text:
Clonidine's adrenonergic nature?
I am little confused here.
I used the term adrenoagonist and sympatholytic to describe the compound.
However, my teacher says that the correct term here is adrenomimetic -term.
My understanding of Terms

Adrenoagonist says that to bind to adrenoreceptor which prolongs the effect of NE in receptor.
Sympatholytic - inhibition of postganglionic fibers of sympathetic nervous system
Adrenomimetic - mimic effects of sympathetic nerve stimulation on pre- / postganglionic fibers.

I still think clonidine is sympatholytic i.e. adrenolytic (not adrenomimetic).
How can clonidine be adrenomimetic?
Why not adrenolytic?

Clonidine is an agonist on the α2 receptor... but then again norepinephrine is also an agonist on the α2 receptor. Then the physiologic ligand of the a2 receptor, norepinephrine is autocrine (meaning it is released from a cell then binds on a receptor on the same cell) causing negative feed back and it inhibits further release of norepinephrine from the neuron thus preventing overstimulation. Clonidine is quite specific to the α2 receptor and it doesn't really stimulate α1/β1/β2. Given a situation  where only the α2 receptor is stimulated and none of the other epinephrine receptors, you would have a net decrease of sympathetic effects since the amount of norepinephrine being released is begin decreased by the stimulation of the α2 receptor on the presynaptic membrane of the sympathetic neuron. Hence clonidine is an α2 agonist that is sympatholytic
I have no clue what the difference are between these

agonist vs mimetic
adreno vs sympatho

So I propose that clonidine is not adrenomimetic but adrenolytic (i.e. adrenonergic and sympatholytic in one word). Do you agree? - Agonist mean to bind etc adrenoagonist to bind to adrenoreceptor. Mimetic means positive ANS effect and/or mimicing the behaviour of the stimuli from ANS. Adreno - just adrenoreceptor where the neurotransmitter is acetylcholine. Sympatho is about if the drug has sympathetic effect and its nature (sympathopositive (-mimetic) vs sympathonegative (sympatholytic i.e. decreasing concentration of acetylcholine etc in case of adrenoreceptor in a synapse)).

I suppose I failed to mention this, but agonist means that it not only binds (as an antagonist binds as well,  both agonist/antagonist bind to either the receptors active site or an allosteric Site, depending on if it's competative/noncompetative) but it stimulates the receptor in a way that mimics the endogenous ligands response. Now the a2 receptors response when stimulated is adrenolytic.

Yes, you are right! Thank you for your answer!

I want to nuance the analysis presented above. Clonidine acts both directly on the alpha-2 receptors of blood vessels (triggering vasoconstriction), and then on the neurons alpha-2 receptors when it gets through the blood-brain barrier (inhibiting norepinephrine release). I think those definitions are too simplistic to fully qualify clonidine action. First reaction is sympathomimetic, prolonged action is sympatholytic.

Wikipedia seems to confirm what you have said. The a2 receptors are found not only in the presynaptic membrane of adrenergic neurons (and in the CNS), but also the vascular smooth muscle. Then there are the 2nd messengers involved, a1 acts via Gq (increasing IP3 and DAG) and a2 acts via Gi (decreasing cAMP). As I understand it, cAMP levels have varied effects on vascular smooth muscle (vasoconstriction/vasodilation) depending about which place int he body we are talking about, but if a1/a2 both worked on cAMP but in contradictory capacities then I would say no, but one is cAMP one is IP3/DAG.


text:
Spironolactone's role with adrenergic agents in heart failure?
I am studying the treatment plan of adrenergic agents for heart failure.
Then, in the group discussion, spironolactone was included.
But I cannot understand how it is relevant when considering adrenergic agents for treatment of heart failure.
It is probably that it was only mentioned because adrenergic agents are usually used in combination with ABC therapy (antiplatelet, beta blockers, ...).
This includes also diuretics.
Spironolactone is diuretic and antihypertensive.
But I cannot understand how one can classify it adrenergic.
What is the role of spironolactone with adrenergic agents in heart failure?

Please could you add a definition of adrenergic and explain why you are asking - ie where is it defined as adrenergic?

@GriffinEvo: adrenergic refers to stuff acting on adrenaline recpetors.

Do you mean SPIRONOLACTONE?

Spironolactone works through a mechanism different than the adrenergics.
You said of the ABC approach, "This includes also diuretics." That's why Spironolactone was included.
Spironolactone is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule. Aldosterone interacts with a cytoplasmic mineralocorticoid receptor to enhance the expression of the Na+, K+-ATPase and the Na+ channel involved in a Na+ K+ transport in the distal tubule . Spironolactone bind to this mineralcorticoid receptor, blocking the actions of aldosterone on gene expression. Aldosterone is a hormone; its primary function is to retain sodium and excrete potassium in the kidneys.

The lack of a decrease in the neuroendocrine prognostic markers, norepinephrine and endothelin-1, suggests that the beneficial effects of spironolactone are mainly related to mechanisms independent of the adrenergic and endothelin systems. The escape of AII and aldosterone, probably reflecting activated feedback mechanisms, confirms the specific activity of spironolactone on the renin-angiotensin-aldosterone system and supports the hypothesis that the beneficial effects of spironolactone on the progression of heart failure are mediated by the blockade of aldosterone receptors.

PubChem
Beneficial neurohormonal profile of spironolactone in severe congestive heart failure: Results from the RALES neurohormonal substudy

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text:
Do both Carbamazepinum and Lamotriginum increase glutamate threshold?
I have in my notes that:

Carbamazepinum increases threshold for glutamate
Lamotriginum delays release of glutamic acid

I would like to simplify these sentences into a single line. I would like to know if it would be correct to say the following:

both Carbamazepinum and Lamotriginum increase glutamate threshold?
"both affect glutamate function" should at least be correct

Do both Carbamazepinum and Lamotriginum increase glutamate threshold?

Characterizing those drugs.
A = group, B = mechanism of action and C = indications.

Carbamazepinum
A. Anticonvulsant, antiepileptic.
B. Block Na+ ion channels and inhibit glutamatergic neurotransmission. Inhibit sustained repetitive neuronal firing.
C. 1st line of Epilepsy grand mall seizures, bipolar disorder, trigeminal neuralgia.
Lamotriginum
A. Unique antiepileptic.
B. Block Na+ ion channels and inhibit glutamatergic neurotransmission. Inhibit sustained repetitive neuronal firing.
C. 1st line Epilepsy - generalized, partial and absence - all types. Bipolar disorder - depression stage. Neuropathy.

Short answer
Both carbamazepine and lamotrigine are listed as Na+ channel blockers. Carbamezipine's action is mainly associated with inhibition of postsynaptic neural activity, while lamotrigine is thought to inhibit glutamate release. Given that glutamate is the principal excitatory neurotransmitter in the brain, and if you insist of using a one-liner I would go for:

Both lamotrigin and carbamazepine can be said to inhibit glutatamatergic neurotransmission, albeit carbamezipine does so in a non-specific way.

Background
My two most beloved drugs in one question!
First off, this answer is formulated from the perspective of both drugs being used as anticonvulsants in generalized tonic-clonic epilepsies. As anti-epileptics, Both lamotrigine (Lamictal) and carbamezipine (Tegretol) are listed as Na+-channel blockers.
Carbamezipine does so quite specifically, and it inhibits sustained repetitive firing by blocking sodium channels. It does so in a very clever way, as it only binds to Na+-channels of rapidly firing neurons, which is exactly what makes it a good anti-convulsant (Courtney & Etter, 1983). It also is believed to have anticholinergic, central antidiuretic, antiarrhythmic, muscle relaxant, antidepressant (possibly through blockade of norepinephrine release), sedative, and neuromuscular-blocking properties (Drug bank). Hence, your note that it increases the threshold for glutamate is true in the sense that it is likely to increase the firing threshold of glutamate-activated neurons.
However, note that carbamezipine (nor lamotrigine) does not increase the threshold for glutamate - glutamate has no threshold and hence it cannot be raised. It is incorrect word use.
Lamotrigine is also listed as a Na+-channel blocker, but the exact mechanism(s) behind its anti-convulsive and mood-stabilizing effects are unknown. In vitro pharmacological studies suggest that lamotrigine's inhibiting effects on voltage-sensitive Na+ and/or Ca2+ channels stabilizes neuronal membranes and consequently modulates presynaptic transmitter release of excitatory amino acids (e.g., glutamate and aspartate). It has also been shown to enhance K+ currents and GABA-ergic inhibition (Coulter, 1997). Hence, your note that it decreases glutamate release is correct.
References
Coulter, J Child Neurol (1997); 12: S2-9
Courtney & Etter, Eur J Pharmac (1983); 88: 1-9.

What do you think about this? Block Na+ ion channels and inhibit glutamatergic neurotransmission stimulating GABA and balancing neuronal excitation and inhibition. I try to make a short one-linear about their common general functioning.

I don't think carbamezipine is generally associated with the GABA system, you have to be very explicit here.

It says it may involve GABA A/B in the mechanism of action here https://pubchem.ncbi.nlm.nih.gov/compound/2554#section=Mechanism-of-Action What do you think?

In lamotrigine, only in vitro studies about GABA here https://pubchem.ncbi.nlm.nih.gov/compound/3878#section=Mechanism-of-Action The exact mechanisms of both these systems are not known. How would summarize this?

I think the question now is: what disease are you looking at? In my answer, I assumed a focus on epilepsy, since the combination of CBZ and lamotrigine is a very successful one. The GABA effect listed is under neuralgia. Both drugs are 'dirty' drugs and will affect many many systems. The question becomes in which context you are comparing them. Again, in my answer, I reasoned mostly from the anti-convulsive perspective.

Again, I wouldn't focus on GABA when talking anti-convulsive therapy.

GABA drugs are contra-indicative for generalized tonic-clonic seizures.

@Masi - thanks for bringing this up - I have adapted my answer intro to specify the pitch of my answer.

I added my summary about those drugs in the body: group, mechanism of action and Indications. Do you agree? I do not know if I can write so many indications if then the mechanism of action is enough general. I am very uncertain about the groups. CYP-450 inductor does not sound good in the first drug.

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text:
Why is Benzylpenicillin better in Bacterial Meningitis than Amoxicillin?
Both are beta lactams.
However, benzylpenicillin, which is also called penicillin G i.e. narrow group antibiotic.
I have now in both the following as a mechanism of action

Binds to PBP in bacterial cell wall, causing deficit in the cell wall and causing cell death.

where I would like to differentiate clearly benzylpenicillin from amocillin.
How is benzylpenicillin better in bacterial meningitis than amoxicillin?

As the term meningitis is pretty broad, you should probably narrow this down to bacterial meningitis. There I would say the antibiotic is used to which the bacteria are sensitive.

@Chris I narrowed it. Specificity of course, but this is a general question. If you have those drugs, give their indications. I see bacterial meningitis in benzylpenicillin as indication, but not in amoxicillin. However, googling shows that amoxicillin has induced some meningitis but I do not know if it has been used in bacterial-meningitis.

Can you share your source that penicillin G is better than amoxicillin? You also stated in your initial revision that you have read about amoxicillin induced meningitis; that amoxicillin can induce aseptic meningitis seems like penicillin G has an advantage. http://m.cid.oxfordjournals.org/content/46/4/642.1.full

@canadiane No, this is a class note. Yes, it may be related to the fact that amoxicillin can even induce meningitis, probably because the increased resistance of the drug (wider spectrum than penicillin G but more resistance also). Good link! Make it an answer with a small summary, please.

Amoxicillin is just penicillin with a hydroxyl group off the ring and an extra amine group..

Their mechanisms of action are the same. Their ability to cross the blood-brain barrier are the same. They can both cause seizures.
Both are used to treat to meningitis. The selection of one over the other would be based on the sensitivity of the infecting organism, and the ability to cross the blood-brain barrier in inflamed meninges.
There are better drugs to treat meningitis.
Penetration of Drugs through the Blood-Cerebrospinal Fluid/Blood-Brain Barrier for Treatment of Central Nervous System Infections

Excellent idea to explain this by structure! Do both work in the similar analogue in Syphilis? Similarly, I think better drugs for that.

benzylpenicillin is actively transported into the brain via the oat‐3 transporters.  Amox is only poorly diffuses through the blood brain barrier. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1471-4159.2009.06451.x

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text:
How many areas are there in Brodmann map?
I read Wikipedia claiming 52.
I heard that this can be extended to 54.
I see there is no limit of having more areas - just better understanding of the neuroblast migration and fibroblast too, probably.
How is this newer classification of Brodmann map done?

Bowmann or Brodmann map?

@potterbond007 Thank you for pointing out the mistake in the body! Brodmann map. I apparently have read too much about kidneys.

I am no expert on the topic, but according to an article published on the centenary of his study, it states that the microscopical structure and classification of these areas are in parallel to the evolutionary distinction between old and new cortical subdivisions. So as and when new subdivisions are deduced (based on its function, cytoarchitecture or the structure and organisation of cells) the map can be extended to include them. There was no upper limit to the number of divisions set in any article I read so it would be nice if you could provide some reference to where it says that the extension can be done to 54. If you are interested, you could have a look at the map published by Constantin von Economo in 1925.

Yes, I agree with you. This is just research talk where I heard people talking about more than 52 areas. I have no idea how they are doing the division. Probably, like you describe, by thinking parallel processes at some point at a particular point in time. I think the amount of these areas i.e. processes vary between different points under considerations.

@Masi basically with the advance of research, even minute differences in any part of an area currently designated due to structural differences or some new functional properties, the map can be further extended to include them as a new subdivision. Rest, I believe it is left to the discretion of the researcher as there is no definite compulsion to map new areas unless significant differences are found. That is my understanding on the subject


text:
What are the physiological roles of Hydrogen sulfide?
I am thinking why hydrogen sulfide has its effects in the body.
For instance, it is one Salmonella's virulence factor.
I am not sure if such a balance equations holds
H2O + H2S ←→ ...
Actually, I miss here some factors because I am not understanding the biochemistry enough to answer this.
I think H2S can exists in some sort of ionic form.
Hydrogen sulfide reminds me of ammonia.
I think it inhibits some systems.
By which mechanisms?
It is mentioned in many places the empirical effects: signaling functions similar to NO and CO.
But I am interested in how this happens.
What is the rate of adhesion of H2S to hemoglobin for instance?
H2S can change to sulfite and thiosulfate in mitochondria which are then excreted into urine.
I think most of the biological effects are done before these forms.
But in which forms?

According to my preliminary reading around this topic, although production of hydrogen sulphide is used as a convenient method for detecting the presence of pathogenic Salmonella, there is nothing to link this trait with virulence. Do you have a reference for this?

You are probably right. I read about this topic in Lange's Medical Microbiology mostly, and I cannot be find any mentioning that directly related to Virulence, but there are mentionings that H2S is related to signalling functions similar to NO and CO, which possibly have virulence roles.

I am not sure about this. I mean, yes it is used to detect sulfide production of Salmonella species (note that not every Salmonella produces H2S), but it is a gasotransmitter in the human body, which has a role for example in regulating immune responses. In small doses it has antiinflammatory effect, while in large doses it has proinflammatory effect. So I think it is possible that H2S is a virulence factor, but it is really hard to find a study about H2S as virulence factor, since it is a relatively new resource area.

$H_2S$ 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.

You are right. This is very new research area (since 2011 most focus put) such that it has not been bound to virulence in any articles. Much discussion about gasotransmitters: http://en.wikipedia.org/wiki/Gasotransmitter but not reached any major textbooks. Feel, free to update your answer when you hear more about this topic and updates.

@Masi "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." - But you are right studies about gasotransmitters and virulence are very rare. Nice question btw., I have not known that gasotransmitters exists until now... :-)

Neither me. I just noticed now that your answer make sense, just because you have this term gasotransmitter. There is no mentioning about them in Mercks' manual nor Harrison. Could not find in any Medical textbooks.

@Masi http://en.wikipedia.org/wiki/Gasotransmitter it is a pretty old word - since 1981. The discovery that H2S is a gasotransmitter is about a decade old story.

Yes, time is relative. Very little has been done in the research of this topic. No mentioning in any major medical textbooks. Thank you for doing some meta-analysis! It would be helpful to all if you could reorganise your answer and make introduction and summary at the end. Now, the main point can disappear.

@Masi It is maybe because H2S is under extensive research but still not in the medical practice. Maybe in 5-10 years... Afaik NO is used in the medical practice currently.

Alan Boyd's answer

Production of hydrogen sulphide is used as a convenient method for
  detecting the presence of pathogenic Salmonella, there is nothing to
  link this with virulence.

which I agree with.


text:
What is the right spelling for this agar?
I could not spell the agar [gonoline-uroline] which I heard yesterday.
My spelling is so wrong that I could not find it in Google.
What is the right spelling for this agar?

Might help if you tell us what it is used for.

It's completely illogical to change the question after a comment and an answer to the original question.

@AlanBoyd I agree, now it looks I did not answer question at all. The authors suggested to open a new questions if the original one has solved and generated other questions.

I rolled back and opened a new a question: http://biology.stackexchange.com/questions/15261/what-is-the-benefit-of-using-gonoline-euroline-in-combination

The first word is ok, there is agar called Gonoline, the second one is probably Euroline and there is an agar with this word too (Liver IgG Euroline).
I've found both of them on the Italian site, probably the are not one, but two agars.

Now, I am thinking why they are using these two agars in combination. The topic was Pathogenous cocci.

I actually don't think this is right (not that it's your fault given the question), but I'm pretty sure Euroline is brand name for a synthetically printed ELISA like assay.  I really don't think there's any agar involved.

Looking at your two questions together, I think you mean gonoline media, followed by blood agar.  To be honest, I feel like this question would be off topic.  You may be referring to a specific blood agar, like Chocolate agar, but that would be wild speculation.
Gonoline media is often used for Neisseriaceae, so perhaps you are specifically looking at Gonorrhea?


text:
Does Sirtuin protein family Sir2 work in low-calorie diet mostly?
I am reading about the protein family in relation to the prolongation of cell life.
It is known that

Sirtuins have been implicated in influencing a wide range of cellular
  processes like ageing, transcription, apoptosis, inflammation and
  stress resistance, as well as energy efficiency and alertness during
  low-calorie situations.

However, I am not sure if these physiologic processes are only during low-calorie situations.
Alertness is at least.
It says in the original paper only that

Our results suggest that in the hypothalamus, SIRT1 functions as a key
  mediator of the central response to low nutritional availability,
  providing insight into the role of the hypothalamus in the regulation
  of metabolism and aging in mammals.

However, it does not specify how the Sir2 works to high-calorie diet.
Therefore, I asked mostly.
When is the protein family active?
Does the Sirtuin protein family work mostly during low-calorie diet?

This is a direct citation from the Wikipedia, which also has a reference for this. Why don't you mark it as this and have a look at the citation? Its this one.

@Chris I clarified the question.

Does sirtuin 1 (SIRT1/SIR1) function to mediate the effects of a low calorie diet? Perhaps, but its really not clear.  Is the function of SIRT1 primarily to mediate low calorie response? Absolutely not.  What does that mean for SIRT2/SIR2 - its probably not more closely associated with calorie restriction signals, though it might be connected in a similar ambiguous way... but see below.
Firstly SIRT1 has also been shown to have many influences in many studies of conditions such as Alzheimers, anxiety and other neuro-functions.  SIRT1 modifies p53 - a bottleneck in cellular reproduction and a key regulator in cancer prevention, but which also an important aspect as to why it is active in calorie restriction conditions.
When reading reference like the one you have here its important to remember that correlation is not causality.  Very few genes in animals function only when specific behavior or conditions are experienced, especially signaling genes.
Examining the OMIM report (see link above) there has been a close examination of the possible role of SIRT1 in calorie restriction since the early 2000s in knockout mice.
SIRT1 would seem to play an important role in embryonic development for instance - cell growth is so important at that point and 80% of mice who are homozygous SIRT1 (-/-) knockouts die before they are born and even more die in the early natal period.  The mice who do survive have problems generating red blood cells which is another important case of cellular reproduction.
Yet the relationship of the knockout mice to calorie restriction has been debated - its been difficult to interpret the activity and the weight loss or gain of the knockout mice compared to wild type mice since the SIRT1 knockouts are smaller.  They may also have genetic traits that compensate for the absence SIRT1 in order to have survived.
More recently mice where SIRT1 expression in the brain have been produced, but the result has been anxiety or anxiousness as opposed to specific calorie restriction diet.
This reminds me of the story of leptin, in the early 90s they found that leptin deficient mice became quite fat, but despite this obvious linkage to obesity, leptin turned out to mediate a lot of other psychological factors as well - it only caused obesity when its function was blocked.  It did not turn out to be an appetite signal.
SIRT2 seems to have similar roles in calorie restriction.

Rogina et al (2002) found that under 2 life-extending conditions, Rpd3 (601241) mutants fed normal food and wildtype flies fed low calorie food, Sir2 expression was increased 2-fold.

But also has similar relationships to Alzheimers.  SIRT2 has not been followed up on as much as SIRT1.  This correlation might not be causal or should be nuanced in a similar way.


text:
Fibrinous inflammation, exudate and scarring in monotonous movements and ageing
I have palpated many hard organs during my work and studies.
I have seen many young and old people who have hard organs, like very hard shoulder - very common.
I have interviewed some of them, some points

only one type of weight lifting
no running
no stretching
no stretching before training
no stretching after training
not age dependent only - very old can be healthy
dynamical movement dependent

There are two mechanisms of fibrinous inflammation

trigger the release of fibrinogen
trigger release of fibrinogen-to-fibrin reaction

which both result in the production fibrin in the interstitium:

The area may also be mixed with serous so two variations of fibrinous inflammation

serofibrinous
fibrinous.

I am interested in the mechanism that leads to this hard tissue throughout the organ.
This raised to me an idea about Fibrinous inflammation in the shoulder.
Robbins say that if the exudate cannot be sucked out, it leads to scarring.
I think this is what is making the organ feel hard.
What is the pathogenesis in such monotonous movements without stretching?

I would now say that the hardening is just local acute venous congestion if in the short term.
Without stretching after practice, it just takes more days to recover.
So lymphatic drainage is the one which helps the muscle get its needs and nutrients.
If this happens during years, it is difficult to say what is the causal factor.
It depends on many factors.
One key factor is how well the lymphatic circulation can recover the body back.
So genomics of the patient comes in the picture.
Many other factors too like anatomical structure of chest.
Then, depending on these factors and other pathological processes may happen many processes like

accumulation of fibrinoid
accumulation of calcium deposits
shorter diffuse distances
smaller total area of cells

which are some adaptation processes to the ageing (also of prolonged monotonous weight lifting).
They can lead to

acute lymphangitis (reddening of the skin)
Chronic lymphangitis
Chronic Granulomatous Lymphadenitis (fibrosis happening between muscles and connection points - not in all cases granulomatous - rare only)
lymphadenopathy (very, very late - after many years)

during ageing (adaptation).
Better question would probably be: what are processes happening during ageing?
And then cover pathologies of ageing separately and also the physiological processes on the weight lifting separately.


text:
Is end-systolic volume (ESV) the same as residual volume?
I am reading this site and my study materials.
The end-systolic volume (ESV), 50-60 ml, is the volume of blood found in ventricles after systole and contraction of ventricles.
I think ESV is the same as residual volume because residual volume is always the volume found in ventricles.
Is ESV the same as residual volume in normal physiological situations?

I am not completely sure that ESV can correspond residual volume in all cases.

The ESV is the residual volume of blood remaining in the ventricle after ejection.
It is the minimum volume of blood in the ventricles (residual volume).
Note that you can also have residual volume of air in the lungs after exhalation.


text:
Which chemical and hormonal effects on heart are by metabolites?
I am thinking which hormonal and chemical effects from:

catecholamines
thyroxin
corticosteroids
sex hormones
prostaglandins
Ca2+
Na+
K+

can be be regarded as metabolites i.e. intermediates or products of metabolism.
I got this question

Account for chemical and hormonal effects on the heart.

and I am thinking if I should include metabolites as a factor as

Metabolites by intrinsic autoregulative system locally

because the autoregulation of heart is very important factor in the physiology of the heart.
Can you regard some metabolites as having hormonal and chemical effects?

Ions are not hormones. Ions are not metabolites either.
Technically, anything that is not directly absorbed from environment but is synthesized/modified in the body is a metabolite.
Even if you don't consider polypeptides as metabolites (which for some reason are not classified as metabolites in scientific parlance), all the molecules that you mention are metabolites with known biosynthetic pathways.

You are right about ions. I missed the word "chemical" in the whole discussion.


text:
What can thrombosis lead to?
I am thinking this question.
Thrombosis can result in

organisation of thrombus,
sepsis
thromboembolism,
fibrinoid swelling
adiposity.

I fibrinoid swelling (edema) (4) can occur.
Also, I think (3) thromboembolism can occur and also (1) organisation of thrombus.
What can thrombosis result in?

I am not sure I understand this question. First, you give the answer. Then, you ask the question. Please note that I am a layman in Biology, absolutely no expert.

@scaaahu this is a homework question. Masi is copying a question he presumably got in an exam and is wondering about it.

Fibrinoid swelling involves necrosis and swelling so no.
Organisation of thrombus refers to some very large space of organising thrombus in different ways - so no, since there is an exact mechanism under.
Based on my interpretation of Robbins -book.
The correct answer is 3. thromboembolism.
Thromboembolism is a combination of thrombosis and its main complication, embolism.


text:
Can acid-fast M. tubercolosis obstruct alveoli?
I am not sure which word is the best here for colonisation of alveoli by acid fast-mycobacteria. I found this question, and I am getting confused by the term obstruction of alveoli because I tend to relate it to COPD which is not a case here:
Which of the following is the predominant pathogenic mechanism of tuberculosis?

a) cell-mediated hypersensitivity
b) obstruction of alveoli by large number of acid-fast mycobacteria

I think the right answer is "obstruction of alveoli by large number of acid-fast mycobacteria", but I am not sure if you can say that acid-fast mycobacteria obstruct alveoli.
Are acid-fast mycobacteria "obstructing" alveoli or just colonizing?

Mycobacteria are on the order of 2µm in length and 0.2µm in diameter.  Alveoli are on the order of 200µm in diameter.  Obstruction is possible, but M. tuberculosis grows rather slowly.  Too slowly, in fact, to avoid being engulfed by alveolar macrophages.
Furthermore, obstruction does not sufficiently explain the predominant symptoms of tuberculosis:  bloody sputum and the tubercles themselves.

I certainly agree it's not the myco colony obstructing the alveoli, but rather the elicited immune response does a pretty good job of that.  Muc5, Il13, etc are all slamming in to cause mucin production and inflammation.

Thank you for your clear answer! So obstruction is possible and it is mostly theoretical model by large number of acid-fast mycobacteria. However, can we still say that obstruction of alveoli by large number of acid-fast mycobacteria is the predominant pathogenic mechanism of tuberculosis?

@AtlLED Is this "cell-mediated hypersensitivity" more right answer? Or what would you say is the predominant pathogenic mechanism?

To answer this homework question, consider "What causes tubercle formation?"
http://en.wikipedia.org/wiki/Tuberculosis

"In most forms of the disease, the bacillus spreads slowly and widely in the lungs, causing the formation of hard nodules (tubercles) in the respiratory tissues and form cavities in the lungs." So the answer must be B, because it implies that bacillus is causing it as a factor. Great! Thank you!

I don't know what all of your possible answers were to this question, but I think you should reread the part about tuberculosis being a granulomatous infection.


text:
Is endoderm visible in the germ layer?
This picture is my drawing about germ layer - not embryonic folding as I wrote initially.

Where exactly is the endoderm here in the picture?
The known things

Ectoderm
Neural tube
Notochord
Endoderm - Where is this?
Somite
Somite leg
Intraembryonic coelom
Embryonic somatopleura
Embryonic splanchopleura (lateral mesoderm)
Endoderm
Mesoderm (intraembryonic)

Ok so that's not the best picture, but I think it would be along the bottom of the top wall there.  Want to give us a few clues with the parts you're sure of?

Another strong possibility is that you're missing it in the inside of 2.

@AtlLED I added clues to the body of the question.

umm... you do note you have endoderm twice, once as 10...

Again you may or may not want to further clarify what slice and when in the germ layer you are looking (might make this a better question). After thinking about it, I think you were going for neural tube and chorda formation (which is exactly what I DDG'ed to pull that image).

I think you're going for a view of tube formation, in which case, here's a good image:

Lateral plate mesoderm
Intermediate mesoderm
Somite mesoderm
Chorda
Endoderm
(Reference)

Again in your drawing I think you correctly have it labeled as 10, and don't really need to put it twice.

Thank you! Of course, I had mistake in numbering and then started to think where the missing number should be, since all known parts were already taken.


text:
Why are new vessels more permeable in microvasculature?
I know for microvasculature

New microvasculature (arterioles, venules) are always more permeable
  as they lack pericytes.

and then I have this sentence about new blood vessels (not specific)

New vessels contain initially only proliferative endothelium, the basement membrane has not formed yet, and pericytes are absent.

However, I think pericytes are only around microvasculature.
I think the second statement is correct for microvasculature too.
Why are new vessels more permeable in microasculature?

Is there something I'm missing to answer your question?  Perhaps I don't understand the question then.  Otherwise, please accept to help our questions/accepted answers ratio.

In adult/pediatric humans, no they don't.  A good figure to get everyone on the same page was made by Cleaver & Melton:

It is important to note that:

In fact, endothelial diversity is reflected by vessel size-specific,
  organ-specific and even age-specific differences. (1)

Developing blood vessels in the fetus can be a bit of a different story, and highlights the fact the one should loose the "inert plumbing" mentality of the previous century.  Modern research tells us that the epithelium is a very dynamic region that participates heavily with signalling.
When large vessels are growing the fetus, mesenchymal stem cells and neural crest cells are the normal precursors to pericytes, but depending on exposure the line between pericyte and smooth-muscle cell can be blurred (2).  I'm assuming it's beyond the scope of the answer to go into the signalling differences.
A good review of endothelium generation, and the surrounding tissue, can be found here.

But think about angiogenesis. There are forming new new vessels in microvasculature which do not have pericytes. I think that should make them more permeable.

Actually they are going to have at least mesenchymal stem cells recruited before the vessel scaffolding is extended.  You might have the order backwards.  I don't know the permeability difference between full differentiated pericytes and stem cells, but it may not be drastic.  I will see if I can find some lit on the subject, but I'm worried there won't be any.


text:
What is a good review book/source for microbiological diagnosis?
I am trying to find the diagnosis figure for different bacteria where phases are illustrated.
I am using at the moment: 1) First Aid for the USMLE Step 1 2013 and 2) Medical Microbiology by Murray et al, 7e.
What is a good review source for basic microbiological diagnosis?

I would suggest:
Koneman's Color Atlas and Textbook of Diagnostic Microbiology
by Elmer W. Konema


text:
Why our body does not produce polyunsaturated fatty acids?
Our body does not produce two polyunsaturated fatty acids (PUFA): linoleic acid and alfa-linolenic acid.
I am thinking reasons for it.
Saturated fatty acids have more energy than unsaturated.
Saturated fatty acids do not need NADPH and some many other enzymes as unsaturated in beta oxidation.
This means that less storage places in the body needed to have energy in the form of saturated fatty acids such as for muscles and heart.
There are four main reasons why our body does not use PUFAs as the primary source of the energy but saturated:

PUFAs lower metabolism and interfere with thyroid function
PUFAs spontaneously oxidize, speed up the process of glycation, since too much glucose
PUFAs decrease mitochondrial respiration - more oxygen and CO2, less lactate

where one reason is missing.
One complication of PUFA is

PUFAs promote diabetes, cancer, inflammation and biological stress

which cannot be thought as a reason why our body does not use PUFAs as the primary source of the energy.
There are positive sides of the PUFAs when they are used in other way.
- PUFAs replace trans fats and saturated fats in certain types of foods.
- PUFAs can help your body to eliminate high cholesterol levels
- PUFAs decrease the risk of heart disease
There are also some types of essential fats that your body cannot produce on its own - omega-6 and omega-3 fatty acids.
PUFAs are used to create these.
You can get PUFAs from vegetable oil, fish and nuts for instance.
Balanced diet is essential.
Normal lipid metabolism depends directly on food lipids.
Both the essential fatty acids and right amounts of PUFAs can be obtained from food.
Body converts the essential fatty acids to long PUFAs, which serve as the precursors of prostaglandins and leucotrienes for instance.
There are so many reasons why our body does not produce polyunsaturated fatty acids.
Why our body does not produce polyunsaturated fatty acids?

I think the framing of this question is wrong. I would guess that our body doesn't produce PUFAs because they were present in adequate amounts in our ancestors' diets, so there was little pressure to gain the ability to synthesize them. The common ancestor of animals probably just didn't possess these enzymes, and we've evolved to make do with what's available in the diet.

I am interested on the biochemical sides, not on epidemiological. However, good point to bring the epidemiological sides too.

Can you pleasse tell me that how PUFA lowers metabolism and how they spontaneously oxidize, speed up the process of glycation, since too much glucose.And howw PUFAs decrease mitochondrial respiration - more oxygen and CO2, less lactate and how PUFAs promote diabetes, cancer, inflammation and biological stress???if you elaborate these points it'll be helpful for me...

@HayaDar Thank you for your notice! I am thinking this thread again. I fixed one thing in the body. More explanation about those specific sentences can be found in some Biochemistry textbooks.

The question is unclear for me as it is mostly an inconsistent alaborate on PUFAs in human body. An example of inconsistency: you write there are four reasons andthen  enumerate only three of them. And there is an especially confusing part "There are so many reasons why our body does not produce polyunsaturated fatty acids. Why our body does not produce polyunsaturated fatty acids?" It suggests the elaborate contains answer to your question, thus it should be an answer.

Simply, it’s because our bodies add double bonds in MUFAs by delta 9 desaturase which adds double bonds between delta 9 and delta 10 carbons, hence additional double bonds can be formed between existing double bond and the carboxilc group but cannot be formed between the existing double bond and the omega carbon. As a result, our body cannon synthesize parent omega 3 alpha linolenic acid and parent omega 6 linoleic acid, but can form timnadoneic acid which is an omega 3 PUFA

Welcome. Can you add sources to your claims,preferably links to journal papers? That way people can background read on your material.

Animals, including fish, do not possess any DNA for producing PUFA. No cultured fish can produce PUFA internally. However, human is known to produce milk containing DHA.  The only explanation is all PUFA synthase enzyme are exogenous.  They come from food.  This explains some people are prone to be obese and some aren’t, but the reason is not in genes.
Dinoflagellates are known to have large DNAs Some have DNA for producing important PUFA such as DHA.  No land plant, nor animals have the DNA for such enzyme.  Only explanation is the enzyme comes through the food chain exogenously.  Fortunately, these dinoflagellates are ubiquitous in ocean, and thus all the sea creatures are benefitted from these enzymes.  Modern food production by human however, strips these good enzymes by heat processing and other extraction processes.

Welcome to Biology.SE! Without supporting references only an expert in this area could evaluate the correctness of your answer. Consequently, your answer is much more likely to receive a favorable response if you include supporting references (primary literature is best). In addition, I don't think your connection to obesity is correct and it isn't directly relevant to the original question. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively and then edit your answer accordingly. Thanks!


text:
Why is Aorta sometimes called Compression chamber?
I find this statement that Aorta is called Compression Chamber in my study materials.
Aorta can

it keeps blood flowing
it can accumulate potential energy for bumping and compression

However, why aorta is called chamber and particularly compression chamber?
I heard this term today first time.

The aorta is a compression chamber because it is an important drive for diastolic perfusion. To keep the blood flowing constantly, and not only during systole (as would be the case with a rigid aorta), the high elasticity of the aortic walls allows it to dilate as a consequence of the high systolic pressure. This allows the aorta to accumulate blood in its proximal part, which is then propelled by the passive elastic contraction of the aorta during diastole.


text:
Can systemic intravascular thrombosis cause brain infarction?
I wonder if the thrombus can pass through the brain-blood barrier because I think small molecules like O2, CO2 and ethanol can pass it.
Probably, in some diseases where the permeability of the barrier changes.
Can systemic intravascular thrombosis cause brain infarction?

This question seems to stem from a misunderstanding of the nature of the Blood-Brain-Barrier, the circulatory system of the brain and of thrombi. The BBB is describes differences in the structure of the walls of the blood vessels of the brain, it is not a barrier to flow within the vessel, but a specialized barrier to flow out of the vessel. In many tissues the walls of capillaries (the smallest vessels) are not tightly adjoined, small molecules and even some proteins from the blood are able to pass through these minute gaps between the endothelial cells and into the tissue.
However, in the brain, these endothelial cells are tightly linked in a specialized fashion that prevents the non-specific travel of solutes between cells. Instead, molecules that cannot diffuse through the membranes of the cells must be actively transported across them (cannot leak across).
An intravascular thrombus is much larger than these minute gaps, it is often considerably larger than these small vessels and becomes lodged in larger arteries, blocking flow. There is no passage through the BBB, but there is no passage of the thrombus through the walls of other capillaries in the body either. The damage caused by the infarct is due to the blockage of flow in the larger vessels.
The circle of Willis is no magical stopping point either. Many important sites of infarct (such as the MCA middle cerebral artery), micro-infarcts in even smaller vessels can also cause difficulties.
In short, thrombi and the Blood-Barrier-Brain exist on different scales, the presence or absence of the BBB is irrelevant when discussing the capacity of a thrombus to occlude arteries.

No, a thrombus would be much too large to pass through the highly selective blood brain barrier.  However, there are some cases where intra-vascular thrombosis can cause stroke.
One example would be non anti-coagulated atrial fibrillation, where the inefficient beating of the heart causes blood to remain stagnant in the left atrium.  This can cause a thrombus to form within the atrium which can then throw off emboli, some of which may enter the cerebral circulation. These may then partially or fully occlude one of the arteries in the Circle of Willis (the brain's circulation system), however the blockage is proximal to the blood brain barrier.
See Management of atrial fibrillation (GY Lip,2007) or for those hitting a pay-wall the professional reference section on AF

It would be great if you can add references for the examples that you mention.

@WYSIWYG duly added a couple of examples of references, the phenomenon is very well known and understood so others viewing the question may find it easier to search for Atrial Fibrillation and Stroke

No, thrombi are far too bulky to cross the blood brain barrier. Now regarding the risk of stroke in case of systemic thrombi Yes, there are 2 situations where this can arise:

floating thrombus of the great circulation proximal to the aortic arch (i.e. Most of the time, chronic atrial fibrillation)
venous thrombus with an associated patent foramen ovale, allowing the thrombi to pass through the atrial septum and get to the great circulation.

It would be great if you can add references to your answer.

The question has a vague term cause which is confusing people here.
For me, it means that the event increases the risk of the outcome.
For some others, it means the event is a definite factor in resulting in the outcome.
So I avoid answering to the question Yes or No because of different interpretations of the term.
The systemic intravascular thombosis increases the risk of stroke, for example, through the two situations as described in Raoul's answer here but those are not sufficient for the accurate risk score of the stroke risk.
The factors of stroke risk interact with each other so we cannot leave this question just only about intravascular thombosis and stroke risk, but must consider stroke risk more generally.
CHA2VASc Score for General Stroke score
The Role of the Left Atrial Appendage in AF-Related Strokes, 2013.
Chads-Vasc score. CHA2 DS2-VASc.
                        SCORE
C    CHF or LVEF < 40\%  1
H    Hypertension        1
A    Age > 75            2
D    Diabetes            1
S    Stroke/TIA/ HF
    thromboembolism/     2
V    Vascular disease    1
A    Age 65-74           1
S    Sex Category female 1
                        Max points 9.

which specificity and sensitivity are not so high which has resulted in many variations of the initial CHAD VASc score, for example in this study:

We studied 94 patients, 66.0% male, mean age 64.4 years (standard
  deviation 14.2). A cardioembolic source was detected in 20 patients.
  ROC curve analysis identified as predictors of cardioembolic source
  CHADS2 score ≥4 (sensitivity of 75.0%, specificity of 66.0%, p=0.014)
  and CHA2DS2-VASc score ≥5 (sensitivity of 83.3%, specificity of 58.0%,
  p=0.009).

To improve this score is ongoing research:

CHADS2 as well as the CHA2DS2VASc risk score can exclude a large proportion of patients from having high risk of stroke or death, here
Negative predictive value for zero as cut off value for the endpoint Stroke between CHADS2 (solid dots) and CHA2DS2VASc (circles) in Figure 1

Figure 1: CHADS2 (solid dots) and CHA2DS2VASc (circles).

Sources of thrombosis

Atrial fibrillation and Left atrial appendix is the source where thrombus can spread into the great circulation
Patent Foramen Ovale and Stroke where risk factors anatomic variation (PFO size, ASA, eustachian valve anatomy), hemodynamic parameters, presence of venous thrombus identified through higher-sensitivity tests such as lower extremity/abdominal/pelvic MRI, and the presence of hypercoagulable genetic variables

BBB's permeability and Stroke risk
The interaction of the permeability of the brain-blood barrier with the stroke risk is much unknown.
The following factors interact with the BBB's permeability

Montelukast (increases)

Cerebral Blood Flow (CBF) and stroke and Stroke Risk
CBF interaction with the risk of stroke is unknown field

Alcohol effects on CBF in subjects with low and high responses to alcohol, here.
carbonated water increases CBF
aging decreases CBF (standard textbook MRI pictures)

Sources

Stoll, Guido. Molecular mechanisms of thrombus formation in ischemic stroke: novel insights and targets for treatment. 2009. Online available.
Homma, Shunichi, et al. Foramen Ovale and Stroke. 2005. Online available.
Citings in the body of this question.

@WYSIWYG Thank you for your comment! I was very young in this field when I first time thought about this issue. I extended my answer little by adding some relevant sources.

You should probably consider the internal carotid arteries and vertebral arteries too as potential sources of emboli

@RoryM Feel free to do so and add relevant references to your answer.


text:
How to measure Na/K channel activation at the membrane level?
Assume that there are two different signals occurring on the ECG - during depolarization and repolarization in the standard ECG.
I was advised not to use the standard ECG in measuring the exact electrical events during:

stages 0-2
3-4

We can get data about the electric activity of neurons in vivo in Fig. 1 where some data about the electric activity of neurons is present.
So my thought is that a similar technique could probably work with cardiomyocytes.
Fig. 1 Example of measurement for electric activity of neurons in vivo

I estimate that there is about 18% uncertainty when using the standard ECG because of the peak in the stage 1 (Gibbs phenomenon) and those two complete different phases.

This is probably not possible in vivo, but there are various methods (voltage clamping, channel blockers) that you can use in vitro with individual cells and perhaps correlate the results with the aggregate activity of a larger piece of heart muscle.

@jonsca I found that we can get data about the electric activity of neurons in vivo. So probably the same technique has been used with cardiomyocytes.

@Masi Neurons are easier because they aren't moving that much.

@NickSandor Can you please make your comment an answer and support it with evidence and/or sources. It is very interesting, but true. Can you say how much neurons and cardiomyocytes move, please. - - I am really interested in on any estimates about the topic because I have overlooked it for long time. - - Can you please state what you expect to be seen in cardiomyocyte activity? What is their metric in time-frequency plane or time-potential plane? I get mostly cloudy areas but different from neuron areas when studying spectrograms and other distributions.

I searched Pubmed for cardiomyocyte+"patch clamp", and read the first ~10 abstracts. Everyone measures plated cells. At best, these cells came from from hearts freshly minced in collagenase / EDTA. See PMIDs 27364017, 27076034, 26142302, 26241168, 26378152, to mention the most recent search results.

@NickSandor Please, see my new question here about the topic http://biology.stackexchange.com/q/50630/86 - - Why are they measuring exactly plated cells?


text:
Hypersensitivity Simultaneously in Ear canals
I got experimental data where hypersensitivity (i.e. tonic pain when touching ear canal) was recognised for about 100 minutes.
I do not know which type of hypersensitivity is this one.
IgM can reach ear canal, I think (not sure) - it is just in the limit.
If IgM cannot reach ear canal, then the hypersensitivity must be caused by

humoral immune system

which is responding slowly to the trigger.
It is proposed that this cannot be contact dermatitis because

the reaction happened simultaneously in both ear canals

after irritating ear canals with plastic the subject is not allergic.
Irritation was also a selected signal which resulted in the dynamic cycle of bass music by Beats earphones.
It was studied the effect of the specific signal with bass music on the movement on the inner membrane on the subject with problem in maintaining the inner physiology of ear itself (also repeated cycle of ear infections during childhood).
Can IgM reach ear canal?
The hypersensitivity was simultaneous in both ear canals.
I did not know before that you can get hypersensitivity reaction in ear canals and also simultaneously.
I think hypersensitivity is not in normal condition.
There must be some etiological factors (probably neuronal) that can cause it.
There are other organs which can have hypersensitivity too.
So I started to think what is the trigger of hypersensitivity.
My conjecture is about Secreted substances of endothelium (EDRF, EDCF).
There are three types of substances secreted by the endothelium

NO
Endothelium hyperpolarising factors
Endothelins

NO is the most important one.
But what is its role in the hypersensitivity of ear canal is unknown to me.
What is the mechanism of hypersensitivity of our body and particularly in the ear canal?

What happened before the hypersensitivity was noticed?

@Chris I answered to your comment. Any allergic reaction caused by the plastic material was minimised. So contact dermatitis not probably.

But you must have a reason to think into the direction of the immune system.

This answer is based on embryological studies and is limited.
I will extend it later when understand better.
Sensory areas

maculae acusticae - walls of utricle and saccule (this most probable area)
cristae acusticae - change in body position

Nerve

vestibular fibers of cranial nerve VIII (TODO each branchial arch has a nerve - how these differentiate between different arches?)

Embryonal Ganglion

statoacoustic (spinal) ganglion (19.5 C Fig)

Embryonal ganglion splits into two

cochlear portion
vestibular portion

which supply sensory cells of organ of Corti, and those of the saccule, utricle and semicircular canals, respectively
Branchial Arches
Each arch has a vessel, cartilage and nerve.
The task is to understand which part of embryonal ear is able to start hypersensitivity reaction.
Middle ear
Tympanic Cavity and Auditory Tube

origin endoderm (1st pharyngeal pouch) - malleus and incus
malleus - 2nd a.a.a.

Eardrum or Tympanic Membrane

ectodermal epithelial lining at bottom of auditory meatus
endodermal epithelial lining of the tympanic cavity
intermediate layer of connective tissue (See Langmans' Fig 19.9B). TODO this part is superficially covered in Langmans.

Auricle

6 mesenchymal proliferations at dorsal ends of 1-2 a.a.a.

TODO I must look again embryonal slides of ear to see where the nerves occur first and how they develop.
Sources

Langmans Medical Embryology, 12th ed, 2011
My notes of Embryology classes, Spring 2014 (I did not have all my notes now so must study these things again after holiday)

Can you be a bit more explanatory? Actually this answer gives a lot of facts without connecting them.

@Chris It is just overview. I will clarify it when I can answer the TODOs. At the moment, I cannot do it.


text:
Staphylococcus AG structure?
I found this statement in my study materials in the section of Staphylococcus

The AG structure:

protein AG (species specific);
polysaccharide AG (serotype specific).

I know what is Protein A/G, a recombinant fusion protein that combines IgG binding domains of both Protein A and Protein G.
What is the point of this AG structure thing in the contex of Staphylococcus?
Can we say that staphylococcus have AG structure?
I think it has properties related to protein A\G and also to polysaccharide A\G.
I know very little about polysaccharide A\G and not sure how it is related to serotype specificity in the context of staphylococcus.
Extension to the question
Antigenic structure of Steptococcus pyogenes:
the group AG is unique, placing streptococcus in group A.

What is the AG here?

After puzzling over this for a while I think I have the answer . It's nothing to do with protein A or protein G. I think that whoever wrote your study materials meant Ag which is a common abbreviation for 'antigen'. I guess this was in the context of immune responses, or strain typing.
Looking back over your last few questions, it seems that you are at the mercy of a teacher who specialises in ambiguity.

I added one more confusing statement which I do not understand about S.pyogenes. Do you understand AG there?

http://en.wikipedia.org/wiki/Lancefield_grouping
"a method of grouping beta haemolytic bacteria based on the carbohydrate composition of bacterial antigens found on their cell walls."


text:
What can cause the bloating in high protein diet of Whey proteins?
I am thinking what can cause the swelling of gastrointestinal system i.e. bloating after high protein diet of Whey proteins.
Liver does breaks those proteins to branched chain amino acids (BCAA), which can cause this swelling.
However, I am not sure if this is the reason.
It may be the carbohydrates which are broken to enable this BCAA synthesis.
If you take the protein diet with carbohydrates, there seem to be less swelling.
So apparently easier energy for BCAA synthesis.
The combination of proteins, carbohydrates and lipids seem to be important.
Creatine should also be mentioned.
Fat burner thing is also important here, I think.
What can cause the swelling of gastrointestinal system after high protein diet of Whey proteins?

What do you mean by "swelling"?

@CaptainCodeman http://en.wikipedia.org/wiki/Swelling_(medical)

Yes but what do you mean by "swelling of high protein diet"?

swelling caused by ... Or Swelling in ...

Still doesn't make any sense.  You're saying the diet swells?  You mean the broccoli I'm eating gets fatter?  Or do you mean there is a part of the body that swells?  I think you're using the wrong terminology to explain something, and it's very unclear what you're trying to say.

There is a part of the body that swells i.e. included in the definition of the process Swelling. I use the question word "what" to ask what is the key factor that can lead to swelling. You can also ask the same by "how swelling in high protein diet ...".

With all due respect, I don't understand a word you're saying.  The definition of swelling means when a part of the body gets larger, but which part are you talking about?

@CaptainCodeman Gastrointestinal system.

Aha, thanks, now it makes sense! I could be wrong, but I think most people call that bloating, not swelling.  I think lactose intolerance has something to do with it as well.

@CaptainCodeman Thank you for the correction! Yes, lactose intolerance and many other diseases like celiac disease contribute to the ethiology of bloating i.e. swelling of abdominal area.

The cause of the swelling is lack of lymphatic carriage capability of proteins to the muscles, because of systemic conditions affecting the circulation of proteins through your lymphatic system.
There will be edema extracellularly because of insufficient carriage of proteins through lymphatic system.
My schematic drawing about the fluid movement between these spaces

I started to think why some people do not observe so much swelling.
I discussed with a few and come to conclusion that the main difference between those people who did not have noticeable swelling was that that they did lymphatic system massage by maximising abdominal breathing after taking whey proteins (before training and after training).
I think it sounds sensible to some extent.
Those people also included lymphatic system massage in their recovery after training.
One video here Lymphatic Drainage for Abdomen and Trunk.
So another reason what may cause the swelling is insufficient drainage of lymphatic system.
The swelling does not happen to the same extent in all people.
Some people swell much after one intake of protein drink.
Some people also do not have to do lymphatic massage.
My conjecture: The reason to this is most probably one glue-gene-group.
Those people who have this genome have other systemic diseases that causes the lymphatic drainage have high proportion of proteins already:

for instance, uncontrolled asthma patients, who are circulating lysed DNAs of lymphocytes from small bronchial tree through the lymphatic circulation

Lymphatic circulation is the system which circulates the proteins to the muscles.
After absorption from the digestive tract, lymphatic circulation carries proteins systemically.
However, since there is already a high proportion of proteins, lymphatic circulation cannot take much more proteins to carry.
Our body has to remove toxic wastes before it can build new materials.
Catabolism then conquers anabolism in some situations.


text:
Can systemic venous congestion caused by tumor?
I am thinking, if 1) little compressed superior caval vena and 2) some vein compression by tumor, can cause systemic venous congestion.
I think this is only in rare occasions.
However, the question is if this is possible.
Can systemic venous congestion caused by these two factors?

No. They increase the risk, but are not the causes.
There must be other factors involved which triggers the systemic venous congestion.


text:
Is Norepinephrine beta2 adrenomimetic?
I know that it has alpha1, alpha2 and beta1 effects.
It has beta2 receptor where epinephrine can effect.
However, to say that it is beta adrenomimetic, I am not sure.
That is ligand binding beta2 receptor causes a stimulatory effect.
Is norepinephrine beta2 adrenomimetic?

Masi, did you try pubchem? Section 14 lists all the biological properties with references. You can do this with any molecular compound.

@anongoodnurse Thank you very much for your excellent comment! I had forgotten this database PubChem. It is so useful!

The answer can be found in PubChem, which is linked in the comment by anongoodnurse.
I would not say that
Norepinephrine is beta2 adrenomimetic

because norepinephrine has many roles such as neurotransmitter.
I would just say that
Norepinephrine is alpha, beta adrenoagonist.

More pieces of information about it from PubChem:


text:
How is Microenvironment strictly defined?
I started to think this definition of Wikipedia:

Microenvironment (biology), a small or relatively small usually
  distinctly specialized and effectively isolated biophysical
  environment (as of a nerve cell)

and I started to think which environments can be examples of its.
Joints, synovial joints with capsule, hyaline cartilage in capsules, ...?
I would like to get more examples of environments so I can think better definition.
What is Microenvironment?

This term is also used in cancer. Cancer cells can go into dormancy.  This is what they used to call remission. No one knows what the trigger is for them to leave G0 and start dividing again. However factors in the microenvironment,  is negativity for Ki-67 (index of proliferation), estrogen positivity are both factors but there are many others.

Is there any energy spectrum classification of these events? For instance, in Fourier spectrum and/or time-frequency joint spectrum? - - It would be very interesting to know more about them in microenvironments. - - However, I have no idea if you can get any 1D signals in such environments.

Excellent answer overall; however, wondering if you could add some references :)

The meaning of the term microenvironment depends on the scale of the system that you're looking at. It's a sort of weasel word that loosely means "context" or "stuff in the immediate surroundings of the system of interest that has some kind of an effect on it". I've seen it used to describe everything from the chemical microenvironment of a cell (e.g. a hormone gradient) to the electrostatic microenvironment of a single amino acid residue in a protein (e.g. the field from nearby charged residues).
Conceptually it's similar to the "surroundings" in the "system and surroundings" framework from statistical physics.

What does it mean in Medicine? I have seen it been used with synovial joints like capsule in the syvovial joint.


text:
Are Purkinje Action Potentials Neuronal and Cardiac?
I first thought that action potentials of His-bundle i.e. Purkinje fibers are Cardiac.
However, I started to think that this is not enough.
I think now that they are neuronal and cardiac.
My conjecture. They have first short-acting neuronal part and then long-acting cardiac part.
Are Purkinje Action Potentials Neuronal and Cardiac?

The His-Purkinje fiber system is a network of one type of specialized conducting cardiac cells that carry an action potential in the heart. There are other cells which perform this function in different parts of the heart. The initiation time, shape, and duration of the action potential are distinctive for different parts of the heart, reflecting their different functions. These distinctions arise because the myocytes in each region of the heart have a characteristic set of channels and anatomy. You can completely dissociate the nervous system from the heart, and the heart will still pace itself. Think of what happens with heart transplants. This completely eliminates neuronal influence. See the following brief excerpt which explains one type of cells conduction method. Please note there is no reference to neurons.

The positive charge that enters cell A not only depolarizes cell A but also produces a flow of positive charge to cell B—intracellular current. This flow of positive charge discharges the membrane capacitance of cell B, thereby depolarizing cell B and releasing extracellular positive charges that had been associated with the membrane. The movement of this extracellular positive charge from around cell B toward the extracellular region around cell A constitutes the extracellular current. The flow of intracellular current from cell A to cell B and the flow of extracellular current from around cell B to around cell A are equal and opposite. It is the flow of this extracellular current in the heart that gives rise to an instantaneous electrical vector, which changes with time. Each point on an electrocardiogram (ECG) is the sum of the many such electrical vectors, generated by the many cells of the heart.

This has been extensively studied, so much so that cardiac electrophysiologists can pinpoint the location of a small group of cells that are misfiring by the nature of the impulse they are giving off. The annual median salary for an electrophysiologist in the US is $480,000. :-( There is a lot of grant money in this area. It's a big deal.
For in-depth study of electrophysiology of cardiac cells, please see Electrophysiology of Cardiac Cells or any other of a number of reliable sources.

Thank you for your answer! The case study does not cancel out my conjuncture. One reason why those neurons have not been found is that they are extremely small. They give signals of very little energy with the same frequency as Purkinje fiber. Other reason is that they are entangled to the Purkinje network together and difficult to separate them when you do not know where to look and how. It would be interesting to study the small group of cells misfiring. I am trying to get a research place in this area so I can start to research better. My options are Norway's research laboratories and USA.

@Masi - If I understand correctly, it is your contention that neuronal cells exist in cardiac muscle but they just haven't been found yet? How do you explain heart transplantation? Are there neurons that exist apart from the nervous system?

I do not know how these neuronal cells exists along cardiac muscle (in, out, near) but I have a clue that they work very closely together. And the only way to do so they should coexist, I think. I have only clues about this coexistent in Purkinje fibers. Person can live without this system some time. These neurons seem to exist in a link with the nervous system. I have not studied any heart transplantation patient. To process such an data (AAMI) similarly would tell me if similar regulation exist. It would be interesting to get such an data to understand your last case better.

Well, Hassall studied this in guinea pigs in the 80's and 90's. I found conflicting studies about it starting in the 2000's on. I don't know much about that. Clearly the nervous system has an effect on the heart. It would be interesting to study the differences in heart transplant patients vs. normal.

Thank you for your excellent comment! I sent requests of data for MIT-BIH's creator (George Moody), my close link of signal processing in Finnish Academy and my Baltic research fellows. The problem has been to get AAMI standard data. Only George's data has passed my validation at this point, although officially, many data are verified so by their AAMI devices.

Can you, please, point me to those conflicting studies from 2000's. I am making an application to my universities for request of data in heart transplant patients for this study.

On the wiki they are called cardiac action potentials. As the generation of the action potentials in the sinoatrial node is mediated by muscle cells, as is the conduction of the action potentials through the purkinje network (see wiki), the action potentials are not neural in nature, but cardiac.


text:
Is this ventricular tachycardia?
I am investigating the public data of this.
Its specification
201 2 360 650000
201.dat 212 200 11 1024 972 -519 0 MLII
201.dat 212 200 11 1024 982 30947 0 V1
# 68 M 1960 2851 x1
# Digoxin, Hydrochlorthiazide, Inderal, KCl
# The PVCs are uniform and late-cycle.  Junctional escape beats occur following
# episodes of ventricular trigeminy.

The data is taken from the interval $[200000, 205000]$ in the following picture with the sample rate 500 Hz.

There seems to be more than Premature Ventricular Contractions (PVC), extrasystoles, so possible ventricular tachycardia.
The same patient has six minutes later this

I think you can see clearer here those PVCs, when the ventricle is starting to contract too early.
Both are very pathological situations.
How can you differentiate between the two?
Are there PVCs in both pictures?

I have looked at this ECG using LightWAVE.
The first part is showing atrial fibrillation or flutter with variable conduction because:

arrhytmia
no P waves or coarse fibrillatory waves
tachycardia at about 95-100 beats/minute
can be seen better in V1

Sample from 00:00:40
The second part is showing premature ventricular contractions with trigeminy because:

different morphology of QRS - ectopic
wide QRS
two normal complexes followed by one ectopic
presence of the compensatory pause after PVC

Sample from 00:09:20
References:

ECG data: PhysioNET MIT-BIH Arrhythmia Database
ECG criteria: LearnTheHeart.com

So the ventricular tachycardia is at about 95-100 beats/minute.

@Masi you can't call it ventricular tachycardia. It appears because of the numerous stimuli generated by atrium. Only a few of these stimuli reach the ventricles because of the atrio-ventricular node. How many - that depends on the subject's age (it lowers the number of stimuli that pass through). At a younger subject atrial fibrillation may cause 150-200 beats/minute or even more.

I am particularly interested in the second part. I completely agree with you about these three findings: different morphology of QRS - ectopic, wide QRS, two normal complexes followed by one ectopic and presence of compensatory pause after PVC. Those two normal QRS complexes seem to different little. Do you see any other else in the second picture? Uneven rhythm, I think. Very low rate tachycardia remnants probably 95-100 beats/second.

@Masi yes they are sometimes different. Are you thinking of ectopic pathways?

Yes, I am thinking ectopic pathways.


text:
How is Calcium regulated in myocardic AP and plateau phase?
The plateau phase is maintained by influx of calcium and outflux of potassium in the second stage:

My conjecture is that calcium transforms between two phases

ionated phase (free calcium from i/c SR and e/c Ca-ATPase)
non-ionated phase (bound to some proteins).

The initial form can be ionated.
The process of deionisation occurs only in all-or-nothing cases - I see no evidence that this process can be continuous in my data.
My another conjecture why this deionisation can occur is because of the vortexes in the diastolic phase of ventricles (T wave; blood bouncing back to the tricuspid valve).
Which sources can correspond to this non-ionated calcium more?
My conjecture is e/c Ca more because longer travelling distance and entry involves accelerative movement.
Actually, this can differ depending on the situation at hand.
The accelerative movement can also contribute more to ionisation process so the situation can be reverse in some cases.
How is Calcium released from Sarcoplasmic reticulum?
Steadily or in accelerative motion or in a vortex.
How are Calcium forms regulated during action potential of myocardial cell plateau phase?
Keywords: Local Ca2+ signaling in health and diseases.

Aren't there models on this already?

@WYSIWYG Thank you for your good comments! This is the question which I leave open or not delete. There are some visualisations about this but not found any good one. I just need to search it with appropriate words probably. One Google search calcium action potential plateau filetype:swf. Probably, muscle contraction action potential better giving http://course.zju.edu.cn/532/study/theory/2/Cell/Action%20potentials%20and%20muscle%20contraction.swf but I have difficulty in playing this. Other SWF's were not from good sources and bad quality. Better search words needed.

I heard many talks on mathematical models for cardiac action potential and the role of calcium waves. You can see this guy's work. I am not sure if there is an animation but he once showed in one of his talks a nice simulation of spatial waves in heart .

@WYSIWYG Thank you very much for the mentioning the name of one relevant researcher here! I just downloaded a bunch of his articles. If you remember anything more, please write an answer or comment. I will write an overview when I understand this topic better.

Other researcher and Eric's coauthor is here https://www.researchgate.net/profile/Long-Sheng_Song?ev=brs_highl

Speaking of non-ionised calcium means that it is available in the form of Ca atoms, which is highly unlikely in an aqueous environment of a cell. I would better write "bound" and "free" calcium.

@Chris can you please make edits directly to body. I do not undestand to whoch part your comment applyes.


text:
Determination of Ageing by ECG inclusions/exclusions?
I am studying ageing and considering ECG signal because of its high sensitivity in theory (escardio). Some factors

Sensitivity
Gender
Medical treatment
...

Benchmark:
RTG dental + wrist uncertainty $\pm$2 years. Etc tooth washing, and hardness of drinking water affect much the dental health. Exposure to the ionisative radiation is problematic so less radiative approach would be nice.
ECG
Cardiac characteristics by ECG signal in power spectrum, having greater uncertainty than RTG dental 2016 because no sufficient exclusions/inclusions and too much exclusions covering data segments of autonomic nervous systems.
Processes to be excluded from the ECG signal

respiratory process
heart beat itself
some cellular-tissue processes

Some cellular-tissue processes

ROS determination ...
some genes about lipids and their characteristics with ageing in metabolic syndrome
decreased replication of cellular ageing
DNA replication stress, genome instability and aging
MICCAI 2012 Workshop on Novel Imaging Biomarkers for Alzheimer's Disease and Related Disorders

Low-Cost Targets

internal physiology of cardiac events in association with ...
cardiac and brain imaging makers related to substance use disorder, HIV, and aging (Stanford)

How can you determine aging by biochemical test and imaging?

I think you need to focus the question a little more. As it stands you list methods to study aging and then summarily ask how to study aging. Perhaps pick a specific technique and ask a specific question about your problems with that specific technique for better reception. I think going down a list of techniques and giving them each a thorough exposition warrants an answer that is too broad.

@Kendall Yes, you are right. I put the focus on Cardiology but including inclusions and exclusions. ECG signal has the great potential in high sensitivity. (escardio)


text:
How to measure GnRH in menstrual cycle?
I am interested in pulse frequencies of GnRH (gonadotropin-releasing hormone) in the menstrual cycle (MC) i.e. 28 +/- 7 days.
I would like to study its pulsatile nature i.e. within one MC, not same as cyclic nature within many MCs; but possible cyclic dynamics could be found in one MC too but not focus there.
GnRH releases human chorionic gonadotropin (hCG) which can be monitored by beta hCG but also by (source DynaMed Plus on Chorionic gonadotropin)

serum progesterone, Luteinizing hormone (LH)
estradiol levels
ovarian US 7-14 MCD i.e. in late follicular phase
onset of ovulation at 14 MCD
pelvic exam
cryptorchidism: signs of precocious puberty

Two articles on GnRH monitoring:

Monitoring gonadotropin-releasing hormone administration by measurement of urinary steroid conjugates in the morning urine samples.
some gene studies: Episodic gonadotropin-releasing hormone gene expression revealed by dynamic monitoring of luciferase reporter activity in single, living neurons

Possible cases to study

Amenorrhea: Kallmann syndrome where congenitally deficiency of GnRH but how low?

However, I did not find any publication describing direct/indirect continuous measurement of GnRH.

How can GnRH be measured continuously during the menstrual cycle?

English-speaking doctors and scientists would never use the word "pulsative." Maybe pulsatile, but not "pulsative."

GnRH is found in very low concentrations (2-10 pg/mL)
Options:

A highly sensitive analytical method (e.g. radioimmunoassay)
To sample directly from the hypophyseal-portal system
A surrogate measure

This abstract: http://www.ncbi.nlm.nih.gov/pubmed/9749566 describes direct measurement.
Direct sampling could only be done under general anaesthesia and in a short window, so I'd avoid that altogether unless you're talking about using an animal model and can surgically impact a cannula.
This abstract: http://www.ncbi.nlm.nih.gov/pubmed/21646369 describes use of the $\alpha$-subunit as a surrogate of GnRH (the $\alpha$-subunit is the same for FSH, LH, and TSH and is released under the control of GnRH).

By the way, GnRH does not promote secretion of hCG so much as it does LH and FSH (LH is fairly homologous to hCG).  For the most part hCG is secreted by trophoblasts (in the placenta) and is quite low except in pregnancy or the presence of certain germ cell tumors, so wouldn't be worth measuring in non-pregnant women or males anyway.
The bigger point is why do you want to measure GnRH pulsatility?  This has been done and the you know that it is pulsatile is because it has been done.

I want to get a 1D signal of this event's potential and study it by FFT. I want to study the fertility by studying GnRH's properties.


text:
How much is local blood non-Newtonian in Pathophysiology?
I am studying the Barus effect / Merrington effect / die swell / extrudate swell, which is a characteristic of non-Newtonian viscoelastic liquids (Introduction to the phenomenon in this video) i.e. the medium responds to the stress $\sigma$ of irritator with a strain $\epsilon (= \Delta l/l)$ that increases until the medium ultimately fails in a local pathology

blood has both viscous and elastic components which it can apply in pathophysiological condition
\begin{equation}
\gamma = \gamma_{v} + \gamma_{e}.
\end{equation}

#1 Maxwell material model

total shear stress if blood behaves like Maxwell material in local pathophysiological regions
\begin{equation}
\sigma = \sigma_{v} = \sigma_{E} = \eta \frac{d \gamma_{v}}{d t} = G_{M} \gamma_{E},
\end{equation}
implying $\sigma = \eta \, d\gamma_{v}/dt$ and $\sigma = G_{M} \gamma_{E}$.

I am thinking when blood is not non-Newtonian etc in muscular pathologies and muscular infections. I want to evaluate how much blood is non-Newtonian in particular situations.
I am interested in muscles and their supply with necessities.
How much is local blood non-Newtonian pathophysiologically?

According to this conference proceeding blood is very nearly newtonian at normal shear rates. More accurately blood is very thick and a shear-thinning fluid, but the shear-thinning effects don't scale with a power law like other non-Newtonian fluids.
In terms of blood changing viscosities, I suspect that in living patients blood viscosity is quite constrained, not only by physiological feedback but by the fact that if the blood viscosity changed very much the patient would become nonliving. Blood circulates constantly, and when it stops circulating it coagulates(which complicates efforts to measure its viscosity, I imagine). Any local effects on blood viscosity would be 'washed away' by the fresh blood arriving every heartbeat. If there's no or very limited blood circulating to the muscular pathology you're interested in the blood viscosity is probably not as significant as the ischemic tissue death that's just about to happen.

Thank you for your answer! Your case is general. You cannot assume that all local effects are always washed away after a new heartbeat. Ischemic tissue death happens lastly. I am interested in what happens between the initiator and ischemia i.e. how much local blood is non-Newtonian.

I'm not sure I understand. Between the initiator and ischemia the blood won't move much/at all, so why would it be interesting to study its non-newtonianness? All fluids at rest are perfectly Newtonian. Studies of blood viscosity next to dead or dying tissue would be pretty interesting but under those circumstances blood clots quickly. I'd start with kinematic blood clotting studies like this one but I think most of this research hasn't been done. With the possible exception of people studying angiogenesis and leaky blood vessels in tumors.

Yes, exactly. Blood at rest is perfectly Newtonian. But I am not considering cases at rest. Consider etc low BP and low Chol cases. Why CVD?