Cord blood or MSC ?

Just 2 very interesting studies :

1) « behavioural deficit was significantly improved with multiple doses of cord blood, but not with a single dose. We also showed that the injury caused significant loss of brain tissue and cell death, which was only improved in the study arm that administered multiple doses of cord blood cells. “


And second :

2) This was made on animal model but UCB seems to be batter choice than MSC….

So a lot to think….

« This study is the first to compare the neuroprotective efficacy ofUCB cells versus MSCs for inflammation-induced preterm braininjury. Both UCB cells and MSCs have protective benefits for thepreterm brain, but their effects on white matter are different.MSCs were strongly anti-inflammatory, dampening multipleindices of brain inflammation at the cellular and gene level. Incontrast, UCB cells showed a reduced ability to mediateneuroinflammation, but importantly, prevented apoptosis-mediated cell death and protected mature myelinating oligoden-drocytes. These differential effects of UCB and MSCs are likely dueto specific actions of an isolated cell population (MSCs) versus astem/progenitor cell mix (UCB). «


In response to LPS-induced preterm brain injury, administration of

MSCs had a global effect on dampening brain inflammation,

which in turn may have detrimental effects on brain repair and

normal development. MSCs did not improve survival of critical

oligodendrocytes and did not prevent apoptosis-mediated cell

death. In contrast, UCB was neuroprotective against cell death and

normalized the number of mature myelinating oligodendrocytes, but did not display the same anti-inflammatory effects as MSCs.

Our results indicate that UCB is a more comprehensive therapy for

protecting white matter brain development, likely contributed by

the mixed cell population in UCB, and their differential actions. »

thé problème i think we need be very careful with dosing MSC:

« In contrast, MSCs require expansion by tissue culture

and are a much larger cell (average 25 μm), limiting the

concentration that can be administered in a single dose without

risk of embolism. »


« Therefore, a global dampening of inflammatory mediators with MSC administration (as seen in the directional change of the bars

in Fig. 4) may interrupt normal brain development and it may be

such that reducing an aberrant pro-inflammatory cerebral

response with cell treatment is preferable. MSC treatment

decreased white matter expression of IGF-1, which is essential

for normal oligodendrocyte maturation produced by multiple cell

types within the CNS, particularly the glial cells.

Indeed, IGF-1 is

proposed as a rescue therapy for hypomyelination,

and protective for oligodendrocytes. »

« The dampening of inflammation and growth factor expression

by MSCs may be a concern, further investigation into this finding

is required. »

Pons and Cp


“It is traditionally considered that a child with cerebral palsy reaches half of its potential to develop motor skills by the age of 5 years and the maximum possible development by 7 years. The potential achieved remains at the same level or may even worsen with age. In our experiments, all children were over the age of 7 years. These results can significantly expand both the scope of this technology in the rehabilitation of children with cerebral palsy and improve the prediction of the effectiveness of the therapy used for older children.

Brain TLNS enhances the effect of physical rehabilitation, activating vast areas of the brain, increases the efficiency of existing neural networks, increases the likelihood of new synaptic contacts (synaptogenesis), enhances the brain’s innate ability to improve motor function. The fMRI data alone confirms that the human brain is plastic at any age and is capable of an amazing reorganization, the mechanisms of which we are just beginning to explore. The dynamics of changes in DMN and functional connections between the first and second timepoints turned out to be more vivid than between the first and third timepoints. That probably indicates a delayed rehabilitation effect.”

Latest publication 2019 with Pons mesures brain activity in high-density EEG

“Microstate effects suggest that even during rest, the PoNS® may elicit functional changes in the brain that are associated with evidence of increased neuroplasticity-related improvements.

Neuromodulation, such as through the PoNS®, has been linked to improved functional outcome in brain injury and disease, but the underlying neural mechanisms remain elusive. We report the initial findings of EEG changes in resting brain activity after a single 20-min session of PoNS®. While both HF and LF PoNS® dosage levels produced significant changes in alpha and theta wave activity, HF stimulation showed differential dosage effects. HF PoNS® also significantly increased attentional microstates suggesting a possible functional mechanism associated with evidence of neuroplasticity improvements. Overall, these findings support continued characterization of the underlying neural mechanisms related to the use of neuromodulation to drive recovery of function through neuroplasticity.”

Fig. 2

a Comparison of alpha EEG power before and after PoNS®, displaying statistically significant main effect of time; (b) Order by time interaction effect on alpha and theta power and Tukey pairwise post-hoc test statistical tests demonstrating a statistically significant increase alpha and theta power when exposed to HF stimulation in the first session; (c) Time-frequency spectral power for each exposure group (HF First and LF First) during each testing session:


We are starting soft hbot for Marc:

I honestly believe that soft chamber can also help in many ways but I think it’s not the best for a period of time right after his injury but on the other hand 100% oxygen has more potential right after an injury from my point of view.

I’ll be honest; I do understand that parents can’t always go to clinics every year, or twice a year for 2 months…. ( in order to do 40 dives).

Just to give you an exemple:

We did four months in Israel’s Hbot back in 2016 ( which was the best thing that could happened to Marc) so it was the period when oxygen 100% helped him mostly and it was more potential because more close to injury in time.

we also did one month in 2017 and then two months in 2018

So in total we did 110hours of hard chamber (1,5ata 100% oxygen) in 3 years.

Both of the two last times, we saw progress which was much less obvious than at his first time in 2016 and it’s totally normal.

So now we are sold on soft chamber: it’s obvious it still helps him but I really think that I would do it now at 1,3 ata without oxygen, not because it’s my favorite protocol, but because it’s safe for home use. In those circumstances it would give less results but everyone is able to do it at home which by the way makes it 50% more oxygen in his plasma that will help him.

So it’s just obvious, we can not escape school every year for 2 months. So I believe that a soft chamber can be THE solution for long term treatment (we are talking years after the acute injury).

And by the way we have some good canadien group testimonials from parents (in french only) who mostly used soft chamber treatments only.

Here’s our chamber installation :


Jean-François Tremblay


It was an exeptional experience, very helpful for installation and for all of my questions and just perfectioning training.


Nous commençons souple hbot pour Marc:

Honnêtement, j’ai la conviction que la chambre souple peut aussi aider de nombreuses manières, mais j’estime que ce n’est pas la meilleure solution pour une période qui suit immédiatement sa anoxie cérébrale , mais que 100% d’oxygène a au plus de potentiel après son arrêt cardiaque (c’est que de mon point de vue) …après 110h chambre dure 100% oxygene et 1,5 ata on passe à chambre souple à la maison 1,3 ata et sans oxygène et après 3 ans!

Je serai honnête; Je comprends que les parents ne peuvent pas toujours aller aux cliniques chaque année, une ou deux fois par an pendant 2 mois … (pour faire 40 plongées).

Juste pour vous donner un exemple:

On a fait pendant 3 ans En Israël, nous avons Hbot dure (1,5 ata 100% oxygène) –

pendant quatre mois en 2016 (ce qui a été la meilleure chose qui puisse arriver à Marc). C’est donc la période où l’oxygène à 100% l’a aidé le plus, ce qui lui donnait plus de potentiel, car il était plus proche de son anoxie cérébrale dans le temps.

nous avons également fait un mois en 2017 puis deux mois en 2018

Au total, nous avons donc effectué 110 heures de chambre dure (1,5% à 100% d’oxygène) en 3 ans.

Les deux dernières fois, nous avons constaté des progrès beaucoup moins évidents que lors de sa première fois en 2016 et c’est tout à fait normal.

Nous sommes maintenant commence le chambre souple : c’est évident que peut l’aider toujours, mais je pense vraiment que je le ferais maintenant à 1,3 ata sans oxygène, non pas parce que c’est mon protocole préféré, mais parce que c’est sans danger pour la maison. Dans ces circonstances, cela donnerait moins de résultats, mais tout le monde est capable de le faire à la maison, ce qui lui donne 50% d’oxygène supplémentaire dans son plasma, ce qui l’aidera.

C’est donc évident, nous ne pouvons pas échapper de l’école tous les ans pendant 2 mois. Je pense donc qu’une chambre souple peut être LA solution pour un traitement à long terme (nous parlons des années après anoxie cérébrale).

Et au fait, nous avons de bons témoignages de groupes canadiens de la part de parents qui utilisaient principalement des traitements de chambre souple :

Voici notre installation de chambre:


Jean-François Tremblay

Si vous voulez contact:

Tel france : 0186655685

Ce fut une expérience exceptionnelle, très utile pour l’installation et pour toutes mes questions et pour perfectionner ma formation.

Here’s the video of Dr. Kurtzberg speaking at the New Horizon Arizona Stem Cells conference -April 2019

Here’s the video of Dr. Kurtzberg speaking at the New Horizon Arizona Stem Cells conference :

(April 2019)

7:30mins discuss male cells getting into brain of CP

Hydrocortisone reduces fevers

12mins starts to talk about autism

19mins only male donors for the cord tissue trial are being used but doesn’t mention if male are better than female. Taken from c-section babies (interesting as c-section implies potential complications). They expand the cells to passage 2. Each cord produces about 60billion expanded cells, amounting to 60 to 100 doses (@ 2million cells per kilo).

23mins one child didn’t use Benadryl and started coughing from transfusion, resolved with the use of Benadryl.

25:40mins hypoxic brain injury helped with cord blood. But beneficial effects stopped when CD14 cells are removed!

33mins slide with cell characteristics for CP trial.

36mins gross motor improvements seen in CP study. Higher doses showed better results. Would love to know what the higher dose is versus the smaller dose.

40:40mins suggesting a cord blood transfusion followed by an MSC booster.

47mins they have over 2000 families on their wait list which is over a years work for them.

If you can’t see hole video on my Facebook please try on YouTube ( I separated in 3 parts):

Part 1:

Part 2:

Part 3:

And I will put all power points Photos ( sorry not in in order of presentation):

PoNS and CP was studed in Russia :

PoNS and CP was studed in Russia :

the latest 2019 study of PoNS:

Officially was published only this yet:

(So just 1-2 November 2018 this cp study was presented to international Congress in Moscow )

If you want to see more -what I posted before read my this article:

But not officially we can find more ( if we can read in Russian 😉 and here link:

Ok this is not yet “official” publication from St Petersbourg where they did CP study for PoNS was done. According to the thesis the situation was not very good ( because author used datas of this study without permission).

Daineko Vadim, is not a doctor, during the practice an instructor without permission of the copyright holders he used the data for his scientific thesis.

Brainport is mentioned in his thesis because from the very beginning they started working with him, and then switched to PoNS. This is a typical mistake in Russia to confuse these devices; but on photos you can see they used PoNS for study. ( old version of PoNS)

But of cause I can’t guarantee that in this thesis will be not others “mistakes” as at any case it’s not official publication yet of this Russian Cp study with PoNS.

So this is not yet officially published data for this study.

Comparison of TR ( traditional rehabilitations) and VTR ( high-tech rehabilitation) groups has shown that VTR has a significantly more significant therapeutic effect in comparison with TR and contributes to a significant development of motor functions.

So it’s comparison of 2 groups:

1) The traditional program of rehabilitation TR group: of children with cerebral palsy (exercise therapy, physiotherapy, hydrokinesiotherapy, therapeutic massage)= all “standard therapies” but intensive for CP

2) VTR group : and the VTR program with the use of high-tech rehabilitation tools (so they also had exercise therapy, physiotherapy, hydrokinesiotherapy, therapeutic massage)= all “standard therapies” but intensive for CP and plus High -technology: Lokomat, Armeo, PoNS)

The obtained therapeutic effect is connected with the application of a complex of high-tech means of neurorehabilitation, providing stimulation of motor centers of the brain and contributing to the more intensive development of compensatory mechanisms.

The final step was a comparison of the therapeutic effects according to the classification scale of movement.

In both groups, the baseline values before treatment improved significantly after the rehabilitation course, but a more pronounced therapeutic effect occurred in the high-tech treatment group.

On the basis of their own observations, children undergoing high-tech treatment were more confident in traveling long distances, climbing independently after falls, overcoming obstacles.

This rehabilitative effect is obviously related to more deep impact of modern high-tech devices on the motor centers of the brain, skeletal muscles and proprioreceptors.

The results of comparing the therapeutic effects of TP and VTR showed that both treatments in children with cerebral palsy have a positive effect on motor function, muscle tone, and balance.

However, VTR has a more pronounced therapeutic effect, especially on the maintenance of vertical position, independent walking and fine motor skills of hands.

The traditional program of rehabilitation TR group: of children with cerebral palsy (exercise therapy, physiotherapy, hydrokinesiotherapy, therapeutic massage)

and the VTR program with the use of high-tech rehabilitation tools (same as TR + Lokomat, Armeo, PoNS)

But in VTR group they had significantly bigger effects in improving balance and walking, reducing spasticity of the upper and lower extremities.

The achieved rehabilitation effects are preserved for six months with continued rehabilitation on an outpatient basis in the variants of individual exercises, hippotherapy and Nordic walking.

The rehabilitation program with the use of high-tech tools (VTR) in comparison with the traditional program of rehabilitation of children with cerebral palsy, has significant advantages in rehabilitation effects that increase the child’s physical activity, as measured by the Berg scale (balance), Ashworth scales for upper and lower extremities (spasticity) , GMFCS scale (motor functions) and classification scale of movement.

So why Hbot works not always same way in brain injury?

So why Hbot works not always same way in children’s? I am not a doctor I am just a mum like you so please I do analyze my son injury I read a lot but I am not a doctor ( take it just only mum reflection on subject) ok?

It’s very difficult question and I think even best Hbot doctors don’t know exact answer honestly

Let’s say : first of all each brain injury is unique and diferent.

I am trying just analyzing what I can as dates but as I said with anoxic brain injuries we don’t have any studies with spect scans so all this discussion just my personal suppositions ok ?

Ok i post mri of Marc before Hbot and after 80h

We have MRI in January 2016 just some days after anoxic injury

And we have MRI June 2017 after 80h Hbot … but without general anesthesia ( so some artifacts)

Be my guest if any radiology specialist want to make professional hole comparison

1. I think Age of child in the moment of injury play very big role : of child very small ( new born or HIE child for example) smaller is a child at brain injury more fragile his brain ( so same 25 minutes without oxygen will be more devastating on smallest child brain at birth or 1 month age than at 4 years old)

Second why age is important – because if child was already walking / full functioning child before brain injury -so after it will be retraining of his lost functions wile in new born it will be just training ( with less neurons in brain) I think it’s more difficult. But it’s just my opinion.

2. Of cause most important factor : it’s volume of Brain which was damaged!!!!

While there is no way of knowing how much recoverable tissue exists in the days, weeks, and years following brain injury , HBOT can increase cell reproduction and administer oxygen to tissue that was previously cut off from blood flow. The dormant cells surrounding the damaged tissue area, also known as ischemic penumbra, are responsible for much of post-stroke dysfunction. If oxygen therapy can revive these cells, lost functionality may return to the individual.

And this you can say only by MRI and Spect. But again for small children’s I am sorry but MRI don’t give exact informations ( that’s why neurologists don’t like to do MRI for cp children’s too early age …. we can really see at age 4-5 years but before it’s very difficult).

But still : Qualitative assessment of brainstem injury on T1 and T2 images in neonates with HIE may provide information on injury severity and risk of death, but objective quantitative data such as ADC values are lacking. ( if you want to read about read this study:

These infratentorial areas have high concentrations of excitatory neurotransmitters (e.g., glutamate) and are especially vulnerable to the profound hypoxia-ischemia that is typical in HIE. The cerebellum acts as a satellite system of established cortico-basal ganglia networks in neonates.

If we talk about MRI of my child ( he had basal ganglia

and thalamus damages) …

In one large study cohort, 60% to 70% of infants who sustained moderate basal ganglia/thalamic injury had cerebral palsy and 35% had developmental quotient less than 70 (40). Cerebral palsy was identified in 98% of infants with severe basal ganglia/thalamic injury 

Before Hbot:

I will post his MRI ( after Hbot a bit father in this article ok?)

3. So here we come fore 3d factor : did child was cooled after brain injury???? I believe that it’s helped to my child ( yes his body temperature was cooled it’s protocol for cardiac arrest but not always for HIE ).

4. Did child had 100% oxygen or just 30% oxygen delivery as Normobaric ? It’s may be has also role to play i think.

( it’s after reading this book I think about )

This lecture is also really good explanation why Hbot is better ( than Normobaric oxygen) we get oxygen in plasma! Lisen at 44minutes :

( and by the way I agree about multiple approach with Sherr – before starting Hbot in Israel’s for my son – we did batteries of blood tests and also tubes in ears – in order to protect them against barotraumatisme).

5. And you see naw what I think about Hbot ( we don’t have real agreement between doctors what is the best protocol for brain injury – and what kind brain injury ? By the way ?) TBI or anoxic? ). Parents has some possibilities: 1,5ata 100% oxygen is most used in hard chambers by centers ( sometimes is more pressure but honestly it’s the mostly use regiment for nerology in hard chambers) and I believe that in case of my son really oxygen in Hbot made biggest changes but as I posted before in Hbot conditions contrary to Normobaric 100% oxygen…

« We found that HBO, but not NBO, reduced oxygen and glucose deprivation-induced cell injury, indicating that passive tissue oxygenation (i.e. without vascular support) of the brain parenchyma requires oxygen partial pressure higher than 1 ATA. »

More about read my post in blog:

About other possibilitiy: 1,3ata without oxygen

Of cause first of all it’s the most “ not risky “ protocol for very injured children’s so may be also that’s why a lot doctors prefer start really very-law presssure ( case child brain really very damaged) and if child very small -very fragile.

So do the 1,3ata without oxygen will give same results for anoxic injury as 1,5ata 100% oxygen??? I don’t know 🤷‍♀️

I believe that in acute period use oxygen after anoxic injury just after it is more beneficial than without oxygen….. but it’s consern acute period 2-6-8 months after injury!!!!)

( I am not talking about CP-ok it’s chronic condition already) this we was discussed in study which compared pressures for cp.

So hope my reflections helps….

So for Marc Sudden cardiac arrest happens to my baby at 4 years old. Because of not diagnosed WPW.

He has cardiac arrest for 25 minutes

I did cpr with fiend ambulance was only after 20 minutes and his heart restarted only after 25 minutes…

He was on the hyperthermic protocol ( cooled)

His child body went through so much:

5 days comas

Blindness for 3 days after coma

He couldn’t talk at all for 2 weeks after ( and restarted very slowly to talk some words)

Wasn’t sitting for 1 month and we was 1 month in Intensive care unit and 4 months in hospital

He had 5 ablations ( for his heart syndrome in 3 years)

He was obliged to learn to do everything again… ( he was just 4 years boy when he has to pass through all this: When My son woke from life support after rewarming his body He had regular heard surveys 24h/24 because of regular SVT , kidney failure, respiratory failure & and he was on a feeding tube as well…. and he was blind and can’t talk….. but constantly crying…..only thing which calm his down a bit was my voice …

He has no memory of what happened but he has PTSD

He couldn’t feed himself

couldn’t stand

couldn’t walk

couldn’t do anything

We passed by phases : wheelchair and walker and he hate both of them….

But yes I am blessed that he is alive.

MRI’s after 80 hours Hbot in Israel:


M’y son Marc avant hbot juin 2016( main gauche)

Après 50 hbot: (septembre 2016)


right – before hbot 1 July 2016

Left – after 15 hours hbot -5 August 2016

PoNS: (started 29 March 2018)

Stairs before Pons (right vidéo septembre 2017)

After 6 months pons (left -September 2018)

Pons 6 mois ( left -June 2018/ right – September 2018)


Stoped using pons from 30 December 2018

So 2 AQM without pons:

AQM 1:(11 January 2019)

Aqm2( 28 January 2019)

Restarted using pons in Russia clinic : 11 February (2 weeks intensive in Moscow clinic with pons):

Aqm 3 (25 February )

I will do 4th AQM in September -October 2019 so hopefully I will get scientific datas for PoNS long therm use ….

If you want more read:

Haw about being accepted by friends in school for « special » children’s ?

I will tell you my point of vue on this question :

Marc has a lot of friends

But honestly I did maximum in order to get all children’s and parents «  on my sight «  after Marc accsident at the beginning it was not obvious …

It’s exactly what I am doing :

Social life is very very important target so during 2 years II worked for this goal for Marc

I see results this year …( I have a chance because I am « not working mum » but in fact I do my job exactly this way : who can invite 5-6 neurological normal friends at home every week and play with them during 3-4 hours per day????….. so I am not working mum who do it for my child… i think I invest better than any proffecionel in this point….)

But I need professionals in parts I can’t do… 😉

Others parents don’t want to do efforts for your child ( or at least not much who will do)

It’s like this

It’s reality

When you know this and do all yourself without counting on them everything is easygoing…

And if it’s interesting to come to your home to theirs children’s they will ask to come from their parents and so … you will start invite for weekend for cake and coffee …. so you start create sosial links with parents and children’s….

Just don’t wait that they will invite you in reteurn

It’s will be always you who will do much more than others parents 😉

Yes it’s the best motivation for my son Marc so that’s why I do my own “friends” programm and every week planing ( yes you need to send messages /phone calls in order to plan 5-6 invitations per week).

Often parents they don’t have time / motivation to play with theirs children’s at home ( I do have this time and my hasbend is playing with kids just exeptional during weekends ! They love to play with him)

I know 11 children’s from his class and parents and we continue doing new friends of cause absolutely!

(so well I know to play with them in social games somtimes can be very boring for adults and we as parents somtimes wants just to rest I know all this! ) I have à chance naw Marc can a bit play just alone between children’s but it wasn’t so evident 2 years ago …

and yes somtimes I am inviting 2 his best friends ( boys) to sleep at home so we can have pyjamas parties 😉 and dansing 😉

Yes I will tell you it’s a lot of job /coking/playing

But it’s worth 😉

But you can’t imagine what I feel this year when children’s I don’t know yet from his class comme to me and ask : “ please can you invite me to eat with Marc?” I am also in his clas I am his friend”… and so – I ask marc” hey you know this boy you want invite him home?”

And his pleasure to tel me yes I want yes he is playing with me at school ….or So other day “mum can you invite this boy …etc…”

This is really cool feeling….

A lot of job but so cool!


It is a long way but it’s worth !

AS said it took me 2 years to get back Marc socialisation after his Sudden Cardiac Arrest.

I started with 2 best friends invited regulary at home ( for 2-3 hours) – weekend.

Than I started to invite friends to eat with Marc at home during lunches ( it’s of cause me who organize all I am going to school taking children’s / make them eat together and playing – and bring them back to school) – parents need only tell to school that they give me permission to take their children’s for lunch ( so not much trouble for other parents or any trouble for their daily plans)

Naw I am in fact : at level 3 lunches per week ( every time I invite only one friend )

And Friday evening – very often he is playing with friends ( after school)

And 2 others children’s for 4 hours invited to play each Saturday and Sunday !

Yah planing for Ministry of Foreign Affaires has less appointments 😉

( exept week-end we travel of cause)

So 6 friends per week!

It’s a real job I have 😉

Kids club

But it’s so worth it!

And if you know haw Marc is happy to has all his friends !

Normobaric or Hyperbaric?

1)Hyperbaric oxygen and hyperbaric air treatment result in comparable neuronal death reduction and improved behavioral outcome after transient forebrain ischemia in the gerbil:

« hyperbaric oxygen may represent a potentially important therapeutic option for post-arrest encephalopathy as well as other forms of brain injury. We also agree that animal studies of global brain ischemia suggest that hyperbaric oxygen may be beneficial with regard to neurologic outcome »

Anoxic brain injury resulting from cardiac arrest is responsible for approximately two-thirds of deaths. Recent evidence suggests that increased oxygen delivered to the brain after cardiac arrest may be an important factor in preventing neuronal damage, resulting in an interest in hyperbaric oxygen (HBO) therapy. Interestingly, increased oxygen supply may be also reached by application of normobaric oxygen (NBO) or hyperbaric air (HBA). However, previous research also showed that the beneficial effect of hyperbaric treatment may not directly result from increased oxygen supply, leading to the conclusion that the mechanism of hyperbaric prevention of brain damage is not well understood. The aim of our study was to compare the effects of HBO, HBA and NBO treatment on gerbil brain condition after transient forebrain ischemia, serving as a model of cardiac arrest.

Source :

2. this one also :Effects of normobaric versus hyperbaric oxygen on cell injury induced by oxygen and glucose deprivation in acute brain slices

« We found that HBO, but not NBO, reduced oxygen and glucose deprivation-induced cell injury, indicating that passive tissue oxygenation (i.e. without vascular support) of the brain parenchyma requires oxygen partial pressure higher than 1 ATA. »

CD14 cells in cord blood that is special and helps repair brain cells from low oxygen in brain or hypoxic injury

About stem cells :

Watch this dr Kurtzberg presentation ( in English from 12 minutes)

From the 20:54, Dr Joanne Kurtzberg says It’s the CD14 cells in cord blood that is special and helps repair brain cells from low oxygen in brain or hypoxic injury

And as I know nobody doing yet hole donor cord blood HLA matched exept Duke ( and yet in clinical trails)….

More on Dr Kurtzberg’s presentation of the good monocytes in cord blood cells:

10:38 [Referring to cord blood cells]…and about 10% are a kind of cells called the monocyte. Monocyte in cord blood is unique and it’s the cell that we think is helping patients with cp and autism. And we don’t think it’s helping because it’s engrafting in the brain or turning into neurons or turning into brain cells. We think it’s helping because it puts out chemicals that signal cells that’s already in the brain to repair damage.

human UCB (hUCB) is a complex internal environment rich in a variety of stem/progenitor cell populations, such as hematopoietic stem cells (HSCs), endothelial progenitor cells (EPCs), UCB monocytes (including T regulatory cells (Tregs) and monocyte-derived suppressor cells (MDSCs)) and MSCs…etc….

UCB mononuclear/ whole blood cells in the perinatal ischemic and hypoxic brain model can reduce the inflammatory response to treat injury. To evaluate whether transplanted cells relieve neuroinflammation, there are two indicators:

(1) reduce the infiltration of CD4 þ T cells into the brain; and (2) reduce microglial activation.

all UCB cell types except EPCs have CNS immunoregulatory capacity.

Tregs and monocytes are present in the normal body at a considerable level, and are indispensable in the regulation of peripheral and central immune responses.

« Currently, the use of UCB-based interventions for CP is limited as the components of UCB are complex and possess different therapeutic mechanisms. These can be categorized by three aspects: homing and neuroregeneration, trophic factor secretion, and neuroprotective effects. »

There are several paper about cord blood CD14+ cells neuroprotective action ( CB Monocytes – CD14+ cells protect brain cells from Oxygen and Glucose Deprivation in Cortex). Even more: cord blood cells contain many neurotrophic factors, which are very important for brain regeneration.

•Brain-derived neurotrophic factor,

Nerve growth factor-

•Neurotrophin-3 –

•Neurotrophin-4 –

•Glial cell-derived neurotrophic factor –

•Cerebral dopamine neurotrophic factor –

•Mesencephalic astrocyte-derived neurotrophic factor

•Pigment epithelium-derived factor.

Latest Duke publication about CD14: