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Neurology - Science topic

Neurology is a medical specialty dealing with disorders of the nervous system. To be specific, it deals with the diagnosis and treatment of all categories of disease involving the central, peripheral, and autonomic nervous systems, including their coverings, blood vessels, and all effector tissue, such as muscle.
Questions related to Neurology
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A patient with desminopathy survived Covid-19 six months ago without pneumonia, but with a temporary loss of smell and taste. After Covid-19, we note an accelerated progression of desminopathy, penetration accelerates, new muscles are quickly involved in the pathological process, muscle mass decreases, and heart function worsens. Perhaps the infection or its consequences are somehow connected with the mechanism of progression of desminopathy?
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To save life in desminopathy, can the body purposefully reduce muscle mass, for example, due to decreased heart function or for another reason?
It is known that when hypothermia, the body sacrifices limbs for survival. Is it possible with desminopathy a similar phenomenon?
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Dear Mozhgan Norouzi, thank you very much for your reply!
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A patient with desminopathy (mutation Thr341Pro DES in a heterozygous state) with the progression of the disease has a decrease in taste and smell, immunosuppression, and an increase in IgA in the blood.
Oddly enough, but all this is characteristic of infections, including viral ones. For example, it is known that if the hepatitis C virus is not treated, then death will occur in 20 years.
In the identified case of late onset desminopathy, muscle weakness manifests itself at the age of 30, and death occurs 20 years after the onset of the disease.
Could the desmin mutation in myofibrillar myopathy be caused by an infection?
Perhaps the infection contributes to the progression of desminopathy?
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A patient with desminopathy survived Covid-19 six months ago without pneumonia, but with a temporary loss of smell and taste. After Covid-19, we note an accelerated progression of desminopathy, penetration accelerates, new muscles are quickly involved in the pathological process, muscle mass decreases, and heart function worsens. Perhaps the infection or its consequences are somehow connected with the mechanism of progression of desminopathy?
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I´m currently in an investigation related to the olfatory system and the possible conexion with empathy in people, so I need a relaible instrument to make the olfatory tests
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Hi,
UPSIT smell test. Follow the link below.
There are some articles on smell tests .Also, look into the cross-references:
Rezende GL, Sarmet M, Sousa GE, Krier FC, Parreira DR, Kuckelhaus SA. Olfactory Performance among Hospital Residents. Int Arch Otorhinolaryngol. 2021;26(1):e032-e037. Published 2021 Feb 19. doi:10.1055/s-0040-1719122
Joseph T, Auger SD, Peress L, et al. Screening performance of abbreviated versions of the UPSIT smell test. J Neurol. 2019;266(8):1897-1906. doi:10.1007/s00415-019-09340-x
Keck JW, Bush M, Razick R, Mohammadie S, Musalia J, Hamm J. Performance of formal smell testing and symptom screening for identifying SARS-CoV-2 infection. PLoS One. 2022;17(4):e0266912. Published 2022 Apr 12. doi:10.1371/journal.pone.0266912
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I may have to get a NL111 electrode holder for the existing NL102G headstage (Digitimer) for building up an ephys recording system. But apparently only the 2 mm pin at the rear of the holder holds the pipette holder assembly in place on the headstage, unlike the design of Axon electrode holder and headstage (Molecular Device). Should I be concerned about the stability of this connection and whether this provides a strong hold of the glass micropipette?
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Good afternoon. I think it's better to use holder
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Dear Neurosurgeons,
Please fill out this survey on research productivity during the pandemic.
Thank you for your time.
#neurosurgery #research #productivity #pandemic #covid #collaboration
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done
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In a patient with hereditary desminopathy (mutation Thr341Pro DES in the heterozygous state) over the past three years, an increase in the blood uric acid level up to 440-480 µmol / l was established by 1.5 times (the norm is 428.4 µmol / l). With the progression of the disease, the level has risen and is above normal. It is known that uric acid is an antioxidant. Is it necessary to reduce the level of uric acid? The patient has no problems with the joints.
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The change in the level of uric acid and biochemical parameters in a patient with an identified case of desminopathy is presented in the article https://www.researchgate.net/publication/357311034_CHANGE_IN_REDOX_STATUS_AND_BIOCHEMICAL_PARAMETERS_IN_PATIENT_WITH_DESMINOPATHY_T341P_SEVERAL_YEARS_AFTER_DISEASE_SYMPTOMS_ONSET
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UCLA and Yale University are conducting a Survey on Postoperative Practices in Evaluating and Treating Patients with Brain Tumors in North America.
We are asking neurosurgeons, (neuro)psychologists, speech-language therapists, and occupational therapists, physiotherapists, or psychotherapists to participate in the survey.
Our goal is to understand common practices, disseminate standards of care, and gather information on post-operative outcomes in patients with brain tumors. We will publish the results from this survey in an open-access journal.
The survey can be accessed here:
BECOME A CO-AUTHOR:
If you are interested in collaborating with us by helping us gather responses from more medical professionals from any of the fields listed above, please email use this email: MPolczynska@mednet.ucla.edu.
Thank you very much for your help!
Monika Polczynska
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Yes I can
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I have an endocast that I am trying to measure the volume of the olfactory bulbs from. I have the data segmented in Avizo, but unfortunately because of the way the specimen was scanned (it was a fluid specimen) the skull was not in anatomical view when it was CT scanned. As a result, it is very difficult to determine where the borders of the olfactory bulbs are.
I am trying to reorient the segmented data so I can get it in standard anatomical view for further analysis, specifically resegmenting the label field to define the olfactory bulbs separately. I know that it is possible to resegment the CT data in Avizo, but I am trying to avoid this as I know it can cause issues with blurring of boundaries between bone and tissue. I was wondering if there is any way to do this with a segmented label field, isosurface, or other data that has already been segmented and thus the anatomy is better defined.
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Hi Russell,
in Amira-Avizo, you can use the Transform Editor of any data-object to change its orientation and position in the global coordinate system.
So, you could use the Transform Editor of your segmented data to rotate it as needed, and afterwards you can use Resample Transformed Image to get get an axes-aligned voxel-grid. (see attached "TransformEditor_snapshot.PNG")
I don't know your workflow, but maybe you could also use the 3D lasso-tool in the Segmentation Editor to select an arbitrarily oriented part of one material and assign that to a new material (see attached screenshot "SegEdit_snapshot.PNG").
For making the selection working only on one specific material, you have to "lock" the other materials appropriately. Remember, you have the "undo" with <Ctrl>+Z ...
There might be some issues with the update of the visualisation when using the 3D-lasso, so it might be necessary to toggle off/on the 3D-view of a material.
Kind regards,
Andreas
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I'm a community Pharmacist and I'm interested in writing, especially writing scientific papers. I'm offering my help and assistance in case you need a hand with your current research. My areas of interest: Pharmacotherapy, psychology, neurology, psychiatry. So send me a message in case you need help.
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I am interested...Kindly contact me after two weeks...
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I am interesting to work in neurology related project. But I can't find any professor or any scope to do that. I want to PhD on it that's why I want to gather so much knowledge. So can we anyone help me about that?
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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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Hi,
Is there anybody who is interested in collaborating with a project regarding neuropsychology of language mechanisms. This work would be a review including papers using fMRI and EEG. We hypothrize the the mutipled demand cortex may play an role in language, but its role is more executive rather than linguistic. Leave your email address if you are interested.
Thanks.
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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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Conversely, rotenone, which is an insecticide, has.
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in fly model MPTP can be used to induce parkinsons disease refer the following article for further clarification.
"Resveratrol prolongs lifespan and improves 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine-induced oxidative damage and behavioural deficits in Drosophila melanogaster"
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Hi all,
I need to learn how to use ImageJ to do colocalization and quantification of my IHC mice brain slides.
I have mice brain sections that I stained with the microglial specific marker iba1, and costained it with M1 and M2 markers iNOS and Arginase-1, with DAPI as a counterstain.
So my slides are as follows:
DAPI
iNOS --> Alexa Flour 488
Iba1 --> Alexa Flour 594
And
DAPI
Arginase 1 --> AF488
Iba1 --> AF 594
I couldn't find a resource on how to quantify this, any help would be appreciated.
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I would recommend that you get the FIJI distribution of imageJ (https://imagej.net/software/fiji/) which includes a number of useful plugins for fluorescence microscopy analysis, including "Coloc2".
An overview of colocalization analays can be found here: https://imagej.net/imaging/colocalization-analysis#methods-of-colocalization-analysis
And directions for using the Coloc2 plugin can be found here: https://imagej.net/plugins/coloc-2#how-to-use-coloc-2
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I know that an infant's brain can repair itself when damaged but why doesn't the same happen in adults after stroke or brain injuries?
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With Regenerative Medicine, using stem cells, the ongoing Programs are doing it, with good results and promising expectations.
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Tensor flow is used in Neurology to see track of water flow
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Satish Narula Tensorflow is the programming framework most machine learning practitioners work with to create ML applications. Generally, Tensorflow is not needed to create any kind of algorithm, it simply makes the process by orders of magnitude faster. Tensorflow (and TF 2) run as a Python 3 module, created by Google.
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Several journals have limitations for article length and number of references. I would like to know if it’s acceptable to add some of the references as supplementary material, if I can’t totally omit them?
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In any case, it will depend on the "Publication Norms" of the Journal in question and the "benevolence" of its Publication Committee ... if the Original has been accepted by its Scientific Committee, after the pertinent revision by the reviewers "ad hoc"; However, I advise adhering to the "Publication Rules" of each Journal, because for something they are done and promulgated
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Dear Colleagues,
Doctors from UCLA and Yale University are conducting a Survey on Postoperative Practices in Evaluating and Treating Patients with Brain Tumors in North America.
We are asking neurosurgeons, (neuro)psychologists, speech-language therapists, and occupational therapists, physiotherapists, or psychotherapists to participate in the survey.
Our goal is to understand common practices, disseminate standards of care, and gather information on post-operative outcomes in patients with brain tumors. We will publish the results from this survey in an open-access journal.
The survey can be accessed here:
Thank you very much for your help! Please reach out with any questions.
Monika Polczynska
UCLA Dept. of Psychiatry and Biobehavioral Sciences
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Shweta Singh Fantastic. Thank you very much. We are asking (neuro)psychologists, neurosurgeons, speech-language therapists, occupational therapists, physiotherapists, and psychotherapists to participate. If you have a few contacts you would like to share, please message me privately. We will be happy to reach out to these people directly, if it helps save your time. I am also providing my email address: MPolczynska@mendet.ucla.edu just in case. Best wishes, Monika
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At the end of The Man Who Mistook his Wife for a Hat, Oliver Sacks cites a number of influential writers who have shaped the direction of his own thinking about neurology; what he refers to as his ‘essential axis of neurology’. As participants within domains of our chosen interest, we are all influenced by the work of previous and/or prominent proponents of the field.
Within education I have been influenced by a number of fields of interest i.e., gifted and talented (Renzulli, Gagne), cognitive psychology (Piaget, Bruner, Paivio), experiential learning (Kolb), disposition and the affective domain (Krathwohl), active agency and learner participation (Dewey), to name a few. Probably the most influential have been those writers who have spelt out the developmental mechanism of learning referred to as construction or constructivism, and the role of action and participatory agency in learning (of course not to reduce learning only to action and agency on the part of the learner!). This influence has been of great use in engaging learners in the classroom.
What would your essential axis of learning be, relative to education, learning and teaching?
And how have these influences shaped your thinking as an education specialist?
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Very philosophical question. My philosophy shapes my practice and this has changed phenomenally over the years due to research and the varying context with in my teaching sphere. I have had to change my dispositions and attitudes towards my students, to become a bit more amenable and understanding especially within the Covid context. My methodology has evolved and now includes engagement, interactivity and more contemporary methods suited to andragogy. Great question Adrian Twissell
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I had a few students help me with a simple but time-consuming task. The data they helped with will be used in a scientific paper. The students are part of the Student Research Program (SRP) at my institution and they received a class credit for their work with me. Should I include these students as co-authors on the manuscript?
I also had a student volunteer help me on the same research project. The student did not get a class credit for their help. Should the student be a co-author on the paper?
Thank you in advance for your opinions/suggestions.
Monika Polczynska
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Co-authorship is not a form of reimbursement (in laboratories and research institutes, all co-authors receive a salary or grants, nevertheless...). If a persons has made a creative contributions, then they are a co-authors. If the work is technical - for example, reprinting a text, or measurements (without processing etc.), then - no. There is another form for highline such participation: acknowledgment.
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Hi all,
I'm interested in ways other clinical researchers or centers quantify/calculate seizure burden for children and adolescents with epilepsy? Any standardized measures and/or clinical algorithms you've found helpful for research purposes?
Thanks in advance,
Andy
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If a seizure as such is not observed, possibly by an EEG and Functional MRI.
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A large majority of intracerebral hemorrhages, especially in younger patients, are due to hypertensive emergency. Often, these patients will get started on a titratable continuous IV drip medication like Nicardipine in the emergency room. However, there was a recent paper in Neurocritical Care journal that suggests that starting oral antihypertensives in conjunction during this very acute stage can lower morbidity, costs, and hospital/ICU stays. The rebuttal is of course that blood pressures on oral antihypertensives are subject to peaks and troughs with medication administration until steady state is reached. During this time, overshooting the target and causing hypotension can cause significant ischemia to surrounding cellular tissue that may be amenable to rehab, and hence worsening long-term outcomes [though this has not yet been systematically analyzed]. What is your opinion on this?
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ESSENTIAL!!
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I am working EEG signal classification. I am using an EEG cap which is having standard 10-10 electrodes placement system. I am not able to find 3D location for the same. .elc file is available for 10-20 but not for 10-10. Has anyone worked with 10-10 electrodes placement system?
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Have you tried different coding snippets in EEGLAB or FieldTrip...?
1. In EEGLAB:
"EEGLAB will automatically read these channel labels. When you then call the channel editing window, the function will look up 10-10 channel locations in a database of 385 defined channel labels, the file “Standard-10-5-Cap385.sfp” in the “function/resources” sub-folder of the EEGLAB distribution. You may add additional standard channel locations to this file if you wish. As of 2021, the default channel location file for electrode position is the MNI file, which is best suited for source localization. Before 2021, it was the BESA spherical location file.
To load or edit channel location information contained in a dataset, select Edit → Channel locations. A dialog box (shown below) will appear, asking you if you want to use standard channel locations based on the imported electrode position labels (for example, ‘Fz’) from a channel locations file using an extended International 10-20 System."
2. In FieldTrip:
3. If I got your other question correctly, for .elc as Cartesian 3D electrode coordinates: EETrak software may help.
See this code:
and
Hope this helps.
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What would land a neuroscience paper in Nature Neuroscience? What is the minimum a paper should have to pass the editorial scrutiny in Nature Neuroscience or the journals around the same cadre? May be a list of things and at the same time explanation of each point would work.
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Hi there,
Basically you need an important topic (most of the articles in Nat.Neurosci. are disease-related) and various, extremely good methods (often collaboration with specialized labs for EM, imaging, electrophysiology, ...).
Moreover, you should be working in a renowned lab, since the reputation of your PI will greatly influence if your paper has a chance to be accepted.
Also, you should think, how the journal would benefit from your paper:
For example, the neurocience community can greatly benefit from a ressource such as a proteomic or transcriptomic database, and such a paper would get a large number of citations, which is also beneficial of the journal.
Eventually, you will still need a good amount of luck to get accepted. ;-)
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I am testing the impedance of a material that will be used for ECoG electrodes.
I was told to test it at a frequency range from 1 Hz - 100 kHz but why is this range used? I wasnt able to find a satisfactory answer.
Which impedance values are good for recording and why? Is there a range ?
Kind regards
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Lester Viray can you help him professor
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Dear Colleagues,
Could you please direct me to studies on the impact of the third language (L3) on the neural organization of the first (L1) or the second language (L2)?
Thank you,
Monika Polczynska
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This is really an interesting question that I want to follow. Besides, may you see studies by Best and colleagues in West Sydney University.
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A patient with hereditary desminopathy (mutation Thr341Pro DES in a heterozygous state) with disease progression has a significant decrease in taste. How can this fact be explained?
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Probably affect facial nerve and glossopharyngeal nerve in the pons and medulla oblongata?
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I would like to ask about how to find other neuroscientists with similar work to professor Henrik Zetterberg? Is there a database that include researchers?
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Get his publications, look for his coauthors and check their profiles. You can learn more about individuals research interests. You can also get to know about their ongoing collaborative researches on their institution websites.
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What are different coil shapes used in Transcranial Magnetic Stimulation? What are their differences (in induced current)? Do they have different applications?
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Hi,
Actually, the influence of inductance value in a coil on TMS is eddy current strength. In addition, the coil design in physical configuration can affect the TMS distribution or depth. The TMS coil with eight shapes is commonly used in clinical application due to better high resolution than the round coil.
You can refer to the article below. Good luck!
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The 10-20 and the Queen Square electrode placement systems both assume a relatively normal head shape. Individuals with very unusual shapes are more likely to require investigations and procedures that require the placement of scalp electrodes. What approaches are people using to compensate for the head shape?
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The international 10-20 system as it is purely based on distances and not on the measure of the head.
Any other way found recently Jonathan A Norton
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In a patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) with disease progression, a significant decrease in olfaction is noted. How can this fact be explained?
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I agree with Japneet Kaur. The problem in the cilia of olfactory sensory neurons. The myofibrilar myopathy is a genetic disease that associated with the primary ciliary dyskinesia. The primary ciliary dyskinesia resulted in defective cilia and olfactory receptors.
Attached, please find the article describing both myofibrilar myopathy and primary ciliary dyskinesia.
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What are the latest updates about the route of transmission and its impact?
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Dear Dr. Ebada,
We know very little about COVID-19 at this moment and its effects on the developing and/or mature brain. In general viral infections can impair charnolophagy (CB autophagy) which is the basic molecular mechanism of intra-cellular detoxification (ICD) for normal function to remain healthy. By attacking the most sensitive neural progenitor cells in the brain, the virus can alter their pluripotency and induce charnolosome (CS) destabilization implicated in inflammasome (particularly NRLP-3) activation to induce hypercytokinemia and charnoptosis (CB apoptosis) implicated in pyroptosis, apoptosis, and necrosis of sensitive hippocampal and other CNS neurons by releasing Panx-1, Viroporine, and gasdermins to cause Charnoly Body Molecular Pathogenesis (CBMP) implicated in early morbidity and mortality through its general (Viral) lytic cycle.
For more details, you may please refer to my books " The Zika Virus Disease: Prevention and Cure" The Charnoly Body: A Novel Biomarker of Mitochondrial Bioenergetics" Fetal Alcohol Spectrum Disorder; and Nicotinism and Emerging Role of E-Cigarettes. I wish I could write more about it.
Dr. Ebada, It is all about Environmental Sanitation, our own Life-Style, Immunity, Mitochondrial Bio-energetics and intracellular detoxification through charnolophagy (CB autophagy), which is compromised by COVID-19 through CS destabilization to cause early morbidity and mortality by infecting the CNS. Thanks.
With Warm regards,
Sushil Sharma, Ph.D; D.M.R.I.T
Academic Dean
American International School of Medicine
Guyana, South America
.
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WHat do you think is the correlation? It's impact? and the possible transmission route?
Neurologic Features in Severe SARS-CoV-2 Infection
DOI: 10.1056/NEJMc2008597
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1. Does consciousness exist?
2. If so, what is Consciousness and what are its nature and mechanisms?
3. I personally think consciousness is the subjective [and metaphysical] being that (if exists) feels and experiences the cognitive procedures (at least the explicit ones). I think that at some ambiguous abstract and fuzzy border (on an inward metaphysical continuum), cognition ends and consciousness begins. Or maybe cognition does not end, but consciousness is added to it. I don't know if my opinion is correct. What are potential overlaps and differences between consciousness and cognition?
4. Do Freudian "Unconscious mind" or "Subconscious mind" [or their modern counterpart, the hidden observer] have a place in consciousness models? I personally believe these items as well are a part of that "subjective being" (which experiences cognitive procedures); therefore they as well are a part of consciousness. However, in this case we would have unconscious consciousness, which sounds (at least superficially) self-contradictory. But numerous practices indicate the existence of such more hidden layers to consciousness. What do you think about something like an "unconscious consciousness"?
5. What is the nature of Altered States of Consciousness?
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Quoting Larry Carlson:
By the way, I am looking for the textual reference, but I read recently that subconscious sensations (e.g., what one might be said to be feeling while having a nightmare), have physical realizers (e.g., neural substrates), similar in structure and function to those associated with conscious experiences (of sensations, thoughts, & emotions). We might call them the neural correlates of the subconscious... e.g., NCS rather than NCC.
  • By what criteria do we distinguish between subconscious, subliminal, or conscious awareness/experience?
  • By what criteria do we distinguish between subconscious or conscious (sense of) self .
  • Is subconsciousness another compartment of consciousness involving a different "I", or else is it just a diminutive form of consciousness.
  • What is the significance of correlating different types of brain "waves" with different forms of consciousness or experience, e.g., waking vs. hypnotic vs. drugged vs. sleeping forms of consciousness.
  • Can we even claim that there are subconscious experiences?
  • Can we claim that subconscious thinking is an experience, as in the case, for example, of those scientists who claim to have solved great mathematical problem in while sleeping, or out of the blue as if their subconscous had been mulling over it, e.g., Poincare stepping off a bus.. a now widely accepted concept
  • Can we draw a distinction between a subconscioius self and a conscious one, e.g., as Freud and Mary Shelley, etc. etc. did.
  • Are we "personally responsible" for our subconscious thoughts and desires, or Freudian slips of the tongue.
  • At what point does my sudden subliminal sensory/cognitive awareness of a McDonald's ad as I drive by a billboard sudden stop being the subconscious experience of hunger (if that's not an oxymoron) and become the P-conscious experience of the sensation of hunger for a cheeseburger in my conscious mind.
  • At what point, then, do I stop being my subconscious I or self, and become my conscious self.
  • At what point can we distinugish between Freud's notion of the Id and that of the Ego, or as Shelly put it, between Mr Hyde and Dr Jekyll.
  • And does it matter whether Dr Jekyll remembers all the terrible things what Mr Hyde did, and is the Dr "responsible?" Can we hold someone responsible for what they did when they were in a blackout state of intoxication, or sleep walking, or overcome with rage?
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Sleep problems can be seen in patients with Parkinson's disease. Can it be about serotonin?
In mice, ablation of the raphe and no production serotonin increases wakefulness and impairs the homeostatic response to sleep deprivation.(DOI:https://doi.org/10.1016/j.neuron.2019.05.038)
Even in the absence of depression, the CSF levels of 5-I-HAA of patients with Parkinson’s disease are lower than those of age-matched controls.
( DOI: 10.1176/jnp.2.1.88 )
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Thank you for great articles. They gave me a new perspective about PD.
I want to suggest an article: Serotonergic dysregulation is linked to sleep problems in Parkinson's disease (doi:10.1016/j.nicl.2018.03.001)
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Honorable Sir Madam
I would be really grateful for your help. To solve problem I need statistical program or statistical operation that are essentially represents reverse process to descriptive statistics.
Example: Because of same event, cases from group D have same chances for either A or B outcome. Outcome A is forming group A. Cases with outcome B are forming group E. Group E is additionally formed with outcome B from group C, but event causing this outcome is different than in group D. If we compare group A with group E (regarding outcome based on different event) we are comparing homogeneous group A with heterogeneous group E. Before comparison, we must subtract from group E subgroup with same characteristics and same number of cases as in group A. Than we must add this subgroup to group A and than we could compare.
My question is: how can we from one larger database extract smaller group if we know number of cases and descriptive characteristics (univariate analysis) of this smaller group?
Yours sincerely
Slobodan Sekulic MD PhD
Child neurologist
Department of Neurology
Medical Faculty
Novi SadSerbia
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Thank you!
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Within three years, a patient with a desminopathy (Thr341Pro DES mutation) was found to have a 17% increase in the level of C4 complement components to 0.41 g / l (Norm 0.1-0.4 g / l).
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Dear Yosvany Castillo! Thank you very much for your answer. Over the past 2 years in this patient with desminopathy (Thr341Pro DES mutation in the heterozygous state), the C4 level of the complement component decreased to 0.36 g/l without taking medications.
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A patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) was recommended to refuse toothpaste. He continued to brush his teeth twice a day with a toothbrush with only water. As a result, within one month we noted a significant increase in strength and muscle mass in this patient. The patient did not take any medications during this period. After 30 days, the muscle condition returned to its original level. How can this positive effect be explained?
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The toothpaste may affect gut microbiota balance of the digestive tract thus affecting natural PH levels. The triclosan is proving s extremely aggressive. https://stm.sciencemag.org/content/10/443/eaan4116
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I really got confused in different protocols
how can I use: Guinea Pig Spinal Cord (GPSC) and
Complete Freund’s Adjuvant (CFA) and
Mycobacterium tuberculosis
what is the real material?
how can I prepare them?
can i use Mycobacterium Tuberculosis H37 Ra, Complete Adjuvant in Oil ( DIFCO 231131)?
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Hello Omid,
I do not have lab experience but I did find an excellent source which describes in detail "active induction by immunization and passive induction through adoptive transfer" (Phelan, 2016). There are also visual aids and graphs as well as a list of references that might help you with your study. Since I am a medical administration student and personally have MS, I plan to take the time to read it as soon as I finish my current assignments. Thank you for alerting me to this type of study for MS and good luck!
Leese
Reference
Phelan, J. (2016, December 19). Generating EAE mouse models of multiple sclerosis. Retrieved from: https://www.taconic.com/taconic-insights/neuroscience/eae-mouse-models-of-multiple-sclerosis.html
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Fungal pathogens have been recently implicated in the development of Alzheimer's and multiple sclerosis. I suspect these illnesses are the terminal stages of a less obvious parasitic relationship between a pathogen and its human host.
References
Benito-Leon, J. and M. Laurence. (2017). The Role of Fungi in the Etiology of Multiple Sclerosis. Frontiers in Neurology 16 October
Pisa, D., R. Alonso, A. Rabano, and I. Rodal. (2015). Different Brain Regions are Infected with Fungi in Alzheimer's Disease. Scientific Reports 5(15015)
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@ Peter Frost. The clinical claim that multiple sclerosis is lacking in any reliable identifying feature and that its neurological incapacitations must not be explained precludes verifying an MS-specific cause.
Isn't a focusing on MS-features such as Dawson's fingers and Steiner's Wetterwinkel lesions, and especially on their specific patterns of growth rather conducive to answering the question of what actually causes MS?
What about the documentation which the book with the ISBN 978-613-9-92056-3 offers on these points?
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I want to test the effect of a neuroprotective drug on rotenone rat model of Parkinson's disease but after reading the related articles about my work, I became doubts about select the best dosage of the drug and treatment methods. in some of the articles they using a low dosage of a neuroprotective drug and in some high dosage and their treatment was different in some cases, they use the oral method and some intraperitoneal injection method.
Does anyone have any suggestions to select the best dosage and treatment (o.p or i.p)?
Many thanks
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Do you know the highest dose that does not produce an adverse effect? If so, this is your NOAEL. A dose 10 fold lower than this should be you maximum dose to ensure a good margin of safety. You will then need to use this a start point for dose response analysis. Starting with the NOAEL dose you need to back down by ten fold increments to the next two lower doses. For example, if the NOAEL is 100 mg/ kg your dose response analysis should start with 1mg/kg, then 10 mg/kg then 100mg/kg. This should give you a good baseline set of data that can be translated to NHP and humans using allosteric modeling.
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In a level one unit of  Complex Neurorehab as an In-patient.
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...how long...years??
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Presentation in last year/years:
Fever with bone and joint pain. Hemorrhage was a common complication and used to occur during afebrile period.
Presentation in present year:
Fever, usually no bone or joint pain. Organ involvement specially cardiac and neurologic involvement is common, Hemorrhage is less common. Complications occur during febrile period. What is /are the factor/factors behind these changes in characteristics?
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Strain variability and host genetic factors.
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Is there a similarity in fMRI between vocalization and sign language?
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MacSweeney, Mairéad, Ruth Campbell, Bencie Woll, Vincent Giampietro, Anthony S. David, Philip K. McGuire, Gemma A. Calvert & Michael J. Brammer. 2004. "Dissociating linguistic and nonlinguistic gestural communication in the brain". NeuroImage 22(4): 1605-1618. doi:10.1016/j.neuroimage.2004.03.015
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In a patient with hereditary desminopathy (Thr341Pro DES mutation in the heterozygous state), a significant loss of muscle mass is observed after a night's sleep, with its replacement by adipose tissue. How to reduce muscle loss during sleep?
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Dear Ali Javadmanesh, Adrian Fierl, Abdulnabi Abdullamer Matruod, thank you very much for your answers!
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Radiosurgery, the therapy of brain tumors, has long been made using a so called Gamma Knife with high activity sealed sources such as Cobalt-60. Nowadays the therapy can also be made with a linear accelerator such as a Cyber Knife. What are your experiences? Can you share advantages and disadvantages of each system. At the end do you think that the use of radioactive sources is still (medically)justified for radiosurgery given the alternative of a Linear accelerator?
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Linear
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Food as a culprit in devolvement of neurologic diseases is not a novel concept, as there is a history of specific neurologic diseases that are caused by deficiencies in nutrition, namely lack of certain foods in human diet, like vitamins. There are also diseases caused by excess of some nutrients, and even vitamins. This review, however, is not about these well-known conditions. It is about potential indirect effect of what is considered a “healthy” balanced diet in development of neurologic diseases. We discuss what is known about gluten sensitivity and neurologic disorders, and we extrapolate that there might be a much wider array of intolerances-sensibilities which don’t have yet an objective marker. We also expanded on a hypothesis that maybe other neurologic disorder with immune mechanism like MS might be a target of immunological overload of other antigens apart from gluten.
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Please go through the following PDF attachments.
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I have received an invitation for member of the editorial board for Advances in Neurology and Neurosciences. I would like to know what do You think about it ? It is worth to accept it ? This journal as I see doesn't have a impact factor and articles published in it are not indexed in Pubmed. Thank You for all opinions and comments. Maybe You have also received such invitations ?
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I receive those invitations almost every single day. I go straight to Beall's list ( https://clinicallibrarian.wordpress.com/2017/01/23/bealls-list-of-predatory-publishers/ ). OPAST (publisher of "Advances in Neurology and Neurosciences ") has been on the list for at least 2 years.
If their email begins with something like "greetings", "good day", or something similar, you can be 99.9% sure that it's from journals referred to as 'predatory'.
I also refer to Shamsheer et al. (2017) which provides a list of items to go through - have a look at Table 10. For example, the opast site shows a plethora of unrelated journals, does not have a contact email address, and the physical address is actually a house in Kansas. Some journals list their address, and when you look it up on google earth it's actually a restaurant. Be careful.
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According to researches, appendix might has connection with Parkinson's Disease but consequences are conflict. One study says, appendix removal reduces risk of PD but another study says that it increases.
Uncovering a Link Between the Appendix and Parkinson Disease Risk
doi:10.1001/jama.2019.9041
Thank you!
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What happen in our brains when we prejudge about someone or something? Our prejudices also affect our decision making mechanism, how does it occur among neurons?
And if you know research that used fMRI, you can share with us.
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Actually, neuroimaging can prove a lot about the structure and function of the brain regions associated with mechanisms underlying complex behaviors like prejudice and discrimination which are convoluted aspects of decision-making under specific circumstances.
For example, there has been a study (using EEG) on gender prejudice (which is one of the major and prevalent types of prejudice) using a completely implicit paradigm to avoid social desirability processes. They demonstrated interesting results as violation of gender-bias prejudices elicited an anterior N400 response followed by left anterior negativity (LAN). For more details check:
Another study (using fMRI) on categorization and stereotyping of faces tested how prejudice affects race category competition and stabilization when perceiving faces varying in racial prototypicality. They indicated that relative prejudice tempers the extent of category competition and response conflict engaged when initially perceiving faces. For further details check:
There are many other studies regarding different aspects of prejudice that you can find and check the results.
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i would like to know about Immediate early genes and neuroplasticity relationship .
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Thanks Daniel Gray for your answer.
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I am a first year medical student looking to learn how to read MRIs over the summer for something to do and I am interested in neurology. What is the best atlas for learning cranial nerve MRI interpretation?
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Check these:
1) MRI of cranial nerves:
2) This article explains MR of each cranial nerve separately:
3) This paper is a model atlas for cranial nerve related disorders:
4) This one also can give you a general view of imaging these nerves:
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The neurologic examination is a powerful tool for urgent bedside assessment of ICU patients with neurologic or neurosurgical illnesses. Assessing cranial nerve function is one of the most vital components In this context. Testing the pupillary light reflex evaluates the status of the second and third cranial nerves. Automated pupillometers have been developed that provide objective measures of size of the pupil and the responsiveness of the pupil to light (neuropupillary index). Although few studies reveal diagnostic and prognostic usefulness in critically ill patients, none of the studies correct/adjust for interfer and confounding effects by for example sympathomimetic or parasympathomimetic drug effects, interference from ambient light, previous cataract operation, etc.
Isn‘t it much too early to reliably use automated pupillometry for diagnosis and prognosis in daily clinical practice in ICUs?
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The size of the pupil, and the responsiveness to light is definitely a key procedure in neurological ICU patients (especially concerning intracranial pressure) as many of the other neurological tests require active participation of the patient. However automated pupillometry has not found the way to our ICU and I think that the amount and quality of studies is not sufficient yet. In my opinion, it's a great approach, as manual pupillary examination shows a great variety between the investigators. On the other hand, many critical ill neurological patients have a external ventricular drainage anyway. So I think more and larger studies are needed, if they show positive results, automated pupillometry could assist the examination in future.
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I want to do primary neuron transfection and then to do live imaging and patch. The neurons need to be healthy after transfection. I tried lipofectamine but it was not that good. I also tried Magnetofectamine, and it was not stable. Sometimes it works, sometimes it kills all the neurons. Could anyone tell me a good method or any tips for transfection?
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Hi Xin
Most of transfection reagent affect the transient cell activity because of cytotoxicity. You could try lipofectamine 3000, which works well in some type of primary cells. In my experience, I would strongly suggest you to use adenovirus to infect primary neuron in vitro and AAV for in vivo infection, these virus have little effect on cell state but can infect primary neuron very well.
Genemedi is very good at AAV/lentivirus/adenovirus production, you could find detail information on their website: www.genemedi.net
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We have many techniques for revascularization [angiplasties, new stents, vascular bypass], yet we are not doing early screening in patients with multiple vascular risk factors.
Should we be more active in our early screening of the carotid and cerebral vessel circulations?
Are we missing the boat?
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We have new innovative patented moleculs who are able to treat Demencia vascular .
Look inside if its possible to participe ( preclinical and clinical developpement needed to dispose of new drug for neurodegenerescences )
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How comes Charcot, that influenced so much psychiatry, by giving an uterine name to a mental disease, to underline it was a female "weakness" related with periods, is respected as an authority and considered as the "father of neurology" or the one that defined Multiple Sclerosis, when no one still today is able to give an exact physiologic definition of what is a "nervous lesion"?
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My own ephemeral opinion, since I begun recollecting data, because not getting the answers to my questions, is MS is a multi-factorial disease and different specialists should work together for getting close to understand it. I find the notion of "MS as a psychosomatic disease" very interesting , but not only. Guts-brain axis is too fascinating, because it almost look like a life lesson: our thoughts are born in our dejection. and what our body rejects feeds our mind. https://journals.sagepub.com/doi/10.1177/1352458517739975#articleShareContainer
And finally, the genetic track should be completed.
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Does any neurolog have any chance to escape the initial report? Why do they always reproduce patterns in their own research? I think the too strict protocols totally ruined in advance any research, forbidding any individual idea and inducing results. Why are neurologs unable to express any novelty? Is there a secret Bible for the human brain, a correct universal way to drive it?
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Dear Fred Romano & André Michaud,
Why not address Fred Romano's hunches in trying to get more concrete?
It is shown below: our advanced, dedicated MR and endoscopic imaging techniques might be far better exploited for unraveling the nature and cause of MS. This would help to avoid mistaken lesion interpretations, brain biopsies, to overcome the pushing of disease-modifying drugs, a commercial monopolizing of MS-research.
Thank you in advance if you are willing to face these problems, to strive to master them in the patients' best interests.
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A patient with hereditary desminopathy (a mutation of Thr341Pro DES in a heterozygous state) with the progression of the disease has been established for a long-term healing of skin tissue when it is damaged, compared with a healthy person. The blood sugar level of a patient with desminopathy is normal.
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informative discussion.
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Brain death is the irreversible and complete loss of cerebral function leading to extinction of brain impulses necessary to sustain life. Its diagnosis is based on the absence of brainstem reflexes and the exclusion of endo- or exogenous factors confounding the clinical presentation [1]. With advances in intensive care medicine and the emergence of organ donation programs worldwide, early and reliable diagnosis of brain death is gaining importance [www.irodat.org]. Howeve, the predefined technical requirements as well as the qualification and number of clinicians to be involved in the diagnostic workup is inconsistent worldwide. This issue is mirrored by an international review, revealing that the conduct of apnea tests, the time to brain death diagnosis, the number of required examiners, and predefined clinical scenarios calling for ancillary tests varied among countries [2]. This variability in combination with the lack of systematic studies regarding the frequency and presentation of specific reversible clinical conditions mimicking brain death further challenge clinicians and put patients at risk.
Are there any systematic studies regarding the frequency and type of clinical conditions mimicking brain death and the reliability of diagnostic procedures when cerebral death is suspected?
1. Wijdicks EF. The diagnosis of brain death. N Engl J Med 2001;344(16):1215-1221.
2. Wijdicks EF. Brain death worldwide: accepted fact but no global consensus in diagnostic criteria. Neurology 2002;58(1):20-25.
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In my hospital caring for the brain dead patient had a multidisciplinary team. And had guideline consistency and comfortable to do.
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There are a growing number of papers related to this topic and I should be glad to know if there are some new agreements related to the heteromeric collectin.
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not my field
kb
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I am working on a forensic case with a psychiatrist regarding a man we evaluated in a psychiatric evaluation who developed complex partial seizures due to clandestine lab exposure, specifically lithium and methamphetamine labs, throughout his career working as a police officer. We reviewed his current list of medications, and he is taking 50 mg of sertraline (Zoloft) once per day.
The research that I found shows that higher doses of sertraline increases the risk of seizure, including partial complex, and that sertraline and methylphenidate (a CNS stimulant) can precipitate seizures. Though, I'm trying to eliminate variables here... 50 mg qd of sertraline is an ordinary prescription. Were the lithium and/or meth vapors interacting with his sertraline, or is there another reason why he was experiencing seizures?
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Marie Humbert-Claude Béatrice Marianne Ewalds-Kvist Thank you for the answers and literature! Will ask more questions with more later when needed.
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Dear Colleagues,
Perhaps you could help me find answers to several questions on the neural organization of alphabet and number recitation:
1. Could recitation of numbers and letters rely on phonological long-term memory without accessing lexical information? Alternatively, could lexical information be accessed only for numbers (since they are words) but not letters (that are not words)?
2. Several neuroimaging studies (including clinical reports) have shown a dissociation between letter and number sequencing (recitation, reading and writing). Why do you think this is the case?
3. A patient could not recite the alphabet but could sing it upon electrical brain stimulation. Any suggestions why this happened?
Help with any of the questions will be greatly appreciated!
Thank you!
Monika
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Dear Monika! Please see related articles in Attachment. All the best. Vladimir
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we can only use 20 percent of the brain's nerve cells to store memories. is there any specific way like shooting electrical current across the brain to increase it's ablility to store memories!?
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Good answer Dr Simon N Young!
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20 years old boy presenting with fever and abdominal pain . Later he lost his consciousness. WBC/CRP/ESR/Creatinine/AST/ALT high
nerve conduction studies  no conduction in all peripheral nerves.
what are the conditions with cause no conduction in all nerves?
Severe GBS?
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Acute GBS is the likely diagnosis
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JAMA Neurology has recently published a phase II clinical trial of 20 mg of atorvastatin in chronic subdural hematoma, with the intention of reducing the surgical risk. The result has been favorable. The study has been done exclusively in Chinese population. Although it will be necessary to confirm this in larger studies and in a non-oriental population, can it be an option?
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it seems quite intresting needs to go for more aggressive study design
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Laughter , mechanism and pathway .
Neurology
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Yes, indeed. An African friend from the Lango tribe in Uganda was so tickled to see us Europeans eating the small bananas. In his tribe, only little children ate them - it was their lolipop!
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We are a team including Epidemiologists, Physicians, Biologists (MSC and PhD), Well-known supervisors from Iran, United States and India and we are writing a lot of articles in these countries.
Now, we need more authors in our team. Motivated, active, Smart and clever authors from everywhere in the world.
Currently we want to form a team and write a new review article in Neuroscience (Especially on Impacts of Nutrients on Brain developments).
Kindly send your request by E-mail or direct message on RG.
Do not hesitate to ask any question.
Best of Luck
Kheirvari JK
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Good Luck
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Mild pressure feeling in the head, not painful but just very aggravating and feeling really strange. Feeling like having an extreme brain fog and like a fuzzy head/ a constant cloud over the brain.
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Brain Fog, feelings of dissociation, mild feeling of head fulness are commonly seen in someone who has a history of Sleep Apnea Syndrome. I certainly would recommend doing a CT of the brain to make sure there is no abnormality of the temporal lobes which can cause complex partial/temporal lobe epilepsy. I am a neurologist and have come across many patients with symptomology like yours. thanks.
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Dear researchers,
1- What is wrong with the spinal interneurons in the stroke patients?How has the stroke affected them?
2- How is the spinal stimulation supposed to affect those problematic interneurons in a way to get them back to normal functioning?
I would appreciate any good papers, books .... to study, or any direct answers.
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The stroke causes loss of the inhibitory effect of the corticospinal tracts on the spinal interneurons (the Renshaw cells). this is the reason for the spasticity after a stroke. the initial flaccidity is due to the spinal "shock" on the spinal reflex arc due to this loss of inhibition. it causes apraxia of the spinal motor neurons leading to the flaccid muscles. but then the spinal reflex arc recovers and we get the spasticity. Hence, you can see there is nothing wrong with the spinal interneurons themselves. we use medications to decrease the activity of these interneurons, including intrathecal baclofen pump, but unfortunately the kind of control that the corticospinal tracts had on them could not be replicated, at least to date. there are many studies that are trying to achieve this with SCI, but the results have been dismal. there seems to be some inhibitory growth factors that prevent the growth of axons when it comes to the CNS. in stroke patients the penumbral neurons would be able to form connections with the interneurons if only we can inhibit these inhibitory growth factors. thanks.
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Over the past three years, a patient with hereditary desminopathy (Thr341Pro DES mutation in the heterozygous state) has an uneven decrease in muscle strength in the hands. In the right hand, the decrease in muscular strength in the last three years is 2.1 times, and in the left one - 1.5 times. In a weaker limb, the disease progresses faster. A similar pattern is observed in the legs. The father of the patient had the same changes.
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The short answer is penetrance variability and phenotypic variability. but in your case there is no phenotypic variability as both the proband and his father had the same phenotype. however, the differences between the cases is likely due to penetrance variability. to do into details about these factors will be too long. thanks.
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What is the definition of a neuron apart from being a cell of the central nervous system? A clear definition of neuron that sets it apart from other cell type unequivocally seems to be conundrum? Any help out there please!
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