostatic load facilitates differential diagnosis near the small ridge between health and disease.

References

Sterling P, Eyer J. Biological basis of stress-related mortality. Soc Sci Med E. 1981 Feb;15(1):3-42. PMID 7020084.
Sterling P. Allostasis: a model of predictive regulation. Physiol Behav. 2012 Apr 12;106(1):5-15. doi: 10.1016/j.physbeh.2011.06.004. Epub 2011 Jun 12. PMID 21684297.
Bizik G, Picard M, Nijjar R, Tourjman V, McEwen BS, Lupien SJ, Juster RP. Allostatic load as a tool for monitoring physiological dysregulations and comorbidities in patients with severe mental illnesses. Harv Rev Psychiatry. 2013 Nov-Dec;21(6):296-313. doi: 10.1097/HRP.0000000000000012. PMID 24201821.
Sagner M, McNeil A, Puska P, Auffray C, Price ND, Hood L, Lavie CJ, Han ZG, Chen Z, Brahmachari SK, McEwen BS, Soares MB, Balling R, Epel E, Arena R. The P4 Health Spectrum - A Predictive, Preventive, Personalized and Participatory Continuum for Promoting Healthspan. Prog Cardiovasc Dis. 2017 Mar - Apr;59(5):506-521. doi: 10.1016/j.pcad.2016.08.002. PMID 27546358.
Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming. Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163. PMID 28775711.