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Stress Response - Science topic

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Hi everyone, I would like to check whether the ER stress response is activated in human fibroblasts. I am particularly interested in the ATF6 signalling pathway. Therefore, I would like to check the protein expression of the cleaved ATF6 by western blot. Unfortunately, I have problems finding a good antibody for this. My current antibodies only show unspecific bands. Do any of you have experience with this and could recommend an antibody or another method?
Many thanks in advance!
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Hi Sarah, I would check citeab.com if you haven’t already.
Best
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We're seeking collaboration to the actual cause of psychophysiological dis-ease. The animal kingdom shakes off stress after being threatened, so why can't we? Is it possible that humans have developed to such a level that stressors are stored extracorporeal, outside of the body and constantly trigger the stress response as a result. Our ability to store and stream data, that is vital to our survival may prove to be the difference that Darwin mist. The ramifications and applications of an informational health based model, will shake the very core of current Western medicine. Ascribing the disease within human-beings to be a dis-ease with their environment rather than, the persons health is defective, is surely a better way for us all to be searching for? Please get in touch to collaborate with a natural, evolutionary approach to physical and mental wellbeing.
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Please have look on our(Eminent Biosciences (EMBS)) collaborations.. and let me know if interested to associate with us
Our recent publications In collaborations with industries and academia in India and world wide.
EMBS publication In association with Universidad Tecnológica Metropolitana, Santiago, Chile. Publication Link: https://pubmed.ncbi.nlm.nih.gov/33397265/
EMBS publication In association with Moscow State University , Russia. Publication Link: https://pubmed.ncbi.nlm.nih.gov/32967475/
EMBS publication In association with Icahn Institute of Genomics and Multiscale Biology,, Mount Sinai Health System, Manhattan, NY, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29199918
EMBS publication In association with University of Missouri, St. Louis, MO, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30457050
EMBS publication In association with Virginia Commonwealth University, Richmond, Virginia, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852211
EMBS publication In association with ICMR- NIN(National Institute of Nutrition), Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/23030611
EMBS publication In association with University of Minnesota Duluth, Duluth MN 55811 USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852211
EMBS publication In association with University of Yaounde I, PO Box 812, Yaoundé, Cameroon. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30950335
EMBS publication In association with Federal University of Paraíba, João Pessoa, PB, Brazil. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30693065
Eminent Biosciences(EMBS) and University of Yaoundé I, Yaoundé, Cameroon. Publication Link: https://pubmed.ncbi.nlm.nih.gov/31210847/
Eminent Biosciences(EMBS) and University of the Basque Country UPV/EHU, 48080, Leioa, Spain. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852204
Eminent Biosciences(EMBS) and King Saud University, Riyadh, Saudi Arabia. Publication Link: http://www.eurekaselect.com/135585
Eminent Biosciences(EMBS) and NIPER , Hyderabad, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29053759
Eminent Biosciences(EMBS) and Alagappa University, Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30950335
Eminent Biosciences(EMBS) and Jawaharlal Nehru Technological University, Hyderabad , India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/28472910
Eminent Biosciences(EMBS) and C.S.I.R – CRISAT, Karaikudi, Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237676
Eminent Biosciences(EMBS) and Karpagam academy of higher education, Eachinary, Coimbatore , Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237672
Eminent Biosciences(EMBS) and Ballets Olaeta Kalea, 4, 48014 Bilbao, Bizkaia, Spain. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29199918
Eminent Biosciences(EMBS) and Hospital for Genetic Diseases, Osmania University, Hyderabad - 500 016, Telangana, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/28472910
Eminent Biosciences(EMBS) and School of Ocean Science and Technology, Kerala University of Fisheries and Ocean Studies, Panangad-682 506, Cochin, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27964704
Eminent Biosciences(EMBS) and CODEWEL Nireekshana-ACET, Hyderabad, Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/26770024
Eminent Biosciences(EMBS) and Bharathiyar University, Coimbatore-641046, Tamilnadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27919211
Eminent Biosciences(EMBS) and LPU University, Phagwara, Punjab, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/31030499
Eminent Biosciences(EMBS) and Department of Bioinformatics, Kerala University, Kerala. Publication Link: http://www.eurekaselect.com/135585
Eminent Biosciences(EMBS) and Gandhi Medical College and Osmania Medical College, Hyderabad 500 038, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27450915
Eminent Biosciences(EMBS) and National College (Affiliated to Bharathidasan University), Tiruchirapalli, 620 001 Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27266485
Eminent Biosciences(EMBS) and University of Calicut - 673635, Kerala, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/23030611
Eminent Biosciences(EMBS) and NIPER, Hyderabad, India. ) Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29053759
Eminent Biosciences(EMBS) and King George's Medical University, (Erstwhile C.S.M. Medical University), Lucknow-226 003, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25579575
Eminent Biosciences(EMBS) and School of Chemical & Biotechnology, SASTRA University, Thanjavur, India Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25579569
Eminent Biosciences(EMBS) and Safi center for scientific research, Malappuram, Kerala, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237672
Eminent Biosciences(EMBS) and Dept of Genetics, Osmania University, Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25248957
EMBS publication In association with Institute of Genetics and Hospital for Genetic Diseases, Osmania University, Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/26229292
Sincerely,
Dr. Anuraj Nayarisseri
Principal Scientist & Director,
Eminent Biosciences.
Mob :+91 97522 95342
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I am interested in learning the relationship between the glucocorticoid hormones and stress response in fish species, and understanding the mechanisms underlying variation in GC levels.
thanks in advance..
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In terms of the role of glucocorticoid hormones (and other stress hormones) in regulating life history strategies in humans, you might want to look at the Adaptive Calibration Model (attached) and the empirical literature it has generated.
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If stress cause depression but individual adapt to decrease dramatically depression symptoms in the cost of anxiety appearance in this case it is active coping or maladaptation or what this situation can be described ?
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Thank you very very very much. Your answer is very helpful.
But could you help me with an updated reference.
Thanks again.
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Hello everybody,
I am writing a UMAT for abaqus, a small strain perfect plasticty code. When i run my code for 4 node single element plain strain condition, i get a stress response higher than my yield stress. However, i get exactly the yield stress when a 3D single element is used. Hence, i am wondering what migth be the difference of same plasticty model according to 2D single element and 3D single element and why is 2D stress response is higher. I am adding a graph so that my question could be understood more easily. Thank you in advance!
Çağatay Kasar
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Dear Cagatay Kasar,
I use the Russian edition of this book, but there is an English thranslation
Kachanov L. M. Foundations of the Theory of Plasticity
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I hear from many senior doctors- more than 20 - 25 years of experience- in residency training clinics and departments that a new generation of assistant doctors are on the rise.
Of course the generations change, and this is normal, but there could be interesting opinions.
Would you like to share?
  • Have you realized behavioral patterns different from "the old times"?
  • Have the expectations/stress responses/ increased work handling of assistant doctors changed recently?
  • Is there a noticeable difference in the way the new doctors treat each other in their daily routines? Are the clinics more or less stressful nowadays?
  • How about medical students?
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I am not an expert in the medical field. However, if you are referring to the workload, it depends on the organizational plan. Usually, organizations have already assigned the worker according to the schedule in one period, determining the number of people with a specific skill in a specific job. But this is not for the emergency. If management thinks the plan is working well (no customer complaint, no rework, no queueing, etc.), the workload will not be considered an issue.
So, in my opinion, organizations have to change themselves first before the employee.
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I am running a trial to evaluate the effect of graded levels of some phytobiotics (black pepper, papaya seeds etc) in diets for broiler chicks during starter period on the activities of some immune enzymes (Catalyze, Superoxide dismutase and Glutathione peroxidase). I also wish to study the effects on the dietary treatments relative to the control the effects on stress response. I am thus seeking suggestions on easy, efficient and practical methods to stress 5 week old broilers so that I may evaluate the stress responses via serum cortisol concentration (if practicable).
Could anyone please suggest to me a method that they adopted or are familiar with that is practicable? I will cite the work if it is already in the literature.
Thank you.
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I following the best answer.
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Hydrogen gas has effects on a range of physiological events in plants. It has been shown to have effects on seed germination, plant growth, and development. It has also been found to be involved in plant stress responses and to be protective against pathological abiotic stress challenges. Similarly, it also has beneficial effects during the post-harvest storage of crops. Therefore, its use in the agricultural setting has great potential as it appears to be safe, with no toxicity or harm to the environment.
This Special Issue aims to bring together a body of papers that focus on the current state-of-play of the molecular biology and possible uses of molecular hydrogen with plants. It is hoped that this Special Issue will highlight the future work which may be undertaken in this field and help to encourage researchers to investigate this exciting field further.
For more information please follow the URL, below.
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I am interested , hope we will get some waiver for processing charges as MDPI are open access
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Hello everyone,
I have the spring stiffness and damper coefficient for the Kelvin-Voigt model and I need to calculate/fit (by using Prony series) the Instantaneous/infinite elastic modulus and decay constant, which are generally derived from the stress relaxation response. Since the Kelvin-Voigt is not able to predict the stress relaxation behavior well, do you have any idea how can I calculate those constants?
Best regards,
Shahab
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Dear Dr.
Ijaz Durrani
,
Thank you so much for the references. I checked them .
As I understood, the instantaneous elastic modulus should be equal to spring stiffness+damper coefficient, and the infinite elastic modulus is equal to the spring stiffness only. Also, since the Kelvin-Voigt considers instantaneous shear relaxation, I need to set the decay constant as big as possible. Please kindly correct me if I am wrong.
Best regards,
Shahab
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I am wondering why the HPA mediated cortisol response only peaks after 20 minutes whereas SNS is quick acting. Is this because SNS is nervous system mediated and HPA is endocrine pathway mediated?
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Thank you. The responses are very helpful. I realize I meant to ask "how" rather than "why". So in simple terms, since SNS is neural based it is faster whereas HPA being a neuroendocrine response takes longer due to the various steps involved.
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Hello, we are a group of students. This year we have a project which deal with the "study of the stress response of micro-organisms for the optimization of food production processes".
It's hard to find real infomations about it, so we need some help. Does someone has already work on this subject o one a similar subject ? or know someone who work on it.
Thank you for your help.
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That's true this mission is not impossible and I agree with chère Carole C Tranchant to select one product/process, e.g. fruit juice/pasteurization, as well as one or two pathogens for evaluating the stress response.
Bon courage :-)
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Hi,
I am looking at a change in protein expression after treatment over time and comparing samples to an untreated control. However, certain proteins i.e. stress response proteins, does not produce protein bands during immunoblotting in untreated samples. I was just wondering how I can calculate fold change or alike, with control samples effectively not showing certain protein due to the absence of stress.
Any relevant thoughts are welcome.
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I think your result does not need to be expressed in terms of "fold-change". The result is very dramatic: no expression (0) versus expression. Do you have a standard for this protein? If you have, do a standard curve and transform your data for picogram/fentogram protein. Anyway your control will be 0, but you may feel better with this way to express results. :)
Housekeeping genes will not work for your specific problem. Why? Because if you do the ratios:
1) control protein signal (0)/housekeeping signal (any number) = 0
2) treated protein signal (any number)/housekeeping signal (any number) = any Real number, lets say 5
fold change = 5/0 - blue windows screen (annoying sound)
The result will be 0. Your problem is the 0. Dividing anything to 0 is impossible. Housekeeping (reference protein) is just for loading control correction.
Best,
Jacó
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I started my PhD study about stress and daily activity and I need to find appropriate device for long measurements (+24). I've found two interesting devices so far: E4 wristband produced by Empatica (https://www.empatica.com/e4-wristband) and BioHarness 3 by Zephyr (http://www.zephyranywhere.com/products/bioharness-3). Did you use one of them during your studies? How do you assess their quality? Or maybe did you use something another? 
I'm interested in measuring such signals as: EDA, heart rate and motion. Thank you for each proposition of device and your opinion.
Mateusz Soliński
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You can see also our work on the E4 validation:
Our results are slightly different from those of Matthijs Noordzij as we found no visual ressemblance between wrist and finger SC, and we found accurate HRV metrics compared to ECG only in motion- and stress-free conditions. Having an adaptation period (e.g., 1 min) before the recording intervals of interest seems to increase the measurement accuracy.
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XRD results indicate that there are significant peak broadening and peak shifting in cold rolled Ti64 alloy (10 % cold rolled).
1- Is it logical to relate peak broadening to the lattice strain during deformation?
2- which kind of stress is responsible for lattice strain ? (plastic or elastic)?
3- Is there any relationship between dislocation density and lattice strain value?
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1- Yes, it is logical. Please see the attached File-1.
2- The residual stresses, which are measured by XRD, are caused by plastic deformation.
3- Please refer to the attached File-2.
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I need a method for postprocessing of fatigue damage, from the random vibration respons result. It should be done in the frequency domain, using proper statistics, for speed and it should be easy to implement. How do you do it? Please share your experience.
Often there is one eigen-mode that dominates the stress response. However, when that is not the case the method must be able to handle complex stress states, including multiaxial stresses with rotating principal directions.
One method that is tempting to use involves the scalar stress PSD, called the 'equivalent von Mises stress PSD' introduced by Pitoiset and Preumont. It is derived using the same quadratic formula as when calculating the common von Mises stress invariant, but using the quadratic operation on the PSD matrix elements instead. The resulting scalar stress PSD can then be interpreted as the the PSD for an uniaxial random stress and 'conventional' relations between PSD and fatigue damage can be used (narrow-band, Dirlik, etc.).
There is a lot of relevant papers to study in Procedia Engineering vol 101 (2015), including a nice review of 'spectral multi-axial fatigue analysis' by Benasciutti, Sherratt and Cristofori. Research is interesting enough, but what method do we find efficient in industrial applications?
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Hi Martin -
Please find attached two papers where I have discussed the use of Von Mises (as per Preumont) in the frequency domain. We have implemented it in fe-safe in 2012 as we've been testing it on loads of industrial cases ever since. It is a reasonable assumption in a lot of cases. I think Professor Braccesi (and Cianetti) would probably agree with me on that.
Regards,
Giovanni.
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Excluding pupilometry, is there any method, how to measure immedate stress response? First I was thinking about hearth rate than about skin conductivity. In both cases there is to long delay between occur of stressor and recorded stress reaction. Do you know about something else? Or how to get more accurate information from hr and sc? Perhaps some reaction in eye tracking?
Thank you very much
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Mia Cobb Thank you for your answer!
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These are theories with which I'm familiar so far:
1) Attention Restoration Theory
2) Predictive and Reactive Control
3) Natural settings evoke meditative-like states (which in turn reduce rumination, which prompts a sympathetic nervous system trend towards a more relaxed state)
What other compelling theories are out there that specifically address (or at least explore) the neural, psychological and/or biological mechanisms by which interaction with nature helps to reduce stress...?
(Responses that include links to quality resources would be appreciated.)
Many thanks!
Catherine
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I think that it can be useful to explore the hypothesis that staying for a while in a natural environment can change our daily activity priority list, inducing us to give more importance to our own material necessities ( food, physical safety, etc.) and less importance to social necessities ( linked to appearance and power for example ). This condition could reset our reward and self esteem psycological balance. .Also, natural environnment for his natural importance and beauty could help us to find a narcisistic balance that in a artificial environnment we could find more difficult to get ( for example, if I enjoiy walking in the wood near my home I dont have to go walking in a crowded and far commercial mall.).
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I want to do single cell RNA-seq with yeast. Droplet-based microfluidic technology is adapted for mammalian cells and the lysis method is therefore unlikely to be sufficient for yeast. Therefore, I'll need to digest the cell walls and submit spheroplasts for scRNA-seq. The problem is that the transcriptomic signature I'm anticipating will largely involve activation of stress response pathways including the cell wall integrity pathway. I therefore need to preserve the cellular RNA prior to processing (including spheroplast prep, live cell sorting by FACS, and transport to scRNA-seq facility).
Any fixation method which permeabilizes the membrane (like alcohol) will be incompatible with my sort (dead cell stain like PI or SYTOX Green). Any fixation method which requires removal of the cell wall (like DSP) won't be sufficient to protect RNA during cell wall digestion. Reagents like RNAlater seem viable but I don't know how I would digest cell walls and sort cells all while constantly keeping the samples in RNAlater.
Any advice is appreciated!
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Hi,
You can add RNAse inhibitor cocktail to your samples and keep them at 4 degrees all the time.
Or you can ask your NGS core to test the drop-seq protocol with a stronger lysis reagent to avoid the initial digestion before the droplet generation.
Or you can do drop-seq from the initial population, before FACS, but with the most intact cells. You will get all the populations present on your PCA clustering and you will need to pick the population of your interest in-silico. Anyway, it will cost more because of deeper sequencing in comparison with the sorted sample.
Best,
Michail
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I am a Crop physiologist and would like to understand stress responses of plants of Indian rice varieties that have been recently developed.
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You can contact Indian Central Rice Research Institute, Cuttack in this regard.
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Hi!
In our psychophysiological stress research, we plan to measure 3 modalities: EDA, ECG, and temperature. However, we also consider EMG as a interesting stress marker. The physiological measurement will last about 20 minutes altogether.
Do you have some experience in measuring EMG (e.g., the activity in upper trapezius muscle) to index stress response to psychological stimuly (e.g., social evaluation, mental load)?
Would you recommend to use EMG signal in a multi-modal assessment of the stress response? Does it provide a valid and reliable measure suitable for indexing the presence (or degree) of acute stress?
Thank you for any relevant advice,
best,
M.
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Hello
If the objective of the psychophysiological evaluation protocol is to evaluate the impact of the stressor (arithmetic task, TSST, cognitive task, etc), of course the EMG; but my suggestion is to measure it in corrugator muscle (if it is a psychological task). If the task requires physical activity (increase-decrease) of the muscles to test the effectiveness of some technique, then the trapezius muscle is more appropriate. It depends on the objective of the study (to assess stress, or deactivation of stress, you have to select the stressor and the measure). In my experience I used the EMG for years, but I have seen that it also limits the movement of the spontaneous response to the emotional task. Then I have replaced it with the infrared thermal image and basically the same thing is found: the corrugator muscle increases the temperature when the subject is stressed, the nose decreases the temperature. In press I have some manuscripts sent with infrared thermal image and blood pressure to assess stress-relaxation in both clinical population and healthy subjects. In short, according to the objective of the study (Evaluation of autonomic and somatic activity?) I suggest the EMG.
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I am interesting to do work on prediction or searching of cis regulatory motifs (stress responsive) from genes(promoter region) in plant resources. so anybody can suggest me a good database of such motifs other than PLACE. or suggest any tool to efficiently predict moist stress/salinity stress responsive motifs or elements.
Thanks in advance.
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Fatigue loading tends to damage the material after a particular number of cycles. Considering the material science and human body in a single frame, imagine a person cycles up a mountain everyday. His knees are exposed to fatigue loading, and is there slow damage happening to his knees due to this fatigue loading? 
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This was explained to us years ago:
Wolff's law, developed by the German anatomist and surgeon Julius Wolff (1836–1902) in the 19th century, states that bone in a healthy person or animal will adapt to the loads under which it is placed. If loading on a particular bone increases, the bone will remodel itself over time to become stronger to resist that sort of loading.The internal architecture of the trabeculae undergoes adaptive changes, followed by secondary changes to the external cortical portion of the bone, perhaps becoming thicker as a result. The inverse is true as well: if the loading on a bone decreases, the bone will become less dense and weaker due to the lack of the stimulus required for continued remodeling. This reduction in bone density (osteopenia) is known as stress shielding and can occur as a result of a hip replacement (or other prosthesis). The normal stress on a bone is shielded from that bone by being placed on a prosthetic implant.
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i am aware that gene expression profiles might differ between cell types and types of mechanical forces. But what are some 'consensus genes' which expression level changes (high chance)  upon mechanical stress? i want to detect some gene expression changes to justify doing RNA-seq later.
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You may find refs in  Communication in plants ...by František Baluška, ‎Stefano Mancuso, ‎Dieter Volkmann - 2007 available on google books p253-
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Hi everyone,
Why is it indispensable to activate the ATF4 during amino acid stress response?
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ATF4 activation is indispensable during AAR due to the importance of ATF4 as a transcription factor in guiding the downstream events.
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Dear fellow researchers,
I am attempting to carry out a thermal stress analysis on a 2d quarter cylinder part model I have attached in the image file. The geometry is in XY plane and I want to apply differential heating in the inner and outer radial surfaces to generate thermal stresses. I want the stress responses for a generalized plane strain configuration. However, the results don't match with my closed form solution. I am positive there is some mistake in my FEM model. Particular queries I have during the modeling are the entries I have attached in picture 2 file. Can someone please tell me the meaning of these fields. For my problem I would like the cylinder to expand freely with a constant strain in the Z direction.
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If your problem is defined in the XY plane then the Z axis is axial.  In this case I think the generalised plane strain boundary conditions should involve the translation UZ and the rotations RX and RY or in ABAQUS speak, U3, UR1 and UR2.  If these freedoms are set to zero then you should obtain the same result as a plane strain model.  
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I have a mutant strain that I have analysed by RNA-seq and when compared to WT, the differentially expressed genes seem to be following the pattern for the yeast environmental stress response (up-regulation of metabolic genes and down-regulation of translation genes etc). Is there a direct way in which I can test whether this mutant is inducing the ESR? for example the phosphorylation of a protein?
Thank you :)
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Hi Julia,
Pol III transcription is known to shut down within minutes of introduction of stress. You might want to look for its negative regulator Maf1 and its phosphorylation.
Good luck.
Yatendra
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It has been reported that excessive inflammatory cytokines such as IL-1beta, IL-6 and TNF-alpha in the serum secreted from the tumor tissues are responsible for the development of weight loss up to 5% decrease within 6 months, also referred to as cachexia. Hyper-metabolism in skeletal muscles and adipose tissues is characterized by promoted beta-oxidation of free fatty lipids in mitochondria. Enhanced beta-oxidation causes accumulated ROS. In addition, the cachexia cancer cells lead to the activation of p38-MAPK signal pathway in skeletal muscle cells. I wonder whether metabolite-induced ROS directly activates p38-MAPK signaling cascade, and furthermore, other stress-response signal pathways are related or not in the cachexic pathophysiology.
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Thank you for the detailed explanation!
CD44 variant-positive normal tissue and/or cancer stem-like cells tend to be resistant to be positive for phosphorylation of p38-MAPK under redox stress.
The IL-6 and/or TNF-alpha inhibitor has attracted attention as the treatment against auto-immune diseases including rheumatoid arthritis and SLE.
These medical agents are alredy used for patients with cachexia?
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The Seahorse kits are so expensive. I was wondering if I could just buy the chemicals and use these in place of the kits. Specifically Oligomycin and 2-DG.
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Oligomycin: 04876
Rotenone: R8875
Antimycin A: A8674
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Hi, I want to use the acute social defeat stress but I don't know which strain should I order, the literature says in general only CD1.
Thanks!
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Ok, thank you very much Beatrice!!!
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I want to establish the high efficient cardiomyocyte differentiation system using mouse embryonic stem cell (mESCs). My colleague told me the hanging drop method (old and classical but famous one). This worked well a little bit but it was not enough efficiency (around 1-5%) to conduct further studies.
 I want to research the stress response of mESC-derived cardiomyocyte. It needs more purity and mass. If you know other better methods, please tell me.
Is there any good cardiomyocyte differentiation system? 
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My previous senior in the lab was working on cardiac differentiation.  He made some series of stable cell lines, one of them which expresses YFP under the control of cardiac specific B-MHC gene promoter.  Using this stable cell line he did FACS and purified cardiomyocytes. He could get approximately 5% pure cardiomyocytes by flow cytometry. 
Also, he made one another stable ESC line with a IRES based vector, which expresses puromycin and GFP under the control cardiac specific a-MHC promoter. The advantage of using this cell line is that, by applying puromycin in the culture media, you could get 100% pure population of cardiomyocytes in culture.
I hope this answers to your question
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If anyone knows anything about salivary alpha amylase, I would be interested to hear your experience with collection and analysis.
Blood pressure will also be measured, but I am not sure that is enough of a stress response measure. 
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The company 'Salametrics' has reliable assays and collection protocols for measuring free cortisol and alpha amylase in saliva.  https://www.salimetrics.com/assay-kit/cortisol-salivary-elisa-eia-kit   They also have protocols for other hormones that can be measured in saliva, just check out their website,
Measuring cortisol doesn't have to be variable, so long as you control for various factors. Time of day that you are sampling, whether the subject has eaten/drank anything immediately before sampling, don't let them smoke before hand, etc. It's not difficult to do, you just have to carefully consider potential confounds and design your study properly.  Look in the literature for studies from David A. Edwards at Emory University.  He has done a lot of research looking at cortisol, testosterone, and other things in saliva. His studies are always well designed, so they will be great examples of how to do the collections properly.  
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I have constructed a rail track model in ABAQUS using dynamic explicit analysis.
Axle loads are positioned at the start of the track and for a period of several seconds the load magnitude rises in amplitude until they reach the required value, to prevent a sharp jump in track inertia. 
The stress response of certain layers in the track is fine initially, but suddenly the response becomes chaotic and very asymmetrical.
I have attached a few images of the ballast layer to show the response. Note that in all of the photos the load remains stationary, albeit the magnitude of the load is increasing from zero to maximum. The photos are from consecutive time increments with the same load step.
Thank you in advance.
Kind regards.
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Since your analysis is dynamics, I would expect these fluctuations to be due to elastic waves.
If your loads are stationary and you are not interested in dynamic effects, consider switching to static.
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There is evidence that stress is mediating the effect of diet on body weight (Peters, A et al). 
Is there  also evidence on whether (reduction of) stress may be involved in the beneficial health effects of leisure physical exercise?
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Please read this article related to stress reduction and weight management. 
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Good morning
I was analysing the literature on stress levels of different professional categories. Unfortunately, I found that the category I am most interested in are sampled for salivary cortisol; the other, which I hoped to use as a benchmark, are sampled for blood or urine cortisol. Is there any way of making findings with these different techniques comparable with each other?
Thank you in advance
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Thanks again, Tim! :-)
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We would like to design an experiment, in which degradation of a certain transcription factor leads to an optically visible (i.e. easily screenable) phenotype in Arabidopsis seedlings (about 3-5 days after germination). The phenotype, however, cannot be light-dependent and the expression of the TF needs to be inducible and not influenced by light either.
We were looking into defense and stress responses to find a good candidate, but havent had a very good idea so far. 
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Thanks for the replies.
Apparently my description was a little ambiguous: What we need is a transcription factor, which is not differentially regulated by light. As COP1 is clearly light-regulated all downstream targets of COP1 (e.g. HY5, LAF1, HFR1) are not suitable. This is why we were looking at stress responses. If we had a transcription factor that could be induced/repressed by a certain stress but in a light-independent fashion, that would be our guy. Ideally the induction/repression would lead to a clear phenotype in seedlings.
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Feedback loops are triggered at
various levels to shut off the axis through inhibition of the
corticosteroid receptor (GR + MR). The loops are activated from the
adrenal gland to the hypothalamus, frontal cortex and hippocampus.
When receiving this information the hippocampus itself also inhibits
the hypothalamus directly (I am not sure how). all this feedback loops
result termination of CRH and in turn ACTH and glucocorticoids
production.
By the way, I think one major out come of a non-working feedback loop
which results accumulation of glucocorticoids is depression.
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Dear Otu, there is a wonderful review paper by James P. Herman that explains the pathways and neurotransmitters involved in hippocampal control of the HPA axis. I am attaching it for your reading. Best of luck!
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I have encountered many articles that have conducted inductive expression of transcription factors by cloning their respective inductive promoters -- constitutive expression is detrimental to plant life. Since the stress response also elevates HSPs in plants that ameliorates plants' response against stresses, and what I believe also induces resistance against pathogens, are there articles regarding overexpression of HSPs in plants that have shown to revamp plant performance?
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Dear Sarbesh,
Please, see the following publications:
1-Plant Cell. 2000 Apr; 12(4): 479–492.
 
PMCID: PMC139847
Heat Shock Protein 101 Plays a Crucial Role in Thermotolerance in Arabidopsis
Christine Queitsch,a Suk-Whan Hong,b Elizabeth Vierling,b and Susan Lindquist1,a
Author information ► Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
 
See attached file.
ABSTRACT
Plants are sessile organisms, and their ability to adapt to stress is crucial for survival in natural environments. Many observations suggest a relationship between stress tolerance and heat shock proteins (HSPs) in plants, but the roles of individual HSPs are poorly characterized. We report that transgenic Arabidopsis plants expressing less than usual amounts of HSP101, a result of either antisense inhibition or cosuppression, grew at normal rates but had a severely diminished capacity to acquire heat tolerance after mild conditioning pretreatments. The naturally high tolerance of germinating seeds, which express HSP101 as a result of developmental regulation, was also profoundly decreased. Conversely, plants constitutively expressing HSP101 tolerated sudden shifts to extreme temperatures better than did vector controls. We conclude that HSP101 plays a pivotal role in heat tolerance in Arabidopsis. Given the high evolutionary conservation of this protein and the fact that altering HSP101 expression had no detrimental effects on normal growth or development, one should be able to manipulate the stress tolerance of other plants by altering the expression of this protein.
2-Role of plant heat-shock proteins and molecular chaperones in the abiotic
stress response
Wangxia Wang1,3, Basia Vinocur1
, Oded Shoseyov1,2 and Arie Altman1,2
Abiotic stresses usually cause protein dysfunction. Maintaining proteins in their functional conformations and preventing the aggregation of non-native proteins
are particularly important for cell survival under stress. Heat-shock proteins (Hsps)/chaperones are responsible for protein folding, assembly, translocation and degradation in many normal cellular processes, stabilize proteins and membranes, and can assist in protein refolding under stress conditions. They can play a
crucial role in protecting plants against stress by reestablishing normal protein conformation and thus cellular homeostasis. Here, we summarize the significance
of Hsps and chaperones in abiotic stress responses in plants, and discuss the co-operation among their different classes and their interactions with other tressinduced components.
See attached file.
3-Small heat shock proteins and stress tolerance in plants
Weining Sun, Marc Van Montagu*, Nathalie Verbruggen1
Vakgroep Moleculaire Genetica, Departement Plantengenetica, Vlaams Instituut voor Biotechnologie (VIB), Universiteit Gent,
K.L. Ledeganckstraat 35, B-9000 Gent, Belgium
Received 8 August 2001; received in revised form 2 May 2002; accepted 4 June 2002
Abstract
Small heat shock proteins (sHsps) are produced ubiquitously in prokaryotic and eukaryotic cells upon heat. The special importance of sHsps in plants is suggested by unusual abundance and diversity. Six classes of sHsps have been identified in plants based on their intracellular localization and sequence relatedness. In addition to heat stress, plant sHsps are also produced under other stress conditions and at certain developmental stages. Induction of sHsp gene expression and protein accumulation upon environmental stresses point to the hypothesis that these proteins play an important role in stress tolerance. The function of sHsps as molecular chaperones is supported by in vitro and in vivo assays. This review summarizes recent knowledge about plant sHsp gene expression, protein structure and functions.
D 2002 Elsevier Science B.V. All rights reserved.
Keywords: Chaperone; Embryogenesis; Transgenic plant
See attached file
Hoping this will be helpful,
Rafik
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Stress response of microbes can decide whether they will be killed by an antimicrobial agent or they will develop immunity ? Is there a way out to use it for efficient killing of microbes?...suggestions...
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What Doesn't Kill Them Makes Them Stronger
Bacteria threatened by antibiotics respond by slurping up bits of DNA from their surroundings, some of which are likely to make them resistant to the antibiotics. That ought to worry people. It probably won’t, one reason why antibiotic resistance is the problem it is.
Many bacteria respond to some stresses with an SOS response. Essentially a heightened ability to repair damaged DNA, the SOS response can also result in rapid changes in DNA that may enable the bacteria not only to survive the immediate stress, but to weather it better in future. A group led by Jean-Pierre Claverys, of the Laboratoire de Microbiologie et Génetique Moléculaires in Narbonne, France, show in a paper in this week’s Science that Streptococcus pneumoniae, which is responsible for a burden of diseases way beyond pneumonia, has something similar that is possibly even more effective.
DNA damage causes S. pneumoniae to change its behaviour, to become “competent for genetic transformation”. The changes are complex. What they mean is that competent cells can absorb DNA from the environment and incorporate it into their own genomes. That DNA might just confer resistance to the antibiotic that damaged the DNA in the first place. Better yet, competent cells can kill their non-competent neighbours. That frees the non-competent cells’ DNA, which may well contain genes for antibiotic resistance, because they would have no reason to become competent if they were resistant to antibiotic damage.
The upshot is that fratricide and competence together act to generate a mass of genetic diversity, a veritable smorgasbord of genes there for the taking. Some of the genes are likely to confer new abilities on the competent cells that take them up. And that is why Claverys and his colleagues sound a bit of an alarm. S. pneumoniae is relatively common, without causing any symptoms. One study in Sweden found that more than a third of children carried antibiotic resistant strains of the bacteria without showing any symptoms. Susceptible strains are even more common. Give those carriers certain antibiotics – for other diseases – and the S. pneumoniae could well pick up additional resistance. As the French team puts it:
[I]nappropirate antibiotic treatments could accelerate the occurrence of additional resistant clones and promote the evolution of virulence.
All of which prompts me to reflect that, as I hinted before, antibiotic resistance is a huge squandered commons. There is no question that pathogens will develop resistance. The only questions are how quickly and how often. And yet patients have demanded them and doctors have prescribed them with little thought for the consequences. In many places the doctor is an unnecessary element in a simple transaction between self-dosing buyer and self-enriching seller. Worse, farmers have strewn the stuff about in search of profits now with no thought of the costs to be paid by the rest of us.
“The world has become a dilute solution of tetracycline,” as one Stuart Levy, one of the few people to sound the alarm, told me many years ago.
Not just tetracycline. And the result is massive multiple resistance. Our best weapons have become useless, by being used both too little and too often.
As a footnote, it is fitting that Claverys studied transformation competence in S. pneumoniae. In 1928 Frederick Griffith injected mice with two forms of the bacteria. One was the normal, virulent and lethal form. The other was a mutant that caused no disease. Griffith killed the virulent bacteria by heating them. Mice that received the dead bacteria stayed perfectly healthy. So did mice that received the non-lethal form. But mice that got a mixture of live, safe bacteria and dead dangerous ones died.
Something – Griffith called it the transforming principle – made the safe bacteria lethal again. That something turned out to be DNA, and Griffith’s experiment was an absolutely vital step in identifying the chemical basis of heredity.
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Traditional paychosocial measures of race based discrimination stress do not take into account biological factors. I am interested in measuring the effecfs of chronic racial discrimination stress on blood sugar control  in diabetic African Americans by incorporating biomarkers of stress response with a questionnaire. What considerations would need to be taken in terms of analysis, choice of questionnaires and appropriate biomarkers for this population? 
Thanks for any guidance you can offer.
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Its best to follow a qualitative to quantitative approach because such issues have a high cultural dimension which can be captured through qualitative research methods only
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If anyone knows something about this topic please answer me. Thank you!
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HI
It a great mistake to use the division physical stress and psychological stress. Stress is stress and it is a very complex phenomenon. It is as two way street. I recommend to read Hans Selye. The father of stress construct.
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In response to stress certain genes are induced. These genes are induced due to some transcription factors (TFs). So how are these particular TFs transcribed in response to that particular stress? Just trying to better understand things. If anyone can give me a good reference, will be thankful.
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Hello Brijesh,
In vertebrates, glucocorticoids (GC) are probably the most well studied hormones that, among other things, increase in response to a stressor. GCs bind with glucocorticoid receptors (GRs) on cell surfaces. This complex translocates to the nucleus where it acts as a transcription factor (TF) to increase or decrease gene expression. It can up-regulate or repress the expression of other TFs that have various actions, including ones that are anti- and pro-inflammatory. GCs are steroid hormones enzematically synthesized from cholesterol, so they are not produce directly via transcription. I am no expert on the mechanistic side of stress physiology, but a quick search for "glucocorticoid transcription factor" produced a number of papers that look like would be good starting points (e.g., http://www.ncbi.nlm.nih.gov/pubmed/11448148). 
Best,
Blake
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I am interested in working in Malawi and would like to use measures that have been adapted appropriately. Any articles welcomed.
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Beatrice,  I can read some German so thank you for that article.  I am particularly thrilled with the Kim article.  Thank you very much for this.  If I may offer anything in return, let me know!
Kim
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I want to know the assay for DNA damage in response to pathogen and heat stress and also due to reactive oxygen species produced in stress response
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Hi,
Comet assay detects single strand breaks, please see my profile to get all the information that you need.
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I’ve run into a problem with a research project that I’m completing.  Previous research has demonstrated a curvilinear relationship between PTG and stress responses, with the relationship resembling an inverted U-shape (e.g., McCaslin et al., 2009; Taku et al., 2015).  The same finding has been found with previous research comparing the relationship of PTG and depression (e.g., Kleim & Ehlers, 2009).  I am working with data from a sample of veterans treated for PTSD in a residential setting, and I’m comparing PTG with depression.  My analysis also produced a curvilinear relationship, but with a U-shape (not inverted-U).   This is very different from previous research.  I have noticed that mean scores for depression are much higher than in previous studies (M  for BDI-II = about 24- moderate depression).  The mean PTGI score is about 55.  I’m not sure what to make of this, and am wondering if I should just scrap my project as it is quite different from findings of previous studies.  Does anyone have a possible explanation as to why the curvilinear relationship might be so different?  Thanks.   
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Interesting patterns, indeed. I wouldn't scrap the project. One issue might be the presence of influential cases that are potentially exerting a strong 'pulling' upward of the curve at the upper end. Also, while I'm less familiar with the PTG literature, it might be that some individuals who experience "growth" also experience a kind of clarity about the realities of their experiences--past and present. I think the findings are fascinating and are worth putting out there for peer review. It might get others to think about the conceptual meaning and implications of "growth" and perhaps the measure itself. Good luck with it. Fascinating project. 
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Hi all,
So I am treating MCF7 cells with a drug and I have a vehicle (DMSO) control. The DMSO in the control is at 0.022% which is below the limit of 0.1% but I am seeing stress responses in my vehicle control, as much as my treated (via western blotting). I am seeing p53 levels for my control at the same levels as my treated, including LC3B, PARP cleavage. Has anyone experienced this?
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What about using ethanol instead of DMSO. may be it would be less toxic
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Dear all, 
I want to test the nitrosative stress response with the fungi.
Can I use sodium nitrite (NaNO2) to be the nitrosative stress?
Thank you all.
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Thank you for your suggestion Mr.Shayan Amiri.
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I want to establish the high efficient cardiomyocyte differentiation system using mouse embryonic stem cell (mESCs). My colleague told me the hanging drop method (old and classical but famous one). This worked well a little bit but it was not enough efficiency (around 1-5%) to conduct further studies.
 I want to research the stress response of mESC-derived cardiomyocyte. It needs more purity and mass. If you know other better methods, please tell me.
 Now I'm planning to try the two following methods; glucose-depleted lactate-added culture (Shugo Tohyama, 2012) and Noggin treatment (Yuasa S, 2005).
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Dear Naoto,
I would strongly recommend you to try out this protocol:
It works very nice with both human iPSCs and embryonic stem cells and it is quite easy and fast.
Good Luck!
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I am looking for an answer to a rather systemic biology question - is there a 1:1 relationship between HPA axis activation and stress response (in terms of the whole body, I mean not the cellular or tissue stress). I mean could an experimental model without functional HPA axis experience stress in its proper sense of word? I know that it depends on what how we actually define stress, but still, is there any possibility of generalized stress response without HPA axis activation? Will be very grateful for any suggestions, Julie
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dear Julie, 
My opinion is that stress in its proper sense involves the activation of the HPA axis. 
Stress is defined as a state of real or perceived threat to homeostasis, which maintenance in the presence of stressors requires activation of  responses involving the endocrine, nervous, and immune systems. 
Dialogues Clin Neurosci. 2006 Dec; 8(4): 383–395.The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress
Sean M. Smith, Wylie W. Vale,
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I am trying to verify if the bulge tester I built is working correctly. The material I am testing is a PP-PE copolymer. 
I have carried out 3 bulge tests. These have shown that the Major and Minor strain vary by about 5% to 8% meaning the stress state is very close to biaxial. I also carried 3 uniaxial tensile tests each in both the transverse and longitudinal direction.
The problem I am facing is that theory states that for metals, biaxial equivalent true strain should be double the uniaxial strain at fracture following the same stress-strain curve. My tests show that true strain in biaxial is about double of uniaxial strain at fracture, but the stress-strain curves do not line up correctly. Please see http://i.imgur.com/CeghDRJ.png for the stress strain curves.
Here is the equivalent strain response: http://i.imgur.com/LSfvHV1.png
One thing to note is that the strain response for the biaxial bulge tests is non-linear. I don't think this is the reason for the difference between uniaxial and biaxial stress-strain curves. Since I am straining much faster during bulge testing, I would expect the stress response to be much higher after .15 strain on the stress-strain plot which is not the case.
Is there something special going on in polymers that explains the difference between the two results? I could not find much research papers that show this difference. 
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This type of material are generally pressure depend which is very different from metal.
You have to use non associative plasticity with two yield surface and take the pressure sensitivity into account with sometimes damage. We have done bulge test on PP and it's the only way to have good results in tension and for the bulge test with the same material parameters.
Good luck
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STUB1/CHIP is a E3 ligase protein that ubiquitylates and tags other proteins for degradation. It is involved in major developmental processes for the downstream expression and/or stabilization of other proteins. But its function is majorly seen in heat-induced stress response, wherein ER stress is regulated by degradation of mis-folded proteins in the ER, after being tagged by STUB1/CHIP.
In fact, in vivo data for STUB1 knock-down in mice, showed increased sensitivity to heat-induced apoptosis and accelerated aging. Putting all this data together, should CHIP/STUB1 be considered pro-survival or apoptotic?
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I believe it depends most on cellular and enviromental context...We have showed that hippocampal slices submitted to ER stress are protected when CHIP is overexpressed and it attenuates pro-apoptotic mediators triggered by ER stress.
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This is going to be the basis of my future research.
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Thanks Laurie for the suggestions.  I was referring to the psychologcal and behavioral determinants.
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We have generated multiple mutant lines (ATAF family) to see some drought stress response in order to undestand some protein interaction. Could you please advise and suggest me some methods to obtain preliminary data regarding drought stress assay?
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Hallo Isura,
Did you read the papers I suggested in an email some weeks ago?  I hope you are making progress.
Regards
David
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Hi friends
I'm writing a user subroutine for a viscoelastic material and material parameters are depend on shear strain rate. I use DSTRAN(3)/DTIME to relate parameters to the shear strain rate in shell element. abaqus solves the problem but during the analysis strain increment becomes zero and parameters and stress response become wrong. Did anyone have such problem with shell elements?
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I am glad that you were able to locate the issue.
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I'm studying the function of a gene whose expression levels are significantly increased in response to different stress-inducing conditions. I would like to assess the presence of stress responsive elements in the promoter. Any suggestion? Thank you.
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I have very less experience to answer your question. But was able to find an article which seems answerable and that could help you. Also login to this website http://caps.ncbs.res.in/stifdb/help.html to get a brief idea about how actually the algorithms for identifying stress responsive elements work .....
All the best
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Hi Everyone,
I am trying to find stress responsive cis elements in the upstream regions of miRNAs in Brassica napus. miRbase gives me the genomic coordinates of miRNA precursor gene, but I am not able to find those in Brassica database.
I am attaching a link for one such miRNA, the coordinates are given in the Genomic Context.
I would highly appreciate if some one could guide me on how to find the upstream region from the coordinates. 
Thanks
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Thanks Ajay. Your suggestion helped me. 
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I am looking for a method to detect stress in response to a fear or pain event. The test will be used to compare the response level of birds to different short term exposure to fear and pain situations.
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There is an absolutely huge literature on corticosterone to assess BOTH acute and chronic "stress" levels. Baseline corticosterone (assessed at <2-4 minutes for most vertebrates) may be indicative on the level of corticosterone for regulation of energy, etc. It may also reflect stressors occurring just before sampling. However, this should be easy to distinguish if you either monitor the individuals in a lab-setting or have made detailed notes of behavior and environmental events prior to sampling (e.g. predation events, loud noises, interactions with conspecifics). The latter will take rather detailed and complex modeling and, to my knowledge, has not been seriously attempted.
There is an old paper in turkeys that used blood-pressure cuffs to measure instantaneous changes in blood pressure in response to acute stressors. Many years ago, I looked into this option for smaller birds, but it just wasn't feasible for me at that point. That would enable you to indirectly assess the rapid portion of the stress response (via catecholamines).
If sampling blood is an acceptable option, I would go the route of measuring corticosterone. It is easy and inexpensive to assay. As I mentioned, there is a nice literature to draw from (see the extensive work of John Wingfield and his many colleagues and students). As you probably already know, you can get a good baseline from control and experimental groups within three minutes, and then you can keep them in a bag for a short period, taking serial samples at some set points (e.g. 5, 10, 30 minutes). Essentially, all you really need is a baseline sample (they should be the same between groups) and a time point after 5 minutes. Simple design.
Other notes:
- If measuring pain thresholds, it may also be good to use some of the collected blood for a testosterone assay, as testosterone may influence pain sensitivity.
- Maybe also measure corticosteroid-binding globulin (also called transcortin), so you can assess free and bound levels of corticosterone available to the target tissues.
All that said, perhaps I've jumped away from your initial question. Are you really wanting to know how to best measure the immediate portion of the stress response? If that is true, I would go with heart rate measures. I feel oddly about this, but you may consider looking at a paper I co-authored on the use of heart-rate telemetry in small passerines (in the field). See my pubs on my profile page.
Sounds like cool research!
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Can anyone recommend literature on the effect of cell sorting on proliferation capacity / stress response / senescence of the sorted cells (especially MSC)?
How is the cell size influencing the stress response? 
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Thank you Robert! What you describe, is what we saw too, but I would need some reference for it... So if you have any tip, I would be very grateful! Kind regards, Mathias
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I think it has also to do with the vocal tone of the handler !!! Some people don't talk much to their mice...But there is a very big difference in mouse when you take him out of his cage...if mouse recognizes the voice he appears to more adaptable to whatever procedure you are performing...which is possibly due to trust...and as mice do communicate with each other in and between cages so the experiences they have are likely to be shared