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- NewSir,I have 38MnSV6 microalloyed steel,what should be its deformation temperature?
and which thermo mechanical treatment is suitable as deformation treatment(rolling or forging)?
Is it possible to take deformation temperature is below 1000 degree celcius for this particular steel?Following
- 4Does the PC12 cell line always need NGF or can it be cultured with RPMI or DMEM with FBS and antibiotic(Penicillin)?
Is PC12 cell line always need NGF or It can be cultured with simply RPMI or DMEM with FBS and antibiotic(Peniciline)?
- NewIs there a consistent relationship between quantity of tree pollen and seed production?
Any information or details of publications concerning this relationship for tree species of temperate/boreal regions of the northern hemisphere would be much appreciated.Following
- 3Dears, Can anyone define the scientific name of this beetle?
I have collected this beetle on Astragalus plant.
This has 1 cm length. I have attached some photos from this insect
Thanks to you both Rinaldo and Vincent. It is nice that you both had the same ideaFollowing
- 4Could you suggest a good source of Identification of macroalgae and bryophytes?
Can someone recommend a good way to identify macroalgae and bryophytes (identification key ...)
Before giving you recommendations of books and keys, it would be important to know in which region you are working, as many books should be used within the appropriate regional context.
All the best,
- NewAnyone else know of a forearm electromyography (EMG) sensor that allows access to data?
Apparently Myo cant let u see EMG data
We need a not-so-expensive EMG device that lets you see and train EMG data for possible research along with brainwaves.Following
- 5In designing a study, when quasi experimental design is appropriately selected?
what are its main advantages, disadvantages?
thanks in advance
I found this book highly readable and informative
Dunning, Thad (2012). Natural Experiments in the Social Sciences: A Design-Based Approach. Cambridge University Press.Following
- NewPlease which of the strain can be used as longitudinal compressive strain in Ansys? Or how can i identify Longitunal conpressive strain in Ansys?
I am actually working on a Tyre-road model affected by the weight of a car. To see its effect on the effective radius, the loaded radius and the amount of deflection.Following
- 3How may I explain the shift in peak positions in radial distribution functions?
I am doing classical MD simulations of crystalline-like FCC nanoparticles at finite temperatures. When analyzing the peak positions of the averaged radial distribution functions over 1000 snapshots at equilibrium, I found the positions of the first peaks (bond length) decreased as T increased, while those of the second, third and fourth peaks increased as T increased. The same trends were observed at two particle sizes. The calculated average bond length (pair-wise distances within cutoff) increased as T increased. So I couldn't think of a reason for the opposite trends of 1st peak vs. others. Would you please shed light on this issue? Thank you very much.
I used NVT ensemble, is it the right ensemble to use please? The attached RDF_varyT.pdf shows the graphs at different T, and the peak positions were read at the maximum, not extracted from fitting. Thanks!Following
- 2How to read values from matrix using UDF programming (as initial condition)?
I have two matrices ones is the u-component velocity and the other is v-component velocity,I am trying to read the values of these two matrices and put them as an initial conditions in the domain of my model. I use the code below but I do not know how to read the values from the matrices and then write them into the model.
#define pi 4.*atan(1.)
real xo1 = 0.00;
real yo1 = 0.00;
/* loop over all cell threads in the domain */
/* loop over all cells */
r1=sqrt(ND_SUM(pow(xc - xo1,2.),
pow(xc - yo1,2.),
pow(xc - 0,2.)));
/* Note xc is x coordinate, xc is y and xc is z */
if ( r1 != 0.0)
C_U(c,t) = 0.0;
C_V(c,t) = 0.0;
thanks in advance for your help
yes, I am using *.txt file format.Following
- 1Can someone really say that a proposition is ´valid´? What is the theoretical basis of making such a statement?
Can someone really say that a proposition is ´valid´? What is the theoretical basis of making such a statement?
The validity of a proposition is the consequence of its meaningfully. In fact a proposition must be meaningful to be valid. A meaningful proposition is a proposition which could be interpreted (and could accept semantical assignments). Accordingly, interpretation is the production of the conceptualisation. Additionally, the described sequence generally specifies the main steps towards defining the semantics of a proposition.Following
- 3How can I find the articles published in previous years in Acta Anaesth Belg?
The main web site does not show archives of published issues. Even table of contents can not be seen. I can only see the years 2015 and 2014. Does any body help with this problem. I mailed to the journal contact address but could not solve this problem. Even if you want to purchase the article you can not find a place. This is a very important problem for people who published their articles in this journal since it is impossible to cite these articles.
Go to PubMed.com and do an advanced search on "Acta Anaesthesiologica Belgica" in the journal field (scroll down to find that in the drop down box). Looks as though there are articles back into the '50s. You can also add additional concepts using the advanced search. As Matthew suggested above, you can request any of these via Interlibrary loan.
Humanities/VetMed/Animal Science Librarian
150 Parks Library
Iowa State UniversityFollowing
- NewAre the "Brand Personality" Scales Reliable Enough?
I am working on brand personality (BP) topic in tourism and hotel marketing field. However I have a serious question related to the scales that measure BP…
Aaker (1997) developed BP Scale, as known well. However, some authors have criticized her scale due to the personality traits she used in her scale (although BP is a metaphoric concept). For example, Azoulay and Kapferer (2003) and Geuens et al. (2009) discussed that BP scales must only include the human personality traits. Because, Aaker used some items that reflects the user imagery, identity or image of the brand lik “feminine, sophisticated, competent” etc. which are not human personality traits at all. Thus, these authors claim that Aaker’s scale is not applicable for measuring BP, because it measures Brand Identity, Brand Image and BP partly. So, we can think that BP scale of Aaker is not strict for BP measures. But many writers have studied BP based on Aaker’s scale, and this compherension seems to continue.
So the question is here: “who is right?”
Do we have to measure BP by using Human Personality traits strictly? Or Is it possible to add items that reflect the brand like Aaker did on her scale?
Thanks for all the responses in advence...Following
- 6How to compute Lambert Function (W)?
Lambert function has been proposed by Jean-Henri Lambert, some times called Omegat function (W).
the equation can be written as following:
xexp(x) = z this means that x= W0(z)
So the question is , how can I compute W0?
Dear Professor B.Achour:
It's great moment to you read, thank you for the contribution.Following
- NewDoes anybody notice here, that massive neutrinos (last nobel price) are incompatible with the break down of parity in weak interaction?
parity is not conserved in weak interaction, like beta decay. this was discovered exactly 60 years ago and since then a fundamental principle in QFT. the nonconservtion of parity comes from the fact, that massless neutrinos can only have two spin positions, parallel or antiparallel to their propagating direction (like photons). the spin of massive particles may point in any direction. A detailed analysis shows (Bjorken&Drell, rel. quantum mechanics, rel. quantum field theory), QED conserves parity, QAD breakes parity.
resume: massive neutrinos (Noble Price) are on the same scale as "neutrinos faster than light" (CERN)Following
- NewDynamic Analysis of Heat Exchanger,Can anybody cast light over it?
How I Can dynamically analyse parallel flow shell and tube type heat exchanger,Can I analyse considering Lumped parameter analysis? I require temperature variation over a definite period of time as well as temperature variation with the length of heat exchanger.Following
- 3What pore size PVDF membrane should I use for 10-100kD range of proteins including Cyt C (12kD)?
For my western blot, all my target proteins are within 10-100kD observed masses. I'm concerned that the lowest is Cyt C at 12kD will transfer through and not stick to membranes with standard 0.45um pore size. I'm planning to use a TGX gel from BioRad as shown by the ladder for SDS PAGE.
Try with 0.2 uM pore size.
In my lab we have successfully transferred 12 KDa protein using Millipore Immobilon 0.2uM PVDF membrane.
- NewWhat are the most relevant aspects of engagement of users and that we have to consider in an immersive educational environment?
What are the most relevant aspects of engagement of users and that we have to consider in an immersive educational environment? And what are the main research and researchers in this area?Following
- 3What mathematical transformation was used on Poisson distribution to derive debye length on semiconductors?
How is this transformation then used to calculate charge excess delta N at band bending with sc of the semiconductor?
Semiconductor Electrochemistry Wiley-VCH, 2001-Rüdiger Memming P.88-91
well, there is a simple answer to your question, although it will not help you at this stage at all. The answer namely is that you can solve the problem numerically, if analytic solution is not available.
So, what else can I suggest to you ? Two things :
1. One of the most simple, beautiful and for most purposes fully sufficient is the way Richard Feynman deals with this problem in his lectures "Feynman Lectures on Physics", volume II, chapter 7, page 7-8. Do not get distracted by the fact that it is the colloidal particle in a electrolyte, the same Maxwell equation is valid (one of the Maxwell equations can be rewritten in form of Poisson equation). The main argument for the form of solution comes from thermodynamics. Once that is introduced , the exponential form of the solution for the potential (and the electrical charge density), together with the characteristic screening length (Debye screening length), result almost automatically. Check that.
2. A word of caution. In semiconductors, the reason for the existence of Debye "screening" length is not the charge on the surface of colloidal particle, it is the difference in the electrochemical potential across the interface (for example metal electrode-semiconductor interface). But be aware, there are in fact two "screening lengths", one which is the Debye screening length Ldebye (high density of mobile charges) and the second one (parabolic approximation), where the density of mobile charges is relatively low and one encounters a full depletion of charges near surfaces. This characteristic length is called the depletion length Ldepletion . Ldepl > Ldebye, but both these characteristic lengths have the same origin, namely the difference in the electrochemical potential across the interface.
I hope this might help.
with best regards
- 6What map sources can be used with GIS modeling for disaster risk assessment?
how can I get them in shape files?
see UN-Satelite based Charter "http://www.un-spider.org" or "http://www.disasterscharter.org"
- 5Any idea about this rock type occurring on the beaches of Maldives?
These structures are about a meter in diameter, displaying striking laminated structure.
My first thought, too, was that it was a stromatolite. But, for the sake of variety -and knowing nothing about the geology of the area- might I also suggest that it could be a mud volcano?
If you go to the wiki page https://en.wikipedia.org/wiki/Mud_volcano and scroll down then eventually you will come across a photo of what is being called a "A cold mud pot in Glenblair, California", which looks very similar.Following
- 6How do I assess the DNA contamination of a protein preparation?
Can we trust the 260/280 ratio?
Do you have an alternative method to propose?
Thank you for your expertise David! Very good to know!Following
- 4What are these bristles on the kudzu bug?
Can anyone tell me what this pair of bristles found associated with every spiracle in the kudzu bug are? A pair is always found near the spiracle and the "crater" around the base of the bristle almost looks like another spiracle.
I strongly believe these are trichobothria. They are basically mechanosensory hairs, like the other contributors mentioned, but with a special function - they respond to air movements (mostly quite finely tuned to certain frequencies) and are thus hearing organs. For Pentatomoidea (where kudzu bug, as all Plataspididae, belongs to), the number and position of the abdominal trichoibothria is an important systematic character.
- 1How can I model growth of copper nanoparticles in water using molecular dynamics simulation?
I would like to know how to model the mean square deviation of copper nanocluster size from its nucleation with time. I am a newbie in this field, and I don't have much idea about how to carry it out. I have LAMMPS package installed in my machine. I have read about umbrella sampling through the paper attached herewith.Following
- 7Are you reasearching the causes for Autistic Savant abilities?
I am interested in connecting with anyone who is researching the causes for the remarkable abilities of autistic savants.
Atemporal. I'm not the only one. My paper covers that. Thanks for the comments. It's appreciated.Following
- NewHow to detect level of phosphorylated PRDX3 in protein samples?
I wanna check the PRDX3 (Peroxiredoxin) and Phosphorylated PRDX3 level in my protein samples, so for that purpose I require antibodies for performing Western blot.
The antibody for PRDX3 is available but I cant find the antibody for phosphorylated Prdx3 (At threonine 146 position).
Is there any other way out besides Western?
- 12What is the evidence that insulin resistance in type 2 diabetes and in metabolic syndrome is NOT caused by hyperinsulinemia?
When I was a medical student at McGill in the late 1970s, we learned a straightforward explanation for the cause of Type 2 diabetes, the most common form of diabetes in adults, accounting for about 90 per cent of all diabetes cases. We were told the insulin resistance responsible for Type 2 diabetes was caused by high levels of insulin. Hyperinsulinemia–increased insulin levels in the blood–was said to “downregulate” insulin receptors, making cells with those receptors less responsive to the insulin message. From a physiology point of view, this makes perfect sense. It’s analogous to the development of tolerance that can happen with regular heroin use when a person no longer responds to the drug in the way they did initially.
Sometime in the 1980s this explanation for the cause of insulin resistance was abandoned. Instead, the medical community adopted a new theory that insulin resistance comes first, and is behind high insulin levels in Type 2 diabetes. To overcome insulin resistance, the pancreas secretes larger-than-normal amounts of insulin, resulting in so-called “reactive hyperinsulinemia.” The cause of this insulin resistance is never clearly explained, although obesity, chronic inflammation, and genes are all said to contribute.
When I ask prominent endocrinologists about how insulin resistance comes about in this new paradigm, they say, sometimes condescendingly: “It’s too complicated for a psychiatrist to understand.” That may be. But I’m also an engineer, and when I studied at the University of Waterloo the saying was “BBB”, short for “Bulls**t Baffles Brains.” I consider myself to be a critical thinker, so if the new explanation for what causes insulin resistance is incomprehensible to me, that’s probably because it’s nonsense.
Why did the medical community make a 180-degree reversal of its theory for the cause of Type 2 diabetes? Why discard a nice, coherent, easy-to-test explanation and replace it with a theory no one seems able to describe in terms that an engineer and physician can understand? Time to apply another useful saying: “Follow the money.”
Who profits from this paradigm shift? To answer this question, let’s compare the consequences of diabetes management approaches under the old paradigm and the new one. If we follow the old theory that high insulin levels cause insulin resistance, then treatment involves lowering insulin levels, assuming that insulin resistance is reversible. Since the main stimulus to insulin secretion is the level of glucose in the blood, we can get the pancreas to release less insulin by decreasing the amount of glucose going into the bloodstream. For people who eat regularly, that main source of blood glucose is carbohydrates in the diet, i.e., sugars and starches.
Treatment options for lowering blood glucose include medications such as acarbose, which reduces the absorption of dietary carbohydrates in the small bowel. Metformin, the first-line treatment of choice for Type 2 diabetes, is believed to have a similar effect and may also contribute to weight loss. Traditional and folk remedies for obesity and Type 2 diabetes, including yerba maté tea and the gourd bitter melon, may act in the same way. An easier route for some would be to lower the amount of carbohydrates in the diet, and/or pick foods with a low glycemic index. Research demonstrates a low-carb diet can reduce or even eliminate the need for medication to control blood sugar, in effect, curing diabetes in some patients, and, more importantly, showing that Type 2 diabetes is likely caused by diet for people with susceptible genes.
If we follow the new paradigm and believe obesity, inflammation and genes cause insulin resistance, what can we do? Lose weight? Many find this impossible. Reduce inflammation? Difficult if we don’t know its cause. Change our genes? Maybe in the future. Typically the victim is blamed for overeating and not exercising enough. In the absence of effective ways to reduce insulin resistance in this paradigm, the usual solution is medication to control blood sugar levels.
Some commonly prescribed anti-diabetic medications stimulate the pancreas to produce more insulin, while others act at the level of the insulin receptor to decrease insulin resistance. And of course, insulin itself, typically given in amounts way larger than what the pancreas secretes in normal individuals, can help people overcome insulin resistance. Yes, blood sugar levels will decrease. But there are side effects: insulin itself, and many of the medications that increase insulin or increase its effectiveness, may cause weight gain. And if obesity is a cause of insulin resistance, there is no way these treatments can stop a patient’s diabetes. Instead, for many victims, the diabetes just gets worse.
So let’s follow the money. If today’s treatment approaches don’t cure diabetes and may even make it worse, who benefits? Drug companies, who gain customers for life due to diabetes and its many complications, including vascular disease, dementia, kidney and eye problems, even cancer. Medical device manufacturers profit when diabetic patients need cardiac pacemakers, artificial valves, and prosthetic limbs. Kidney failure requires expensive machines, products and dialysis facilities. Many professions, including physicians, pharmacists, dietitians, physiotherapists, social workers, occupational therapists, and others are called upon to provide care and diabetics need hospitals, clinics, blood test labs, MRI machines, offices, exercise machines, and more. Simply put, the new paradigm is good for the economy. It’s too bad that patients must suffer.
If the theory that high insulin levels cause insulin resistance has no scientific basis, where is the research disproving this hypothesis? And why aren’t the current treatment approaches truly helping Type 2 diabetics fight a disease that has huge health consequences? I don’t mind being wrong. Show me the evidence!
Thank you, Dr. Nunemaker, for the Hansen reference - I had not come across that paper before.
Here are some other references supporting the hypothesis that hyperinsulinemia precedes insulin resistance:
Pettitt DJ, Moll PP, Knowler WC et al. Insulinemia in children at low and high risk of NIDDM. Diabetes Care. 1993;16:608-615.
Arslanian SA, Saad R, Lewy V, Danadian K, Janosky J. Hyperinsulinemia in african-american children: decreased insulin clearance and increased insulin secretion and its relationship to insulin sensitivity. Diabetes. 2002;51:3014-3019.
Kim B, McLean LL, Philip SS, Feldman EL. Hyperinsulinemia induces insulin resistance in dorsal root ganglion neurons. Endocrinology. 2011;152:3638-3647.
Marangou AG, Weber KM, Boston RC et al. Metabolic consequences of prolonged hyperinsulinemia in humans. Evidence for induction of insulin insensitivity. Diabetes. 1986;35:1383-1389.
Gray SL, Donald C, Jetha A, Covey SD, Kieffer TJ. Hyperinsulinemia precedes insulin resistance in mice lacking pancreatic beta-cell leptin signaling. Endocrinology. 2010;151:4178-4186.
Kelly CT, Mansoor J, Dohm GL, Chapman WH, Pender JR, Pories WJ. Hyperinsulinemic syndrome: The metabolic syndrome is broader than you think. Surgery. 2014
Iozzo P, Pratipanawatr T, Pijl H et al. Physiological hyperinsulinemia impairs insulin-stimulated glycogen synthase activity and glycogen synthesis. Am J Physiol Endocrinol Metab. 2001;280:E712-9.
Del Prato S, Leonetti F, Simonson DC, Sheehan P, Matsuda M, DeFronzo RA. Effect of sustained physiologic hyperinsulinaemia and hyperglycaemia on insulin secretion and insulin sensitivity in man. Diabetologia. 1994;37:1025-1035.
Rizza RA, Mandarino LJ, Genest J, Baker BA, Gerich JE. Production of insulin resistance by hyperinsulinaemia in man. Diabetologia. 1985;28:70-75.
Garvey WT, Olefsky JM, Marshall S. Insulin induces progressive insulin resistance in cultured rat adipocytes. Sequential effects at receptor and multiple postreceptor sites. Diabetes. 1986;35:258-267.
- 7Why, can small amounts of O2 cause production of acetic acid in culture media of bacteria?
Why does acetic acid cause inhibition of bacterial growth?
its now clear
thank you a lotFollowing
- NewIs there any possibility to calculate UV-Visible spectra of compound in different solvents?
I installed GABEDIT and tried. i got absorbance spectra of my compound. is there any possibility to find the absorbance in different solvents by using any software without using Gaussian.Following
- 3Is there any conclusion on whether a symmetric matrix with zero diagonal entries is positive definite or not?
Say A=B*B^H (^H means conjugate transition)
C=A - (diagonal of A).
So C is a symmetric matrix which diagonal entries are all 0.
I wondering whether there is any study on how to judge C is positive definite, or not
I don't have an answer for a generalized case. However, for 2 x 2 matrices and 3 x 3 matrices with real entries , they are neither positive definite nor negative definite.
If you consider C = [0 a;a 0], then Eigenvalues of C is +a or -a, so neither positive definite nor negative definite.
If you consider C = [0 a b; a 0 c; b c 0], then the characteristic equation to find the Eigenvalues is -l^3+(a^2+b^2+c^2)l+abc=0. From the relation between roots and coefficients, it is clear that l1+l2+l3=0, l1l2+ l1l3+ l3l2=-(a2+b2+c2) and l1l2 l3=abc. From the second relation, it is clear that, it is neither positive nor negative.Following