Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, January 11, 2023

The Stressed Gut: Region-specific Immune and Neuroplasticity Changes in Response to Chronic Psychosocial Stress

It is your doctor's responsibility to make sure you are under no stress as a result of your stroke. And the only way to do that is for your doctor to have EXACT STROKE REHAB PROTOCOLS LEADING TO 100% RECOVERY. Less than that and your doctor is incompetent.

 The Stressed Gut: Region-specific Immune andNeuroplasticity Changes in Response toChronic Psychosocial Stress


Beatriz Lobo,1,5,6,7
* Mónica Tramullas,1,8  
Beate-C Finger,1  
Kevin W Lomasney,1,3 
 Caroll Beltran,1,9  
Gerard Clarke,1  
Javier Santos,5,6,7,10
Niall P Hyland,1,2  
Timothy G Dinan,1,4 4
nd John F Cryan1,3 *
1
APC Microbiome Ireland, Departments of 2
Physiology, Anatomy and Neuroscience, Psychiatry and Neurobehavioural Science, University
College Cork, Ireland; 5
Digestive System Research Unit, Laboratory of Neuro-Immuno-Gastroenterology, Vall d’Hebron Institut de Recerca (VHIR),
Vall d’Hebron Hospital Universitari, Barcelona, Spain; 6
Department of Gastroenterology, Vall d’Hebron Hospital Universitari, Passeig Vall
d’Hebron Barcelona, Spain; 7
Facultat de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain; 8
Departamento de Fisiología
y Farmacología, Facultad de Medicina, Universidad de Cantabria, Santander, Spain (Current address); 9
Laboratory of Immunogastroenterology,
Gastroenterology Unit, Hospital Clinico Universidad de Chile, Faculty of Medicine Universidad de Chile, Santiago, Chile; and10
Centro de
Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
Background/Aims
Chronic psychological stress affects gastrointestinal physiology which may underpin alterations in the immune response and epithelial transport, both functions are partly regulated by enteric nervous system. However, its effects on enteric neuroplasticity are still unclear. This study aims to investigate the effects of chronic unpredictable psychological stress on intestinal motility and prominent markers of enteric function.
Methods
Adult male C57BL/6J mice were exposed to 19 day of unpredictable stress protocol schedule of social defeat and overcrowding. We investigated the effects on plasma corticosterone, food intake, and body weight. In vivo gastrointestinal motility was assessed by fecal pellet output and by whole-gastrointestinal transit (using the carmine red method). Tissue monoamine level, neural and glial markers, neurotrophic factors, monoamine signaling, and Toll-like receptor expression in the proximal and distal colon, and terminal ileum were also assessed.
Results
Following chronic unpredictable psychological stress, stressed mice showed increased food intake and body weight gain (P < 0.001), and reduced corticosterone levels (P < 0.05) compared to control mice. Stressed mice had reduced stool output without differences in
water content, and showed a delayed gastrointestinal transit compared to control mice (P < 0.05). Stressed mice exhibited decreased mRNA expression of tyrosine hydroxylase (Th), brain-derived neurotrophic factor (Bdnf) and glial cell-derived neurotrophic factor(Gdnf), as well as Toll-like receptor 2 (Tlr2) compared to control (P < 0.05), only proximal colon. These molecular changes in proximal colon were associated with higher levels of monoamines in tissue.
Conclusion
Unpredictable psychological chronic stress induces region-specific impairment in monoamine levels and neuroplasticity markers that may relate to delayed intestinal transit.
(J Neurogastroenterol Motil 2023;29:72-84)

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