Effect of Pulsed Electromagnetic Field (PEMF) on Infarct Size and Inflammation After Cerebral Ischemia in Mice

 It's been 7 years, where is the followup research in humans? Or did this fall thru the cracks like everything in stroke since there is NO LEADERSHIP?

Effect of Pulsed Electromagnetic Field (PEMF) on Infarct Size and Inflammation After Cerebral Ischemia in Mice

• Juan Carlos Pena-Philippides,
• Yirong Yang,
• Olga Bragina,
• Sean Hagberg,
• Edwin Nemoto &
• Tamara Roitbak 

Translational Stroke Research volume 5, pages 491–500 (2014)Cite this article

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Abstract

Pulsed electromagnetic fields (PEMF) have been demonstrated to have anti-inflammatory and pro-regenerative effects in animals and humans. We used the FDA-approved Sofpulse™ (Ivivi Health Sciences, LLC) to study effect of PEMF on infarct size and poststroke inflammation following distal middle cerebral artery occlusion (dMCAO) in mice. Electromagnetic field was applied within 30–45 min after ischemic brain damage and utilized twice a day for 21 consecutive days. Ischemic infarct size was assessed using MRI and histological analysis. At 21 days after dMCAO, the infarct size was significantly (by 26 %) smaller in PEMF-treated animals as compared to controls. Neuroinflammation in these animals was evaluated using specialized cytokine/chemokine PCR array. We demonstrate that PEMF significantly influenced expression profile of pro- and anti-inflammatory factors in the hemisphere ipsilateral to ischemic damage. Importantly, expression of gene encoding major pro-inflammatory cytokine IL-1α was significantly reduced, while expression of major anti-inflammatory IL-10 was significantly increased. PEMF application significantly downregulated genes encoding members of the major pro-apoptotic tumor necrosis factor (TNF) superfamily indicating that the treatment could have both anti-inflammatory and anti-apoptotic effects. Both reduction of infarct size and influence on neuroinflammation could have a potentially important positive impact on the poststroke recovery process, implicating PEMF as a possible adjunctive therapy for stroke patients.

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Glucose Modifies the Effect of Endovascular Thrombectomy in Patients With Acute Stroke

WHOM  is the person responsible for shepherding this through human clinical studies to a translational protocol?  With no one identified it will fall thru the cracks like the thousands of other research studies that showed promise.

 

Glucose Modifies the Effect of Endovascular Thrombectomy in Patients With Acute Stroke

A Pooled-Data Meta-Analysis

Ángel Chamorro

,

Scott Brown

,

Sergio Amaro

,

Michael D. Hill

,

Keith W. Muir

,

Diederik W.J. Dippel

,

Wim van Zwam

,

Ken Butcher

,

Gary A. Ford

,

Heleen M. den Hertog

, … Show all Authors

Originally published19 Feb 2019https://doi.org/10.1161/STROKEAHA.118.023769Stroke. 2019;0

Abstract

Background and Purpose—

Hyperglycemia is a negative prognostic factor after acute ischemic stroke but is not known whether glucose is associated with the effects of endovascular thrombectomy (EVT) in patients with large-vessel stroke. In a pooled-data meta-analysis, we analyzed whether serum glucose is a treatment modifier of the efficacy of EVT in acute stroke.

Methods—

Seven randomized trials compared EVT with standard care between 2010 and 2017 (HERMES Collaboration [highly effective reperfusion using multiple endovascular devices]). One thousand seven hundred and sixty-four patients with large-vessel stroke were allocated to EVT (n=871) or standard care (n=893). Measurements included blood glucose on admission and functional outcome (modified Rankin Scale range, 0–6; lower scores indicating less disability) at 3 months. The primary analysis evaluated whether glucose modified the effect of EVT over standard care on functional outcome, using ordinal logistic regression to test the interaction between treatment and glucose level.

Results—

Median (interquartile range) serum glucose on admission was 120 (104–140) mg/dL (6.6 mmol/L [5.7–7.7] mmol/L). EVT was better than standard care in the overall pooled-data analysis adjusted common odds ratio (acOR), 2.00 (95% CI, 1.69–2.38); however, lower glucose levels were associated with greater effects of EVT over standard care. The interaction was nonlinear such that significant interactions were found in subgroups of patients split at glucose < or >90 mg/dL (5.0 mmol/L; P=0.019 for interaction; acOR, 3.81; 95% CI, 1.73–8.41 for patients < 90 mg/dL versus 1.83; 95% CI, 1.53–2.19 for patients >90 mg/dL), and glucose < or >100 mg/dL (5.5 mmol/L; P=0.004 for interaction; acOR, 3.17; 95% CI, 2.04–4.93 versus acOR, 1.72; 95% CI, 1.42–2.08) but not between subgroups above these levels of glucose.

Conclusions—

EVT improved stroke outcomes compared with standard treatment regardless of glucose levels, but the treatment effects were larger at lower glucose levels, with significant interaction effects persisting up to 90 to 100 mg/dL (5.0–5.5 mmol/L). Whether tight control of glucose improves the efficacy of EVT after large-vessel stroke warrants appropriate testing.

Footnotes

Guest Editor for this article was Harold P. Adams, MD.
The online-only Data Supplement is available with this article at https://www.ahajournals.org/doi/suppl/10.1161/STROKEAHA.118.023769.

Correspondence to Ángel Chamorro, MD, Hospital Clinic of Barcelona, Villarroel 170, 08036 Barcelona, Spain. Email achamorro@clinic.cat

Repairing the Brain by SCF+G-CSF Treatment at 6 Months Postexperimental Stroke

Now we just need to update and execute that stroke strategy and run human clinical trials on this. Followup which will never occur under current stroke leadership. It will fall thru the cracks like thousands of other studies. Incompetence reigns supreme in the stroke medical world.
Repairing the Brain by SCF+G-CSF Treatment at 6 Months Postexperimental Stroke

Mechanistic Determination of the Causal Link Between Neurovascular Regeneration and Motor Functional Recovery

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Lili Cui, Dandan Wang, Sandra McGillis, ...

First Published August 9, 2016 Research Article

Article information

Abstract

Stroke, a leading cause of adult disability in the world, is a severe medical condition with limited treatment. Physical therapy, the only treatment available for stroke rehabilitation, appears to be effective within 6 months post-stroke. Here, we have mechanistically determined the efficacy of combined two hematopoietic growth factors, stem cell factor (SCF) and granulocyte-colony stimulating factor (G-CSF; SCF + G-CSF), in brain repair 6 months after cortical infarct induction in the transgenic mice carrying yellow fluorescent protein in Layer V pyramidal neurons (Thy1-YFP-H). Using a combination of live brain imaging, whole brain imaging, molecular manipulation, synaptic and vascular assessments, and motor function examination, we found that SCF + G-CSF promoted mushroom spine formation, enlarged postsynaptic membrane size, and increased postsynaptic density-95 accumulation and blood vessel density in the peri-infarct cavity cortex; and that SCF + G-CSF treatment improved motor functional recovery. The SCF + G-CSF-enhanced motor functional recovery was dependent on the synaptic and vascular regeneration in the peri-infarct cavity cortex. These data suggest that a stroke-damaged brain is repairable by SCF + G-CSF even 6 months after the lesion occurs. This study provides novel insights into the development of new restorative strategies for stroke recovery.

Repairing the Brain by SCF+G-CSF Treatment at 6 Months Postexperimental Stroke

Now we just need to update and execute that stroke strategy and run human clinical trials on this. Followup which will never occur under current stroke leadership. It will fall thru the cracks like thousands of other studies.
http://journals.sagepub.com/doi/full/10.1177/1759091416655010?utm_source=Adestra&utm_medium=email&

Mechanistic Determination of the Causal Link Between Neurovascular Regeneration and Motor Functional Recovery

Show all authors

Lili Cui¹²

Lili Cui

1Department of Neurosurgery, State University of New York Upstate Medical University, Syracuse, NY, USA2Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, LA, USA
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, Dandan Wang¹

Dandan Wang

1Department of Neurosurgery, State University of New York Upstate Medical University, Syracuse, NY, USA
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, Sandra McGillis¹

Sandra McGillis

1Department of Neurosurgery, State University of New York Upstate Medical University, Syracuse, NY, USA
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,

Michele Kyle¹

Michele Kyle

1Department of Neurosurgery, State University of New York Upstate Medical University, Syracuse, NY, USA
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, Li-Ru Zhao¹²

Li-Ru Zhao

1Department of Neurosurgery, State University of New York Upstate Medical University, Syracuse, NY, USA2Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, LA, USA
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...

First Published August 9, 2016 Research Article

https://doi.org/10.1177/1759091416655010

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Article Information

Volume: 8 issue: 4,

Article first published online: August 9, 2016; Issue published: June 1, 2016
Received: February 16, 2016; Accepted: April 19, 2016

https://doi.org/10.1177/1759091416655010

Lili Cui¹, ², Dandan Wang¹, Sandra McGillis¹, Michele Kyle¹, Li-Ru Zhao¹²

¹Department of Neurosurgery, State University of New York Upstate Medical University, Syracuse, NY, USA

²Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, LA, USA

Corresponding Author: Li-Ru Zhao, Department of Neurosurgery, State University of New York Upstate Medical University, 750 East Adams Street, Syracuse, New York, USA. Email: ZHAOL@upstate.edu

This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).

• Abstract
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Abstract

Stroke, a leading cause of adult disability in the world, is a severe medical condition with limited treatment. Physical therapy, the only treatment available for stroke rehabilitation, appears to be effective within 6 months post-stroke. Here, we have mechanistically determined the efficacy of combined two hematopoietic growth factors, stem cell factor (SCF) and granulocyte-colony stimulating factor (G-CSF; SCF + G-CSF), in brain repair 6 months after cortical infarct induction in the transgenic mice carrying yellow fluorescent protein in Layer V pyramidal neurons (Thy1-YFP-H). Using a combination of live brain imaging, whole brain imaging, molecular manipulation, synaptic and vascular assessments, and motor function examination, we found that SCF + G-CSF promoted mushroom spine formation, enlarged postsynaptic membrane size, and increased postsynaptic density-95 accumulation and blood vessel density in the peri-infarct cavity cortex; and that SCF + G-CSF treatment improved motor functional recovery. The SCF + G-CSF-enhanced motor functional recovery was dependent on the synaptic and vascular regeneration in the peri-infarct cavity cortex. These data suggest that a stroke-damaged brain is repairable by SCF + G-CSF even 6 months after the lesion occurs. This study provides novel insights into the development of new restorative strategies for stroke recovery.

Keywords brain repair, chronic stroke, G-CSF, hematopoietic growth factors, SCF, live brain imaging

Introduction

Stroke is a cerebrovascular disease in which brain tissue death (infarct) and neurological deficits occur from the sudden interruption of blood flow to a specific region of the brain. Stroke progresses through three phases: the acute, subacute, and chronic phase. The pathological profiles of the three phases appear to be quite different. Unlike in the acute and subacute phases, when massive neurons undergo primary and secondary damage (Parsons et al., 2000) in the chronic phase, a stroke patient’s neurological status becomes relatively stable and the surviving neurons establish new networks in an effort to take over the function of the dead neurons (Tombari et al., 2004; Carmichael, 2012; Cui et al., 2013; Zhao et al., 2013). The duration and pathological severity of the three phases vary between individuals and depend on the infarction size, infarct location, cerebrovascular collateral response, patient’s age, and medical comorbidities. Generally, the chronic phase begins 3 months after stroke onset (Hara et al., 1993; Parsons et al., 2000).
Stroke is an enormous public health problem and the leading cause of persistent disability worldwide. Today, there is a large population of chronic stroke patients in the world suffering from stroke-induced disability. A recent study shows that in 2010, there were 102 million disability-adjusted life-years lost in the world (Feigin et al., 2014). In the United States alone, about 6.6 million stroke survivors are suffering from persistent disability (Mozaffarian et al., 2015). Targeting brain repair in chronic stroke is a highly important but much less investigated field in stroke research. Speech and physical therapies appear to be the only therapies available for chronic stroke patients. Since it would be unfeasible for stroke patients to spend every hour with physical therapists for physical performance, developing alternatives, such as a pharmaceutical approach, to help in restoring motor function for stroke survivors is needed. Importantly, the therapeutic window for traditional physical therapy appears to be limited within 6 months after stroke onset (Hendricks et al., 2002; Schaechter, 2004). Over 50% of chronic stroke patients, who are discharged from rehabilitation therapy at 6 months post-stroke, still show significant motor impairment (Gresham et al., 1975; Hendricks et al., 2002; Kelly-Hayes et al., 2003). Currently, therapies that can further improve functional restoration 6 months after stroke occurs have not yet been developed.
Recently, we have demonstrated the therapeutic efficacy of stem cell factor (SCF) and granulocyte-colony stimulating factor (G-CSF) on brain repair and functional restoration in animal models of chronic stroke. SCF and G-CSF are well-characterized hematopoietic growth factors and play an essential role in controlling bone marrow stem cell growth, survival, and differentiation into blood cells (Welte et al., 1985; Zsebo et al., 1990). Increasing evidence, however, shows that SCF and G-CSF are also involved in neuronal plasticity, neuronal network formation, and neuronal function in learning and memory (Hirata et al., 1993; Motro et al., 1996; Katafuchi et al., 2000; Diederich et al., 2009; Su et al., 2013). Our earlier study revealed that systemic administration of combined SCF and G-CSF (SCF + G-CSF) 3.5 months after induction of cortical brain ischemia led to much greater functional improvement than SCF or G-CSF treatment alone (Zhao et al., 2007). However, it remains unanswered whether administration of SCF + G-CSF at a much-delayed time, 6 months after stroke, would be effective in brain repair.
Neurovascular network remodeling has been proposed to play an important role in stroke recovery (Moskowitz et al., 2010). Nuclear factor-κB (NF-κB), a transcription factor, is involved in synaptogenesis (Meffert et al., 2003; Memet, 2006; Boersma et al., 2011; Imielski et al., 2012) and angiogenesis (Stoltz et al., 1996). Our recent findings revealed that NF-κB mediates SCF + G-CSF-promoted neurite outgrowth in cultured primary cortical neurons (Su et al., 2013). The purpose of the present study was to determine whether administration of SCF + G-CSF at 6 months after experimental stroke would be effective in enhancing functional improvement and neurovascular network remodeling and whether NF-κB would be involved in the restorative process of SCF + G-CSF in such a delayed treatment.

More at link.

Biomarkers of stroke recovery: Consensus-based core recommendations from the Stroke Recovery and Rehabilitation Roundtable

The bolded line is a major problem in stroke research that Rebecca and I have commented on; cherry picking of research subjects. I was rejected from a TMS study because I did not have enough voluntary hand opening movement. We need to do complete research that leaves no survivor behind.  But since we have NO stroke leadership and NO stroke strategy this great idea will fall thru the cracks. 

Biomarkers of stroke recovery: Consensus-based core recommendations from the Stroke Recovery and Rehabilitation Roundtable

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Lara A Boyd, Kathryn S Hayward, Nick S Ward, ...

First Published July 12, 2017 Research Article

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Abstract

The most difficult clinical questions in stroke rehabilitation are “What is this patient’s potential for recovery?” and “What is the best rehabilitation strategy for this person, given her/his clinical profile?” Without answers to these questions, clinicians struggle to make decisions regarding the content and focus of therapy, and researchers design studies that inadvertently mix participants who have a high likelihood of responding with those who do not. Developing and implementing biomarkers that distinguish patient subgroups will help address these issues and unravel the factors important to the recovery process. The goal of the present paper is to provide a consensus statement regarding the current state of the evidence for stroke recovery biomarkers. Biomarkers of motor, somatosensory, cognitive and language domains across the recovery timeline post-stroke are considered; with focus on brain structure and function, and exclusion of blood markers and genetics. We provide evidence for biomarkers that are considered ready to be included in clinical trials, as well as others that are promising but not ready and so represent a developmental priority. We conclude with an example that illustrates the utility of biomarkers in recovery and rehabilitation research, demonstrating how the inclusion of a biomarker may enhance future clinical trials. In this way, we propose a way forward for when and where we can include biomarkers to advance the efficacy of the practice of, and research into, rehabilitation and recovery after stroke.

Neuroprotective compound could save brain cells during stroke, rat study shows

WHOM do we talk to to get this followed up in humans? Or will this fall thru the cracks like most promising stroke research due to our fucking failures of stroke associations? I bet the lasting effect is because there are less dead and damaged neurons because of the treatment. It stopped some part of the neuronal cascade of death.

The latest here:
Neuroprotective compound could save brain cells during stroke, rat study shows

Researchers from the University of Iowa Carver College of Medicine and the University of Miami Miller School of Medicine have shown that a neuroprotective compound tested in rats provides two-pronged protection for brain cells during stroke and improves physical and cognitive outcomes in the treated animals.
Every year, nearly 800,000 Americans have a stroke and almost 130,000 die. Survivors often are left with long-term physical and cognitive disability that significantly alters their lives.
When a stroke interrupts the brain's blood supply, mature brain cells (neurons) die. In addition, reestablishing blood flow, known as reperfusion, also leads to processes that cause cell death. A part of the brain's natural response to stroke injury is to increase production of new brain cells in two specific regions (the subgranular zone of the hippocampal dentate gyrus and the subventricular zone of the lateral ventricles), which normally make a smaller number of new brain cells every day. Unfortunately, the vast majority of these newborn cells die within one to two weeks, limiting the benefit of this potential repair process. Minimizing the loss of brain cells is a primary goal for new stroke therapies.
"If we could prevent the mature brain cells from dying that would be beneficial," says Andrew Pieper, MD, PhD, professor of psychiatry in the UI Carver College of Medicine and co-senior study author. "But if we could also support or enhance this surge in neurogenesis (birth of new neurons), we might be able to further foster recovery, especially in terms of cognitive function, which is critically dependent on the hippocampus."
Using rats, Pieper and his colleagues Zachary B. Loris and W. Dalton Dietrich, PhD, tested the effects of a compound called P7C3-A20 on these two aspects of neuroprotection following ischemic stroke. Blood flow to the rats' brains was interrupted for 90 minutes and then the blockage was cleared allowing reperfusion. One group of rats was given the P7C3-A20 compound twice daily for seven days following the stroke. P7C3-A20 has previously been shown to prevent brain cell death in other animal models of neurologic injury, including Parkinson's disease, amyotrophic lateral sclerosis, stress-associated depression, and traumatic brain injury.
In terms of the brain itself, the P7C3-A20 compound reduced loss of brain tissue (atrophy) and increased survival of newborn neurons six weeks after stroke. In addition to the improved survival of both mature and newborn neurons, rats that received the P7C3-A20 compound for seven days after stroke also had better physical and cognitive outcomes than untreated rats. Treated rats had improved balance and coordination one week after stroke, and improved learning and memory one month after stroke. The findings were published recently in the journal Experimental Neurology.

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"There is no previous demonstration of a pharmacologic agent that both protects mature neurons from dying and also boosts the net magnitude of neurogenesis," Pieper says. "Our compound is beneficial in this animal model of stroke, and we're hopeful that it might eventually benefit patients."
"Currently there are limited treatments for acute stroke that make a real difference in patient's lives. There is an urgent need to identify, test, and translate new therapies to the clinic," adds Dietrich, co-senior study author and Scientific Director of The Miami Project to Cure Paralysis, professor of neurological surgery, neurology, biomedical engineering and cell biology at the University of Miami where the studies were conducted. "The ability to both protect and repair the injured nervous system has major implications on how we think about improving outcomes in millions of people each year with acute neurological injuries."
The neuronal protection provided by the P7C3-A20 compound was also associated with a boost in the levels of a substance called nicotinamide adenine dinucleotide (NAD) in the rats' brains. NAD is emerging as an important player in neuronal health and survival. Levels of this substance are depleted during stroke, and it has been proposed that increasing NAD levels may be a therapeutic target for treating stroke. In this study, P7C3-A20 treatment restored NAD to normal levels in the rats' cortex after a stroke.
Importantly, the study examined the effects of P7C3-A20 on cognitive and physical outcomes well beyond the time of the initial stroke. The sustained physical and cognitive improvement seen in the rats up to one month after the stroke suggests that the P7C3-A20 compound provides a long-term benefit.
"We found we can give the compound in this critical period immediately after the stroke and it has a lasting effect," notes Pieper, who also is a professor of neurology, radiation oncology, and a psychiatrist with the Iowa City Veterans Affairs Health Care System.
In recent years, advances in treatments that break up or remove stroke-causing blood clots have reduced the death rate for stroke and are improving outcomes for patients. The researchers hope that a treatment based on P7C3-A20 used in addition to the clot-clearing therapies might further improve outcomes by protecting brain cells during the traumatic ischemia/reperfusion period.

Source:

University of Iowa Health Care

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Posted in: Medical Science News | Medical Research News | Medical Condition News

Tags: Adenine, Blood, Brain, Brain Cell, Cell, Cognitive Function, Compound, Cortex, Depression, Disability, Health Care, Heart, Hippocampus, Ischemic Stroke, Nervous System, Neurogenesis, Neurology, Oncology, Paralysis, Parkinson's Disease, Psychiatry, Sclerosis, Stress, Stroke, Surgery, Traumatic Brain Injury, Veterans Affairs

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Feasibility and efficacy of a robotic device for hand rehabilitation in hemiplegic stroke patients: A randomized pilot controlled study

Is this enough to scream it out to all stroke hospitals worldwide? Or will this once again fall thru the cracks? Because we have NO stroke leadership pushing such knowledge out to stroke medical professionals?
http://cre.sagepub.com/content/early/2016/04/06/0269215516642606.abstract

1. Fabio Vanoglio1
2. Palmira Bernocchi2⇑
3. Chiara Mulè3
4. Francesca Garofali1
5. Chiara Mora1
6. Giovanni Taveggia3
7. Simonetta Scalvini2
8. Alberto Luisa1

1. ¹Neurological Rehabilitation Unit, Fondazione Salvatore Maugeri, IRCCS, Institute of Lumezzane, Brescia, Italy
2. ²Care Continuity Unit, Fondazione Salvatore Maugeri, IRCCS, Institute of Lumezzane, Brescia, Italy
3. ³Habilita Hospital, Sarnico, Bergamo, Italy

1. Palmira Bernocchi, Unit of Care Continuity, Fondazione Salvatore Maugeri, IRCCS, Via Giuseppe Mazzini 129 – 25066 Lumezzane, Brescia, Italy. Email: palmira.bernocchi@fsm.it

Abstract

Objective: The purpose of the study was to evaluate the feasibility and efficacy of robot-assisted hand rehabilitation in improving arm function abilities in sub-acute hemiplegic patients.

Design: Randomized controlled pilot study.

Setting: Inpatient rehabilitation centers.

Participants: Thirty hemiplegic stroke patients (Ashworth spasticity index <3) were recruited and randomly divided into a Treatment group (TG) and Control group (CG).

Interventions: Patients in the TG received intensive hand training with Gloreha, a hand rehabilitation glove that provides computer-controlled, repetitive, passive mobilization of the fingers, with multisensory feedback. Patients in the CG received the same amount of time in terms of conventional hand rehabilitation.

Main outcome measures: Hand motor function (Motricity Index, MI), fine manual dexterity (Nine Hole Peg Test, NHPT) and strength (Grip and Pinch test) were measured at baseline and after rehabilitation, and the differences, (Δ) mean(standard deviation), compared between groups.

Results Twenty-seven patients concluded the program: 14 in the TG and 13 in the CG. None of the patients refused the device and only one adverse event of rheumatoid arthritis reactivation was reported. Baseline data did not differ significantly between the two groups. In TG, ΔMI 23(16.4), ΔNHPT 0.16(0.16), ΔGRIP 0.27(0.23) and ΔPINCH 0.07(0.07) were significantly greater than in CG, ΔMI 5.2(9.2), ΔNHPT 0.02(0.07), ΔGRIP 0.03(0.06) and ΔPINCH 0.02(0.03)] (p=0.002, p=0.009, p=0.003 and p=0.038, respectively).

Conclusions: Gloreha Professional is feasible and effective in recovering fine manual dexterity and strength and reducing arm disability in sub-acute hemiplegic patients

Discovery of a "neuronal Big bang"

This should be useful for the strategist in stroke to know which research should be followed up on for neurogenesis. But since we seem to have no strategy in stroke this will fall thru the cracks.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=161704&CultureCode=en

Our brain is home to different types of neurons, each with their own genetic signature that defines their function. These neurons are derived from progenitor cells, which are specialized stem cells that have the ability to divide to give rise to neurons. Today, neuroscientists from the Faculty of Medicine at the University of Geneva (UNIGE) shed light on the mechanisms that allow progenitors to generate neurons. By developing a novel technology called FlashTag that enables them to isolate and visualize neurons at the very moment they are born, they have deciphered the basic genetic code allowing the construction of a neuron. This discovery, which is published today in Science, allows not only to understand how our brain develops, but also how to use this code to reconstruct neurons from stem cells. Researchers will now be able to better understand the mechanisms underlying neurological diseases such as autism and schizophrenia.

Directed by Denis Jabaudon, a neuroscientist and neuroscientist at the Department of Basic Neurosciences at UNIGE Faculty of Medicine and neurologist at the University Hospitals Geneva (HUG), the researchers developed a technology termed FlashTag, which visualizes neurons as they are being born. Using this approach, at the very moment where a progenitor divides, it is tagged with a fluorescent marker that persists in its progeny. Scientists can then visualize and isolate newborn neurons in order to dynamically observe which genes are expressed in the first few hours of their existence. Over time, they can then study their evolution and changes in gene expression. «Previously, we only had a few photos to reconstruct the history of neurons, which left a lot of room for speculation. Thanks to FlashTag, there is now a full genetic movie unfolding before our eyes. Every instant becomes visible from the very beginning, which allows us to understand the developmental scenario at play, identify the main characters, their interactions and their incentives», notes Denis Jabaudon. Working in the cerebral cortex of the mouse, the scientists have thus identified the key genesto neuronal development, and demonstrated that their expression dynamics is essential for the brain to develop normally.

A very precise primordial choreography

This discovery, by giving access to the primordial code of the formation of neurons, helps us to understand how neurons function in the adult brain. And it appears that several of these original genes are also involved in neurodevelopmental and neurodegenerative diseases, which can occur many years later. This suggests that a predisposition may be present from the very first moments in the existence of neurons, and that environmental factors can then impact on how diseases may develop later on. By understanding the genetic choreography of neurons, the researchers can therefore observe how these genes behave from the start, and identify potential anomalies predicting diseases.

After successfully reading this genetic code, the scientists we able to rewrite it in newborn neurons. By altering the expression of certain genes, they were able to accelerate neuronal growth, thus altering the developmental script. With FlashTag, it is now possible to isolate newborn neurons and recreate cerebral circuits in vitro, which enables scientists to test their function as well as to develop new treatments.

A website open to all

The UNIGE team posted a website where it is possible to enter the name of a gene and observe how it is expressed, and how it interacts with other genes. «Each research team can only focus on a handful of genes at a time, while our genome is made up of close to 20,000 genes. We therefore made our tool available for other researchers to use it, in a fully open way,» highlights Denis Jabaudon.

• Full bibliographic informationSequential transcriptional waves direct the differentiation of newborn neurons in the mouse neocortex; Ludovic Telley, Subashika Govindan, Julien Prados, Isabelle Stevant, Serge Nef, Emmanouil Dermitzakis, Alexandre Dayer, Denis Jabaudon; Science; March 3 2016

A single blind, clinical trial to investigate the effects of a single session extracorporeal shock wave therapy on wrist flexor spasticity after stroke

Since this seems to work, WHO is going to research this in larger trials and see if this can be extrapolated to other spasticity areas? WHO is going to create the stroke protocol on this? But this won't occur because we have NO stroke strategy or stroke leadership in any part of stroke and this will fall thru the cracks. You are fucking screwed.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J72272&phrase=no&rec=129122
NeuroRehabilitation , Volume 36(1) , Pgs. 67-72.

NARIC Accession Number: J72272.  What's this?
ISSN: 1053-8135.
Author(s): Daliri, Seyedeh S.; Forogh, Bijan; Razavi, Seyedeh Z. E.; Ahadi, Tannaz; Madjlesi, Faezeh; Ansari, Noureddin N..
Publication Year: 2015.
Number of Pages: 6.
Abstract: Study examined the effects of extracorporeal shock wave therapy (ESWT) on wrist flexor spasticity after stroke. Fifteen patients with poststroke wrist flexor spasticity (12 male and 3 female with a mean age of 54 years) were enrolled. Patients received 1 sham ESWT followed by 1 active ESWT 1 week later. The outcome measures were the Modified Modified Ashworth Scale (MMAS), the Hmax/Mmax ratio, and the Brunnstrom motor recovery stage. Results showed that the sham ESWT had no effects on the outcome measures. After active ESWT, the MMAS scores of spasticity and the Hmax/Mmax ratio improved. The improvements were maintained 5 weeks after active ESWT. No significant improvements were observed for the motor recovery after sham or active ESWT. In this study, a single session of active ESWT resulted in significant improvement in wrist flexor spasticity and alpha motor neuron excitability in adult patients after stroke.
Descriptor Terms: ELECTRICAL STIMULATION, INTERVENTION, LIMBS, MOTOR SKILLS, MUSCULAR IMPAIRMENTS, OUTCOMES, SPASTICITY, STROKE.

Can this document be ordered through NARIC's document delivery service*?: Y.

Citation: Daliri, Seyedeh S., Forogh, Bijan, Razavi, Seyedeh Z. E., Ahadi, Tannaz, Madjlesi, Faezeh, Ansari, Noureddin N.. (2015). A single blind, clinical trial to investigate the effects of a single session extracorporeal shock wave therapy on wrist flexor spasticity after stroke. NeuroRehabilitation, 36(1), Pgs. 67-72. Retrieved 1/14/2016, from REHABDATA database.