text:
Free Version
Moderate

# Average Speed: With and Without Breaks

ACTMAT-GVJIKJ

The following graph depicts miles walked by Scott over a period of 12 hours, including breaks:

Scott calculated his average speed, both with and without his breaks.

Approximately how much faster was Scott’s average speed when he did not include his breaks, in miles per hour?

A

$0.21$

B

$0.48$

C

$0.36$

D

$5.17$

E

$4.33$


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# How can I prevent PrintWriter from printing a blank line at the beginning of each file?

I'm trying to write a couple of methods to save a binary tree to a file. They work correctly, except for a slight problem. The problem is that a blank line is inserted at the beginning of each file that's created. Why is PrintWriter doing this, and how can I prevent it from happening?

Here's my code:

import java.io.*;

void callSaveGame(String fileName) throws IOException {
PrintWriter out = new PrintWriter(new FileWriter("X:\\path\\to\\save\\directory\\" + fileName)); // associate PrintWriter with file

saveGame(root, out);

out.close();
}

void saveGame(Node current, PrintWriter out) {
if (current != null) {
out.println(current.getData()); // print node to file

saveGame(current.getLChild(), out); // call for left child(ren)

saveGame(current.getRChild(), out); // call for right child(ren)
}
}

-

It is not PrintWriter that is inserting the blank line. PrintWriter won't do that.
The actual cause of the problem is not shown in the code snippet you provided, but if the code is an accurate reflection of your real application, then the offending blank line is already in the result of the first getData() call.

format: plain


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Address 545 Mutts Rd, Sayre, PA 18840 (570) 882-8851

# error propagation division equation Lockwood, New York

This ratio is called the fractional error. These instruments each have different variability in their measurements. as follows: The standard deviation equation can be rewritten as the variance ($$\sigma_x^2$$) of $$x$$: $\dfrac{\sum{(dx_i)^2}}{N-1}=\dfrac{\sum{(x_i-\bar{x})^2}}{N-1}=\sigma^2_x\tag{8}$ Rewriting Equation 7 using the statistical relationship created yields the Exact Formula for Propagation of All rules that we have stated above are actually special cases of this last rule.

A. (1973). Now consider multiplication: R = AB. They do not fully account for the tendency of error terms associated with independent errors to offset each other. So the fractional error in the numerator of Eq. 11 is, by the product rule: [3-12] f2 + fs = fs since f2 = 0.

Keith (2002), Data Reduction and Error Analysis for the Physical Sciences (3rd ed.), McGraw-Hill, ISBN0-07-119926-8 Meyer, Stuart L. (1975), Data Analysis for Scientists and Engineers, Wiley, ISBN0-471-59995-6 Taylor, J. Mathematically, if q is the product of x, y, and z, then the uncertainty of q can be found using: Since division is simply multiplication by the inverse of a number, Also, if indeterminate errors in different measurements are independent of each other, their signs have a tendency offset each other when the quantities are combined through mathematical operations. The derivative with respect to t is dv/dt = -x/t2.

External links A detailed discussion of measurements and the propagation of uncertainty explaining the benefits of using error propagation formulas and Monte Carlo simulations instead of simple significance arithmetic Uncertainties and Introduction Every measurement has an air of uncertainty about it, and not all uncertainties are equal. The error propagation methods presented in this guide are a set of general rules that will be consistently used for all levels of physics classes in this department. They are, in fact, somewhat arbitrary, but do give realistic estimates which are easy to calculate.

Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. In Eqs. 3-13 through 3-16 we must change the minus sign to a plus sign: [3-17] f + 2 f = f s t g [3-18] Δg = g f = When a quantity Q is raised to a power, P, the relative error in the result is P times the relative error in Q. General functions And finally, we can express the uncertainty in R for general functions of one or mor eobservables.

doi:10.1007/s00158-008-0234-7. ^ Hayya, Jack; Armstrong, Donald; Gressis, Nicolas (July 1975). "A Note on the Ratio of Two Normally Distributed Variables". For example, a body falling straight downward in the absence of frictional forces is said to obey the law: [3-9] 1 2 s = v t + — a t o If R is a function of X and Y, written as R(X,Y), then the uncertainty in R is obtained by taking the partial derivatives of R with repsect to each variable, Contributors http://www.itl.nist.gov/div898/handb...ion5/mpc55.htm Jarred Caldwell (UC Davis), Alex Vahidsafa (UC Davis) Back to top Significant Digits Significant Figures Recommended articles There are no recommended articles.

p.2. Then σ f 2 ≈ b 2 σ a 2 + a 2 σ b 2 + 2 a b σ a b {\displaystyle \sigma _{f}^{2}\approx b^{2}\sigma _{a}^{2}+a^{2}\sigma _{b}^{2}+2ab\,\sigma _{ab}} or For example, lets say we are using a UV-Vis Spectrophotometer to determine the molar absorptivity of a molecule via Beer's Law: A = ε l c. We'd have achieved the elusive "true" value! 3.11 EXERCISES (3.13) Derive an expression for the fractional and absolute error in an average of n measurements of a quantity Q when

What is the average velocity and the error in the average velocity? Such an equation can always be cast into standard form in which each error source appears in only one term. Therefore the fractional error in the numerator is 1.0/36 = 0.028. To fix this problem we square the uncertainties (which will always give a positive value) before we add them, and then take the square root of the sum.

The previous rules are modified by replacing "sum of" with "square root of the sum of the squares of." Instead of summing, we "sum in quadrature." This modification is used only Uncertainty, in calculus, is defined as: (dx/x)=(∆x/x)= uncertainty Example 3 Let's look at the example of the radius of an object again. The average values of s and t will be used to calculate g, using the rearranged equation: [3-11] 2s g = —— 2 t The experimenter used data consisting of measurements We will treat each case separately: Addition of measured quantities If you have measured values for the quantities X, Y, and Z, with uncertainties dX, dY, and dZ, and your final

And again please note that for the purpose of error calculation there is no difference between multiplication and division. Since the uncertainty has only one decimal place, then the velocity must now be expressed with one decimal place as well. The result is most simply expressed using summation notation, designating each measurement by Qi and its fractional error by fi. © 1996, 2004 by Donald E. Pearson: Boston, 2011,2004,2000.

In problems, the uncertainty is usually given as a percent. It will be interesting to see how this additional uncertainty will affect the result! In both cases, the variance is a simple function of the mean.[9] Therefore, the variance has to be considered in a principal value sense if p − μ {\displaystyle p-\mu } The absolute error in g is: [3-14] Δg = g fg = g (fs - 2 ft) Equations like 3-11 and 3-13 are called determinate error equations, since we used the

That is easy to obtain. Retrieved 2016-04-04. ^ "Propagation of Uncertainty through Mathematical Operations" (PDF). Retrieved 2013-01-18. ^ a b Harris, Daniel C. (2003), Quantitative chemical analysis (6th ed.), Macmillan, p.56, ISBN0-7167-4464-3 ^ "Error Propagation tutorial" (PDF). The system returned: (22) Invalid argument The remote host or network may be down.

Correlation can arise from two different sources. A one half degree error in an angle of 90Â° would give an error of only 0.00004 in the sine. For example, if you have a measurement that looks like this: m = 20.4 kg Â±0.2 kg Thenq = 20.4 kg and Î´m = 0.2 kg First Step: Make sure that The end result desired is $$x$$, so that $$x$$ is dependent on a, b, and c.

Therefore we can throw out the term (ΔA)(ΔB), since we are interested only in error estimates to one or two significant figures. In a probabilistic approach, the function f must usually be linearized by approximation to a first-order Taylor series expansion, though in some cases, exact formulas can be derived that do not This makes it less likely that the errors in results will be as large as predicted by the maximum-error rules. Hint: Take the quotient of (A + ΔA) and (B - ΔB) to find the fractional error in A/B.

Given the measured variables with uncertainties, I Â± ÏƒI and V Â± ÏƒV, and neglecting their possible correlation, the uncertainty in the computed quantity, ÏƒR is σ R ≈ σ V


text:
### Weekly Challenge 43: A Close Match

Can you massage the parameters of these curves to make them match as closely as possible?

### Weekly Challenge 44: Prime Counter

A weekly challenge concerning prime numbers.

### Weekly Challenge 28: the Right Volume

Can you rotate a curve to make a volume of 1?

# Weekly Challenge 37: Magic Bag

##### Stage: 5 Challenge Level:

A magic bag contains some black and white balls, all of the same size and shape.

I put my hands in the bag and simultaneously and randomly pull out two balls. They are both the same colour and the magic bag tells me that the chance of this occurring was exactly $0.5$.

I wonder to myself how this condition constrains the numbers of black and white balls.

At the same time, the bag, who can read minds, says "I'll give you a hint: it's got something nice to do with triangle numbers."

Did you know ... ?

Probability theory has many overlaps with the study of combinatorics. Is it fascinating how beautiful and tricky the consequences of counting become!


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### Part 3: Light-controlled cell biology (revisited)

Your cells are constantly being shed and replaced—so is your body ever completely refreshed? Does anything remain of the body that existed on Jan. 1, 2017? 2007? The day you were born? (video)

Out of Order: Undaunted

…as I prepared for this issue’s Special Report on Microbiomics (starting on page 19), I am stunned by what I am only starting to understand. That our individual existence as humans may only be 10 percent of what we see in the mirror—and that perhaps only 1 percent of our personal ecological genome is a human genome…

When you understand the concept of biophysically constrained energy-dependent ecology (Frohlich, 1968), you may begin to understand the difference between ecological adaptation and evolution. Each cell type represents biophysically constrained viral latency, not mutation-driven evolution.

Outside the context of energy-dependent RNA-mediated DNA repair (aka autophagy), no cell types exist. Bacteria become archaea and archaea become L-forms and the L-forms become non-cells. The energy for cell type differentiation comes from sunlight or from food. It is biophysically constrained by the pheromone-controlled physiology of reproduction in species from microbes to humans.

Theorists used the term “de novo” in the context of de novo transcription and other aspects of energy-dependent cell type differentiation that they cannot explain with their ridiculous theories. For instance, David Sinclair has touted pseudoscientific nonsense until now.

He knows that the cell biology game, “Cytosis” for ages 10+ has exposed him to ridicule, and obviously won’t go away without a fight to maintain some scientific credibility.

State of art:
TDP-43 and FUS, two RNA-binding proteins (RBPs), have been recently the subject of increased attention due to their role in Amyotrophic Lateral Sclerosis (ALS) and FrontoTemporal Lobar Degeneration (FTLD). In non-pathological conditions, these proteins are mostly found in the nucleus where they participate to mRNA biogenesis and regulation of alternative splicing. However, TDP-43 and FUS are also present in the cytoplasm and they are able to shuttle from one compartment to another. TDP-43 and FUS notably participate in cytoplasmic functions such as mRNA transport and localized translation, which are of critical importance for neuron physiology. In neurons of ALS and FTLD patients, TDP-43 and FUS form insoluble cytoplasmic aggregates with fibrillar structure that can further spread the disease to other areas of the brain.

If this is the state of the art, was the information used to treat the late Stephen Hawking, or was he left to suffer unnecessarily until he died?

Neo-Darwinian theorists and Big Bang cosmologists seem to have no sense of pattern recognition in the context of Olfaction Warps Visual Time Perception

See for comparison: What Stephen Hawking’s Final Paper Says (And Doesn’t Say)

The claims in “Olfaction Warps Visual Time Perception” link the sense of smell in bacteria to our visual perception of energy and mass in the context of the space time continuum and biophysically constrained viral latency. Everything known to Hawking’s co-authors Roger Penrose and George FR Ellis has since been linked from what organisms eat to the physiology of reproduction via the creation of sunlight and biomolecules.

The difference between Hawking’s ridiculous theories and biologically-based facts will place the claims about his intelligence and insight into the historical context of how celebrity scientists have led to our unnecessary suffering and premature death. It’s ironic that Hawking could have been effectively treated with food energy-dependent microRNAs, but instead got stuck with a useless theoretical approach to life. I would not want that to happen to my children or grandchildren (if I had any). What are your children being taught to believe in: theories or experimentally established facts?.

### Thinking about energy is not radical re-thinking

The brain: a radical rethink is needed to understand it

…Optogenetics, a technique that uses genetic modification of neurons so that their electrical activity can be controlled with light pulses – can help us to explore their specific contribution to brain function.

Optogenetics links the speed of light on contact with water to what is known about all energy-dependent cell type differentiation in all individuals of all living genera. Serious scientists, for example, have linked angstroms to ecosystems in all living genera because they know that brain function is experience-dependent and RNA-mediated.

Even in organisms that have no brain, cell type differentiation occurs in the context of biophysically constrained RNA-mediated protein folding chemistry. All chemistry is energy-dependent quantum chemistry and chemistry links quantum physics from the de novo creation of G protein-coupled receptors to the biological basis for all biodiversity on Earth.
For example, food odors link natural selection for energy-dependent codon optimality to the metabolism of food to pheromones. Biophysically constrained RNA-mediated feedback loops link the metabolism of food from the physiology of reproduction to supercoiled DNA, which protects all organized genomes from virus-driven entropy.
Simply put, quantum physics, quantum chemistry, and energy-dependent quantum biology prevent virus-driven entropy, which links everything known to serious scientists about niche construction to consciousness.
The Penrose Institute was established to link that fact to human consciousness in the context of everything known about cell type differentiation to everyone since the time that Lewis Thomas began making claims olfaction and smell.
A Fear of Pheromones (1971)
On Smell (1980)

The act of smelling is remarkably like the act of thinking itself.

I should think we might fairly gauge the future of biological science, centuries ahead by estimating the time it will take to reach a complete comprehensive understanding of odor. It may not seem a profound enough problem to dominate all the life sciences, but it contains, piece by piece, all the mysteries.  —  as cited in The Scent of Eros: Mysteries of Odor in Human Sexuality

In 1991, Roger Penrose, summarized what was known about all the mysteries in his forward to the reprint of Schrodinger’s “What is Life?”

How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?

For comparison, see this comment by “Sonny” Williams to the International Society for Human Ethology’s yahoo group:

The empirical evidence is overwhelming that the brain is composed of highly specialized regions, whose neuronal members are unique in their cytoarchitecture (down to the molecular level).  Moreover, empirical evidence reveals that genes have directed these neural variations during corticogenesis; that is, most specialized neurons are differentiated early during development and directed to their place in the brain by intrinsic cues, and not activity-dependent cues.  This fact does not preclude later “rewiring,” or changes that are activity-dependent (plasticity), but this range of plasticity is constrained by the genetically derived regions.

Thus, the metaphor that the brain is “modular” is as accurate as any other metaphor.  HOWEVER, “modular” and functionally specialized regions has always included the fact that functional outcomes require a widely distributed network of specialized regions.  That is, modules do not exist in isolation, as islands of specialized function, but rather there existence as a specialized region is predicated upon their iterative communication with many other equally specialized regions.

I cannot recall any comment by Clarence “Sonny” Williams that might ever have made sense to a serious scientist. He is, in my opinion, a biologically uninformed science idiot. I once wondered who could have taught anyone to believe what biologically uninformed people believe in, or why they think what they were taught makes sense to serious scientists.
Then, I tried to discuss what I know about the energy-dependent links from angstroms to ecosystems in all living genera with the senior author of Complex Spike Patterns in Olfactory Bulb Neuronal Networks by Alister U Nicol, Anne Segonds-Pinchon, and Magnus S. Magnussen. It was also published as a book chapter in Discovering Hidden Temporal Patterns in Behavior and Interaction: T-Pattern Detection and Analysis with THEME™
Background:

T-pattern analysis is a procedure developed for detecting non-randomly recurring hierarchical and multiordinal real-time sequential patterns (T-patterns).

CONCLUSIONS:

We conclude that such sequences are an important physiological property of the neural system studied, and suggest that they may form a basis for encoding sensory information.

My summary: They link everything known to serious scientists about energy as information to non-randomly recurring patterns of biophysically constrained RNA-mediated protein folding chemistry and “…characterize these patterns in light of their putative role in processing sensory information.”
They ignore the fact that sunlight is the anti-entropic virucidal source of the energy that prevents genomic entropy via the pheromone-controlled physiology of reproduction in all living genera.
Apparently, like other biologically uninformed theorists, they did not realize what Dobzhansky (1973) did when he linked the light of evolution to all biophysically constrained biodiversity via the nutrient energy-dependent pheromone-controlled physiology of reproduction.
Dobzhansky was one of the first self-declared Creationists to level the playing field with his joke about evolution as if it occurred over billions of years.

I am a creationist and an evolutionist. Evolution is God’s, or Nature’s, method of Creation. Creation is not an event that happened in 4004 B.C.; it is a process that began some 10 billion years ago and is still under way.

Anyone who followed Dobzhansky’s works probably got the joke. He knew there was experimental evidence of God’s Creation. For example, he linked sensory input from what organisms eat and their physiology of reproduction to amino acid substitutions that differentiate all cell types in all living genera. He also knew that theorists had not found experimental evidence of biologically-based cause and effect that supported their claims about millions to billions of years of evolution.
All serious scientists were made aware of Dobzhansky’s rabbinical form of debate in 1964. He began by referring to theorists as bird-watchers and butterfly collectors.  A rather well known form of rabbinical begins with: “Thou fool….”
Dobzhansky was far less damning when he started his address with this:

The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists! I have heard a man whose official title happens to be Professor of Zoology declare to an assembly of his colleagues that “a good man cannot teach zoology. A good man can teach, of course, only molecular biology.

Dobzhansky probably was referring to himself in the third person when he made the claim about the unidentified Professor of Zoology. Still, to avoid ridicule by biologically uninformed theorists, he tempered the claim.

Such pronunciamentos can be dismissed as merely ridiculous. They are, however, caricatures of opinions entertained by some intelligent and reasonable people, whose views deserve an honest and careful consideration and analysis. Science must cope with new problems that arise and devise new approaches to old problems. Some lines of research become less profitable and less exciting and others more so.

Clearly, Dobzhansky knew that his claims about amino acid substitutions would be accepted by serious scientists and rejected by pseudoscientists, who have continued to reject the claims of all serious scientists. That’s what pseudoscientists have always done.
See for instance:

3/09/17 Jay Feierman: One can’t have Darwinian evolution by natural selection without either “random” mutations or directional selection. They are both necessary, proximate, contributing causes for genes and the proteins they code for changing in frequency over time in a population and by which the population becomes adaptively configured to the current environment.

3/17/17 Jay R. Feierman [NEW]: We are adaptively configured to the current environment because we are the most successful mammal on earth by any measure. There are 7 billion of us and we inhabit every continent on earth. We accomplished this by Darwinian natural selection adaptively influencing the structural design features we call genes and the proteins they make as well as the extra-genetic structural design features developed through our creativity and ingenuity where we pass the instructions on how to make them across generations by social learning. An iPhone is an example today and an obsidian arrow head was an example in the past.

My comment:  After attempts to discuss energy-dependent biophysically constrained RNA-mediated cause and effect with Magnus S. Magnusson, I was not surprised to find support for some of Feierman’s claims about human adaptations in:

Complex spike patterns in olfactory bulb neuronal networks

Indeed, adaptations occur. But, in the same article, they failed to support Feierman’s claims that the adaptations randomly occur.

Abstract excerpt:

BACKGROUND:

T-pattern analysis is a procedure developed for detecting non-randomly recurring hierarchical and multiordinal real-time sequential patterns (T-patterns).

Conclusion: We conclude that such sequences are an important physiological property of the neural system studied, and suggest that they may form a basis for encoding sensory information.

My conclusion: People like Jay R. Feierman should try to support their assertions about adaptations with experimental evidence of biologically-based cause and effect like the evidence that was cited in the article linked above.

Any claims about how a population becomes adaptively configured to the current environment are not true outside the context of what is known about energy as information and biophysically constrained RNA-mediated protein folding chemistry. If those ridiculous claims were true, the experimental evidence of top-down causation that theorists think support the claims could be used to convince serious scientists that something besides natural selection for energy-dependent codon optimality and the physiology of pheromone-controlled reproduction could replace facts to support theories about mutation-driven evolution.

### Allen Institute confirms food energy is information

See also: Theistic evolutionists fight back and lose
Excerpt: Predictably, Paul Allen will be the next to start funding works that might help to prevent the viral apocalypse, now that Bill Gates is mentally prepared to do so.

### Allen Institute FB page

3/3/17 Fascinating new research on stem cell division
Scientists discover an unexpected influence [of food] on dividing stem cells’ fate

One particular protein, Pex11b, caught her attention. It is associated with the membrane that surrounds the peroxisome, an organelle that helps to free energy from food.

“While some evidence already suggested the distribution of organelles, including energy-producing mitochondria, can influence the outcome of cell division, we have shown for the first time that this phenomenon is essential to the proper behavior of and formation of the tissue,” says Fuchs, who is also a Howard Hughes Medical Institute Investigator.

This unexpected influence of food energy on endogenous RNA interference and cell type differentiation in skin cells from mice was first reported one month ago. However, the influence of food on the survival of all species is known to all serious scientists.

For example, see Schrodinger (1944). He linked the anti-entropic energy of sunlight from all energy-dependent biophysically constrained viral latency to healthy longevity before Roger Penrose (1991) mentioned this in his forward to the reprint edition:

How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?

In 1991, Penrose reduced the systems complexity of biophysically constrained top-down energy-dependent viral latency to the question of where the energy in a hydrogen atom comes from.comes from. Schrodinger suggested it came from sunlight in an attempt to stop the pseudoscientific nonsense about mutations that was touted after de Vries defined “mutation” in 1902. So far, no experimental evidence of biologically-based cause and effect has limited the claims about mutations and evolution that are made by biologically uninformed theorists.

See for comparison:

A mystery concerning the structure of protons is a step closer to being solved, thanks to a seven-year experiment led by researchers at MIT. Credit: Christine Daniloff/MIT

The resulting values of R2γ, presented here for a wide range of virtual photon polarization 0.456<ε<0.978, are smaller than some hadronic two-photon exchange calculations predict, but are in reasonable agreement with a subtracted dispersion model and a phenomenological fit to the form factor data.

The phenomenological fit links the claims of Schrodinger and concerns of Penrose to this report on the Lepton-Proton Scattering. The title includes the joke about the link from sunlight to evolution that Dobzansky (1973) reported as: Nothing in Biology Makes Any Sense Except in the Light of Evolution. Dobzhansky’s clever creationist attack on neo-Darwinian theorists, who failed to link the creation of the sun to all biologically-based cause and effect went virtually unnoticed despite his claim:

I am a creationist and an evolutionist. Evolution is God’s, or Nature’s, method of Creation.

No experimental evidence of biologically-based cause and effect links Dobzhansky’s claims about amino acid substitutions to evolution. For contrast, all claims made by other serious scientists link sunlight to energy-dependent changes in angstroms to ecosystems in all living genera.

The two-photon contribution to the structure of protons and the biophysically constrained functional structure of supercoiled DNA was reported as:

OLYMPUS experiment sheds light on structure of protons

…experiments had previously led researchers to assume that the electric and magnetic charge distributions are the same, and that one photon—an elementary particle of light—is exchanged when the protons interact with the bombarding electrons.

…two photons are indeed exchanged during electron-proton interactions.

However, unlike the theoretical predictions, analysis of the OLYMPUS measurements suggests that, most of the time, only one of the photons has high energy, while the other must carry very little energy indeed…

Natural selection for the higher energy photon is the most likely link from the anti-entropic effects of sunlight to energy-dependent codon optimality and cell type differentiation in all living genera via the physiology of pheromone-controlled reproduction and endogenous RNA interference.
The links from higher energy photons to energy-dependent changes in chirality and autophagy extend what is known about RNA-mediated DNA repair. The molecular mechanisms of DNA repair helped to establish sunlight as the energy source for hydrogen-atom transfer in DNA base pairs in solution. The most recent report on one carbon metabolism also extends what is known about subatomic particles to the creation of the energy in hydrogen atoms and differences in the structure of teeth.
See: Evidence for dietary change but not landscape use in South African early hominins (2012)
Reported as: Millions of years of evolutionary history recorded in teeth (March 3, 2017)
The nonsense about the evolutionary history was refuted in 2013. See: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes
A change in diet was linked to differences in C. elegans and a predatory nematode with teeth. They claimed that the differences emerged during 200 million years, but no experimental evidence of biologically-based cause and effect has ever supported such ridiculous claims.
Subatomic Particles, Part 1: Leptons
Subatomic Particles, Part 2: Baryons, the Substance of the Cosmos
Subatomic Particles, Part 3: Mesons
See also: Feedback loops link odor and pheromone signaling with reproduction

Please place the feedback loops into the context of how PCR applications are linked to what is known about cell type differentiation via virus-driven degradation of messenger RNA (mRNA), or linked by nutrient energy-dependent endogenous RNA interference to healthy longevity.

A snapshot of the most common PCR application

1) “Another possible application: looking for an RNA target, either viral or an endogenous mRNA.”
2) “…the IC [internal control] should be RNA to reflect the desired sample type.”
3) Conclusion: An understanding of the overall method workflow and some of the possible causes of false positive or negative results is thus beneficial in appropriately interpreting test results in the full clinical context.The light energy as information-induced de novo creation of RNA, protein, and lipid precursors links the common origin of amino acids to cell type differentiation in all living genera via endogenous RNA interference and the physiology of reproduction, which links supercoiled DNA to chromosomal inheritance.
See: Common origins of RNA, protein and lipid precursors in a cyanosulfidic protometabolism
John Brunstein indirectly suggests that supercoiled DNA prevents mutation-driven evolution. Unless the mutations can be linked from amino acid substitutions to pathology, he also seems to also be suggesting that neo-Darwinian theories are sources of errors.  Researchers are virtually guaranteed to fail, if they start with theories and try to link the possible causes of energy-dependent  false positive or negative results from the National Microbiome Initiative cell type differentiation in the context of the Precision Medicine Initiative.
I hope that someone like John Brunstein will comment on facts about the degradation of messenger RNA (mRNA). For example, virus-driven energy theft appears to link mRNA degradation to all pathology.  If he does not agree, I hope he knows of an alternative model that links energy-dependent RNA-mediated amino acid substitutions to all healthy longevity and something else to all pathology.
In any case,  I believe it is past time to eliminate neo-Darwinian theories, which link beneficial mutations to the stability of organized genomes in all living genera, but link amino acid substitutions to the stability of viruses.
See: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

Watch Jason Silva tell you about the importance of fire in an attempt to link the pseudoscientific nonsense touted by theorists to survival of all species except those that do not need to eat. Those species must have emerged and automagically evolved to become people like Jason Silva who can tell others how that happened, but won’t.

He can tell others about the importance of fire. Watch as everyone else in the world starts to link energy-dependent endogenous RNA interference to biophysically constrained gene activation and link virus-driven energy theft to all pathology during the cell type differentiation of all species from microbes to humans.

See for example: Services – QuantSeq 3’ mRNA-Seq Libraries

Lexogen provides a fully integrated service-workflow for generation of QuantSeq 3’ mRNA-Seq libraries, multiplexed sequencing, and data analysis. QuantSeq libraries are produced from total RNA to yield Illumina-compatible sequences close to the 3’ end of polyadenylated RNA.

Then wait for someone to tell you more about the importance of fire.

See also this video representation of the link from sunlight to biodiversity in marine life.
Alternatively, place everything known about energy-dependent RNA-mediated cell type differentiation back into the context of “Nature.”
See: Nature Fights Back Against Gene Editing
Then, stop calling it “Nature” and learn what serious scientists already know about the energy-dependent links from angstroms to ecosystems in all living genera. If not, now that the Allen Institute has linked food energy as information to brain development, you will be asked to tell others how “Nature” created everything from subatomic particles to the hydrogen-atom energy. Then, the next question will be about how the energy is transferred in DNA base pairs in solution to allow natural selection for energy-dependent codon optimality and the physiology of reproduction in all living genera.
See also: The Persistent Contributions of RNA to Eukaryotic Gen(om)e Architecture and Cellular Function
See also: A Revised Tree of Life
See also: A Chat with Leeuwenhoek Medalist Jeffery Errington

Suzan Mazur: Do viruses play a role in regulating L-form bacteria?

Jeffery Errington: That’s a good question. Of course, much of the research on bacteriophages has shown that they tend to bind to components of the cell wall, so certainly you’d anticipate that L-forms would be resistant to many forms of virus. But I don’t know if much work has been done on this.

Anyone who does not know how much experimental evidence links food energy to all biodiversity via the pheromone-controlled physiology of reproduction is not likely to know enough about anything that could be linked from bacteriophages to all pathology via the degradation of messenger RNA.

### Theistic evolutionists fight back and lose (3)

See also: Theistic evolutionists fight back and lose
See also: Theistic evolutionists fight back and lose (2)
For succinct representations of the claims made by people who are obviously biologically uninformed, see:

7/25/13
Jay R. Feierman: Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding [of] Darwinian biological evolution.
See for comparison:

7/26/13
Jay R. Feierman: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.
See for comparison:

See also: Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation (August 3, 2013)
Abstract excerpt:

Resurrected proteins reveal that ancestral uricases have steadily decreased in activity since the last common ancestor of mammals gave rise to descendent primate lineages. We were also able to determine the 3D distribution of amino acid replacements as they accumulated during evolutionary history…

The amino acid substitutions are not accumulated during evolutionary history. The substitutions link nutrient energy-dependent RNA-mediated top down causationk from ecological variation to ecological adaptation via the creation of heat shock proteins. The heat shock proteins “buffer” organized genomes to protect them from virus-driven energy theft and genomic entropy via the physiology of reproduction, which is controlled by pheromones in species from microbes to humans.
See also this discussion attempt: An epigenetics gold rush: new controls for gene expression
Sonny:

The other day, I read a new paper from a sociologist who wrote that epigenetics reveals that the environment is “more important than genes” in constructing the phenotype.  That is an egregiously misleading statement.

James Kohl

m6A is the link from energy-dependent changes in angstroms to ecosystems via learning and memory, which links ecological variation to ecological adaptation in the context of the physiology of pheromone-controlled reproduction.

Experience-Dependent Accumulation of N6-Methyladenosine in the Prefrontal Cortex Is Associated with Memory Processes in Mice

Excerpt: “The differential effects of m6A may depend on distinct cis-acting elements that are present on the RNA molecule which may interact with m6A, including micro-RNAs (Alarcón et al., 2015; Chen et al., 2015).” p. 6776

James Kohl: Ultimately, the biggest embarrassment to scientists who have linked energy-dependent changes from angstroms to ecosystems via chirality, autophagy, and supercoiled DNA is that other scientists start with the de novo creation of copy variants.

Sinclair et al., (January 25, 2017) Nucleic and amino acid sequences support structure-based viral classification

They conclude that no discussion of nutrient energy-dependent species-specific pheromone-controlled viral latency should allow others to challenge their claims about the energy-dependent RNA-mediated signals that link virus-driven energy theft to dysfunctional relationships among structure, amino acid sequence, and coding sequences.

They prefer that others, like Masatoshi Nei in “Mutation-driven evolution” (2013) place their claims into the context of how discussions about signaling between viruses and the supercoiled DNA of all organized genomes can be placed into the context of possible evolutionary relationships.

The evolutionary relationships do not link energy-dependent changes in chirality from autophagy via the innate immune system to endogenous RNA interference and all biodiversity on Earth.

Without the energy-dependent changes, the virucidal effects of femtosecond blasts of UV light on energy-dependent codon optimality and DNA repair cannot link the de novo creation of the energy in hydrogen atoms to the biophysically constrained coding sequence in all living genera via the physiology of reproduction.

See for comparison: Nutrient-dependent/pheromone-controlled adaptive evolution: a model and this presentation. Energy as information and constrained endogenous RNA interference

Keeping up-to-date with the primary literature just got a little easier

Today, Springer Nature is pleased to announce the launch of an innovative service which we believe will significantly improve the workflows of researchers by saving time and enabling access to the most relevant content, allowing users to access a new way to keep up to date without visiting any new websites.

Recommended is a service which we believe will help all primary researchers in the natural sciences keep up to date with the literature that really matters to them.  It is a personalised service that suggests relevant papers for users, regardless of publisher, based on what they have previously read across all Springer Nature services.

The “Nature Publications Group” banned me from commenting on their publications several months ago.
Comments on this news are disabled for everyone, which means the Nature Publications Group knows how to hide from any accountability for the lies they have told in the context of gene-centric theories.
See: The RNA code comes into focus Published online

The presence of an N1 methyl group on adenine bases in DNA and RNA was thought to be a form of damage. Results now show that it also occurs at specific sites in messenger RNAs, where it affects protein expression.

This nutrient energy-dependent methyl mark link RNA methylation from learning and memory to biophysically constrained RNA-directed DNA methylation, which is now represented in the context of endogenous RNA interference (RNAi). The link from the epigenetic landscape to RNAi and to the physical landscape of supercoiled DNA has repeatedly been placed into the context of via RNA-mediated protein folding chemistry and amino acid substitutions that differentiate all cell types in all living genera via the physiology of reproduction.
Typically, the physiology of reproduction prevents the transgenerational epigenetic inheritance of virus-driven pathology in all living genera — until the landscape changes to one in which energy-dependent RNA-mediated DNA repair can no longer keep up with the virus-driven energy theft.

## for the design and synthesis of molecular machines

Excerpt:

They have developed molecules with controllable movements, which can perform a task when energy is added.

My comment: When energy is added is the key to understanding healthy longevity in the context of popular information
Popular information (link opens pdf)
Excerpt:

All chemical systems strive for equilibrium – a lower energy state – but this is somewhat of a stalemate. We can take life as an example. When we eat, the body’s molecules extract the energy from the food and push our molecular systems away from equilibrium, to higher energy levels. The biomolecules then use the energy to drive the chemical reactions necessary for the body to work. If the body was in chemical equilibrium, we’d be dead.
Just like the molecules of life, Sauvage’s, Stoddart’s and Feringa’s artificial molecular sytems perform a controlled task. Chemistry has thus taken the first steps into a new world.

My comment: All steps that were designed to link energy as information to the physiology of reproduction and healthy longevity existed at the dawn of creation.  Chemistry finally links the differences between Old Earth Creationists (OEC) and Young Earth Creationists (YEC). The OEC appear to have assumed that the reaction times Schrodinger (1944) placed into the context of his claims in “What is Life?” occur across billions of years.
Excerpt:

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight.)

In that context the emergence of energy automagically linked the “Big Bang” to theories about all reaction times. The reaction times linked what organisms eat to natural selection for mutations. Theorists may still think that de Vries 1902 definition of ‘mutation’ links their assumptions to the evolution of all biodiversity.
In 1991, Roger Penrose succinctly addressed that problem with the theorists claims in the forward to the reprint edition of “What is Life?

How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?

My comment: The answer to that question was placed into the context of “…his discoveries of mechanisms for autophagy,” when Yoshinori Ohsumi won the 2016 Nobel Prize in Physiology or Medicine.
Virus-driven energy theft is the link to all negative outcomes in the context of autophagy. The nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to mammals is the link from RNA-mediated protein folding chemistry to all biophysically constrained limits on life.
Life exemplifies natural selection for codon optimality, which links RNA-mediated amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven entropy.  The virus-driven theft of quantised energy links changes in base pairs to amino acid substitutions in viruses that facilitate their energy dependent replication. Differences in their rate of replication can be compared to differences in rates of energy-dependent cell type differentiation and proliferation in all cell types of all individuals of all living genera.
That has already been done in the context of the Precision Medicine Initiative and National Microbiome Initiative, which link energy-dependent differences in metabolic networks to genetic networks via the pheromone-controlled physiology of reproduction in species from microbes to humans.  If the fine-tuned balance of life in all its diversity is not maintained by the proper use of available energy, nutrient-stress and/or social stress link energy-dependent viral latency to all pathology.
See: Epigenetics and Genetics of Viral Latency

… viral latency is responsible for life-long pathogenesis and mortality risk…

My comment: When the 2017 Nobel Prizes in the hard sciences are again awarded to those who are Combating Evolution to Fight Disease, which is what happened in 2015, how many more times will neo-Darwinian theorists and “Big Bang” cosmologists try to dumb-down the findings on how energy as information biophysically constrains cellular differentiation and proliferation in the context of ecological variation and energy-dependent ecological adaptations?

## Templeton grant funds evolution rethink

Excerpt:

The extended evolutionary synthesis is a term coined in 2007 to imply that the preeminent current evolutionary theory, the so-called modern synthesis, needed to broaden its focus because it concentrated too much on the role of genes in evolution and lacked adequate incorporation of new insights from development and other areas of biology.

My comment: That is an understatement! The problems with the so-called modern synthesis are perfectly clear:
1) [W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. Assumptions, made but not verified, were taught as fact.
2) The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis…
3) …evolutionary science has now “moved on to such an extent” that she and Peter Saunders don’t really care anymore about “trying to convince the neo-Darwinists.”
All serious scientists have since linked angstroms to ecosystems via what is known about the biophysically constrained chemistry of energy-dependent protein folding and links from the innate immune system to supercoiled DNA, which protects all organized genomes from virus-driven energy theft and entropy in the context of the physiology of reproduction.
See for example:

See also: Precision Medicine Program to Get $9.3M in NHLBI Funding for Omics Research One of the things they are asking for is: “Causal modeling using whole genome sequences and functional genomics data to enhance discovery of influential genetic and epigenetic variants that influence [heart, lung, blood, and sleep] HLBS disorders;” My comment: They are asking for what has already been included in every model of biologically-based cell type differentiation that has ever been detailed by serious scientists. Now, the Templeton Foundation has awarded$8.7M to fund research that can only benefit humanity by answering Schrodinger’s question “What is Life?” in the context of what is known about how the energy-dependent RNA-mediated innate immune system and supercoiled DNA protect life from virus-driven energy theft.”How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?” — Roger Penrose

## How to lie by telling the truth

Excerpt:

People… trot out half-truths, in full expectation and knowledge that they will create a false impression. And then, when others act on the false impression, the “truth-telling liars” can sit back and pretend that they aren’t liars. They get the benefit of lying, without any damage to their precious self-image.

My comment: It is more difficult for others to determine who benefits from half truths when more than one individual or research group fails to link biologically-based cause and effect. When two groups use the same model organism, but no model, they are not likely to report the truth about biologically-based cause and effect, .

## Craig Venter’s Synthetic Genome 3.0 Evokes Classic Experiments

Venter’s group seems to have run into a common problem with attempts to explain nutrient-dependent RNA-mediated cell type differentiation. They try to keep it constrained by evolution, which leads them to use terms like mutation instead of amino acid substitution. See their references for a link to work on viruses that should have led to recognition of the difference between the amino acid substitutions the cause changes in virulence and the mutations, which are biophysically constrained.
Dobzhansky (1973) used “amino acid” and “mutation” in the context of claims that we know can be supported only with experimental evidence that links atoms to ecosystems in all living genera via the physiology of reproduction. The nutrient-dependent physiology of reproduction is biophysically constrained by the innate immune system, which is the RNA-mediated link to supercoiled DNA. Supercoiled DNA protects all organized genomes from virus-driven entropy.
See also: A Tunable Mechanism Determines the Duration of the Transgenerational Small RNA Inheritance in C. elegans
Excerpt:

Synthesis of dsRNA is required for replication of RNA viruses and transposons, and therefore dsRNA constitutes a ‘‘danger signal’’ in many organisms, including humans, where it activates the interferon response (Wang et al., 2002). As in worms, RNAi is important for anti-viral defense (Lu et al., 2005); it is possible that the mere ‘‘sensing’’ of dsRNA (for example, by pattern recognition mechanisms [Melo and Ruvkun, 2012]) is sufficient to activate the RNAi system, regardless of whether the dsRNA molecule is further processed to trigger an RNAi response or not.

My comment: Nutrient-dependent pheromone-controlled RNA-mediated cell type differentiation in the nematodes, C. elegans and P. pacificus clearly shows how the innate immune system links metabolic networks and genetic networks to supercoiled DNA that protects the organized genome of all living genera from virus-driven entropy.
See: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes
Reported as: The neurobiological consequence of predating or grazing
Excerpt:

While C. elegans feeds exclusively on bacteria, P. pacificus is able to switch its behaviour to prey on other worms if bacterial food gets scarce.

Classical olfactory imprinting drives approach behavior, such as homing to the natal stream for salmon (Nevitt et al., 1994), bonding between mammals and their young (Lorenz, 1935), kin recognition in zebrafish (Gerlach et al., 2008), and acceptance of imprinted foods (Wilson and Sullivan, 1994). Positive imprinting to odors experienced early in life also has been described in C. elegans, although little is known about its mechanisms beyond a requirement for the orphan G protein-coupled receptor SRA-11 in AIY neurons (Remy and Hobert, 2005).

My comment: The nutrient-dependent de novo creation of G protein-coupled receptors links classical olfactory imprinting to supercoiled DNA via everything known about RNA-mediated cell type differentiation, which is controlled by the physiology of reproduction. Examples link all invertebrates to all vertebrates via the conserved molecular mechanisms we detailed in our section on molecular epigenetics in the Hormones and Behavior review.  From Fertilization to Adult Sexual Behavior
Excerpt:

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

Rechavi’s group recognizes the fact that RNA-mediated events are important for anti-viral defense. Bargmann’s group ignores the fact that virus-driven energy theft links perturbed protein folding chemistry to mutations and gene loss.
But her group does not link what nematodes eat to nutrient-dependent biodiversity via the de novo creation of olfactory receptors, which are G protein-coupled receptors. Instead, Bargmann wins another award.  McGovern Institute awards prize to neurogeneticist Cori Bargmann
Excerpt:

Building on her olfaction work, Bargmann has also studied the neural basis of social behavior, which in worms is strongly regulated by chemical cues. In one set of papers, for example, she identified a single neuron that integrates information from multiple chemical cues including food, oxygen and pheromones, to control the expression of social behavior.

My comment: Her award-winning works fail to link virus-driven energy theft from perturbed protein folding chemistry to mutations and gene loss.  Perhaps no one else but me will ever know that she could have linked the works from Rechavi’s group from what is known about how olfaction and the immune system enable the fine-tuning of metabolic networks and genetic networks, which is linked from the physiology of reproduction to supercoiled DNA.
She could have stopped the threat of the Zika virus and other viruses by acknowledging the fact that supercoiled DNA protects all organized genomes in all living genera from virus-driven entropy. Instead, her works will continue to be well-funded.
Others will be forced to increase their efforts and focus on Combating Evolution to Fight Disease.

### Viruses, amino acids, and somatic cell types (3)

A co-author of our 1996 Hormones and Behavior review of hormone-organized and hormone-activated behaviors gave her permission to add additional items of interest to this series of blog posts about viruses, amino acids, and somatic cell types. Teresa Binstock is largely responsible for my knowledge of RNA-mediated cell type differentiation. She introduced me and others to the complexity in the section of our review with the title Molecular epigenetics.
Excerpt:

It is now understood that certain genes undergo a process called “genomic or parental imprinting.” Early in embryonic development attached methyl groups become removed from most genes. Several days later, methyl groups are reattached in appropriate sites. Fascinatingly, some such genes reestablish methylation patterns based upon whether the chromosomal segment carrying the gene came from maternal or paternal chromosomes. These sexually dimorphic patterns are labeled genomic or parental imprinting, and these imprintings are inheritable but non-genetic modifications of specific genes…

See also: “RNA mediated DNA methylation” and “RNA mediated
From Teresa:
1) Here’s how I repackaged the exciting news [which links RNA-mediated DNA methylation to cell type differentiation in all genera]:
Expanding the brain: Research identifies more than 40 new imprinted genes
http://medicalxpress.com/news/2015-07-brain-imprinted-genes.html
* * * *
open access:
Quantitative and functional interrogation of parent-of-origin allelic expression biases in the brain.

Perez JD, Rubinstein ND, Fernandez DE, Santoro SW, Needleman LA, Ho-Shing O, Choi JJ, Zirlinger M, Chen SK, Liu JS, Dulac C.
Elife. 2015 Jul 3;4. doi: 10.7554/eLife.07860.

The maternal and paternal genomes play different roles in mammalian brains as a result of genomic imprinting, an epigenetic regulation leading to differential expression of the parental alleles of some genes. Here we investigate genomic imprinting in the cerebellum using a newly developed Bayesian statistical model that provides unprecedented transcript-level resolution. We uncover 160 imprinted transcripts, including 41 novel and independently validated imprinted genes. Strikingly, many genes exhibit parentally biased-rather than monoallelic-expression, with different magnitudes according to age, organ, and brain region. Developmental changes in parental bias and overall gene expression are strongly correlated, suggesting combined roles in regulating gene dosage. Finally, brain-specific deletion of the paternal, but not maternal, allele of the paternally-biased Bcl-x, (Bcl2l1) results in loss of specific neuron types, supporting the functional significance of parental biases. These findings reveal the remarkable complexity of genomic imprinting, with important implications for understanding the normal and diseased brain.
* * * *

• Wang L, Zhang J, Duan J, Gao X, Zhu W, Lu X, Yang L, Zhang J, Li G, Ci W, Li W, Zhou Q, Aluru N, Tang F, He C, Huang X, Liu J. Programming and inheritance of parental DNA methylomes in mammals. Cell. 2014a;157:979–991. doi: 10.1016/j.cell.2014.04.017.

• Wang SS, Kloth AD, Badura A. The cerebellum, sensitive periods, and autism. Neuron. 2014b;83:518–532. doi: 10.1016/j.neuron.2014.07.016.

• Wang X, Sun Q, McGrath SD, Mardis ER, Soloway PD, Clark AG. Transcriptome-wide identification of novel imprinted genes in neonatal mouse brain. PLOS ONE. 2008;3:e3839. doi: 10.1371/journal.pone.0003839.

2) Each is open access:
Sex-specific processing of social cues in the medial amygdala.
Bergan JF, Ben-Shaul Y, Dulac C.
Elife. 2014 Jun 3;3:e02743.
Animal-animal recognition within, and across species, is essential for predator avoidance and social interactions. Despite its essential role in orchestrating responses to animal cues, basic principles of information processing by the vomeronasal system are still unknown. The medial amygdala (MeA) occupies a central position in the vomeronasal pathway, upstream of hypothalamic centers dedicated to defensive and social responses. We have characterized sensory responses in the mouse MeA and uncovered emergent properties that shed new light onto the transformation of vomeronasal information into sex- and species-specific responses. In particular, we show that the MeA displays a degree of stimulus selectivity and a striking sexually dimorphic sensory representation that are not observed in the upstream relay of the accessory olfactory bulb (AOB). Furthermore, our results demonstrate that the development of sexually dimorphic circuits in the MeA requires steroid signaling near the time of puberty to organize the functional representation of sensory stimuli.
Neural control of maternal and paternal behaviors.
Dulac C, O’Connell LA, Wu Z.
Science. 2014 Aug 15;345(6198):765-70.
Molecular organization of vomeronasal chemoreception.
Isogai Y, Si S, Pont-Lezica L, Tan T, Kapoor V, Murthy VN, Dulac C.
Nature. 2011 Sep 21;478(7368):241-5.
The vomeronasal organ (VNO) has a key role in mediating the social and defensive responses of many terrestrial vertebrates to species- and sex-specific chemosignals. More than 250 putative pheromone receptors have been identified in the mouse VNO, but the nature of the signals detected by individual VNO receptors has not yet been elucidated. To gain insight into the molecular logic of VNO detection leading to mating, aggression or defensive responses, we sought to uncover the response profiles of individual vomeronasal receptors to a wide range of animal cues. Here we describe the repertoire of behaviourally and physiologically relevant stimuli detected by a large number of individual vomeronasal receptors in mice, and define a global map of vomeronasal signal detection. We demonstrate that the two classes (V1R and V2R) of vomeronasal receptors use fundamentally different strategies to encode chemosensory information, and that distinct receptor subfamilies have evolved towards the specific recognition of certain animal groups or chemical structures. The association of large subsets of vomeronasal receptors with cognate, ethologically and physiologically relevant stimuli establishes the molecular foundation of vomeronasal information coding, and opens new avenues for further investigating the neural mechanisms underlying behaviour specificity.
4) More on imprinting. Different folks, different lab.
Parents’ Genes Vie to Influence Offsprings’ Brain, Behavior
July 31, 2015
http://www.genengnews.com/gen-news-highlights/parents-39-genes-vie-to-influence-offsprings-39-brain-behavior/81251577/
Genomic imprinting, a mechanism that mutes gene expression in a parent-of-origin manner, can be highly targeted, affecting not just particular tissues, but even tissue subregions, mere clusters of cells—to subtle effect. Subregion-specific imprinting in the brain, for example, has been shown to influence behavior.
This finding emerged from a study conducted at the University of Utah School of Medicine, where researchers focused on a kind of targeted genomic imprinting they call noncanonical imprinting. They used an RNA-sequencing-based approach to detect even modest maternal or paternal allele expression biases at the tissue level….
* * * *
open access:
Paul J. Bonthuis, Wei-Chao Huang, Cornelia N. Stacher Hörndli, Elliott Ferris, Tong Cheng, Christopher Gregg.
Noncanonical Genomic Imprinting Effects in Offspring
.
Cell Reports, 2015
http://www.cell.com/cell-reports/abstract/S2211-1247%2815%2900757-3
——————————————————————–
My comment: Teresa continues to pleasantly provides links to pertinent publications, without comments about the ongoing claims of theorists.
I’ve continued to invite anyone else who is following the current literature on RNA-mediated cell type differentiation to comment here or on my FB pages. Typically, however, my frustration with the theories and the theorists is manifested in the content of my posts.
Pheromones Research
RNA-mediated
It is obvious to me that evolutionary theorists are not going to acknowledge the paradigm shift, which — largely due to Teresa Binstock’s initial efforts —  is now more than two decades old. Instead, people like Jay R. Feierman, who banned me from participation on the ISHE’s Human Ethology yahoo group, continue to try and sneak in the back door, by posting links to articles that attest to the facts about RNA-mediated cell type differentiation, which he has previously ignored and/or criticized.
Earlier today, for example, he posted links to
Using modern human genetics to study ancient phenomena

Chemosensory discrimination of identity and familiarity in koalas

Experience may allow increasing accuracy of the innate chemosensory recognition of snake predators by Iberian wall lizards

Explaining large-scale patterns of vertebrate diversity

Study of birds’ sense of smell reveals important clues for behavior, adaptation

Excerpt:

Now, a large comparative genomic study of the olfactory genes tied to a bird’s sense of smell has revealed important differences that correlate with their ecological niches and specific behaviors.

My comment: What made biologically uniformed human ethologists, like Jay R. Feierman, think that the sense of smell in birds was any less important to RNA-mediated cell type differentiation and ecological niche construction than it is to all other invertebrates and vertebrates? Had other human ethologists and theorists never heard the term “bird flu” or did they simply attribute the virus-driven pathology to mutations in the context of their ridiculous theories about evolution? Is it a wonder that the theorists have not already led to the death of us all. See for comparison: Combating Evolution to Fight Disease.
Excerpt:

It’s time for biophysicists to tell theorists and pathologists how to differentiate between theories about the genesis of different cell types and the biological facts about the nutrient-dependent pheromone-controlled ecological adaptations that enable the genesis of different cell types in individuals of different species. Simply put, it’s time to stop trying to explain ecological adaptations in the context of mutations and evolution.

Summary: Biology to most physicists has much in common with biology to human ethologists and evolutionary theorists. They look at a bird and see a bird. They’ve learned nothing about the bird’s nutrient-dependent pheromone-controlled physiology of reproduction, and cannot link anything known to serious scientists about physics, chemistry, or molecular biology to RNA-mediated events and ecological speciation in birds. Many of them probably still think that birds “evolved” from dinosaurs.
Addendum: After I posted this to my blog, Jay R. Feierman posted a link to this article to the evolutionary psychology yahoo group. Genetics and genomics of autism spectrum disorder: embracing complexity.
In Feierman’s ongoing attempts to obfuscate what is known to serious scientists about medical genetics and biologically-based cause and effect, he presents results from disparate research that most people cannot connect to the validations of our model of RNA-mediated events, which Teresa Binstock helped to integrate earlier today, by adding the reference to:

• Wang SS, Kloth AD, Badura A. The cerebellum, sensitive periods, and autism. Neuron. 2014b;83:518–532. doi: 10.1016/j.neuron.2014.07.016.

What motivates an MD/Ph.D to attempt to disparage others who might otherwise begin to put their own ideas about biologically-based cause and effect into a complete model linked to autism and other disorders, with origins that must start with gene activation by sensory stimuli, not with mutations?
Could it be Feierman’s oft touted claims about mutations and natural selection?
On 11/1/12: “Random mutations are the substrates upon which directional natural selection acts.
On 2/16/13 : “Random gene mutation is the variance generator upon which natural selection operates.
On 2/23/13: “…random genetic mutations generate the substrate upon which natural selection can act. Random genetic mutations create structural variations in protein enzymes…
Alternatively, could it be the claims made by bird-brained butterfly-watchers who think dinosaurs evolved into birds. See, for example: Birds inherited strong sense of smell from dinosaurs (w/ video)
I think that Dobzhansky would agree with me, if he was not still dead.  The problem seems to be that Feierman, and others like him, never became serious scientists. See BIOLOGY, MOLECULAR AND ORGANISMIC (1964)
Excerpt:

The notion has gained some currency that the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists! I have heard a man whose official title happens to be Professor of Zoology declare to an assembly of his colleagues that “a good man cannot teach zoology. A good man can teach, of course, only molecular biology.
Such pronunciamentos can be dismissed as merely ridiculous. They are, however, caricatures of opinions entertained by some intelligent and reasonable people, whose views deserve an honest and careful consideration and analysis. Science must cope with new problems that arise and devise new approaches to old problems. Some lines of research become less profitable and less exciting and others more so.”

My comment: The attempts of neo-Darwinists, who never learned anything about how viruses are linked to perturbed cell type differentiation, which links them to all pathology, have been wasted on the biologically uninformed. Billions of research dollars also have been wasted on attempts to link beneficial mutations to evolution.
See for comparison: A review of transgenerational epigenetics for RNAi, longevity, germline maintenance and olfactory imprinting in Caenorhabditis elegans
My comment: Catherine Dulac and others have linked olfactory imprinting to imprinted genes in the human brain via the nutrient-dependent pheromone-controlled behavior of nematodes and the development of their primitive nervous systems. How much longer will people like Feierman continue to tout the pseudoscientific nonsense of their ridiculous theories, as if they ever made sense to any intelligent scientist.
No Genetics without Epigenetics? No Biology without Systems Biology?
How does the social environment ‘get into the mind’? Epigenetics at the intersection of social and psychiatric epidemiology
Brain on stress: How the social environment gets under the skin
Mae-Wan Ho: No Boundary Really Between Genetic and Epigenetic
Excerpt 1)

…when we eat food nucleic acids can get into our cells. Also, there is a theory that our cells in the body keep sending out nucleic acids and one theory has it that it seems to correct the mistakes that other cells have suffered from mutations. . . .

1) It is not a theory: it’s a model. Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Excerpt 2)

evolutionary science has now “moved on to such an extent” that she and Peter Saunders don’t really care anymore about “trying to convince the neo-Darwinists.

2) Neo-Darwinists, like Feierman, prefer their ridiculous theories.
See for comparison: How keeping active pays off in the olfactory system
Excerpt:

This ‘use it or lose it’ model explains previously observed changes in olfactory receptor frequency that occur with age (Rodriguez-Gil et al., 2010), or with exposure to odorants (Jones et al., 2008).
Importantly, this model provides an elegant balance between plasticity and adaptation; although the potential to detect a wide range of odours, afforded by the exceptional number of genes for receptors, remains intact, the sensory organ becomes ‘tuned’ and sensitized to odorants relevant to its habitat.

My comment: Food odors and RNA-mediated gene duplication are linked to the experience-dependent de novo creation of olfactory receptor genes. RNA-mediated amino acid substitutions link the de novo creation of olfactory receptor genes and virus-perturbed mutations. If nutrient-dependent organized genomes are not protected from entropy by the availability of food and nutrient-dependent microRNAs viruses link viral microRNAs from entropic elasticity to genomic entropy.
The fact that what organisms eat prevents genomic entropy via the controlled physiology of nutrient-dependent reproduction can be placed into the context of claims that something must prevent mutation-induced damage to organized genomes.
See for instance: He proposed that our scientific understanding of reality is radically incomplete, and that some sort of anti-entropy, order-generating force remains to be discovered.
The discovery that food prevents genomic entropy links Darwin’s ‘conditions of life’ to his theory of how ecological variation leads to ecological adaptations. That fact may be a bigger embarrassment than anyone who has touted the pseudoscientific nonsense about mutations and evolution could ever imagine.
See also: Feedback loops link odor and pheromone signaling with reproduction
Estrogen Permits Vasopressin Signaling in Preoptic Kisspeptin Neurons in the Female Mouse
Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes
Excerpt: The ZAL2 and ZAL2m ER! Alleles Encode Alternative Protein Isoforms.
Alignment of the translated ER! alleles revealed no differences between ZAL2 and ZAL2m in the DNA and ligand-binding domains, which are typically highly conserved across species. For example, ZAL2 and ZAL2m show 77% sequence identity with human ER! across the entire protein and 100% and 94% sequence identity in the DNA and ligand-binding domains, respectively. The ZAL2 and ZAL2m alleles code for 597 amino acids, with two fixed differences driving a Val73Ile and Ala552Thr polymorphism in
ZAL2m.
My comment: Anyone who claims that the role of fixed amino acid substitutions cannot explain both morphological and behavioral development during life history transitions in all vertebrates and invertebrates, may want to see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults, or familiarize themselves with everything else known to serious scientists about how medical genetics is linked from nutritional epigenetics to pharmacogenomics in the context of what is currently known about personalized medicine.

## Phage spread antibiotic resistance

Excerpt 1)

nearly half of the 50 chicken meat samples purchased from supermarkets, street markets, and butchers in Austria contained viruses that are capable of transferring antibiotic resistance genes from one bacterium to another—or from one species to another.
Excerpt 2)
Until recently, transduction of antibiotic resistance via phage was assumed to be a very minor source of the spread of resistance, said Hilbert.

My comment: Bacteriophages were linked to cell type differentiation in species from microbes to humans via RNA-mediated events, which were detailed in the molecular epigenetics section of our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior. The fact that a science fiction author was the first to make that connection to biodiversity may be why it has been ignored for nearly two decades.
Claiming “…antibiotic resistance via phage was assumed to be a very minor source of the spread of resistance…” is like claiming that antibiotic resistance was assumed to be caused by mutations. Serious scientists don’t make such ridiculous assumptions and neither did Greg Bear. See: The Darwin Code. For comparison, Richard Lenski can be credited with touting the pseudoscientific nonsense about mutations and antibiotic resistance. See: The Man Who Bottled Evolution See also: Combating Evolution to Fight Disease.
On May 15, 2015, an antagonist asked: “Can you even tell me what scientists have got wrong about the reasons that proteans are folded at all?
My response: Nutrient-dependent RNA-mediated protein folding protects all cell types from the damage to their DNA caused by viral microRNAs. Biophysically constrained RNA-directed DNA methylation links thermodynamic cycles of protein biosynthesis and degradation to RNA-mediated amino acid substitutions that stabilize the organized genomes of all genera.
See: The Strange Inevitability of Evolution.
Most discussants do not seem to realize that only ecological adaptation is inevitable. Organisms and species adapt or species become extinct. Organisms and species do not evolve into other species. Only the biologically uninformed and intellectually handicapped believe in the pseudoscientific nonsense about the evolution of increasing organismal complexity via mutations — or whatever other ideas theorists think sound convincing enough to tout and teach others to believe in. Thank God that the Israeli middle schools have begun to teach the theory of evolution at the same time their students are learning about ecology. That’s how several generations of scientific progress have been made by those who were not taught to believe in ridiculous theories. See: Israeli Middle Schools School to Include Theory of Evolution
Excerpt:

“…learning about evolution is not the primary function of the decision, but rather to use it as a building block for students to learn more about their ecology.”


text:
# Linear algebra vector space

1. Aug 10, 2010

### SpiffyEh

1. The problem statement, all variables and given/known data
I uploaded the problem because its easier to see.

2. Relevant equations

3. The attempt at a solution

The solution is there from a practice exam. I don't understand the x,y,z part and how it fulfills the multiplication requirement of a vector space. Could someone please explain to me why it does?

#### Attached Files:

• ###### problem.png
File size:
37.6 KB
Views:
84
2. Aug 10, 2010

### hgfalling

In the solution they are handling the addition and multiplication at the same time.

They define u and v as vectors in the space, then show that u + dv (where d is any real) is also in the space.

So after multiplying and adding the vectors, you have a new vector:

$$\left(\begin{array}{cc} 4(a + da') + 3(b + db')\\0\\(c + dc') - 2\\(a + da') + (b + db')\end{array}\right)$$

So now all we have to do is show that all three (a+da'), (b+db'), (c+dc') are real numbers. Since a,b,c,d are all real, this is obviously the case, and hence the space is closed under addition and multiplication.

In the solution, they converted these expressions to (x,y,z), but that's unnecessary.

3. Aug 10, 2010

### SpiffyEh

oh! That makes sense, i didn't see where they came from. Thank you


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# How do I solve for the voltage on a geometry that has varying thickness of a conductive metal?

I currently have a 3D geometry which is made from an isotropic material. In my case this material is simply a highly conductive metal. We can think of this geometry almost as a thin film with slightly varying thickness throughout. I am told that the thickness at a point on the film correlates with its conductance there. Simply put the thicker the section the better conductance it has.

Here is what a 2D projection of my geometry looks like. For the moment ignore the grid lines inside.

What I am trying to solve is a boundary valued problem for a 2D model of this 3D geometry in MATLAB. The top curved edge has a voltage of +V0 applied to it and the bottom curved edge has a voltage of -V0 applied to it. These are my Dirichlet boundary conditions. The left and right sides have a boundary condition of zero flux (I think this means electric field flux but it may be current flux) and these are my Von Neumann boundary conditions.

So far this makes sense to me. It's when I try solving the governing equation that I become a bit lost. It seems I need to solve 2 partial differential equations simultaneously.

The first equation is Poisson's electrostatic equation shown here, note V(x,y) represent the voltage as a function of x and y,:

$$\nabla^2V(x,y)=-\frac{\rho}{\epsilon}$$

The other equation I think I need to solve is the continuity equation shown here:

$$\nabla \cdot \vec{J} = -\frac{\partial \rho}{\partial t}$$

Now I will explain what my misunderstandings are. First off, since we are dealing with a static case I believe that both $$\frac{\partial \rho}{\partial t}$$ and $$\frac{\rho}{\epsilon}$$ (might be wrong to assume this is zero) are zero meaning both of the right hand sides of the PDE go to zero.

Secondly for isotropic materials (which this should be since its all the same metal) we can relate the electric field and current density as $$\vec{J} = \sigma \vec{E}$$. Does the thickness not effect this equation at all?

Based on my equations and understandings of the problem I do not see how the thickness is coming into play. Is it a mistake to be treating this 3D geometry as a 2D one with different conductances at different regions?

One person mentioned that if the thickness is a function like $$\delta(x,y)$$ where it varies based on my 2D location then the actual equation I should be solving is

$$\nabla \cdot \big(\sigma \delta(x,y) \nabla V(x,y)\big) = 0$$

but $$\sigma$$ should be constant so that just falls out. If someone could provide some help I would greatly appreciate it. Thank you and sorry for this long winded post.

• It should be clear to you that the current is not equal through all parts of your film. Consider the case of an array of resistors of linearly-varying resistances. Go from there. – Jon Custer Dec 14 '18 at 15:19
• @nick2225 Why not use a 3D model? – Alex Trounev Dec 14 '18 at 16:13
• @JonCuster I think I get your idea. I tried to derive a similar expression by representing the film as infinitesimal squares with various heights. So in a 2D projection it would look like squares with side lengths of dl, differential length, and height delta. However, getting an expression for the conductance of a single infinitesimal doesn't shed light for me on the governing PDEs above. I tried performing a current balance at the same scale but I am afraid it was not too informative to me as I could not get my derivation to match any of the PDEs above, I can include my notes later. – nick2225 Dec 14 '18 at 17:45
• Why is $\rho=0$ in static case? – Kyle Kanos Dec 18 '18 at 11:11


text:
a743. 10420 - List of Conquests
Tags :
Accepted rate : 1215人/1297人 ( 94% ) [非即時]

Content

In Act I, Leporello is telling Donna Elvira about his master's long list of conquests:

This is the list of the beauties my master has loved, a list I've made out myself: take a look, read it with me. In Italy six hundred and forty, in Germany two hundred and thirty-one, a hundred in France, ninety-one in Turkey; but in Spain already a thousand and three! Among them are country girls, waiting-maids, city beauties; there are countesses, baronesses, marchionesses, princesses: women of every rank, of every size, of every age.'' (Madamina, il catalogo è questo)

As Leporello records all the beauties'' Don Giovanni loved'' in chronological order, it is very troublesome for him to present his master's conquest to others because he needs to count the number of beauties'' by their nationality each time. You are to help Leporello to count.

Input
The input consists of at most 2000 lines, but the first. The first line contains a number n, indicating that there will be n more lines. Each following line, with at most 75 characters, contains a country (the first word) and the name of a woman (the rest of the words in the line) Giovanni loved. You may assume that the name of all countries consist of only one word.
Output
The output consists of lines in alphabetical order. Each line starts with the name of a country, followed by the total number of women Giovanni loved in that country, separated by a space.
Sample Input #1
3
Spain Donna Elvira
England Jane Doe
Spain Donna Anna
Sample Output #1
England 1
Spain 2

Hint ：
ACM 10420 UVa
Tags:

[管理者： taichunmin(和風信使) ]

 ID User Problem Subject Hit Post Date 33770 wrr606@gmail...(Not Exist) a743 150 2023-02-01 16:40 33089 howie13579(技職水龍頭) a743 248 2022-11-29 17:51 30521 s411085056@g...(小宥) a743 616 2022-05-27 15:55 29120 Imcyj123(cyj891023) a743 357 2022-01-30 22:35 29095 406490150@gm...(我是朱朱) a743 394 2022-01-28 22:07


text:
# Probability of Normal Distribution

Test scores on a standardized test have mean 55 and variance 64. What is the probability that a random sample of 256 scores will have a sample mean score between 53 and 57

I attempted the problem and came up with this:
u=55 and sd = 8 (Square root of 64)
$$\mu=55 \sigma=\sqrt{64}=8$$
$$P(53< \bar{X} < 57) = P(\frac{53-55}{\frac{8}{\sqrt{256}}}<Z<\frac{57-55}{\frac{8}{\sqrt{256}}})=P(-4<Z<4)$$

What am I doing wrong?

vela
Staff Emeritus
Homework Helper
Your work looks fine to me. Why do you think there's something wrong?

I felt like it was off because 4 is off the charts, so I figured I managed to perform a miscalculation somewhere

vela
Staff Emeritus
Homework Helper
Yeah, I know the feeling. These statistics and probability problems can really test your intuition quite a bit.

$$\Phi(4)-\Phi(-4) = 1 - 0 =1$$

So is this correct?

vela
Staff Emeritus


text:
# Limit from the right

• April 8th 2010, 12:01 PM
sfspitfire23
Limit from the right
Hey guys,

Show that $\lim_{x \to a^+} \sqrt{x} = 0$ with a delta epsilon proof.

I first took $|\sqrt{x}-0| \rightarrow |\sqrt{x}|\times (|\sqrt{x}-0|) \rightarrow |x-0|< |\sqrt{x}| \times \epsilon$. So, $\delta = |\sqrt{x}| \times\epsilon$...is this right? How do I get the result to follow?
• April 8th 2010, 02:20 PM
(Assuming the limit is to 0+). Um, let $\epsilon > 0$. We must find a $\delta > 0$, s.t. if $0, $\sqrt{x}<\epsilon$. Since $\sqrt{\;\cdot\;}$ is increasing, $\sqrt{x} < \sqrt{\delta}$. So chuse $\delta \le \epsilon^2$ and it should follow...


text:
## Cryptology ePrint Archive: Report 2013/220

Towards Efficient Private Distributed Computation on Unbounded Input Streams

Shlomi Dolev and Juan Garay and Niv Gilboa and Vladimir Kolesnikov and Yelena Yuditsky

Abstract: In the problem of private swarm'' computing, $n$ agents wish to securely and distributively perform a computation on common inputs, in such a way that even if the entire memory contents of some of them are exposed, no information is revealed about the state of the computation. Recently, Dolev, Garay, Gilboa and Kolesnikov [ICS 2011] considered this problem in the setting of information-theoretic security, showing how to perform such computations on input streams of {\em unbounded length}. The cost of their solution, however, is exponential in the size of the Finite State Automaton (FSA) computing the function.

In this work we are interested in efficient (i.e., polynomial time) computation in the above model, at the expense of {\em minimal} additional assumptions. Relying on the existence of one-way functions, we show how to process unbounded inputs (but of course, polynomial in the security parameter) at a cost {\em linear} in $m$, the number of FSA states. In particular, our algorithms achieve the following:

\begin{tiret}

\item In the case of $(n,n)$-reconstruction (i.e., in which all $n$ agents participate in the reconstruction of the distributed computation) and at most $n-1$ agents are corrupted, the agent storage, the time required to process each input symbol, and the time complexity for reconstruction are all $O(mn)$.

\item In the case of $(n-t,n)$-reconstruction (where only $n-t$ agents take part in the reconstruction) and at most $t$ agents are corrupted, the agents' storage and time required to process each input symbol are $O(m{n-1 \choose n-t})$. The complexity of reconstruction is $O(mt)$.

\end{tiret}

We achieve the above through a carefully orchestrated use of pseudo-random generators and secret-sharing, and in particular a novel share re-randomization technique which might be of independent interest.

Category / Keywords: cryptographic protocols / Secure-Multi-Party-Computation, Streamin Input

Publication Info: A brief announcement of the paper was published at DISC 2012, and a version of the paper was accepted to ACNS 2013


text:
## Boole’s Inequality

Boole’s Inequality The Boole’s Inequality Theorem states that "the probability of several events occuring is less than or equal to the sum of the probabilities …

## Weibull Distribution Examples | Calculator | Two Parameter

Weibull Distribution Calculator Use this calculator to find the probability density and cumulative probabilities for two parameter Weibull distribution with parameter $\alpha$ and $\beta$. Weibull …

## Bonferroni Inequality

Bonferroni’s Inequality For $n$ events $A_1,A_2,\cdots, A_n$ $$$$\label{bof} P\big(\cap_{i=1}^n A_i\big)\geq \sum_{i=1}^n P(A_i) -(n-1).$$$$ Proof For $n =2$,  \begin{equation*} P(A_1\cup A_2)= P(A_1)+P(A_2) …


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# 1.9 Vector (cross) product

 Page 1 / 2
Vector multiplication provides concise and accurate representation of natural laws, which involve vectors.

The cross product of two vectors a and b is a third vector. The magnitude of the vector product is given by the following expression :

$\begin{array}{l}|\mathbf{c}|=|\mathbf{a}×\mathbf{b}|=ab\mathrm{sin}\theta \end{array}$

where θ is the smaller of the angles between the two vectors. It is important to note that vectors have two angles θ and 2π - θ. We should use the smaller of the angles as sine of θ and 2π - θ are different.

If " n " denotes unit vector in the direction of vector product, then

$\begin{array}{l}\mathbf{c}=\mathbf{a}×\mathbf{b}=ab\mathrm{sin}\theta \phantom{\rule{2pt}{0ex}}\mathbf{n}\end{array}$

## Direction of vector product

The two vectors ( a and b ) define an unique plane. The vector product is perpendicular to this plane defined by the vectors as shown in the figure below. The most important aspect of the direction of cross product is that it is independent of the angle, θ, enclosed by the vectors. The enclosed angle , θ, only impacts the magnitude of the cross product and not its direction.

Incidentally, the requirement for determining direction suits extremely well with rectangular coordinate system. We know that rectangular coordinate system comprises of three planes, which are at right angles to each other. It is, therefore, easier if we orient our coordinate system in such a manner that vectors lie in one of the three planes defined by the rectangular coordinate system. The cross product is, then, oriented in the direction of axis, perpendicular to the plane of vectors.

As a matter of fact, the direction of vector product is not yet actually determined. We can draw the vector product perpendicular to the plane on either of the two sides. For example, the product can be drawn either along the positive direction of y – axis or along the negative direction of y-axis (See Figure below).

The direction of the vector product, including which side of the plane, is determined by right hand rule for vector products. According to this rule, we place right fist such that the curl of the fist follows as we proceed from the first vector, a , to the second vector, b . The stretched thumb, then gives the direction of vector product.

When we apply this rule to the case discussed earlier, we find that the vector product is in the positive y – direction as shown below :

Here, we notice that we move in the anti-clockwise direction as we move from vector, a , to vector, b , while looking at the plane formed by the vectors. This fact can also be used to determine the direction of the vector product. If the direction of movement is anticlockwise, then the vector product is directed towards us; otherwise the vector product is directed away on the other side of the plane.

It is important to note that the direction of cross product can be on a particular side of the plane, depending upon whether we take the product from a to b or from b to a . This implies :

$\begin{array}{l}\mathbf{a}×\mathbf{b}\ne \mathbf{b}×\mathbf{a}\end{array}$

Thus, vector product is not commutative like vector addition. It can be inferred from the discussion of direction that change of place of vectors in the sequence of cross product actually changes direction of the product such that :

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text:
# Another centripetal Acceleration problem

1. Jun 7, 2014

### BrainMan

1. The problem statement, all variables and given/known data
(a) What is the tangential acceleration of a bug on the rim of a 78 rpm record 10 in. in diameter if the record moves from rest to its final angular velocity in 3 s? (b) When the record is at its final speed, what is the tangential velocity of the bug? Its tangential acceleration? Its radial acceleration?

2. Relevant equations
ω = ωo + $\alpha$t

3. The attempt at a solution
I have solved everything in the problem accept the second and third part of (b). I managed to calculate the tangential velocity of the bug just fine. The way I read this question is that once it hits 78 rpm it stops accelerating and that becomes the final velocity. This would cause the tangential acceleration in part (b) to be zero which my book agrees with. The third part of (b) I don't understand though. The book says that the radial acceleration at that point would be 8.39 m/s. If the tangential acceleration is zero, how could there be a radial acceleration and how would I calculate it?

2. Jun 7, 2014

### Nathanael

It's talking about the inward acceleration needed to move in a circle at a constant speed

(The centripetal acceleration from "uniform circular motion")

3. Jun 7, 2014

### SammyS

Staff Emeritus
Does an object undergoing uniform circular motion have a non-zero acceleration?
If no: isn't its the direction of its velocity changing?

If yes: What is that acceleration called, & what is its direction?

Darn !!
Nathanael beat me !

4. Jun 7, 2014

### BrainMan

I wonder why they would call it the radial acceleration instead of the centripetal acceleration? I followed the formula for centripetal acceleration which is
a = v2/r
(1.04)2/.127 = 8.52 m/s which is not the correct answer the correct answer is 8.39. I am using the velocity that I solved for in the first part of (b) which the book says is correct. The radius I calculated by converting inches to meters
10/39.37/2 = .127

Last edited: Jun 7, 2014
5. Jun 7, 2014

### SammyS

Staff Emeritus
It's the component that's along the radius. It's perpendicular to the tangential acceleration.

6. Jun 7, 2014

### Nathanael

It basically just means "along the radius" which is a way of saying "towards the center" which is what centripetal means.

It's just terminology

This time you beat me, Sammy! Hahah

7. Jun 7, 2014

### BrainMan

check out my edited post

8. Jun 7, 2014

### Nathanael

Weird. I would say the book made a mistake. I have no idea why it would be 8.39

I used a more specific velocity (1.037) and the answer came out to 8.47 which is a little closer. I don't know why the book says that it's 8.39, I really think it's just a mistake.

9. Jun 7, 2014

### BrainMan

OK cool. Thanks!

10. Jun 7, 2014

### BrainMan

Just as an additional question if the centripetal force is the force pulling inward to the center what is the force pushing out that keeps it in equilibrium? The only other acceleration is the one tangent to the circle and its not pulling outward.

11. Jun 8, 2014

### Nathanael

If there was an equal force outward then it would just move in a straight path.

The centripetal force is the required net force to move in a circle.

(Centripetal force is not really a "force" in the sense that gravity is a force, it's just the net force that is required for uniform circular motion. It could be caused by tension, friction, gravity, etc.)

(An example of tension causing it would be spinning an object around on a string. An example of friction causing it would be a car driving in a circle. An example of gravity causing it would be an object orbiting a planet.)

12. Jun 8, 2014

### SammyS

Staff Emeritus
(78/60×2 π)^2×5×2.54 = 847.325...

The book's answer must have some rounding at an intermediate step, or steps

13. Jun 8, 2014

### BrainMan

Oh I get it now. Thanks!