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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.
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.
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
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.
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.
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?
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
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
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?
(i.e. Without any artificial interventions)
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.
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?
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.
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?
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.
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 ?
I'm interested in natural history, time course development of symptoms and any management strategies for rehabilitation of this condition.
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?
Is the educational programme used in this article related to neuroscience education ? Thank you for the answer.
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?
There is always cost to interrupting the normal function of the body. What are the consequences of manipulating the neuro system in delaying dementia?
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.
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! =)
How is cortical surface area related to cortical folding (e.g. measured by FreeSurfer) and what is the additional value in measuring both variables?
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.
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?
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.
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?
Article Zinc and the aging brain
Can anyone point out any resources focusing on the neurological processes and structures involved in interoception and bodily self-awareness?
For example, for ECG signal, R peaks are considered, and ECG time series are constructed by RR intervals.
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.
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?
Does their role in calcium entrance lead to these conditions?
