text:
How can low cholesterol cause mortality?
I am studying processes 1. stroke, 2. heart disease, and 3. cancer, and their mechanisms associated with low cholesterol which is a result of lowering cholesterol especially in elderly, Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study.
Stroke's manifestation is primary intracerebral hemorrhage ICH confirmed by many exclusion articles of other factors such as liver disease).
In the heart disease, there CAD and ischemia.
In the cancer, metastasis.
I started to think what could be enough general for all of these.
In the energy sense, one possibility could be glycogen, since it is used as an acute energy storage in all those organs.
Mechanisms could be the macro/microstructures of storage which are mostly unknown, presenting roughly 80/20 proportions.
So I propose that the lack of energy causes those conditions.
I noticed that many authors use the word remnant cholesterol when speaking about the subject. I did not understand its biophysical meaning.
Remnant cholesterol is an independent factor of cardiovascular manifestations apparently through the larger triglyceride-rich lipoproteins' (TRL) remnant kinetics.
Remnant cholesterol does not seem to cover all aspects of low cholesterol.
How can you low cholesterol cause stroke, heart disease and cancer?

can you please clarify your question above? Especially the very last sentence where it says "how can you low cholesterol cause stroke… "– That doesn't even make any sense. Did you mean to say how can lower cholesterol cause stroke? Or, why would lowering cholesterol cost stroke? I'm not sure what you're talking about (?) Would be happy to take a stab at answering this question if I could understand what you're actually asking.

@VanceLAlbaugh I attached the full title of the publication which says that low cholesterol is associated with mortality from stroke, heart disease and cancer. I think it is not only stroke that is associated with low cholesterol especially with elderly. Yes, you are right that the situation is caused by lowering cholesterol.

Cholesterol provides rigidity to plasma membrane and is also essential for certain cell-signalling pathways.

What you have asked for is a causal answer to correlated findings. There is no cause-effect evidence (at least from my searching) showing low cholesterol will indeed cause stroke. Associations like this are dangerous in the sense that we shouldn't think that one causes the other. But, we can speculate on how they are linked, which is always fun.
I'll be going off my understanding of cholesterol transport and will include the reference at the bottom. Essentially, cholesterol is used in the cell membrane to change the permeability of the membrane. The more cholesterol, the less permeable the membrane is to water. However, this also changes the physical properties of the cell membrane, making it more rigid and structured. If I had to guess (which is again PURE SPECULATION) I would think that decreasing the cholesterol to the point of a dangerous level would increase the cell permeability of vital cells, the most sensitive would be neurons who depend on ion based signaling to perform primary functions. Since ions are very small and easily pass through the membrane if the membrane is leaky, they might be the first indicator that the something is wrong and the membrane isn't strong enough. Again, purely speculative with no evidence. An experiment one could do is examine the amount of cholesterol required in a cell to keep ions from crossing the membrane and see if there are any other effects that occur within or around the cell before ion passing. If you aren't in this type of research yourself, maybe you can fund it!
Source= Cassarett and Doul's Essentials of Toxicology. Textbook, 12th edition

Interesting answer! I need to classify first how cholesterol presents in imaging. And also its subtypes. Do you know any 1D signals which has a high focus about cholesterol?

I had an old professor (Bruce Hammock) that used to do mass spec quantification of lipid concentrations. Check out his papers. Here is also a paper for reference and good measure: http://onlinelibrary.wiley.com/doi/10.1111/j.1742-4658.2009.06869.x/pdf

Is there any raw data about these mass spectrometry results? Some 1D data. I want to characterize it my way.

I'm not sure if there is any out there. Most mass spec data is priority classified due to the specific methodology each person uses. Aka. often most people don't post mass spec stuff because they don't want other people analyzing their data in a different way, thus generating a different result (one of the faults of mass spec). Your best bet is to look at publications and see if they added supplement info (http://www.ncbi.nlm.nih.gov/pubmed/16458590 another ex). Or check the ncbi bioinformatics database


text:
Pathogenesis of Cardiac Atypia?
I am studying the pathogenesis of atypia in cardiac cells where the etiology is most commonly irritation or infection and where the precancerous risk depends on the context of diagnosis.
This fact motivates me to think how they can generally arise, from superficial or stromal origin, and how - multifactorial and/or polygenic.
Cardiac tumours are mostly secondary (30x1) in comparison to primary tumours.
I am thinking the sources of these metastases.
I did not understand if benign tumours can be secondary such as myxoma. Therefore, I assume now that myxomas (superficial) and stromal origin can be secondary.
I am mostly interested in superficial changes of the heart in atypia.
It is interesting to notice that benign cardiac tumours originates from the left side of the heart mostly, while the malignant from the right side.
I am thinking the mechanisms here and how the myxoma could be related to the pathogenesis of stromal procesesses in the right part of the heart and the pacemakers' function (AV, SA).
It would be nice to understand the links between myxoma, AV and SA.
Myxoma in the left chamber

Benign.
Origin - superficial mostly in left atrium.
Pathogenesis - polygenetic and/or multifactorial. Mobile mass obstructs blood flow in chambers and cause an increase in pulmonary capillary wedge.
Myxoma (benign tumor of connective tissue containing mucus and gelatinous material) most commonly in left atrium, fossa ovalis in septum.
Imaging DX sound after S2 in ECHO and sometimes ECG; ECHO heterogenic mass.
Differential DX lipomas, rhabdomyomas, teratomas.

Stromal Processes

Malignant diagnostically mostly.
Right side of the heart mostly.
Most commonly haemangiosarcoma (= angiosarcoma).
Pathogenesis. There can be some pathways which are activating atypia such as lymphoma.

Myxoma and Stromal Processes?
I did not understand the link between these two processes.
The former resides mostly in the left side of the heart, while the latter in the right side of the heart.
Their link or their individual links to the pacemaking (SA, AV) would be nice to understand.
I am not sure if we can exclude Purkinje cells, although they reside physically far from the atrias because their low conduction frequency and because the myxoma is about benign tumor of connective tissue which would well reside there, probably even better energetically than in SA/AV.
Sources

DynaMed Plus Lymphoma, sarcoma, ..., visited 25-February 2016.
Orlandi A, Ferlosio A, Angeloni C, et al; Cardiac tumors. Pathologica. 2005 Jun;97(3):115-23.
Patient.co.uk. Visited 30.12.2014. URL: http://www.patient.co.uk/doctor/cardiac-tumours
Cleveland Clinic. Visited 30.12.2014. For Diagnosis. URL: http://my.clevelandclinic.org/services/heart/disorders/cardiac-
tumors
http://www.learningradiology.com/lectures/cardiaclectures/insideoutflash.swf, visited 13.1.2015.
Emilsson, Medscape. The Characterisation and Risk Factors of Ischaemic Heart Disease in Patients With Coeliac Disease.
P. e. a. Whorwell, DEATH FROM ISCHMIC HEART-DISEASE AND MALIGNANCY IN ADULT PATIENTS WITH CLIAC DISEASE. Institute of Cancer Research, Sutton, Surrey, United Kingdom: The Lancet, 1976, volume 308, Issue 7977, p. 113 - 114.

How can you describe the pathogenesis of Cardiac Atypia?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Average Beginning of Action Potential in ECG by t-f HRV
I have some ECG data where I am estimating the average beginning of the action potential.
I am interested in the discrete Fourier analysis of joint t-f HRV when input data is ECG.
Frequency domain method here - a simplification of the joint t-f HRV.
However, I am uncertain how this method works because I see several limitations and mistakes in designs of several systems. There are also several publications about the topic, but little has been peer-reviewed. Also little data and research systems are publicly available for reviews.  According to @Christiaan (see comments), ECG shows compound action potential which is most likely detected by detecting R peaks.
In HRV analysis, they do currently
Estimate R-R interval in time and frequency domains:
Consider an estimate of R peaks.
It is not always the maxima.
There can be two peaks of equal length at maximum.

I think, in including two R peaks, they think they cancel the error of estimating the start of R peak, although the uncertainty actually increases. I think this is wrong in ignoring the uncertainty about the estimate of the start of R-R or simplifically the start of AP.
I think we should be able to estimate the precise location of action potential better.
They are using commonly exclusion principles which lose much original signal and decrease sensitivity

by excluding small time, frequency $|x|, |\eta| \in \mathbf R$ by choosing the window $w$ such that $w(t) \approx 0 \approx \hat{w}(\eta)$.
by excluding one beat normal beat before and after each ectopic beat.
system fails if more than 20% of ectopic beats.
system fails in 24h recordings because of computational issues of longer segments - so limiting to 5 minutes and averaging.

My Exclusions and Hypothesis
To detect the exact beginning of the action potential $s$ value $s(x) \in \mathbf R$ at exact instance $x \in \mathbf R$ is unpractical.
Instead, I measure some averages of the signal: $A_{\sigma} s(x) := \int_{\mathbf R} x(y) \varphi_{0,\sigma}(y-x) dy$ where $\varphi_{0,\sigma}$ is 0-average-valued $\sigma$-variance of normal density function.

$A_{\sigma} s(x) := \int_{\mathbf R} x(y) \varphi{0,\sigma}(y-x) dy$.
No windowing function so including also small time, frequency $|x|, |\eta| \in \mathbf R$.

Processes limiting to detect the beginning of action potential

Technical processes (fine with these)
HR Saturation process.
HR Recovery process.

I am very interested in how you can characterize HR saturation process and the HR recovery process.
I think they are using individual signals measure in three circumstances: Paced, Exercise and Recovery, here.
How can you characterise differences between such circumstances?
Views
Labview (most likely LabVIEW Biomedical Toolkit) or Matlab (which should be fine!)

ECG,
R-wave detection,
IBI signal (Inter-Beat Interval),
Expanded ECG,
HRV spectrum.

I do not understand the reason which component is requiring to use Labview here and most likely its Biomedical Toolkit in the analysis like in 4. I sent a message to the developer about the thing but waiting for an answer. Why? I would like to use Matlab, but I need to know if there can be some electronics that limits you and is only suitable for Labview. I have built my own ECG boards and systems with mostly Analog Devices' electronics.
How is the R-wave detection done? I think this can describe the challenge better about the beginning of the action potential.
Which channel(s) is/are used precisely in the view ECG? How can the electrical activity view be created? Summation of all channels in steady intervals? I think we should not exclude things now but it can be later done if some some anatomical/physiological reason is found.
What is precisely the Expanded ECG?
How does the expanded ECG allow you to evaluate the mean electrical axis?

I think another problem with such views is that they are not fixing the mean electrical axis. However, I may be wrong, since I do not understand the definition of ECG view and expanded ECG view. How are you considering ECG channels here?
Joint time-frequency domain HRV
I am interested in how you associate frequencies (high, mid, low) with different intrinsic, autonomically-modulated periodic rhythms.
I only see in slides the following link without an association
High Frequency = 0.25 Hz (15 cycles/min
Low Frequency = 0.1 Hz (6 cycles/min)
Very Low Frequency = 0.016 Hz
(1 cycle/min)

Adapted from the presentation here and here but changed for t-f
N-N - normal-to-normal
To calculate a standard deviation of a series of numbers:
[0. missing step about location of action potential]
1. Find the average in R-R intervals [4]
2. Calculate the differences between each number and the average
3. Square each difference (so they don’t cancel out)
4. Sum
5. Divide by number of datapoints
6. Take square root
...
n. no interpolation because FFT

How can you estimate the average beginning of the action potential in the joint t-f domain?
I think you measure the distance between two peaks and count the variance.
Sources

https://www.heartmath.org/research/, organisation about the field.
Pruneti, C. A, and McCraty, R. Very interesting presentations about the topic.
www2.unipr.it/~cprunet9/files/Heart-Rate-Variability.ppt, one example of HRV presentation.
BME 333 Biomedical Signals and Systems, J. Schesser. https://web.njit.edu/~joelsd/signals/classwork/BME314signalscw12a.pdf About R-R intervals in time and frequency domains

The question is unclear; 1) ECGs don't show action potentials, but compound action potentials. 2) an image of a waveform would help 3) what is some analysis of channels' function? and 4) with sensitivity - sensitivity is dependent on the hardware, you might be talking about accuracy? And that is a subjective term, what is accurate? And for that matter, what is sensitive? Explain please.

A start of something in the frequency domain is impossible. That's why it is called frequency domain.

There is no time interval in the frequency domain.

@Christiaan Yes, you are right. There is a time interval in the joint t-f.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Is Rheumatic fever more Chronic than acute?
It follows from the complication of S.pyogenes' pharyngitis.
I am thinking how the inflammatory response behaves: acute or chronic or something between.
I think chronic disease is better description here than acute, however not sure.
What is the type of inflammatory response in the Rheumatic fever?

the inflammatory response it autoimmune reaction, thus it occurs 4 weeks after the Strep infection.
please, look at the picture from the "Nature" -

So it is chronic, since not rapid.


text:
To define the total Resistance of Systemic Blood Circulation
Some systems are in parallel.
For instance, the resistance of lungs $R_{\text{lungs}}$.
Assume here for simplicity that these parallel systems can be handled linearly.
We also consider only Total Vascular Resistance for simplification.
So we have now only systems in series under consideration.
Linear system  for Systemic Vascular Resistance
Formula for the total resistance as mechanical definition as assuming linear connections between those systems:
$$R_{\text{total}}=R_A+R_a+R_c+R_V+R_v$$
where appropriate resistances are

$R_c$ capillaries,
$R_a$ arterioles,
$R_A$ Small artery,
$R_v$ venules and
$R_V$ vein.

Nonlinear system for Systemic Vascular Resistance
There are many factors involved in these locations:

permeability
vasoconstriction
...
growth factors (FGF) for renewal of the vessel wall
different channels (activated, deactivated - mostly potassium channels)

where I skip the consideration of vasoconstriction, growth factors and different channels.
Permeability is one which applies to all types of vessels.
Change in permeability of one location does not mean a linear change in permeability in another.
A change in the permeability of small arterioles does not lead to a similar change in the arteries or venules.
The vessel is permeable to gas and liquid.
Let's consider only these components.
I want to include these facts into the definition because, in the pathological situations, different state of inflammation for instance can apply to a vessel.
Let's call total permeability $S$ which is dependent on gas and liquid components, first on liquid component (so inner integral).
I could give you the nonlinear formula of the total resistance but I think it goes over the skills most here.
Let's call the nonlinear resistance dependent on permeability of the vessel, $W(x,y)(t,f)$ in time and space.
So consider only the nonlinear component of the permeability formula after parametrisation i.e. permeability, let's call it $T$, which is dependent on changes in water (w) and gas (g) components over a path integral.
The path covers all components in the vascular system that are in series.
So total resistance defined nonlinearly
$$W(x,y)(t,f) = \int_{\gamma} T(u) \frac{1}{u} \int_{t-u/2}^{t+u/2} T(w) \, S(x,y)(t,f) dw \, du$$
where the inner integral corresponds to the water component while the outer integral to the gaseous component.
There is only an averaging in the inner integral when the width of the window is $u$.
However, we do not any windowing here actually, just because of this averaging, so we lose no data and can handle the total resistance as a single process.
Notice that change in $T(u)$ leads to a change in $T(w)$ nonlinearly.
I skip the nonlinear definition of $S(x,y)(t,f)$ which stands for the energy in time in each instance - you can think it as the amount of permeability in each position of the vessel.
Actually, I also skipped the explicit definitions of the water and gaseous components too.
I have not found any work done on the nonlinear development of the resistance.
I think this is necessary for defining inflammation explicitly.
How can you describe the total resistance as an nonlinear operation better?

Most people talk about SVR/TPR (systemic vascular resistance/total peripheral resistance) and PVR (pulmonary vascular resistance). You're welcome to re-name the variables, but how this culminates in the question about a "way to define system circulation" I don't know. (Maybe you just forgot the word "resistance" there?) This wikipedia article gives a good overview of the formulas that can be brought to bear.

@Susan I really had a completely different target here for getting some nonlinear definition of the systemic vascular resistance. You will not find pieces of information about this in literature.

Can you shorten the question with just the essential elements. Also please add a reference for the equation. I did not understand your final question — How can you describe the total resistance as an nonlinear operation better?... Are you asking why nonlinear model is better than linear model or how to make the nonlinear model better?

We do not need to compare apples and cars. Linear case is straightforward. Thinking now the presented question. This applies necessary dependences and connections, mostly in electrophysiological level now.

I see no reason to model the components of the vascular system as a series circuit. Also, I see no reason to model the system's components as "gas" and "liquid" because the gases are all dissolved (until they're outside the system). I think the systemic blood circulation is analogous to the movement of air through the pulmonary tree. You should locate those references, which definitely treat the flow as turbulent. Also, defining "inflammation" in terms of this quantity "resistance" is confusing.

@Ryan Good comment! I cannot agree with the analogy to pulmonary tree and blood circulation because of inflammation and other processes in vessels. The turbulence absolutely should be taken into account in the definition. It actually inside the energy term S(x,y)(t,f) which I have not explicitly defined here but where the separation of different flows is done. Actually, I do not define inflammation into resistance; I used inflammation's effect on permeability (T) for water and gas in the definition.


text:
Calling for Free Online Data for Paediatric ECG?
I need free online data about heart murmurs to study these:

heart murmur frequency , S2 heart sound frequency and its split,
  murmur timing, and duration, murmur intensity, S3 sound presence and
  intensity, S1 presence and intensity, presence of ejection sounds and
  arrhythmias

I will cite your source then if I can use your data freely.
I would really have the same data as used in this paper:

Heart energy signature spectrogram for cardiovascular diagnosis
  Vladimir Kudriavtsev, Vladimir Polyshchuk and Douglas L Roy

No pediatric ECG data here

beecardio (aggregation of many ECG databases)

Does anyone have simple data for my task?
I remember that some CD of some book has some standardised nicely organised sounds that you can use freely.

Where does ECG come into this?  It seems like a question about auscultation.  What sort of data are you actually looking for?

Normalised and well measured. This type of data: https://dl.dropboxusercontent.com/u/62073194/bmt-2012-4075.pdf They do not share their data publicly. I have asked for the data, but they have ignored my request and do not want to share it.

I recognize this was asked like 7 months ago, but in case you're still looking for a good resource:
I used a CD of heart sounds that is called something like "Harvey Heart Sounds," which I got with the purchase of my stethoscope.  If you can find a copy of this, I found it an excellent tool when training to recognize the differences.
These are good heart sounds: http://depts.washington.edu/physdx/heart/demo.html
If you were looking for something other than the sounds themselves, then I'm not sure if you're asking about.  There are all sorts of good ECG references, especially Dale Dubin's EKG Interpretation book.  And Kablunde was the cardio textbook I used, which I liked.

Thank you for your good answer! It is never too late. This is a research topic. I need so clean sounds as possible and preferably many so I can then compare and contrast and decide which one is the most cleanest.

Hmm. I am not sure if these sounds are pediatric. Do you know who has recorded them? Any confirmation about how old the patient has been? I am thinking about the normal heart sound.


text:
Voltage-gated Potassium channels in the action potential of cardiomyocyte?
There is one type of potassium voltage-gated channels open in Phase 1 too.
Some call them early repolarization channels.
I am not convinced that the channels are different in different phases: 0, 2, 3 and 4.
I think all these potassium channels are voltage-gated.
However, they probably differ in some places.
I am not sure if one type of channel can be open in all these five phases.
Which types of potassium channels are open during the action potential of cardiomyocyte?


text:
Late control mechanisms of blood pressure (arterial) level?
I first covered the fast and moderate control mechanisms which I think are

Fast control: Baroreceptive reflex (tonus), Chemoreceptive reflex
  (CO$_2$).
  Moderate control:  Bicarbonate
  (ECF), Phosphate buffer (ECF), Proteins (ICF).

then late control mechanisms about which I am unsure

Capillary fluid shift mechanisms
Stress-relaxation of the vasculature
RAA

What are the late control mechanisms of blood pressure?

Capillary fluid shift mechanisms
If the pressure of the blood is high, there is high hydrostatic pressure. Simply put, this means fluid exits the capillaries at the arterial side due to this pressure, and less fluid returns at the venous side. With less fluid in the circulation, blood pressure falls.
Stress-relaxation of the vasculature
Imagine the arteries are like springs. The more you pull them the stronger the recoil force. However if you stretch them too much for too long, they stay stretched.
Renin-Angiotensin-Aldosterone system
When the blood pressure is high, there is less release of renin from the kidneys. This means less angiotensin II production. Angiotensin acts to increase blood pressure by increasing vasoconstriction and increasing retention of fluid and salt (via aldosterone). With less RAA system activation, the blood pressure drops.

Can you say about the stress-relaxation of vasculature that high ICF leads to increased diameter and length of arteries?


text:
What are the movement mechanisms of thrombus?
I am thinking how thrombus (veins, arteries and heart) can move.
Secondary mechanisms come to my mind only:

some enzyme which lyses it, probably adhesion mechanism.
Blood circulation (flow rate) is one secondary measure, I think.

I am not sure if there exist any primary mechanisms:

In veins, there are valves which probably can help thrombus go forward by pushing.
Veins can also dilate so dilation of vessel can help.

Arteries do net dilate their diameter.
So aim would be there to maximise laminar flow, and decrease turbulence.
So probably the question is related somehow to the laminar flow which could help thrombus to move.
How can thrombus move in veins, arteries and heart?

Have you found the answer of this one? Is this the thing :http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681659

@DevashishDas I considered your pointed paper. I added my considerations about it. I think the paper makes big simplifications about the processes in movement of thrombus.

This answer aims to list existing models and do meta-analysis about them.
This answer is a draft.
There are many models made based on the thrombus movement.
One of them is proposed by DevashishDas' answer but it seems to focus only on the first stage of hemostasis:

The model assumes thrombin is generated on the surface of activated
  platelets in the thrombus core and is transported through the fibrin
  network that surrounds the core both by advective flow of fluid
  permeating through the fibrin network and by diffusion through the
  fibrin gel.

and particularly the model keeps these values constant and simplifies

To calibrate the model, we experimentally determined fibrin clot
  permeability and thrombin diffusion rates through a fibrin network.

which I think should be dynamic (not constant) because of the three endothelium main factors listed below.
Endothelium is a dynamic structure controlling the fibrin clot.
Thrombus Hemodynamics Model

Fibrin Networks Regulate Protein Transport during Thrombus Development by  diffusion-advection equation (Stokes, continuity, Brinkman equations)

which is about the first stage of hemostasis because of its simplification about fibrin clot permeability and thrombin diffusion rates.
Hemostasis
There are three stages of hemostasis altogether which work parallel together:

primary (formation of the platelet plug)
secondary (formation of fibrin through the coagulation cascade)
tertiary hemostasis (formation of plasmin for breakdown of the clot)

Primary hemostasis is the formation of the primary platelet plug.
It involves

platelets
blood vessel wall
von Willebrand factor

Normal endothelium prevents hemostasis.
Injury of endothelium

involves vasoconstriction (local)
enhances adherence of platelets to exposed platelet subendothelial surfaces
and activation of coagulation process

The formation of primary platelet plug involves

Platelet adhesion,
Platelet activation, and
Platelet aggregation.

Main steps in blood coagulation:

Formation of prothrombin activator complex (thrombokinase)
Conversion of plasma protein prothrombin into thrombin
Conversion of dissolved plasma fibrinogen into fibrin (makes filamen- tous skeleton of fibrin clot)

Clot retraction

The platelets in the clot contain contractile proteins.
They bring the edges of the wound together, which also reduces the chance of further bleeding - not vasoconstriction here!
The contraction process also supports the wound healing process as it brings the ends of the wound together.

Clot retraction is the process of getting clot towards fibrinolysis process. Fibrinolysis is the process where a fibrin clot (product of coagulation) is broken down. Its main enzyme plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidney and liver. Clot retraction and fibrinolysis are necessary to remove clot so wound healing can proceed.
Myogenic and metabolic autoregulation by endothelium
Myogenic control involves the localized response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relax- ation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.
Myogenic and metabolic Autoregulation is the automatic adjustment (local) of blood flow to each tissue in proportion to its needs (oxygen, nutrients, ...), and is controlled intrinsically by modifying the diameter of local arterioles. It involves localised response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relaxation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.
There are three types of substances secreted by the endothelium (1):

NO
Endothelium hyperpolarising factors
Endothelins.

where I think the modelling should focus on these three factors.
Sources

My discussion with a researcher in this field 7/2014
My notes in three Physiology courses during years 2011-2014
Costanzo, Physiology, book
Guyton, Physiology, book


text:
What is it the most common reason for community acquired pneumonia?
This is a difficult question because there are many types of community-acquired pneumonia (CAP): typical acute, atypical acute and chronic.
Most common microorganisms are also different among different groups: children, adults, elderly, immunocompromised and people at risk of different diseases.
Some options:

Streptococcus pneumoniae
Hemophilus influenzae
Escherichia coli
Klebsiella pneumoniae
Pseudomonas aeruginosa
bronchiectasis
Chlamydia pneumoniae

Not any virus, since they are present in only about 20% of diseases.
Streptococcus pneumonia is probably a good choice.
What is the most common reason for community acquired pneumonia?

Are these being pulled from Medical Microbiology, and if so which edition?

I cannot find this from my edition. I do not know which edition of the book it is, but its cover is this: https://dl.dropboxusercontent.com/u/62073194/Screen%20Shot%202013-08-29%20at%2011.18.58%20AM.png

You are right in that there are several ways to split down CAP, and plenty of different pathogens to look at.  But then we are looking for the most common.  Pnumonia is most common in children and adults over the age of 75 (or 65 depending on who's counting).  Luckily there are plenty of good reviews for both populations.
From the pediatric side we have Iroh Tam PY(1):

Pneumonia occurs more often in early childhood than at any other age,
with the exception of adults older than 75 years, and kills more
children than any other disease worldwide

As far as pathogens:

Streptococcus pneumoniae and Haemophilus influenzae type b (Hib) have
been characterized as 2 bacteria predominately responsible for cases
of fatal pneumonia in children.  However, widespread introduction
of Hib and pneumococcal conjugate vaccines has led to significant
declines, especially of Hib, although Streptococcus pneumoniae is
still the predominant bacteria isolated from bacterial CAP in
children.  There is increasing recognition of the prevalence of mixed
bacterial and viral infections, which have been documented in 23% to
33% of cases of pneumonia.

Then we move to the geriatric side of things with Falcone et al (2):

Common pathogens include H. influenzae, enteric gram-negative bacilli,
the atypical organisms, S. aureus, Pseudomonas aeruginosa, and M.
catarrhalis, although the relative prevalence of each tends to vary
among studies. Among elderly individuals with aspiration pneumonia,
gram-negative bacilli are the predominate organisms (49 %), followed
by anaerobic bacteria (16 %) and S. aureus (12 %).

Though I should note, having done them myself, getting accurate cultures is difficult, and viral levels a very likely to be under reported because of handling and skill.

For example, in different prospective studies in which the
microbiologic etiology of CAP was systematically sought in the
elderly, a definite or presumptive pathogen was often reported in <60
% of the patients. (2)

And again in children:

There are 2 main challenges in the diagnosis of CAP: the first is the
definition of CAP, particularly in young children, in whom bacterial
and viral infections can occur with similar frequencies, and in whom
overdiagnosis of mild symptoms and signs may lead to unnecessary
antibiotic use; the second is the identification of a causative pathogen, which is frequently impractical and inadequate in children, and
in whom the failure to isolate an organism can result in unnecessary
antibiotic use. (1)

Taking into account more global sources, I'm actually thinking Hib infection has dropped more due to vaccination than I gave it credit for, putting my bet on S. pneumoniae, and showing my regional experience may not be representative (3, 4, 5, 6).
(1) Iroh Tam PY. Approach to common bacterial infections: community-acquired pneumonia. Pediatr Clin North Am. 2013 Apr;60(2):437-53. doi: 10.1016/j.pcl.2012.12.009. Epub 2013 Jan 12
(2) Falcone M. et al. Pneumonia in frail older patients: an up to date. Intern Emerg Med. 2012 Oct;7(5):415-24. Epub 2012 Jun 12.
(3) Brown JS. Community-acquired pneumonia. Clin Med. 2012 Dec;12(6):538-43.
(4) Kurutepe S, Ecemiş T, Ozgen A, Biçmen C, Celik P, Aktoğu Özkan S, Sürücüoğlu S. [Investigation of bacterial etiology with conventional and multiplex PCR methods in adult patients with community-acquired pneumonia]. Mikrobiyol Bul. 2012 Oct;46(4):523-31.
(5) Tao LL, Hu BJ, He LX, Wei L, Xie HM, Wang BQ, Li HY, Chen XH, Zhou CM, Deng WW. Etiology and antimicrobial resistance of community-acquired pneumonia in adult patients in China. Chin Med J (Engl). 2012 Sep;125(17):2967-72.
(6) Capelastegui A, España PP, Bilbao A, Gamazo J, Medel F, Salgado J, Gorostiaga I, Lopez de Goicoechea MJ, Gorordo I, Esteban C, Altube L, Quintana JM; Poblational Study of Pneumonia (PSoP) Group. Etiology of community-acquired pneumonia in a population-based study: link between etiology and patients characteristics, process-of-care, clinical evolution and outcomes.  BMC Infect Dis. 2012 Jun 12;12:134. doi: 10.1186/1471-2334-12-134.

I had a question in exam where Chlamydia pneumoniae was the most common reason for CAP in the situation. I cannot remember the situation. Can you think any situation where Chlamydia is the most common pathogen?

@Masi The only possible thought is a-typical with myco ruled out.  Another possibility is with a sub-section of patients who develop low risk CAP.  If you look at any of the sources I posted world wide, not one of them found C. pneumoniae as most common.


text:
Which pathways/mechanisms could control some Synaptic clefts in series by Somatic Nervous System?
I listened a talk where the speaker said that this can probably be possible by Weak Quantum Cognition Theory.
I see that there is no evidence at the moment, only theory.
I see no pathways by which this could happen directly such that the quantum entanglement and quantum superposition could happen.
They should happen in a series, but I see no system holding the signal going on.
I think this is a only a hypothesis, without any supportive  evidence.
Probably, some type of synaptic cleft can be controlled, but still I see no evidence or no pathway or pathways.
I do not understand which pathway/pathways this could happen.
What is the target mechanism? Presynaptic membrane or postsynaptic neuron?
Which are possible pathways that could control the secretion of synaptic cleft?


text:
How can an infection of lower respiratory tract lead to a skin infection?
I am interested in the multifactorial process about infectious diseases of the lower respiratory system and their progression to a skin infection.
Possible agens are zwitterions, viruses, fungi, amoebas, bacteria and/or parasites.
Zwitterions
Small protein segments, much unknown but their importance is much greater than known.
Viruses
Parvovirus B19

Example of a case: 5 children develop a bright red rash on the face and turns violet after a few days and then disappears. Then maculopapular rash appears on the trunk, buttocks and extremities. It soon fades from the trunk but persists on the thights and forearms. Two children have also had a slight fever and a sore throat, but all were not terribly sick. What is the genetic material of the most likely causative agent?
It is a skin infection. Not so severe. Little upper respiratory infection but not necessary caused by the agent. Infects many so spread probably by respiratory droplets. **But how a respiratory infection can lead to a skin infection?*

Bacteria
....
Amoebas
...
Fungi
....
Parasites
...

I don't have the time to answer this now, but you're thinking about it just in the context of the question which is limiting.  Check out Mycoplasma pneumoniae.

So, my question is are we limiting ourselves to the example case, which seems to have nothing to do with respiratory infection (unless it's measles, but the statement "not terribly sick" somewhat precludes this, and the measles rash turn dark brown, not violet).  Or are we just generically asking the question "how can a respiratory infection lead to a skin infection." which is very different.  I also don't see what your attempt to answer the question has been.

cf. Parvo, Erythema infectiosum, Rubella, and viremia.  You're going to have to give me more before I'm enticed to come back.

Have you determined the the most likely causative agent first?  This still feels like a homework question that hasn't been addressed fully.  I've given you 4 different respiratory infections that causes rashes (M. pneumoniae, measles, parvo, and rubella).  Start with figuring out the causative agent, then ask the question, "How does [P] pathogen cause a rash?"  If you show your effort in answering that, and have trouble, I'd be happy to come back and help.

Perhaps we should continue the discussion in chat?

One might argue that since replication takes place in erythroblasts (Brown, Anderson, & Young, 1993), that it's not actually a respiratory infection either.  Fluids are simply more hospitable to the virus and more transmissible.
As for the rash, perhaps it is because the P antigen receptor that erythrovirus uses to infect erythroblasts is also expressed on endothelial cells, like those in skin (and alveolar) capillaries .


text:
Which immunosuppression caused by long-term usage of these antibiotics in untreated celiac disease?
These antibiotics include

amoxicillin + acidum clavulanicum (beta-lactam, inhibit cell wall synthesis, broad specturm, 3rd gen aminopenicillin) / last part preventing the resistance
ceftriaxone (3rd gen cephalosporine, inhibit cell wall synthesis, broad spectrum)
clarithromycin (macrolide, inhibit protein synthesis by binding to ribosomal subunit S50)

used regularly for cyclic middle ear infections for years during the childhood - ages 2-10 for a patient with untreated celiac disease.
I am thinking what kind of immunosuppression can this lead to.
I think it mostly conquered by suppression of adaptive immune system.
Little lowered innate immunity lowered too.
I am especially interested in the antigen-presenting cells (mostly dendritic cells) and their function in an immunosuppressed patients of the antibiotics.
There may be other factors which I have not mentioned related to this kind of immunosuppression.
Feel, free to propose.
How can dendritic cells work in an immunosuppressed patients?
You can assume any combination of cases for the three antibiotics: 8 possible cases.
For instance,

(1) and (2) high antibiotic resistance, and only susceptible to (3)
High antibiotic resistance to (1)-(3)
...

Possible cases which reminds

this immunosuppression can remind this one: immune reconstitution syndrome like in HIV but milder

Amoxicillin is often combined with a beta-lactamase inhibitor like clavulanic acid. This oversomes the problems with the resistance, but can cause problems in patients which are sensitive to this additive. It can cause vomitting.

@Chris Thank you for your comment! Yes, indeed - Acidum clavulanicum added next to Amocillinum.

I am a bit confused by your question. So you want to know if and how immunosuppression by antibiotics work and how APC are involved or affected?

One further question: What are your references for these antibiotics beeing immunosuppressive? There are some, which have this effect, but these are not widely used to fight infections.

@Chris. Yes to first question. Please, open me on this topic. There may be other antibiotics in the case. There may also be cases that such antibiotics cause immunosuppression in some patients - this is what I am studying now. I am just not understanding the mechanism.

Off the top of my head, chloramphenicol is the only antibiotic I know of that causes immunosuppression (by causing aplastic anemia).

I don't think these antibiotics has immunosuppressive effects. There are immunosuppressants which are completely different drugs... Antibiotics simply kill pathogens, or stop/slow down their growth and multiplication. I think you should clarify your question, at least I don't understand how using antibiotics can lead to immunosuppression...

I added the case to be with a patient with untreated celiac disease during that time.

Thanks. Interesting question, I'll check it when I have a little free time...

One possibility is that these antibiotics could disrupt your normal gut bacteria. Given that your gut has the surface area of a tennis court and is typically coated with symbiotic microbes, antimicrobial therapies could dramatically change the population dynamics of your gut ecosystem. One might imagine that the immune system of the gut is in homeostasis with these gut microbes, and if they all die off all at once because you're taking some sort of 'cillin, your immune system might suffer for lack of stimulation. Fewer immune cytokines released by your intestinal immune cells into your blood => systemic reduction in immune function.
Other possibilities could include: the drug just randomly fits into a bad spot on some important immune protein; the drug targets bacterial-related genes in the mitochondrial genome and disrupts the metabolism of the immune cells; the drug disrupts your ability to absorb nutrients required for immune function...the list of potential mechanisms is undoubtedly long.

Thank you for your answer! I added untreated celiac disease to the description which disrupts the normal gut bacteria.


text:
What are the mechanisms of disabling extrinsic control of heart?
I started this thread by thinking this question but I developed it further below

What is the mechanism maintaining refractory period of pacemakers?

My conjecture is that the mechanism is the simultaneous depolarisation of at least SA node and AV node.
I am not convinced yet about the Purkinje fibers' participation.
Bigger question from this is:
How do pacemakers work under threshold without action potential?
There are continually leaking Funny channels (Na+) in pacemakers.
There has to be chemical changes intrinsic changes

change in the permeability of Funny channels or
active pumping of Na+ out OR pumping something negative inside the cell (probably Cl-, not sure) and

extrinsic changes

reflex arch blocking the action potential of pacemakers when enough preceeding sensitisation of AV node

I have no evidence for that this kind of sensitisation would happen in SA node or in Purkinje fibers.

which all seem to be working together in firing recovery mechanism through AV node without specific SA node stimulation.
Example logic tree for a myocardial infarction patient of 68 years old:

R wave of atrial fibrillation and flutter
extrinsic stimulus to start sensitisation of AV node
intrinsic sensitisation of AV node
extrinsic stimulus through reflex arch
systole and upper-systole of AV node starting
lower-systole of AV node

intersection of upper- and lower-systoles

unstable end of lower-systole
unstable systole
extrinsic firing simultaneous SA and AV node (similar extrinsic regulation as in the beginning of this logic tree)
prolonged and stable refractory period and long compensatory pause

It is debated whether the pathophysiology of IST and POTS results from abnormal autonomic regulation or abnormal sinus node function.

My conjectures based on my logic tree

Pathophysiology of IST results from normal extrinsic (recovery) mechanism of autonomic regulation which body uses to recover from abnormal stimuli (etc atrial fibrillation and flutter)
Pathophysiology of POTS results from abnormal extrinsic mechanism of autonomic regulation when there is no stimuli after abnormal stimuli

What is causing the abnormal autonomic mechanism in POTS?
I would say that IST precedes POTS.
Prolonged IST seems to be going to POTS.
Physical explanation is that the body cannot last regular IST so it goes to POTS, since losing its normal extrinsic regulation.
What is this (apparently cumulative, not necessarily long-term) trigger of disabling the extrinsic autonomic regulation of the heart?


text:
What is the nature of action potentials in autonomic nervous system?
My conjecture is that the natures of sympathetic and parasympathetic action potentials are different.
My findings propose me that

sympathetic action potential is little longer lasting than parasympathetic

there may be another mechanism in sympathetic action potential - some sort of plateau phase which does not exist in parasympathetic action potential
however, I have not managed to gather any convincing evidence on this claim

parasympathetic action potential has greater energy per one time instance, while the energy of sympathetic AP is distributed along wider time space

My hypothesis is that the energy of parasympathetic and sympathetic action potentials is equal.
This would suggest me that the action potentials of the autonomic nervous system are coming from the same source.
Their nature is just different.
What can this source be exactly?
I have read the recent Physiology and Pathophysiology books where this topic was not covered rigorously.
I did not manage to find any good publication about the topic, probably, I missed something.
What is the nature of autonomic nervous system action potentials?
You can select what ever condition you want and see if you can get some findings as I have got.

What makes you say the action potentials are different? From my knowledge APs are uniform across all nerves

See the energy spectrum of APs. You have to define uniform. They seem to have the same energy (uniform; thing which has confused people to think that they are uniform also in nature), but different energy spectrums.


text:
Does the Parasympathetic Tract of Colon Sigmoideum Travel with Nervus Vagus and its Nucleus Dorsalis Nervi Vagi?
I have the following tractus now:

nucleus parasymphaticus sacrales -> nervus splanchnic -> ganglion
  terminalis -> colon sigmoideum

The tract is parasympathetic.
It suggests me that it should travel along CN 9 or CN 10, most likely with CN 10.
Does tractus colon sigmoideum travel with CN 10 and its nucleus dorsalis nervi vagi?

I found the following from Wikipedia:

Pelvic splanchnic nerves are the primary source for parasympathetic innervation [for Sigmoid colon].

The non-cranial nerve is extending the scope of the cranial nerve by a synapse between the two neurons. The neurons are transmitting the electrical impulse from one neuron to another.
So this way the splanchnic nerve does not need to be with CN 10 in the region of impact.
The parasympathetic tract of colon sigmoideum can travel with nervus vagus by having a synapse between pelvic splanchnic nerve and CN 10. I verified this from my professor.


text:
Elevated position effect on recovery times from upper respiratory infections at rest?
In nursing school, they advice for people with upper respiratory infections to be in a slightly elevated position at the head region when sleeping.
My intuition of the reason is that the lymphatic drainage to the venous arch works better; gravity helps to drain the lymph to the venous system; not only the heart.
Bacterial infection of the pharynx occurs in a prolonged exposure of the concentrated lymph.
I got today exact information about exact positions to relieve the body most when sleeping:

5-10 % angle to relieve body most, while gravity helping to suck the lymph from the throat; can be helped with the hormone motilium (domperidone)
more than 10 % is for other conditions

Is there any studies about the effect of elevated sleeping position on the recovery time from the upper respiratory infection?

Physiology
My conjecture.
The slightly elevated position causes greater venous return (work against gravity by smooth musculature and thoracic pump).
Why this is happening this way is partially based on my question here about Fast standing and the heart's insufficient accommodation of the increased venous return.

where the venous return reacts first the change in the position from supine by shifting the VR1 to VR2.
The stroke volume increases initially to SV1 to SV2, while the end diastolic volume from EDV1 to EDV2.
The increased stroke volume cannot be maintained long time so the cardiac output shifts to the right from CO1 to CO2.
So the initial stroke volume SV1 is the same as SV3 (not in the picture).
However, the EDV has increased (EDV3 >> EDV1) which increases much the lymphatic drainage.
Lymphatic drainage is not dependent on the stroke volume.
Increased lymphatic drainage then again increases the circulation of lymph.
This then again supports the recovery from the upper respiratory infection where the fine regulation between

the thoracic pump,
respiratory pump, and
smooth musculature

determine the final effect of the body position on the recovery times.
The size of the thoracic cavity puts some limitations, for instance.
Cardiology
In some cases, the upper respiratory infection can cause myocarditis.
This will decrease the functioning of the heart and cause possible

premature atrial contraction, and/or
premature ventricular contraction.

Elevated position helps small arterioles of left ventricle supply preload.
Otherwise, ectopic beat can be heard or also called "epics beat" which is sign of the two previous conditions.
The nurse is educated to listen to the patient and ask for possible jolts and flips in the chest.
Elevating position in such a case can help because of better supply for preload in the left ventricle.
Pathophysiology
Upper respiratory infection is often acute respiratory infection (acute respiratory distress syndrome).
There is an increased permeability of the vessels.
The fluids and plasma proteins are going through alveoli.
Acute hyaline membranes are formed.
Cytokines play a big role in this process.
To maintain lymph retention, the result of increased venous return compensates.
These patients can breath normally in the sitting position.
There are also other reasons for the infection:

overweight - the greater intra-abdominal pressure $\to$ more liquid diffused into the lungs OR other organs are suppressed.
Big chest suppresses lungs such that the architecture can change.

Pharmacology
There are different drugs which effect is dependent on posture and position of the body.
Hypertension is a common disease which amount increases during ageing in population.
Let's take hypertensive drugs as a case study.
Peripherally acting sympathoplegic drugs are generally dependent on posture more than centrally acting ones.
In hypertension treatment, the peripheral acting sympatholegic drugs are used often in combination with diuretics.
Blood pressure can be under control when blood volume is 95% of normal, but much too high when blood volume is 105% of normal.
So this study should be considered with no hypertension and hypertension.
Sources

For Pharmacology, Basic and Clinical Pharmacology, 11th edition, Katzung et all.


text:
Vitamin D oral intake, transportation and absorption
Several factors affecting vitamin D and its active form absorption and storage

acidity of stomach (not significant effect)
cytopathic effects of viruses
cytopathic effects of bacteria

where the last two reasons can be some reasons which may explain why vitamin D should be administered with bread; to make a surface covering around out vitamin D molecules.
Probably, the fibers also work in some short of transport media.
They can also partially explain why big dose of vitamin D does not last long time in the normostenic body.
Summary of procedures in administrating vitamin D orally

with bread (carbohydrates; fibers) - possible protection, better transportation and more to absorbtion
with oils (fat metabolism could help in destroying extra free radicals; but I see no other sense in administrating vitamin D with fish oils)
daily (not weekly)

Why does the lipid-soluble vitamin D not last in the body long time?


text:
To have TBE vaccine during allergic times with mild asthmatic symptoms?
My assistant says that if you have asthmatic symptoms you cannot have TBE (Tick Born Encephalitis) vaccine, although you are living in the active zone of TBE.
Cases

mild allergic symptoms
allergic symptoms under control of Montelukast (asthma in control)
asthmatic symptoms (bronchitis, rhinosinutis, repeated cough)

What are the risks of having this vaccine during allergic symptoms when you have mild asthma medication (Montelukast)?
I still think the risk of encephalitis is higher if you get TBE from nature than from vaccine.
Are there really some cases where encephalitis is caused by the TBE vaccine?

Can you define the acronym TBE in the question?

Interesting question!
The Tick Borne encephalitis vaccine is an inactivated vaccine. It is therefore impossible to get the infection from the vaccine. Reports of fever have been noted but that is due to the body mounting an immune response not due to infection. There are therefore no reports of encephalitis or other markers of infection following the vaccine.
Not only may you have the TBE vaccine if you are asthmatic, but if you are at risk due to your lifestyle and location then, particularly if you have chronic asthma, the TBE vaccine might be a good idea.
Asthma is usually treated by inhalers and montelukast is reserved for uncontrolled/severe asthma. However in the rarer case of aspirin induced asthma, it is much more first line and used for mild asthma. Montelukast is not considered a mild medication.
I hope this answers your question :) if not, comment below!


text:
ECG of heart transplant patients
I am studying ECGs of heart transplant patients.
The difficult thing is that there is so little available data publicly.
I must apply for data in my universities.
It would be also great if something is public.
I have searched several databases and contacted some authors directly.
Some findings

No heart transplant data in Physionet, online search tool here.
No heart transplant data of ECGI with Dr Rudy (personal email)

I am waiting answers or working with application for

Dr Rudy's company
University of Helsinki's database (under process for application)
Some technical universities in Finland (these have connections where are good data but they do not hold data themselves)

Is there any ECG data about heart transplant patients?

This might get you started on how to look for such (it's also interesting). I don't know if the National Center for Biotechnology Information might be a resource.

Thank you for the comment! Interesting. Citing articles are also good resources: http://scholar.google.com/scholar?start=0&hl=en&as_sdt=0,5&sciodt=0,5&cites=http://circ.ahajournals.org/content/81/3/821.abstract&scipsc= Let's see if any data is public.

are you looking for images or anything in particular coz I found a bunch after a google search. Most of them are heterotrophic heart transplants though

@TheLastWord I am looking for data (raw numerical data). Not pictures. Feel free to propose any data which you found so I can take a look at them if they are appropriate.


text:
Does transplanted heart have full sympaticus without medication?
I am reading this and this where I am considering this sentence

[N]o baseline parasympathetic innervation [in transplanted heart].

Does this sentence imply that the heart work then in full sympaticus all the time?
Probably, through altered systems, but still.
At least the regulation of blood pressure strongly supports this, here for the generic medication plan.
Does transplanted heart have full sympaticus without medication?
Notification of terminology. I tend to use overloading in writing.
For instance, I can say that there is sympathetic and parasympathetic supply to the heart i.e. innervations of S and PS through endocrine system to the heart.
I am not yet completely sure how the recipient's body can target the alpha and beta receptors of donors in heart. Are there any variations of these receptors? If yes, then the effect of sympathetic stimulation would also differ from the original stimulation.
So full sympaticus (or original) may not be present.
The new stimulation may lead to greater or smaller activation of sympaticus.

Downvoter! Leave, a feedback.

The parasympathetic supply to the heart is by nerves and that is truncated during surgery as pointed out.
The sympathetic supply to the heart is by two means:

Through sympathetic nerves from the sympathetic trunk
From the adrenal medulla which secretes both adrenaline and nor-adrenaline directly into the blood stream

The heart contains the beta receptors for the sympathetic system, especially the ventricles and nodes (SA) and conducting fibers. These receptors respond to the presence of adrenaline and nor-adrenaline in blood. Thus the sympathetic response is preserved while the parasympathetic responce is lost.
There is a minimal level of nor-epinephrine in blood at all times which thus influences the heart.
Receptors in Heart:
The heart contains adrenergic (sympathetic) and cholinergic (Parasympathetic) receptors. When the heart is transplanted, the donor heart also contains the same receptors. The only thing missing are the nerves.
The sympathetic system does not suffer as much as the parasympathetic system, because of the adrenal medulla which secretes the nor-epinephrine (same as nor-adrenaline) into the blood, which upon reaching the heart can stimulate the beta receptors on the heart.
There is no organ which releases acetyl-choline into blood, (fortunately, as such a release would be disastrous leading to shock and rigor, possibly death). So the parasympathetic receptors in the heart do not receive any stimuli.
Edit 1:
In response to your edit, yes there are polymorphisms in all receptors. But the structure of adrenaline and nor-adrenaline are pretty much constant. This means that the donor heart will be at a similar level of sympaticus as it was in the donor when (s)he was alive. Although this will not be the same as the recipients pre-surgery sympaticus state of the now removed heart.

Excellent answer! So the type of sympathetic stimuli is from adrenal medulla in transplanted heart. In normal heart, two types - from the former and from sympathetic trunk.

Yes, adrenal medulla is kind of a sympathetic endocrine system, stimulating the whole body at times of need

Assume adreniline/stimulates tissue. There are alpha and beta receptors. How is the sympathetic action potential generated? From receptor to periphery and to heart? Can you see this action potential generated by adrenaline and noradrenaline clearly in some channel of ECG? Probably, II or MLII. I would like to find the channel and situation where action potential from sympathetic trunk is not visible.

I think I gave you the wrong idea. I will explain further in the answer

I don't understand your comment. There are no nerves to heart and thus no action potential in generated in any nerves. The receptors are in the heart muscle cells and conducting fibers. The effects are as described above

There is vagus nerve to the heart so I think action potential is generated through the release of acetylcholine in heart. There is sympathetic trunk to the heart similarly neuronal. What do you mean that there are no nerves "to" the heart? I mean by this that there is the neuronal component combined with the endocrine system + receptors i.e. something to heart.

In that case you are correct, there is no parasympathetic supply to heart.

In your definitions, is there sympathetic supply to heart? I tend to overload terms and say that there is both S and PS supply to heart through endocrine system.

Yes, maybe that's why I was confused. I also confused myself with the term 'action potential' I forgot about the muscle action potential. Did that answer your question?

I am not yet completely sure how the recipient's body can target the alpha and beta receptors of donors. Are there any variations of these receptors? If yes, then the effect of sympathetic stimulation would also differ.


text:
Theranos blood test's Specificity and Accuracy?
I am studying the limitations of Theranos device.
They have 238 documents in Google Patents Search (Inassignee as Theranos), here.
Which patents are relevant for their device?
They have 70 tests which are not necessary to consider now.
Just the basics of the device.
My intuition says that it uses PCR to multiply the microliter of blood for the analysis.
What are limiations of multiplying so little blood?
I think this is where their engineering work applies.
What components do you need to multiply?
I think all is not necessary.
Otherwise, the specificity and accuracy can be difficult to hold.
How can Theranos blood test's be specific and accurate compared to conventional full blood test?
I suspect if you can do the conventional full blood test with Theranos device with the same accuracy and specificity as the conventional one.

Which patents are relevant for their device?

They currently only have about 27 issued patents (US)
Of those patents about 10 of them are related to network/internet/health record/algorithm (so not really about their device)
The remaining patents focus on a few areas: sample acquisition (getting the blood drop and handling of it), Patch based technology (before they pivoted), sample quality analysis (this is key to making sure the small sample is good quality), microfluidics/modular device (these are the patents relating to the actual testing and device)

What are the limitations of multiplying so little blood?

From a molecular standpoint (PCR) the smaller sample you start with, the less of the original nucleic acid template you have to start with.  Lower end PCR testing uses 10uL of sample.  This is ok when you are trying to bring molecular diagnostics to the point of care or developing markets, but the best PCR tests use 50uL of sample (more than a drop of blood which is traditionally 25uL or so),  regardless of how good your device is, at some point you start amplifying junk. The better the primers and other reagents the less junk you amplify, but at the end of the day you want more sample to be more sensitive.
From a NON-molecular standpoint (chemistries, cellular analysis, coag, etc.), they aren't/can't multiply the analyte of interest.  In these tests, they rely more on dilution or small volumes to perform detection.  This is where their ability to reliably dilute and correct for the dilution comes into play. Although there is certain limits to this.  Coagulation tests would not be representative if you diluted the sample so in this case they will have to rely on working with a small volume.  Cellular analysis can only be diluted so much as you get to a point where you miss important but less common cell types.  Take eosinophils (a type of WBC) while they can get to 15 or 20 percent of all WBC cell types, in general they only make up a couple percent.  Assume that 2% of all your WBCs are eosinophils.  If you only have 3500 WBCs per 1uL of blood (which is on the lower end of normal), you have approximately only 70 of these cells in that same volume.  If you dilute the sample so that way there is more of it available for other tests like electrolytes, but you still analyze 1uL, The number of those cells is even less.  If you had perfect detection you might be ok, but you generally want to analyze more blood so that statistics work in your favor and your performance goes up. Most of the other chemistries, proteins, and as mentioned earlier, electrolytes will probably be ok for dilution and detection and in fact this is why there are plenty of small devices already out there that use a drop of blood and perform the same tests.
Their issue in diluting or amplifying analytes of interest is that biology still is governed by the laws of physics and even though technology may allow you to analyze samples down to 10nL, that just isn't use full in biology, and limits their their capability to perform the supposed menu of tests from one microtainer of blood.  They don't publicize that they may need to draw a venous sample (needle in your arm) for some tests and depending on what tests you order, you may need a separate finger prick for each test.

How can Theranos blood test's be specific and accurate compared to conventional full blood test?

If they reliably control dilution of the small sample, they maybe able to provide high quality results for some tests.
Finger pricks actually can be easily skewed via technique.  Theranos has specially trained people to draw these samples, but it is time consuming >5 mins and until it is fully automated this is one variable that no matter how good sensors are, you can't correct for variation pre-analytically when you have that small sample.  Finger pricks also skew certain tests even when technique is good such as platelet and WBC values in the CBC.
I discussed the sample volume issue above regarding PCR amplification and how good tests use up to 50uL.  So if they compare to a 10uL test, they may be able to compete, but not full lab quality.
A lot of the future techniques they have regarding small techniques (in their applications) like their coagulation tests work great in an academic setting, but they fail to be able to handle the full range of blood samples they will see, so it will be interesting to see how that plays out.

Takeaway

Theranos is working on modular micofluidic devices/cartridges that will use small sample
There are certain biological limitations that stand in the way of them performing all the tests in their catalog with only a drop of blood
The FDA will eventually be requiring them to submit their tests for approval as they are currently doing tests that are available on commercially and FDA approved devices already (this makes sense because LDTs were never ment to be used in place of standard tests and equipment and since there is NO published data on their performance it can be worrisome to providers and payer)
Their true business plan has yet to be elucidated, but if they really did have a box that did all this, they would be selling them to physicians and clincs where those results could actually be used in diagnosis rather than 4 hours later.
I hope they succeed, but there is just way too much hype to buy in on it yet.

I am sorry I don't have sources, most of this is from intimate knowledge of the space and from the little info available on them so I could definitely be wrong on some of this.  I hope this helps!

Thank you very much for your excellent answer with outstanding details and analysis! I am interested in in the Biological and Physical limitations here, particularly. They do not cover anywhere the uncertainties of their tests. I would like to work for a review about uncertainties in sampling small volumes of blood in different tests. How did you find the pieces of information about their patents? Google patents with Theranos gives 10 international classifications: A61B5/00, A61M5/172, B01J19/00, A61B5/15, B01L3/00, A61M5/142, A61M37/00, A61M5/145, G01N35/00 which I think are their patents

Issued Patents:https://www.google.com/?tbm=pts&gws_rd=ssl#q=inassignee:%22Theranos,+Inc.%22&tbs=ptso:us,ptss:g&tbm=pts  Applications:https://www.google.com/?tbm=pts&gws_rd=ssl#q=inassignee:%22Theranos,+Inc.%22&tbs=ptso:us,ptss:a&tbm=pts&start=10

Wow! This is insightful answer, clear expert on this area! I tried to summarise this answer in my answer related to sensitivity and amplification. I cannot fully understand them. Perhaps you could preview them? +1 for the awesome work already!

I haven't seen their device and I won't want to see it, I want to first understand the concept better independently. I am not an expert in biology but I have feeling how such device could be done.
Noname covers sensitivity and new concept "amplification" raising a new puzzle: is amplification done by analog methods (op-apms), digital methods, dilution or/and some other methods?

Summarising the Noname to sensitivity, amplification and background

(I added bolding)

"Theranos is working on modular micofluidic devices/cartridges"

"regardless of how good your device is, at some point you start amplifying junk. The better the primers and other reagents the less junk you amplify, but at the end of the day you want more sample to be more sensitive."

"they aren't/can't multiply the analyte of interest. In these tests, they rely more on dilution or small volumes to perform detection. This is where their ability to reliably dilute and correct for the dilution comes into play. -- if you had perfect detection you might be ok, but you generally want to analyze more blood so that statistics work in your favor and your performance goes up. Most of the other chemistries, proteins, and as mentioned earlier, electrolytes will probably be ok for dilution and detection and in fact this is why there are plenty of small devices already out there that use a drop of blood and perform the same tests."

"They don't publicize that they may need to draw a venous sample (needle in your arm) for some tests and depending on what tests you order, you may need a separate finger prick for each test."

where by (2) more sensitivity can actually be a good thing; by (3) same tests already done by other devices in small size: what is so special with Theranos device? and by (4) one drop of blood not enough for all tests.
"What are limiations of multiplying so little blood?"

Decision Analysis (DA) and Compositional Blood Analysis (CBA): I see such a device as a Decision Analysis (DA) device where you need to do compositional blood analysis (CBA). You get a lot of vague information on which you do sensitivity analysis. Conventional full blood tests can be seen as devices where the sensitivity is very very low to other factors. It is not surprising that development has lasted about 10 years, sensitivity analysis is very low research project. For example, Chevron's DA model started 1990 and continuing, implementation takes time. For example, scale hydration level to some level in all samples. When you have low-quality information, you need to use ad hoc models (often based on high-quality samples) such as supposed correlations between things to improve prediction accuracy.

1.1. What are Decision factors?

1.1.1. Rheology of blood? Dry or liquid phase samples?
1.1.2. Correlation of red/white shells: I don't use the word "approximation" because the number of red shells correlated with the number of white shells
1.1.3. Density (~1.05 kg/l)
1.1.4. Colour of blood
1.1.5. Hydration level
1.1.6. other factors?

"How can Theranos blood test's be specific and accurate compared to conventional full blood test?"

I think this question mis-framed. It is better to ask "How much extra value does such a device can offer?"
Smaller size and less blood mean convenience. It may be useful with athletes, new markets. More convenient to patients/users even though suffering from some abnormalities due to its intrinsic limitations related to its small-volume measurement method.

What components do you need to multiply?

I think this is an important insight: is it possible to multiply blood somehow ensuring its quality for testing? This would make blood tests less painful for patients. Perhaps this is related to stem-cell research? Perhaps not, the Noname covers this in terms of dilution more closely.

Using ">" indicates that you are citing a source. Are you? If so please provide a link. Otherwise please format your post differently.

Please, see Noname's answer. I think you need to revise your answer accordingly.

@Masi Christian: done done, ">" changed to "---" and the Noname summarised related to sensitivity and amplification. I think the Noname adds more insight to sensitivity on this process. The DA and CBA are still the underlying processes in building the product -- where I think most other small-size products fail (it requires capital/time/creativity/teamwork/etc).

-1 I think your answer is too much business-minded: Extra value of device. Specificity and accuracy of the device in some test is very relevant here. I think you are little bit lost in your last big title question - PCR is for multiplying  blood parts. Those patents seem to apply too it and to multiply just some parts of blood - see Noname's answer. Rheology of blood should be able to maintained by pharmacological methods and by method of educating personnel who take the blood. So no coagulation problems. I think your listed factors are not keys here. Those "other factors" are most relevant.


text:
Differentiation of norepinephrine and epinephrine in indications
Norepinephrine is less beta2 adrenomimetic than epinephrine so more selective so less bronchospasm so may be therofore better in treatment of cardiac failure and different shocks.
However, I am not sure.
I have some intuition that some of them is somehow analog of the other one.
PubMed about norepinephrine in Pharmacology

Sympathomimetics
Adrenergic alpha-Agonists
Vasoconstrictor Agents

PubMed about epinephrine in Pharmacology

Bronchodilator Agents (beta2)
Mydriatics (beta2)
Adrenergic alpha-Agonists
Sympathomimetics
Adrenergic beta-Agonists (this causes those two first indications)
Vasoconstrictor Agents

which is logical because epinephrine is nonselective beta2.
However, I am not sure if those properties include all accepted indications.
This proposes me that norepinephrine can be used better in acute situations.
However, I know that epinephrine injections are more given to allergic people to carry for anaphylactic shock.
Why so?
Probably, because of price.
How does the indications of norepinephrine differ from those in epinephrine?

You're proposing several problems: cardiogenic/septic shock, bronchospasm, and anaphyllaxix. Cost isn't the factor. Epinephrine is the drug of choice for anaphyllaxis because it decreases edema through its alpha-1 adrenergic vasoconstrictor effects on the small arterioles and precapillary sphincters in most body organ systems. If blood pressure were the major consideration, another agent would be used. Dobutamine is used for cardiogenic shock because it is also a positive inotrope. You can't pick two drugs and ask how they differ (too broad) without the effect (indication?) you're looking for.

The differences in the action/indication is because of differential affinity of the two molecules to different adrenergic receptors. The wikipedia page on Ardenergic receptor has a table which summarizes this.
Wikipedia doesn't cite references for it. You may have a look at some of the following old articles.

α- and β-Adrenergic Receptor Subtypes

In the periphery, α1-receptors are located postsynaptically, mediating the excitatory effects of catecholamines at α-receptors. α2-Adrenoceptors, on the other hand, are autoreceptors involved in the regulation of noradrenaline (norepinephrine) release. In the central nervous system, both α1- and α2-receptors exist on postsynaptic cells; there are also 2 principal subtypes of β-adrenoceptors. β1-Receptors have a high affinity for both noradrenaline and adrenaline (epinephrine) and are found in the heart, brain, and adipose tissue. β2-Receptors have a low affinity for noradrenaline and are involved in mediation of relaxation of vascular and other smooth muscles and in many of the metabolic effects of catecholamines.

β-Adrenergic Receptor Subtypes: Properties, Distribution, and Regulation

                  NE=Norepinephrine, EPI=Epinephrine, ISO=Isoprenaline

NE properties seem to go little over each other: its alphanergic properties cancel out some of its betanergic properties. This may result in the fact that epinephrine is more potent drug than norepinephrine. At least, it is used more widely and has more indications including PCR and acute anaphylaxis, in contrast to norepinephrine. I wonder if there are any indications of norepinephrine where you cannot use epinephrine. Probably, one such a property is acute hypotension. Probably some stability issue with the epinephrine or something.

@Masi α-receptor mediated responses would be more responsive to NE; I don't think it will cancel out. α-receptor mediated responses are synaptic. Very localized and not endocrine....... I don't think there is a stability issue. NE is specifically administered for acute hypotension. There are other synthetic agonists that target only one type of receptor like salbutamol.


text:
How to manage fat-gluten oxidation in celiac disease?
Assume you have been in non-gluten diet 20 years.
You built mass 8 mass with substances containing gluten (endogenous gluten stored in fat).
Then, celiac disease is diagnosed.
You have been 3 months in gluten free diet.
After mass period, you go to fat burning period.
The challenge starts: endogenous gluten stored in fat.
It is painful if too intensive training program.
Even little amount of gluten causes enteropathy.
What are the protectant methods for burning fat containing gluten?
How can you prove that there are no gluten-derived peptides that accumulate somewhere?
Since the cellular receptors for gluten have been identified, I think this may be over-complicating things. - Ryan's answer
I have not found any good solution for this, since I do not understand the pathophysiology enough well.
Toxic factors related to celiac disease

gliadin
...

How is endogenous gluten released from fat?

Do you have any evidence that gluten is stored in fat cells? As far as I know, it can only be synthesized by certain plants...

@MattDMo No. This was just a wild conjuncture. Probably, better one is gluten staying on the fat cells, but this would not apparently last long.

Gluten is a protein. The textbook answer is that protein is not stored in fat cells.
Proteins are hydrolyzed into amino acids through digestion; some amino acids are ketogenic, and can contribute carbon towards fat biosynthesis. So some of the carbon that originates in gluten may be incorporated into a fatty acid. But the carbon has no 'memory' of its previous role in a gluten molecule, and could not act as gluten when the fat is subsequently oxidized.
One can imagine an undigested gluten molecule (or its peptide fragments) binding to the exterior of a fat cell, but there's no mechanism for it to get incorporated into fat as an intact protein.

Thank you for your answer! I think you are correct. Is there any other way how gluten can remain in the body, like in some compartments? I think this is possible in stomach itself for some hours. I approximate that enough-digested-gluten-for-symptoms remain in the body at least 5 hours or better said its effect. Of course, this is relatively for each individual. To know where gluten stays would help to think better the mechanisms of gluten interaction with the body.

"Is there any other way how gluten can remain in the body, like in some compartments?" I think so, as I allude to in my last sentence. It's an interesting enough question to stand on its own. A problem is that the question is structured as an appeal to ignorance...how is one to conclusively prove that there are no gluten-derived  peptides that accumulate somewhre? Since the cellular receptors for gluten have been identified, I think this may be over-complicating things.

Thank you very much for your excellent comment! It is true. There must also be other aspects in this fat burning where gluten may remain stored.


text:
How can succinylcholine cause myorelaxation?
I first thought that this is because of prolonged depolarisations.
However, I am not sure anymore, because after reading PubChem, the only possible pathways are are Choline agonist.
So I would say that succinylcholine cause myorelaxation by some cholino-receptor agonists.
I do not think it is about depolarisation and how long it is.
How can succinylcholine cause myorelaxation?

Succinycholine, as its name might suggest, is a cholinergic agonist indeed. It acts on the neural plate of skeletal muscles, where it activates the muscle cholinergic receptors.
Phase 1 block due to succinylcholine thus occurs by activating so many receptors at once, that the whole muscle gets desensitized and therefore paralyzed. A corollary of that is that muscle will twitch during activation, thus accounting for the reason why people twitch shortly before becoming paralyzed after a succinycholine iv injection. This phase 1 block will resolve in 2-5 minutes.
Now an interesting phenomenon is that if you go on stimulating the muscle with more cholinergic agonists (for example, a second iv dose of succinylcholine), you may end up provoking endocytosis and degradation of the cholinergic receptors. This is called phase 2 block, and in contrast to phase 1, it will take at least several hours to resolve. This is why we never use a second dose in the clinics, except in very special cases.
You can also read about it all on wikipedia

What is the event called that causes such a phenomena as phase 1 block and phase 2 block? Do other adrenoergic drugs and Cardiac drugs have such characteristics? How such an event documented for instance in PubChem, for instance in the link in the body of my question? I want to be aware of such events for each drug.

So the short answer to my question is that the succinylcholine cause myorelaxation because of cholino-receptor antagonism with big dose or second dose; stimulated by endocytes and degradation of the cholinergic receptors.

NOT THAT KIND OF CHOLINERGIC RECEPTOR!!! think autonomic nervous system, not autonomic nervous system... he is talking about nicotinic cholinergic receptor on the SKELETAL MUSCLE, not the muscarinic cholinergic receptors on cardiac conducting cells and muscle... this is a drug to temporarily paralyze the skeletal muscle for the sake of the surgeon doing the operation.. this is an anesthesia drug, not a cardiology drug...

secondly, this phase 1  vs phase 2 is to distinguish it from the curare-derived neuromuscular blockers which ONLY act as antagonists on the nicotinic cholinergic receptor (aka exhibit phase 2 type effects)... the phase-1/phase-2 type drugs are called depolarizing neuromuscular blockers... the curare derrived ones are nondepolarizing... here is an article listing more depolarizing types with this phase-1/phase2 type effects: http://en.wikipedia.org/wiki/Neuromuscular-blocking_drug#Depolarizing_blocking_agents another example of a drug is Decamethonium

I see what your saying, masi... the downregulation of receptors that are overstimulated is pretty common throughout pharmacology, and upregulation with blocking a receptor... for example (1) the dopamine receptor is up/down regulated with levodopa/carbidopa and it causes cycling... in typical psychotics it causes extrapyramidal symptoms... (2) it's also a proposed mechanism of the SSRIs, downregulating the seratonin receptor is what mediates the antidepressant action, supposedly... (3) also thats why going off of a betablocker quickly is very dangerous for patients... the list goes on...

oops, for "typical psychotics" it's supposed to say "typical ANTIpsychotics"...

@JasandPruski Please, make your comments an answer, since they are good and make sense.

@Masi Actually, those comments you propose to turn into an answer do not directly answer your primary question, even if they are good comments. On the other hand, I did answer your primary question and you did not mark it as accepted... just saying :-)

@Raoul The reason is that I am not satisfied enough. It seems too be too much cardiac. I may be wrong. I need something more etc references, images or anything so that I can be certain about your answer. You have now only a reference to Wikipedia which is not enough. I want to understand this topic.

@Raoul don't be upset with Masi, he is notoriously finicky... he once down voted a 1 page length answer I posted (which in ym opinion was very good) because it didn't please him... Masi simply wants to learn more and sometimes it's hard to say what he wants to learn... though his questions may be off beat and poorly worded I still feel there is a thread of insight, which always attracts me to them...

I think Masi's question was this: how is it possible for us to have a drug where the mechanism of the drug is to cause the opposite of what it actively does? the answer: to exhaust the receptor or maybe downregulation of receptors

@jasand well I'm not upset. It was just a remark. I'm not that eager for fame and reputation.

@jasand oh, and BTW both elements you cite are in my answer

I think he wanted to hear about SSRIs, Parkinson med cycling, extra pyramidal symptoms, etc... As I understand it tolerance can be more tricky... Thats it


text:
Why are melodies/harmonies perceived as pleasurable by humans?
Is there any evolutionary advantage to finding melodies or harmonies pleasurable? Does the ear pick up these particular oscillating waves differently from other sounds, and if so, how does that affect our perception of pleasure? I'm looking for some sort of signalling pathway (most likely involving neurotransmitters I realize).

Why was this asked on Biology and not [cogsci.se]?

There are strong connections between the auditory cortex and the limbic system, which includes such structures as the hippocampus and the amygdala.
A recent paper [1] builds on earlier notions of emotional "significance" of music without any lyrics.  It adds in lyrics, so giving a perspective of which portions of the brain are reacting to which component of the music.

Additionally, contrasts between sad music with versus without lyrics recruited the parahippocampal gyrus, the amygdala, the claustrum, the putamen, the precentral gyrus, the medial and inferior frontal gyri (including Broca’s area), and the auditory cortex, while the reverse contrast produced no activations. Happy music without lyrics activated structures of the limbic system and the right pars opercularis of the inferior frontal gyrus, whereas auditory regions alone responded to happy music with lyrics.

One of the limitations of this particular study is that the subjects self-selected their own pieces, which may limit the reliability of the results.  Of course, defining "happy" or "sad" for every individual is slightly subjective and difficult.  They cited an earlier "pioneering" study which standardized the musical selection between subjects.  Without consideration of the lyrics:

The first pioneer study using functional magnetic resonance imaging (fMRI) by Khalfa et al. (2005) chose a controlled manipulation of two musical features (tempo and mode) to vary the happy or sad emotional connotations of 34 instrumental pieces of classical music, lasting 10s each. Sad pieces in minor-mode contrasted with happy pieces in major mode produced activations in the left medial frontal gyrus (BA 10) and the adjacent superior frontal gyrus (BA 9). These regions have been associated with emotional experiences, introspection, and self-referential evaluation (Jacobsen et al., 2006; Kornysheva et al., 2010).

As an aside to answer your final thought, in cases like this I think trying to jam everything under an umbrella of one "neurotransmitter system" or another can make things overly simplistic to the point where you lose focus of the diversity of receptors expressed.  You can say a system is driven by Dopamine, but D1 and D2 receptors have exactly the opposite effects on the neuron.

[1] Brattico, E., Alluri, V., et al (2011) A functional MRI study of happy and sad emotions in music with and without lyrics.  Frontiers in Psychology, 2: 308.  doi: 10.3389/fpsyg.2011.00308 (free pdf)

(see also, http://www.sciencedirect.com/science/article/pii/S0028393206003083 and related)

In music, harmonies are simultaneous combination of tones or chords that are concordant.
In physics, each note is actually a vibration with defined wavelenght, the concordance can be explained in mathemathical terms, for instance with regard to coincidence of phase oscillation.
In physiology, the ear perceives air vibrations and send them to the brain by means of trains of pulses.
According to some scientists, a music providing regular train of pulses (like harmonic music and rhytmic music) should be more pleasing, probably because of stimulation of the limbic system, as the other answer explains.
Source: Ushakow et al. 2011, Physical Review Letters, DOI 10.1103/PhysRevLett.107.108103
Lay explanation: Why harmony pleases the brain, New Scientist, Sept 2011


text:
How can I predict DNA binding affinities from a protein sequence?
Are there any computational tools to predict the binding affinity to specific DNA motifs from protein domain sequence information?

Those that come up from a Google search ("predict DNA binding from protein domain tool") seem pretty well suited to your question.

BindN
DNAbinder

Depending on your computational/statistical know-how you might also find these papers relevant

Huang et al, Predicting and analyzing DNA-binding domains using a systematic approach to identifying a set of informative physicochemical and biochemical properties
Gao et al, A threading-based method for the prediction of DNA-binding proteins with application to the human genome

The OP is not asking to find which residues interact with DNA, but which DNA motifs are preferred by a given binding protein.


text:
All or nothing phenomena
We know that an action potential is produced by an active cell membrane when the stimulus reaches a certain threshold. When it does, an action potential fires, and when it doesn't, nothing happens.
There are dozens of videos online painstakingly illustrating this point, using examples going from plumbing to pebbles falling down a paper towel.
But this is such a simple idea. There doesn't need to be analogies. When I push a button, something moves, when I don't push it, nothing moves.
But what is the fundamental principle behind this? What biochemical device causes this all or nothing phenomena?

The fundamental principle behind this is a "sensor" or the excitation-contraction coupling, regardless where you are.
Let's consider the striated muscle and the cardiac muscle.
The function of excitation-contraction coupling in skeletal muscle is as voltage sensor to tell the SR, "We have got an action potential; release Ca2+ for contraction".
This is a contrast to a heart muscle which works like a Ca2+ channel (i.e. Ca2+ is flowing in cardiac muscle continuously).
Similarly, xcitation-contraction coupling in cardiac muscle translates the action potential into the production of tension.
There are individual steps in this process of cardiac muscle:

The cardiac action potential is initiated in the myocardial cell membrane, and the depolarization spreads to the interior of the cell via the T tubules.
Recall that a unique feature of the cardiac action potential is its plateau (phase 2), which results from an increase in Ca and an inward Ca2+ current in which Ca2+ flows through L-type Ca2+ channels (dihydropyridine receptors) from extracellular fluid (ECF) to intracellular fluid (ICF).

Entry of Ca2+ into the myocardial cell produces an increase in intracellular Ca2+ concentration.
This increase in intracellular Ca2+ concentration is not sufficient alone to initiate contraction, but it triggers the release of more Ca2+ from stores in the sarcoplasmic reticulum through Ca2+ release channels (ryanodine receptors).
This process is called Ca2+- induced Ca2+ release, and the Ca2+ that enters during the plateau of the action potential is called the trigger Ca2+.
Two factors determine how much Ca2+ is released from the sarcoplasmic reticulum in this step: the amount of Ca2+ previously stored and the size of the inward Ca2+ current during the plateau of the action potential.

and 4. Ca2+ release from the sarcoplasmic reticulum causes the intracellular Ca2+ concentration to increase even further.
Ca2+ now binds to troponin C, tropomyosin is moved out of the way, and the interaction of actin and myosin can occur.
Actin and myosin bind, cross-bridges form and then break, the thin and thick filaments move past each other, and tension is produced.
Cross-bridge cycling continues as long as intracellular Ca2+ concentration is high enough to occupy the Ca2+-binding sites on troponin C.

A critically important concept is that the magnitude of the tension developed by myocardial cells is proportional to the intracellular Ca2+ concentration.
Therefore, it is reasonable that hormones, neurotransmitters, and drugs that alter the inward Ca2+ current during the action potential plateau or that alter sarcoplasmic reticulum Ca2+ stores would be expected to change the amount of tension produced by myocardial cells.

I like this figure about the topic in summarising stimuli in the smooth muscle:

In heart

In the gastrointestinal tract, we have then again special cells, Cajal cells, that work as "pacemakers" of the GI tract.
Myenteric Interstitial cells of Cajal [ICC-MY] serve as a pacemaker which creates the bioelectrical slow wave potential that leads to contraction of the smooth muscle.
This activity differs along the length of the system

3 per minute in the stomach
11-12 per minute in the duodenum
9-10 per minute in the ileum
3-4 per minute in the colon

You can see them as to work analogously through the "all-or-none" principle.
Sources

Costanzo, Physiology
Pocock, Physiology
My notes during during years 2011-2014 (in three Physiology courses and research)


text:
Will an 11W UVC lamp kill bacteria?
If I shone a UVC lamp (11W) on something (say for example a plastic phone case) for an hour, would that kill off a noticeable amount of bacteria? That is, if I were to go over the case with a cotton swab before the hour and swipe the cotton swab over a petri dish with nutrients and if I were to do the same after the hour with a different cotton swab and a different petri dish. Do you think that after a week there would be a noticeable difference in bacterial growth between the dishes? I think it should, since some filters for ponds work the same way, but I'm not sure, since in my case, the light needs to penetrate about 10 inches of air first and the environment isn't as closed off. What are your ideas on this?

I think you should add distance parameter to it because it has inverse relation with any rays that use for such uses

Some physical methods of sterilisation are in hospitals

Steam autoclaving
Dry heat – thermostat
White light / UV light sterilization

where continuous UV light has poor penetration.
UV radiation heat is absorbed by proteins and nucleic acid.
All micro-organisms contain tehm.
They inactivate the DNA.
There will be electronic and photochemical reactions by

photolysis
loss of colony-forming ability
enzyme inactivation
destruction of nucleic acid.

If I shone a UVC lamp (11W) on something (say for example a plastic
  phone case) for an hour, would that kill off a noticeable amount of
  bacteria?

Direct answer: Not all bacteria, but some.
UV light has poor penetration so it will not expose all bacteria.
Most prevalent bacteria there

streptococci,
staphylococci and
some others.

I estimate that the majority of the bacteria will remain because the light cannot reach each corner of the object.
In clinics, many hours and high temperatures are used to kill bacteria.
UV light is not efficient there.
I think the problem is that you cannot reach each corner of the object.
The high temperature and disinfectants can then again reach the clinical instruments throughly.
Manual work is however still needed.
You can then take examples of bacteria.
Search their corresponding temperature ranges.
The survival can also be dependent on the nature of the light of the bulb.
Each bacteria has an individual structure.
We can manipulate the environment to make bacteria more vulnerable to the heating i.e. to change the structure of the bacteria.
We can increase the duration of the heat exposure to make kill of the bacteria more effective.