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I plan to inject poly I:C via i.p to induce immune responses. What I have now is the Polyinosinic-polycytidylic acid potassium salt from Sigma (P9582, with buffer salt). The product information from sigma has the following description:
'The products require ionic strength to maintain the double-strand structure. To prevent denaturation, reconstitute Catalog Numbers P1530 and P0913 in solutions with physiological salt concentrations (e.g., saline solution). Reconstitution may prove difficult, and require heating (50°C) and cooling to achieve re-annealing.
Reconstitution of Catalog Numbers P9582 and I3036 at ∼10 mg/ml of water yields a polynucleotide in physiological phosphate buffered solution'
So is there anyone who has experience in poly I:C injection can tell me how to prepare the poly I:C? Do I need to prepare it immediately before the injection?
Thank you!
Yuhui
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Hi Yuhui,
Thanks a lot for asking this question!
Just wondering could you please share your final protocol for poly(I:C) preparation.
I'm still confusing should I prepare it just before injection (i.p. 4mg/ml) or it's fine to make a stock (10mg/ml).
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I am a nurse who is researching why some cancer patients are not reporting the same dramatic effectiveness of high-dose cannabinoid extracts on causing tumor regression as some others. Here is the best current article I know of which explains the Anticancer Mechanisms of Cannabinoids and includes the information about THC-resistant glioma cells that overexpressed Midkine (MDK) and became sensitive to the THC after pharmacologic ALK inhibition. Velasco G, Sánchez C, Guzmán M. Anticancer mechanisms of cannabinoids. Current Oncology. 2016;23(Suppl 2):S23-S32. doi:10.3747/co.23.3080.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791144/
 
We know there are different rates of over-expression of CB1 and CB2 which appear to play at least a partial role but, of course, the various tumor microenvironment factors, mutations and, especially, this information about MDK/ALK as a mechanism of resistance to THC should soon produce much more clarity about this problem.
 
I am intrigued by the knowledge that Non-Small-Cell Lung Cancer and many Breast Cancers often have ALK mutation (and there are significant patients with NSLC and Breast Cancer who do not seem to get as much/any tumor regression yet others get dramatic regression and even No Evidence of Disease with high-doses of THC and CBD). The NSLC patients with ALK mutations are suddenly becoming more treatable after addition of an ALK inhibitor crizotinib, ceritinib, alectinib and others. I have been unable to find any research assessing ALK mutation status and THC resistance or sensitivity for tumors from other tissues than the brain.
 
I can't help but wonder if research could show if there are THC-resistant tumors of lung and breast ++ that are also ALK mutated or Midkine overproducers that may regain their sensitivity to THC as the glioma cells did after pharmacological ALK inhibition.
Thank you for your assistance.
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HA, I know exactly what you mean! Had similar cases and the delusory stuff is widespread thanks to the unethical "cannabiz" b.s. Would love to chat. I'm in a home office these days, based in S.Oregon ie pacific time zone. My cell is 541 326 6082. Afternoons best. Around most of the day tomorrow wed 5th but can call you to suit if you are still a busy onc nurse. Let me know what works. Best JT
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Hello
In different literature it has been concluded that there is a significant inverse correlation between SUV_mean and ADC_mean.
I need to know about metabolic energy in different parts of tumor (qualitatively of semi-quantitatively) but I only have Average diffusion coefficient maps. Since FDG-SUV is related to metabolic energy somehow and since there is an inverse but significant correlation between SUV and ADC, I wonder if I can use ADC maps for mapping tumor's activity or not? (For example in parts with lower ADC, I assume higher SUV (activity) vice versa)
Any help would be appreciated.
Thanks in advance.
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Although apparent diffusion coefficient (ADC) value can be used as a valuable biomarker for tumor detection, grading, prognostication, and response to therapy; it is not an indicator of tumoral metabolic activity. This value depends mainly on the tumor cellularity and integrity of cell membrane (pathodynamic environment), which determine the magnitude of water molecule diffusion. As you mentioned we expect the value to be lower in high cellular parts of a tumor, but for example the ischemic parts may cause a reduction of water diffusivity and hence a lower ADC value as well.
Some studies have concluded that there may be a negative (inverse) correlation between standard uptake value (SUV) and ADC value; however, a recent large meta-analysis by Shen et al. concluded that correlation between these two parameters is generally poor (you may find the link of the paper as an attachment to my answer).
In summary, you cannot determine metabolic activity of the tumor by ADC mapping. SUV [measured by positron emission tomography (PET) scan] and ADC value [measured utilizing magnetic resonance imaging (MRI)] may be used as complementary information to diagnose tumoral lesions and predict their behavior, which is currently performed on multiparametric hybrid PET-MRI machines particularly in neurooncologic imaging.
Among all advanced MRI techniques, MR spectroscopy is best correlated with the cellular metabolism of a tumor especially if it is performed by multivoxel technique (because of the high spatial heterogeneity within tumors).
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Currently trying to slice mice brain from 200um slices into 40um slices for IHC. At times it works perfectly fine, but other times there are complications where the slices do not stay intact, or the whole 200um brain slice falls off. We use 30% sucrose and dry ice as a glue to the machine. I would like to ask if anyone has some tips and tricks to improve the quality of the slices. 
The 200um slices were introduced to dopamine and then left in PFA. In case of not proceeding to slicing immediately, we store them in Anti-freeze and then wash it with pbs thoroughly prior to slicing.
- Any environmental factors that may have a big affect on the slicing (perhaps temperature wise)?
-Any blades that are optimal?
-The timing of PFA incubation?
Any tips would be very appreciated!!
Thanks,
Lynn
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How long do you fixed in PFA? or did you perfused the animal? I have not used the anti freeze, but I can reccomend the last wash be with 30% surcose before embede in OCT medium to slice.... I have did it already and it works.... you have to make sure to extend your 200um slide in an uniform position before freezze... in order to obtain your 40um slices. Good luck!! 
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Thank you Rafael
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Synasthesia is a neurological phenomenon where stimulation of one sensory or cognitive modality leads to automatic, involuntary experiences in a second sensory or cognitive pathway/modality. It has been observed that around 4% population have this feature and connection of words/numbers to colours (grapheme-colour synaesthesia) is one of the commonest observed types. Studies have shown that rTMS applied over a right parieto-occipital region disrupts performance on a synaesthetic priming task indicating the role of this region in building up of this phenomenology (Muggleton et al, 2007; expected as the cross talk between visual and somatosensory spatial reference regions). But are you aware of any studies using M1-TMS as the measure of altered excitability while responding to any 'so called' non-specific stimuli (colors/sounds)? Further these or other stimuli could be used to modulate the excitability of brain regions in synesthetes or in other conditions. 
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fMRI may be the answer to this I guess
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We know neuronal pools communicate through electrical signal transmission or neurotransmitters and electophysiologically we can measure oscillations of these neuronal pools as signals. To understand the neuronal communication, we can use imaging (fMRI, PET, default mode network...), electrophysiological techniques (local field potentials, EEG, MEG..and coupling of signals: phase-amplitude, cross-frequency..) and neurochemical analysis at different levels (system, tissue, cellular and molecular..). I would like to know how to integrate all these to better understand the physiology of neuronal communication effectively. That would solve many puzzles in this field and provide some remedies for neurological disorders which are the results of degeneration of some of these causing these mis-communications between neurons. 
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You may find some of the our observations interesting that we made when combining TMS and fMRI: It turns out that at an individual level some areas that correlate in Resting State respond to TMS stimulation in a very similar way indicating a very direct connection between these areas, while other nodes of the RS network seem to have a more complex response pattern indicating a modulatory / cross-network hub role. Also different nodes of the network seem to respond to 1Hz stimulation than to 10Hz stimulation. Acquiring EEG data in the same subjects might help us to understand this frequence dependency.
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I want use Beta amyloid 25-35 as a neurotoxin for SHSY5Y cells.Although in articles 10 microM of it for 24h is used and cell viability of them decreased approximately  20% but in my experiments with two bath from different company even in 200 microM of it  , there was no decrease in cell viability. my protocol is: Briefly, Aβ25–35 was initially dissolved in double-distilled water to 1 mM. The peptide solution was divided into aliquots and stored at −20°C. Before use, the Aβ25–35 solution was incubated at 37°C for 7–10 days to form aggregated diffusible oligomers, then diluted in medium to the indicated concentration. When I treated cells with BA i tested 10% and 2% FBS in media and both of them has the same result. what  is your recommendation?
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Maybe your peptide is too aggregated and your cells are not able to internalize it?
I had the same problem in the past, but with abeta 1-42...
Take a look at this article: "Oligomer-specific Abeta toxicity in cell models is mediated by selective uptake"  http://www.ncbi.nlm.nih.gov/pubmed/18602001
Hope it helps!
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In clinical settings?
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Olá Almir,
Look these papers which I sent to you. I think that you should find your response.
I hope this helps.
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Relapsing Chronic Nephrotic Syndrome for the last 4 years
Intermittent flare-ups, taking prednisolone
Current albumin levels normal
Renal function tests normal
Generalised tonic-clonic seizures for the last 4-months
MRI Brain for intracerebral sapce occupying lesions, MRV for evaluating venous sinus thrombosis
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thanks very much for your enlightening responses
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We know that melanopsin is sensitive to blue light with a peak around 480 nm and that melatonin suppression is most sensitive to blue light with a peak around 460 nm. Furthermore, it seems that melanopsin is important but not essential to circadian photoentrainment. I have found some older reports showing that circadian phase shifts are more sensitive to short wavelength light.
Does anyone have any idea of how important blue light is to circadian photoentrainment, preferably based on recent research?
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Lots of experimental evidence are available to support that monochromatic light shift the clock, especially blue light compared to red light. Blue light shifts the clock (circadian locomotor activity rhythm)  but not red light. When we keep animals in constant DD, people have been using constant red light.  if you keep the animal in DD, blue light exposure definitely shifts the clock. 
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(i.e. Without any artificial interventions)
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The short answer is yes. SNS can have increased local activity. i.e. heart, muscle activity (forearm) . For humans it can be measured by either catheterisation or radioisotope dilution. For animals neurographic measurements are also possible.
/Rune
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We recently concluded a study on the prevalence and characteristics of maxillofacial injuries in patients with mTBi,  and analysed the possible influence  of maxillofacial (MF) trauma over specific cognitive deficits post trauma (namely executive function, memory and attention). We also looked out for WM tracts that were affected both in the acute and follow up phase [controlling for both the presence of maxfac injuries and as well as the CT imaging findings (intracranial lesion vs. none)]. The results were quite interesting and seem to challenge the conventional understanding and management of patients with mTBI.
We found that patients with maxillofacial injuries without intracranial lesion doing significantly worse over time in the domains of executive function and memory. Miscrostructurally, these patients seem to have poorer WM integrity especially involving the projection and association fibers (mainly corona radiata, cingulum, superior longitudinal fasiculus, optic radiation and genu of the corpus callosum).
Would appreciate your thoughts on the biophysics and biomechanics of maxillofacial trauma in mTBI  and how that could explain the findings.
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Also the energy used in the process of breaking such hard bones is not available to go through to harm the underlying tissue (that's what a safety helmet does or a football helmet, for example - helmet is toast so the tissues underneath are not).  It is also why you have to replace a bike helmet every 3 years or after any accident - the lining materials are no longer useful as an energy trap and the energies of a blow go right through.  But the majority of the brain parenchyma is only loosely associated with the pia mater so it is the blood vessels (which run through the arachnoid and have to deal with entrances and exits through bones) and the white matter tracts (which are ultimately attached through the brain stem to the spinal cord and which run through longer spaces within the brain, connecting grey areas) that are vulnerable to the energies of an acceleration/deceleration injury.  The exception of course is the olfactory bulb and tract which run through bone and get sheared off leaving folks unable to smell in frontal injuries and accel/decel ones all the time.  Have you thought about doing a simple olfactory screen with your patients to document that kind of injury?
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I'm currently working on a project to identify possible predictors for the level of cognitive functioning in patients matched for the degree of cerebral atrophy. I was planning on operationalizing cerebral atrophy as gray matter volumes. But to account for head size, I would correct this gray matter volume by intracranial volume which gives the fraction of the total volume which consitutes gray matter and thus corrected gray matter volume..
The problem is that I want to examine intracranial volume itself as a possible predictor for cognitive function with corrected gray matter volume as a covariate. Is it valid to use intracranial volume and corrected gray matter volume (GM/ICV) in one regression model as predictors or would this somehow lead to statistical difficulties?
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You have to check your VIF and tolerance values in you regression analysis and then you probably see that the correlation between the two is too high?
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I converted some EEG time series to their related visibility graphs, now I need to find correlation between each 2 graphs, please note that there is no any interlink between each 2 graphs hence I'm not sure if it is possible to use some synchronization methods of complex networks.
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It depends. Are the periods iqual? If the time series has some similar trend, then its better to remove the trend at first. Are the time series stationary? Did you make an unit root test? I think it is appropriate to make also a co-integration test, in case they are not stationary.
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Instead it causes right sided constant rigorous spinning .. would the occipital eventually deteriorate and the spinning ever stops or the person will eventually be blind, if at all?
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The most common non-penetrating injury produced by any blow to the head is a contrecoup injury to that part of the brain OPPOSITE the blow.  This is because the brain is accelerated into the skull by the blow.  In this case, a patient who has struck the back of his head by falling over backward would likely have the most injury to the frontal lobes, and might have problems with executive functions like memory rather than vision.  It sounds like vertigo has been a serious problem in the case you describe.  This certainly implies a problem with the vestibule, the vestibular nerve, or the vestibular nucleus.  Careful neurologic evaluation, including brain imaging if appropriate will help clarify the prognosis.  I hope there is rapid recovery.   
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Cannot figure out why my PTZ is not producing a score of 5 during acute seizure experiment even when i am using dose of 90 mg/kg. 
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thank you john !! 
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I am interested in developing a cortico striatal stimulation protocol, in horizontal slices of rodents where the synaptic connection between the cortex and striatum are perserved. I will like to record the glutamatergic evoked responses (I/O curve) in the striatum after constant current stimulation in layer V of the cortex. Could anyone provide me the information of what kind of stimulation electrode to use, most of the reference papers are using bipolar electrode, but what type ? concentric, parallel..? will these electrodes make a difference in stimulation? (I know that you need to stimulate a large population of glutamatergic cells to wake up an MSN. What is the scientific reason to use Constant current vs voltage current ?
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Constant current is typically preferred, especially for I/O comparisons, because the current supplied will always be 'constant' even if there are slight variations in resistance between slices (for example, due to buildup of extracellular debris on the electrode surface).  The output voltage will adjust accordingly in order to pass identical current.
With constant voltage, you might apply 5 V in two different recordings, but due to differences in resistance, one area might "see" higher current than another, making direct comparisons difficult.
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I'm interested in natural history, time course development of symptoms and any management strategies for rehabilitation of this condition.
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Vincent Blok...very good article...thanks again...
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I want to preserve major mouse organ, like brain, liver, lung, heart, kindney, and spleen. It will contain certain organic dye. Is it possible to store mouse organ in deep freezer (-70C) for a month? What would be the best method?
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I agree with both Marthe-Susanna and Richard, first you should snap freeze the tissues in liquid nitrogen (for about 2-3 days), then transfer them immediately into -70 or -80 freezer, it will be preserved for years
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Thank you. 
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Ref # 1
Fly Larvae And Pupae As Vectors For Scrapie
Transmission of 3 mouse-adapted scrapie strains to murine neuroblastoma cell lines ... developmental stages caused scrapie in hamsters after they ate fly extracts. ... of scrapie-infected hamsters (scrapie strain 263K) or healthy control brains. ..... at the endoplasmic reticulum, causing a higher percentage of PrP molecules to ..
Ref # 2 
Protein Structure and Biology
www.ncbi.nlm.nih.gov › NCBI › Literature › PubMed Central (PMC)
by AJ Green -
Apr 1, 2013 - PS.03: Size, not density of strain-specific prion particles determines their .... Cell cultures treated with prions show an increase of ER stress markers. .... we have created cloned cell lines expressing transmembrane (TM) and ..... their relative infectivity using the 263K strain of hamster-adapted scrapie.
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Is the educational programme used in  this article related to neuroscience education ? Thank you for the answer.
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HI Jan ,
Thanks for the heads up. To bad I only saw your message today , chekking unknown authors and sources is indeed a verry good idee. I ended up not including this study because the educational program i'm researching is not described in this article.
Thanks again for the great advice!
Greetings,
Haytem 
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There are a lot of animal models of Parkinson's Disease. I'd like to know whether Parkinson's disease develops spontaneously in monkeys or not. Are there any reports?
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Perhaps you should also look into papers of de Hartog Jager, dutch prof in neuropathology and in those of Vianny de Jong. They worked together on Parkinson in monkeys.  Don't have them here, but you easily can find them.
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There is always cost to interrupting the normal function of the body.  What are the consequences of manipulating the neuro system in delaying dementia?
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At least one study has shown that higher cumulative anticholinergic use is associated with an increased risk for dementia.
see Gray et al., 2015
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Hi everyone!
I got a bit of an issue with my radioligand receptor binding. I've started with standard kinetic and saturation experiments to determine the incubation time and Kd. The thing is that in the kinetic experiment the association curve increases linearly and does not reach steady state even after 12h of incubation at 35deg.! The same thing happens with the saturation curve, that refuses to go hyperbolic. The non-specific binding (hot and cold are the same molecule) is about 20% of total binding at 60min. incubation in the association experiment so at least it competes with the hot ligand for the binding site. I tried to increase ligand concentration, buffer composition and pH in hopes that it will equilibrate faster, but no luck so far. Has anyone of you guys experienced this problem? I was thinking about running a homologous competition experiment, but I do not know whether the hot does not bind to several binding sites or there is no cooperativity.
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Thanks for all your valuable suggestions! I'll try isolating and purifying mitochondrial membranes.
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This is an excellent question.  For me, the major ethical implication involves the concepts of moral responsibility and voluntary action.  As neurocriminology  becomes more sophisticated, neuroscientists will become more capable of identifying features of the brain, both organic, neuro-chemical, and genetic which are statistically associated with the commission of crime.  One implication of this development is bound to be strategies aimed at preventing crime before it is committed.
I can imagine strategies of this sort which would threaten the freedom and dignity of the individual.  The relationship between the brain and its functions and mind which is the realm of intention, consciousness and conscience is one of the most persistent philosophical problems.  One cannot be reduced to the other. Mind cannot be reduced to the psycho-physical, and the psycho-physical cannot be reduced to the mind and its features.
The relationship is, at the least, complex and sophisticated.  Any crime prevention strategies which seek to identify and/or engage those persons seen as potential offenders, before they offend, are a danger to the concept of the moral responsibility and the human capacity to choose our voluntary actions, as well as to the concept of free will, which is another important and persistent philosophical problem, which as such, is associated with what it means to be both human and a moral agent.  In short, I am concerned with the potential for developments in neurocriminology to arise with could threaten human freedom.
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We are trying to isolate dorsal root ganglion neurons from guinea pigs. Can anyone suggest the age of animal to go for which may be easier to dissect and give nice quality and purity of cells? Thanks for any inputs! =)
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Thank you very much for your information! That's very helpful! Seems it's more common to use mice and rats for the isolation. Did anyone have any experience with guinea pigs?
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How is cortical surface area related to cortical folding (e.g. measured by FreeSurfer) and what is the additional value in measuring both variables?
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My impression is that surface area is literally that, if the cortical mantle was spread out into a sheet what would the surface area at. The folding instead is the pattern of folks that make of the gyri. Neither are measures that most labs look at when using Freesurfer (thickness and volume are most common). I would take a look at this paper to get a sense of what Freesurfer means by cortical folding.
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A 19 years old male patient feels muscle function loss on the right side accompanied by parasthesia to the right of the mandibula, which occurs for approximately 20 seconds. It relapses many times a day. In addition there is alveolar bone loss without tooth mobility and bleeding.
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This patient need to scanned for any Infra temporal Fossa lumps that can affect the main trunk of mandibular division containing  both sensory and motor fibres. I also seen a lady with same manifestation turned to have a nasopharyngeal Carcinoma.so do not lgnor these possibilities 
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I could find articles and reports of gamma secretase inhibitors used for toxicity and efficacy in Zebrafish models but not for Beta secretase (BACE1).
What data will I be able to collect from the Zebrafish models with my compounds in general?
I am planning a behavioral assay, a neurotoxocity based approach.
I would also be interested in the efficacy of my compound as a BACE1 inhibitor, but how do i proceed?
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Hallo,
this is an extremely interesting question, since BACE1 inhibitors are being discussed for the therapy of Alzheimers disease for years now. Unfortunately preclinical studies (e.g. in mouse "models" for AD or in drosphila) were quite disappointing because of BACE-related undesired effects (off-site effects and /or off-target effects). These included -amongst others- retinal pathology and myelinisation abnormalities. In a clinical Phase II study hepatotoxicity was observed (which is not necessarily related to a reduction of BACE activity)When assessing toxicity you should not only look for behavioral deficits (which are unlikely to occur) but specifically for lesions in the peripheral nervous system. An extensive phenotyping may be necessary. The literature is confusing, since BACE1 KO mice were reported to be entirely "normal".
Good luck for your research and your zebrafish!
Just
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I would like any information dealing with the neurosciences, because material on this epidemiological and scientific field is lacking in my country. All contributions will be interesting for this project.
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Parasitosis is one of the best epidemiological topics in which neuroscientists should be very interested. For instance, the presence of certains forms of T. brucei gambiense in the choroid plexus and cerebrospinal liquid may activate the glial environment of the brain, leading to the release of pro-inflammatory cytokines and the subsequent sickness behavior in infected subjects. Playing a role in nervous-immune interactions, cytokines would somehow help building an anti-parasitic memory to avoid reinfections. I would just highlight the importance of revealing processes that underlie the bidirectional memory transfer between nervous and immune systems in case of infectious diseases.
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Many studies have implicated accumulation of metals in Alzheimer's pathology and this has been used to justify the use of metal targeted therapies in clinical trials. A quantitative meta-analysis suggests this data has not been consistent and demonstrated a citation bias for papers that found increased iron levels. This study found that cortical copper levels were actually lower and zinc levels were only increased in the parietal lobe. Zinc supplementation may have therapeutic affects associated with decreasing circulating copper levels in Alzheimer's patients. Mechanistic research supports a model where accumulating zinc leads to neuronal cell death by: targeting Amyloid beta to stimulate NMDARs, inhibiting the ferroxidase activity of Amyloid Precursor Protein, and stimulating hyperphosphorylation of Tau. If we accept this pathological role of brain zinc, how can we explain beneficial effects of zinc supplementation?
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How Strong? Very Strong
I a have listed just a few refs from our group
1: Rembach A, Hare DJ, Lind M, Fowler CJ, Cherny RA, McLean C, Bush AI, Masters
CL, Roberts BR. Decreased copper in Alzheimer's disease brain is predominantly in
the soluble extractable fraction. Int J Alzheimers Dis. 2013;2013:623241. doi:
10.1155/2013/623241. Epub 2013 Oct 21. PubMed PMID: 24228186; PubMed Central
PMCID: PMC3818847.
2: Hung YH, Bush AI, La Fontaine S. Links between copper and cholesterol in
Alzheimer's disease. Front Physiol. 2013 May 16;4:111. doi:
10.3389/fphys.2013.00111. eCollection 2013. PubMed PMID: 23720634; PubMed Central
PMCID: PMC3655288.
3: Rembach A, Doecke JD, Roberts BR, Watt AD, Faux NG, Volitakis I, Pertile KK,
Rumble RL, Trounson BO, Fowler CJ, Wilson W, Ellis KA, Martins RN, Rowe CC,
Villemagne VL, Ames D, Masters CL, AIBL research group, Bush AI. Longitudinal
analysis of serum copper and ceruloplasmin in Alzheimer's disease. J Alzheimers
Dis. 2013 Jan 1;34(1):171-82. doi: 10.3233/JAD-121474. PubMed PMID: 23168449.
4: Ayton S, Lei P, Bush AI. Metallostasis in Alzheimer's disease. Free Radic Biol
Med. 2013 Sep;62:76-89. doi: 10.1016/j.freeradbiomed.2012.10.558. Epub 2012 Nov
9. Review. PubMed PMID: 23142767.
5: Greenough MA, Camakaris J, Bush AI. Metal dyshomeostasis and oxidative stress
in Alzheimer's disease. Neurochem Int. 2013 Apr;62(5):540-55. doi:
10.1016/j.neuint.2012.08.014. Epub 2012 Sep 8. Review. PubMed PMID: 22982299.
1: Biran Y, Masters CL, Barnham KJ, Bush AI, Adlard PA. Pharmacotherapeutic
targets in Alzheimer's disease. J Cell Mol Med. 2009 Jan;13(1):61-86. doi:
10.1111/j.1582-4934.2008.00595.x. Epub 2008 Nov 18. Review. PubMed PMID:
19040415.
2: Adlard PA, Cherny RA, Finkelstein DI, Gautier E, Robb E, Cortes M, Volitakis
I, Liu X, Smith JP, Perez K, Laughton K, Li QX, Charman SA, Nicolazzo JA, Wilkins
S, Deleva K, Lynch T, Kok G, Ritchie CW, Tanzi RE, Cappai R, Masters CL, Barnham
KJ, Bush AI. Rapid restoration of cognition in Alzheimer's transgenic mice with
8-hydroxy quinoline analogs is associated with decreased interstitial Abeta.
Neuron. 2008 Jul 10;59(1):43-55. doi: 10.1016/j.neuron.2008.06.018. PubMed PMID:
18614028.
3: Barnham KJ, Kenche VB, Ciccotosto GD, Smith DP, Tew DJ, Liu X, Perez K,
Cranston GA, Johanssen TJ, Volitakis I, Bush AI, Masters CL, White AR, Smith JP,
Cherny RA, Cappai R. Platinum-based inhibitors of amyloid-beta as therapeutic
agents for Alzheimer's disease. Proc Natl Acad Sci U S A. 2008 May
13;105(19):6813-8. doi: 10.1073/pnas.0800712105. Epub 2008 May 7. PubMed PMID:
18463291; PubMed Central PMCID: PMC2383936.
4: Barnham KJ, Bush AI. Metals in Alzheimer's and Parkinson's diseases. Curr Opin
Chem Biol. 2008 Apr;12(2):222-8. doi: 10.1016/j.cbpa.2008.02.019. Review. PubMed
PMID: 18342639.
5: Smith DG, Cappai R, Barnham KJ. The redox chemistry of the Alzheimer's disease
amyloid beta peptide. Biochim Biophys Acta. 2007 Aug;1768(8):1976-90. Epub 2007
Feb 9. Review. PubMed PMID: 17433250.
6: Crouch PJ, Barnham KJ, Bush AI, White AR. Therapeutic treatments for
Alzheimer's disease based on metal bioavailability. Drug News Perspect. 2006
Oct;19(8):469-74. Review. PubMed PMID: 17160147.
7: White AR, Barnham KJ, Bush AI. Metal homeostasis in Alzheimer's disease.
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For example, for ECG signal, R peaks are considered, and ECG time series are constructed by RR intervals.
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Brain activity is not inherently periodic and regular like cardiac, so signals are usually analyzed relative to some exogenous signal. This is called ERP, "evoked response potentials" (or "event-related potentials"). The classic approach is to just average the epoch surrounding an event (for repeats of the same event type). It is common practice to use a small pre-stimulus period (say 150ms) which is thought of as a baseline. There is a substantial literature, dating back many decades, about the features that appear from this kind of averaged, stimulus-locked EEG and how these features are distributed over the scalp, and how they change in response to manipulation of the stimulus. Of course, ERPs differ greatly depending on the sensory modality of the stimulus.
This whole body of practice is tied to the hypothesis-testing approach and, although it can sometimes encompass analysis of single trials, it does not provide much insight into the spontaneous wiggles of non-stim-locked free-running EEG. The classic example of this is to epileptic seizures, though they are pretty much impossible to miss. There is a body of literature, more from a clinical perspective (not as much experimental or hypothesis-driven) that studies "rhythm" or frequency (and sometimes phase) components of ongoing "spontaneous" activity.
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I recently finished analyzing longitudinal data on the influence of a patient's and their proxy/care taker's mindfulness on recovery from severe traumatic brain injury. The patients are not veterans. A multilevel modeling approach was used to analyze the data.
I'm looking for a journal that would be interested in publishing a manuscript of this nature.
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I recommend JCCP BRAT.
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mu waves in the pre-frontal cortex are dependent on attention and consciousness. I am trying to create a protocol based on the article: Mirror neuron function, psychosis and empathy in Schizophrenia (McCormick et al., 2012), however I am having a hard time designing a protocol that will standardize attention in schizophrenics. Do you have any suggestions? Could I employ a neurocognitive test such as the Trail Making test or the Stroop test before recording the EEG mu wave response to live biological movement?
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Hi Carolina,
Thanks for the response. I would agree with you on your interpretation of these papers. I would say that the group differences between the patient group and healthy group, seen in the Singh et al paper and the Kim et al paper, may be a result of the nature of the stimuli used (i.e. moving points), and therefore may just be reflecting an information processing deficit in the schizophrenia group rather than a difference in perceiving biological motion per se.
I thought it was quite strange that the McCormick et al paper actually found greater mu suppression in the patient group with more severe symptoms. This seems to contradict the general hypothesis that impaired social functioning in schizophrenia is coupled with degraded mirroring, and therefore we should expect lower mu suppression in the patient group. Do you have any ideas why there might be greater mu suppression in the patient group? I think the interpretation that McCormick et al gives in their paper is not so convincing. Incidentally, from the data I have collected so far (15 schizophrenia patients and 15 controls) it seems like the patient group does have a lower mu suppression, but the difference is not reaching significance. Though interestingly, there appears to be a strong correlation between the mu suppression and (negative) symptoms, but in the negative direction, so this means that patients with more severe negative symptoms have greater mu suppression. Strange also. I need to collect more data to get a clearer picture on this. I would be keen to hear your ideas on the McCormick finding.
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Does their role in calcium entrance lead to these conditions?
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Yes, NMDA receptor are the major mediators for memory and synaptic plasticity (change in strength between two neuron upon synapsis), NMDA receptor plays a role in opening up of voltage gated ion channels by influx of Na+ and ca+ and efflux of K+ ions through co-activation of glutamate and serine. several studies reported that overexpression of glutamate also increases the severity of alzheimer disease. Hence expression of NMDA receptor mediated glutamate is needed for above said memory cirteria also its overexpression lead to alzheimers disease.