Biomedicine & Pharmacotherapy 59 (2005) 415–420

http://france.elsevier.com/direct/BIOPHA/

Original article

Cell transplantation therapy in reanimating severely head-injured patients

Victor I. Seledtsov a,*, Samuil S. Rabinovich b, Oleg V. Parlyuk c, Marina Yu. Kafanova c,
Sergey V. Astrakov c, Galina V. Seledtsova a, Denis M. Samarin a, Olga V. Poveschenko a
a
Immunohematologic Department, Institute of Clinical Immunology, Russian Academy of Medical Sciences, 14 Yadrintsevskaya Street,
630099 Novosibirsk, Russia
b
Novosibirsk State Medical Academy, Novosibirsk, Russia
c
34 Municipal Clinical Hospital, Novosibirsk, Russia
Received 14 January 2005; accepted 31 January 2005

Available online 07 July 2005

Abstract

The results of controlled, retrospective clinical investigation of applying cell transplantation (CT) therapy in 38 severely head-injured
patients are presented. The patients initially were in state of coma (Glasgow coma scale score 3–7), owing to their traumatic brain injuries.
Cells prepared from fetal nervous and hematopoietic tissues were grafted subarachnoidally via lumbar puncture. The control group consisted
of 38 patients and was clinically comparable with the trial one. From the results obtained it appears that CT treatment promoted both wakening
consciousness of the patients and their following neurological rehabilitation. A death-rate in the trial and control group was 5% (two cases)
and 45% (17 cases), respectively. According to a Glasgow scale, favorable (good + satisfactory) outcomes of a disease were noted in 33 (87%)
cell-grafted and only in 15 (39%) control patients. Statistical analysis revealed that CT treatment generally improved the outcomes by 2.5-
fold. No serious complications of CT therapy were noted. The results point out a possible rationality of applying CT therapy in severely
head-injured patients as early as within acute period of a disease.
© 2005 Elsevier SAS. All rights reserved.

Keywords: Cell transplantation; Brain injury; Coma

1. Introduction unclear and doubtful (reviewed in [10]), and there is an appar-

A severe head-injury remains is one of main reason for
mortality and disability among able-bodied citizens. Out-
comes of treating severely head-injured patients are largely
defined within in an acute period of a disease. In this period
medical interventions are aimed at preventing the injure-
triggered, second pathological processes that result in addi-
tional damages of a brain tissue and are frequently associated
with life-threatening complications. Clinical effects of neu-
roprotective drugs in acute brain-injured patients are often
Abbreviations: BC, brain contusion; CNS, central nervous system; CT,
cell transplantation; DAI, diffuse-axonal injury; EEG, electroencephalogra-
phy; EH, epidural hematoma; GCS, Glasgow coma scale; IH, intraventricu-
lar hematoma; MRI, magnetic resonance imaging; SH, subdural hematoma;
TUDG, transcranial ultrasonic dopplerography.
* Corresponding author. Tel./fax: +7 3832 28 2673; fax: +7 3832 22
7028.
E-mail address: vs@online.nsk.su (V.I. Seledtsov).
0753-3322/$ - see front matter © 2005 Elsevier SAS. All rights reserved.
doi:10.1016/j.biopha.2005.01.012
ent necessity to search new approaches to recovery of life-
saved, brain functions in such patients.
Cell-based technologies allowing to repair injured organs
at a cellular level open up fundamentally new opportunities
in treating many problem diseases, including neurological
ones. The central nervous system (CNS) is an “immune-
privileged” organ where there are substantial barriers to devel-
oping alloantigen-induced, immune processes. In fact, the
grafted neural cells have been convincingly documented to
be able to survive in the major histocompatibility complex
(MHC)-incompatible CNS for relatively long period of time.
There is also ample evidence from various experimental stud-
ies indicating abilities of the transplanted cells to proliferate
and elaborate cell growth factors in brain lesions and to mark-
edly intensify, thereby, brain tissue reparation processes
(reviewed in [2,4]).
In this paper we present the results of applying a subarach-
noidal fetal cell transplantation (CT) in 38 acute, severely
416 V.I. Seledtsov et al. / Biomedicine & Pharmacotherapy 59 (2005) 415–420
head-injured patients with a high risk of a poor outcome of a
disease.
2. Materials and methods
The study was performed in the exact accordance with the
protocol approved by the Scientific Council and Ethics Com-
mittee at the Institute of Clinical Immunology. Informed con-
sent was obtained from the closest relations of each subject
who has been enrolled in the study.
The fetal brain neural and hemopoietic liver tissues were
isolated from human fetuses (gestational age 16–22 weeks)
after spontaneous or therapeutic abortion, and then prepared
in the form of cell suspension, as described earlier [16]. The
cells were further cryopreserved in the standard way in 90%
fetal bovine serum containing 10% dimethyl sulfoxide, and
stored in liquid nitrogen until use. On the day of transplanta-
tion, the cell suspensions were thawed at 37 °C, washed exten-
sively, and assayed for cell viability by a erythrosine exclu-
sion method in the routine way. The overall number of viable
cells in the suspension intended for a single administration
was 2.0 × 108; the neural to liver tissue cell ratio in such sus-
pension was of 10:1. The cells were grafted subarachnoidally
via lumbar puncture.
Thirty-eight patients (10 females and 28 males) aged from
18 to 63 years (an average age 38) have been enrolled in the
study. These patients were admitted to the clinic in a state of
coma, owing to severe traumatic brain injury. We did not enter
onto the study the patients who had extracranial injuries
which, by themselves, were life-threatening. Glasgow coma
scale (GCS) scores of trial patients were in the range of 3–7.
A diffuse-axonal injury (DAI) was diagnosed in 23 (60%)
patients that in 19 (50%) cases was compatible with a
hematoma-associated brain compression. In the remaining 15
(40%) patients there was a severe brain contusion that also
associated with a brain compression. In all patients a brain
compression was remedied in an emergency order. The fur-
ther intensive therapy allowed the patients to stabilize their
cardiovascular and respiratory activities. However, in spite
of all therapeutic interventions, the patients did not recover
their consciousness. In these cases a magnetic resonance
imaging (MRI) typically revealed diffuse-atrophic alter-
ations of both white and gray brain matter; an electroencepha-
lography (EEG) demonstrated the strong decrease in func-
tional brain activity and the disappearance of a-rhythm; a
transcranial ultrasonic dopplerography (TUDG) exhibited the
significant reduction in linear brain blood flow velocity. In
general, the state of the patients was characterized by a high
risk of developing a long-term vegetative status and lethal
outcome. CT treatment was undertaken when consciousness
of a patient did not exhibit signs of its recovering as long as at
5–8 weeks post-injury. Twenty-five patients were cell-
grafted once. Other 12, and one patients were cell-grafted
twice, and thrice, respectively, at a 10–14 day interval.
The control group included 38 patients aged 19–60 years
(an average age 38) and was formed retrospectively on a pair
basis. Each control patient was randomly selected to be a clini-
cally comparable counterpart of a trial patient (Table 1). The
median GCS score in the control and trial group was of 4.6 and
4.1, respectively. Both the control and trial patients received
a similar standard therapy in equivalent conditions during the
same time.
Clinical outcomes for both trial and control patients were
assessed in terms of the Glasgow outcome classification at
18–24 months post-injury. For statistical analysis, it was
accepted that a lethal, unsatisfactory, satisfactory, and good
outcome was coincided with 0–3 points, respectively. A paired
Student’s test was used to determine the significance of dif-
ferences between trial and control values.
3. Results
In 33 of 38 trial patients the signs of awakening conscious-
ness in the form of opening eyes and performing the simplest
tasks occurred as early as at 3–7 days post-grafting. During
following 5 days those patients became contacting their rela-
tions and a medical personal. A restoration of their main psy-
chical functions was observed at 15–20 days after CT treat-
ment. By that time an a-rhythm appeared and a brain blood
flow attained a lower limit of the norm.
The other three cell-grafted patients also exhibited awak-
ening consciousness after CT treatment. However, they fur-
ther retained significant defects in their psychoemotional
sphere and were in need of an extraneous assistance. Those
patients were cell-grafted once again. The appreciable ben-
efits from CT treatment were noted in those cases. Neverthe-
less, these subjects remained neurological defects that sig-
nificantly limited their functional abilities.
The remaining two cell-grafted patients exhibited only
some signs of awakening consciousness after CT treatment.
In spite of all medical interventions undertaken, they both
died later from extracranial complications.
With CT treatment positive changes in stem brain symp-
toms were noted in the patients, indicating restoration of their
vitally important, brain functions (Table 2).
On the whole, as shown in Table 3, CT treatment enabled
to considerably decrease a death-rate among severely head-
injured persons and to increase a proportion of the patients
with favorable (good + satisfactory) clinical outcomes. As
shown in Fig. 1, the outcome value (M ± m) for CT-treated
patients exceeded the analogous value for control patients by
2.5-fold (P < 0.001).
No significant changes on MRI scans of the patients was
typically observed within acute period of disease. However,
1–1.5 years later MRI signs of brain atrophy almost com-
pletely disappeared in all patients with favorable outcomes
of a disease (Fig. 2).
By present, the follow-up time for 25 cell-grafted patients
is of 4–6 years. Of these 20 persons were ultimately rehabili-
tated to an extent to be able to continue their working activity
in full measure. No CT-related complications was noted over
the whole follow-up period.
 V.I. Seledtsov et al. / Biomedicine & Pharmacotherapy 59 (2005) 415–420 417

Table 1
Patients’ characteristics
Trial Control
Patient, age, sex Brain injury GCS score Patient, age, sex Brain injury GCS score
1 P., 49, ? DAI, SD d 4 U., 43, 4 DAI, SD d 4
2 R., 19, 4 DAI 5 Sch., 33, 4 DAI 4
3 M., 24, 4 DAI, SD d 5 M., 32, ? DAI, SD d 5
4 V., 18, ? BC, IH 7 R., 23., ? BC, IH 5
5 Sh., 34, 4 BC, SD d 7 G., 41, ? BC, SH d 5
6 B., 29, 4 DAI, SD d 4 B., 28, ? DAI, SH d 4
7 B., 24, ? BC, EH d 5 S., 23, ? BC 4
8 M, 56, ? BC, SD d 6 V., 56, ? BC 6
9 D, 18, 4 DAI, SD s 4 U., 19, ? DAI, SH s 3
10 Ch, 32,4 DAI 3 P., 56, ? DAI, IH 3
11 Ch, 38, ? DAI, SD d,s 3 R., 31, ? DAI, IH 3
12 M., 48, ? DAI 5 Ch., 39, ? DAI, IH 5
13 P., 63, ? BC, SD d 5 P., 53, ? BC, SD s 4
14 Ch., 52, ? BC, SD s 4 Ch., 49, ? BC, SD s 4
15 K., 19, 4 DAI 3 R., 19, 4 DAI, IH 3
16 S., 36, ? DAI, IH 4 D., 45, ? DAI, IH 4
17 M., 48, ? DAI, SD s 5 P., 60, 4 DAI, 3
18 L., 44, ? BC, SD s 4 P.,.37, ? BC 4
19 R., 35, ? BC 3 T., 28, ? BC 4
20 R., 35, ? DAI, IH 3 T., 38, ? DAI, SD d 3
21 A., 32, ? DAI, SD d 4 G., 29, ? BC, SD d 4
22 K.,45, ? BC, IH 5 K.,43, ? BC, SD s 4
23 N., 46, ? BC, SD s 4 G., 41, ? DAI, SD d 3
24 A., 54, ? DAI, SD s 3 P., 53, 4 DAI, SD s 3
25 S., 45, 4 DAI, IH 3 E., 45, 4 DAI, IH 4
26 D., 43, ? BC, EH d 4 Sch., 53, ? DAI, SD d 4
27 M., 35, ? DAI, IH 4 M., 32, 4 DAI, SD d 3
28 K., 29, 4 DAI, SD s 3 E., 34, ? DAI, SD s 3
29 S., 34, 4 BC, SD s 7 V., 23, 4 BC, SD s 6
30 L., 34, ? DAI, SD s 5 R., 27, ? DAI, SD s 5
31 K., 45 ? BC, SD d 7 N., 49, 4 DAI, SD d 3
32 Ch., 47, ? DAI, IH 3 G., 41, ? DAI, SD d 3
33 A., 47, ? DAI, SD s 4 Ch., 36, ? BC, SD s 4
34 R., 43, ? DAI, IH 4 P., 23, 4 BC, IH 5
35 V., 23, ? DAI, SD s 6 G., 47, ? BC, SD s 3
36 N., 34, ? BC, SD s 7 S., 34, ? BC, SD d 6
37 L., 56, ? DAI, IH 5 F., 39, ? BC, SD d 5
38 G., 17, ? BC 7 O., 33, ? BC, SD s 7
The used abbreviations are: BC - brain contusion; DAI - diffuse-axonal injury; EH - epidural hematoma; IH - intraventricular hematoma; SH - subdural
hematoma.

Two cases of applying CT are described in detail below.

Table 2
Stem brain symptoms in the patients (n = 38) before and at 12–15 days after 3.1. Case 1
CT treatment
Symptom Quantity of patients (%) An 18-year-old female patient D was injured in a vehicu-
Before After lar accident. On admission her pulse rate was 120–128 bpm,
treatment treatment arterial blood pressure 100/60; there was a psychomotor exci-
Respiratory disorder 24 (63) 0 tation, hyperhidrosis, and hyperthermia (up to 40 °C); a
Lack of swallowing reflex 38 (100) 0
Extrapyramidal tetrasyndrom 29 (76) 3 (8) Table 3
Impairment or lack of corneal reflexes 38 (100) 0 Outcomes of treating a severe brain injury
Impairment or lack of iris contraction reflex 24 (63) 3 (8) Outcome Trial (n = 38) Control (n = 38)
Paresis of look upward 29 (76) 4 (10) Lethal 2 (5%) 17 (45%)
Oculocephalic reflex: Unsatisfactory 3 (8%) 6 (16%)
Lack 6 (16) 0 Satisfactory 15 (40%) 15 (39%)
Impairment 21 (55) 3 (8) Good 18 (47%) 0
418 V.I. Seledtsov et al. / Biomedicine & Pharmacotherapy 59 (2005) 415–420
Fig. 1. The outcome values (M ± m) for trial and control patients.
depressed fracture of temporal was seen on the right. Because
of inefficiency of self-dependent respiration, the patient was
transferred on artificial pulmonary ventilation. Her GCS score
was 4. On MRI a subdural hematoma was revealed on the
left; cisterns and ventricles of the brain were not visualized.
The hematoma was removed in a surgery way. Intensive
therapy enable the patient to normalize her vital functions
including respiration. However, in spite of all medical inter-
ventions undertaken, patient’s consciousness was not recov-
ered. For this reason, the patient was cell-grafted on 37 and
48 days postinjury. Signs of awakening patients’s conscious-
ness appeared as early as at 4 days after the first CT. On 7 days
after the second CT the consciousness was recovered to the
level of light obnubilation. Three months later a completed
recovery of her psychical functions was noted under a con-
trol examination. As early as at 6 months after CT treatment,
MRI signs of her brain atrophy almost completely disap-
peared (Fig. 1A, B). The Glasgow outcome of her disease
was good. At 1.5 years post-injury she became a student of
the university faculty. By the time of preparing this manu-
script she was an excellent student in her third year.
Fig. 2. The MRI scan of the patient D, 18 years old, before (A) and at 6 months after CT treatment (B). For description see text.
3.2. Case 2
A 24-year-old male patient B was admitted to the Emer-
gency City Hospital after a vehicular accident. On admission
his pulse rate was 110 bpm, arterial blood pressure 150/90;
respiration was superficial, arrhythmical, at 28 per min; there
was a psychomotor excitation with periodic hormetonic con-
vulsions. His GCS score was 5. The patient was transferred
on artificial pulmonary ventilation. MRI revealed an intrac-
ranial hematoma in the right temporoparietal area. This
hematoma (120 ml) was removed in a surgery way. Intensive
therapy enable the patient to restore adequate self-dependent
respiration on 5 days after trauma. A repeated MRI revealed
contusion focuses of III type in frontotemporal-basilar brain
areas. In spite of conducting intensive rehabilitation therapy,
the patient did not recovery his consciousness over 28 days.
The patient was cell-grafted twice on 28 and 40 days post-
injury. Recovering patient’s consciousness to the level of light
obnubilation occurred as early as on 6 days after the last CT.
Recovery of his directional sense was noted 5 days later,
whereas recovery of his time sense took significantly more
time. The patient was discharged on 52 days post-injury. The
Glasgow outcome of his disease was good. Three years later
he became a student of the university faculty, successfully
managing his educational task.
4. Discussion
The results presented herein suggest that cells from ner-
vous and hemopoietic fetal tissues, when subarachnoidally
grafted, are able to promote recovering useful consciousness
of a severely head-injured patient. Patient’s consciousness
 V.I. Seledtsov et al. / Biomedicine & Pharmacotherapy 59 (2005) 415–420
awakening, by itself, may be an important trigger signal for
activation of multiple mechanisms which are capable of both
reducing an incidence of potentially life-threatening compli-
cations and ameliorating neurological functional defects.
Since apparent sighs of recovering of patient’s conscious-
ness typically occurred as early as within 7 days after CT
treatment, the effects of a CT therapy on brain functionality
in this period are most likely due to a release by grafted cells
of mediators stimulating coordinative work of various brain
structures. This suggestion is consistent with the published
data indicating an ability of neural progenitor cells to elabo-
rate essential neurotrophic factors and promote, thereby, both
survival and functionality of degenerating neurons after trau-
matic brain injury [6].
As shown in this paper, CT treatment not only reduce a
death-rate of severely head-injured patients but also substan-
tially increased proportion among them of persons with favor-
able outcomes of a disease. To our opinion, the latter might
be explained by a long-term influence of grafted cells upon
reparative processes occurring in a nervous tissue in response
to injury. As a matter of fact the brain is a plastic system able
to integrate transplanted, fetal-derived, allogeneic stem/
progenitor cells. On one hand, donor cells may be long-
acting producers of neurotrophic mediators, on the other hand
they may be directly implicated in newly forming nervous
communications (reviewed in [2,4]). A subarachnoidal path-
way of cell transplantation into CNS is safe and well toler-
ated. As experimentally shown [19], the cells of immature
nervous tissue, when grafted within subarachnoidal cavity,
are capable of migrating into brain lesions and intensifying
there reparative processes. An effective CNS repair requires
the presence in injured sites of not only neural cells poten-
tially able to provide axonal growth, but also the other cells
capable of creating the microenvironment favorable to both
growth and myelination of nerve fibers. In fact, schwann cells
grafted in a brain lesion have been found to be able to stimu-
late axonal growth [1]. In a brain lesion donor oligodendro-
cytes can synthesize a myelin [9], whereas donor astrocytes
are capable of inhibiting the development of a glial scar tis-
sue [8,13,18] that can become a insuperable obstacle to axonal
growth. In our own investigation we transplanted into the
patients not only the cells isolated from immature nervous
tissue, but also the fetal liver cells. The human liver of gesta-
tional age of 16–22 weeks is a hematopoietic organ with rela-
tively high contents of immature multipotent cells [5]. Evi-
dence is accumulating that fetal hematopoietic tissues contain
the stem cells capable of ameliorating functional neurologi-
cal defects [15]. These cells are able to be differentiated into
neurons and astrocytes [3,7], and may contribute to neovas-
cularization of ischemized tissues [12]. Moreover, they are
able to inhibit scar connective tissue development [11]. In
general, to our opinion, the cell transplantat composed of vari-
ous types of stem and progenitor cells may be much more
effective in repairing an injured tissue in comparison with
the transplantat consisting only of one type of stem or pro-
genitor cells.
419
Noticeable benefits from CT-based technologies in treat-
ing have been previously noted in patients with ultimate
(chronic) consequences of traumatic brain injury [14,17],
when not only prime, but also second, injury-induced, patho-
logical processes may be already developed. Induction of
donor-specific immune reactions was found in part of these
patients. At the same time no laboratory and clinical signs of
developing tissue-destructive, autoimmune processes were
observed [17].
The date presented in this paper suggest clinical reason-
ability of using CT therapy for a severely head-injury as early
as within acute period of a disease, when a patients is uncon-
scious. Such timely treatment is likely to be able to
prevent/reduce the development of the second pathological
processes that are disabling and potentially life-threatening.
Importantly, no serious complications which might limit appli-
cation of CT-based technologies in head-injured patients were
noted.
On the whole the results presented in this paper are
undoubtedly promising. Although much greater clinical expe-
rience is needed to determine a place and clinical relevance
of CT-based therapy in overall complex treatment of the
patients with brain. It is reasonable to anticipate that devel-
oping CT-based approaches may provide much progress in
the management of multiple neurological diseases including
those which are now considered as uncurable. Novel tech-
niques of preparation and propagation of multi- and unipo-
tent cells, which are being now actively developed, enable to
solve not only technical, but also ethical problems confront-
ing progress in cell transplantology (reviewed in [3]) and,
thereby, may promote widespread adoption of CT-based
advances in clinical practice.
References
[1] Azanchi R, Bernal G, Gupta R, Keirstead HS. Combined demyelina-
tion plus Schwann cell transplantation therapy increases spread of
cells and axonal regeneration following contusion injury. J Neu-
rotrauma 2004;21:775–88.
[2] Cova L, Ratti A, Volta M, Fogh I, Cardin V, Corbo M, et al. Stem cell
therapy for neurodegenerative diseases: the issue of transdifferentia-
tion. Stem Cells Dev 2004;13:121–31.
[3] Eglitis MA, Mezey E. Hematopoietic cells differentiate into both
microglia and macroglia in the brains of adult mice. Proc Natl Acad
Sci USA 1997;94:4080–5.
[4] Favcett JW. Spinal cord repair: from experimental models to human
application. Spinal Cord 1998;36:811–7.
[5] Golfier F, Barcena A, Cruz J, Harrison M, Muench M. Mid-trimester
fetal livers are a rich source of CD34+/++ cells for transplantation.
Bone Marrow Transplant 1999;24:451–61.
[6] Hagan M, Wennersten A, Meijer X, Holmin S, Wahlberg L, Mathie-
sen T. Neuroprotection by human neural progenitor cells after experi-
mental contusion in rats. Neurosci Lett 2003;351:149–52.
[7] Hao HN, Zhao J, Thomas RL, Parker GC, Lyman WD. Fetal human
hematopoietic stem cells can differentiate sequentially into neural
stem cells and then astrocytes in vitro. J Hematother Stem Cell Res
2003;12:23–32.
[8] Hatton JD, Garcia R, Sang H. Migration of grafted rat astrocytes
depends on source/target organ. Glia 1992;5:251–8.
420 V.I. Seledtsov et al. / Biomedicine & Pharmacotherapy 59 (2005) 415–420
[9] Lachapelle F, Gansmuller A, Baulac M, et al. Transplantation of
oligodendrocytes in the CNS. Acta Cytobiol Morphol 1989;1:24–30.
[10] Maas AIR, Dearden M, Servadei F, Stocchetti N, Unterberg A. Cur-
rent recommendations for neurotrauma. Curr Opin Crit Care 2000;6:
281–92.
[11] Moiseev A, Samarin DM, Kustov SM, Senyukov VV, Seledtsova GV,
Kozlov VA. Fetal cell transplantation in the treatment of scarring
processes in gynecology. Bull Exp Biol Med 1998;126(Suppl
1):129–30 [in Russian with English abstract].
[12] Murohara T, Ikeda H, Duan J, Shintani S, Sasaki K, Eguchi H, et al.
Transplanted cord blood-derived endothelial precursor cells augment
postnatal neovascularization. J Clin Invest 2000;105:1527–36.
[13] Nguyen HM, Alksne HSUJF, Hatton JD. Migration of rat neonatal
cortical, hippocampal and hypothalamic astrocytes transplanted into
neonatal rat cerebrum. J Cell Biol 1990;111:490–5.
[14] Rabinovich SS, Seledtsov VI, Poveschenko OV, Senuykov VV, Tara-
ban VY, Yarochno VI, et al. Transplantation treatment of spinal cord
injury patients. Biomed Pharmacother 2003;57:428–33.
[15] Saporta S, Kim JJ, Willing AE, Fu ES, Davis CD, Sanberg PR. Human
umbilical cord blood stem cells infusion in spinal cord injury: engraft-
ment and beneficial influence on behavior. J Hematother Stem Cell
Res 2003;12:271–8.
[16] Seledtsov VI, Avdeev IV, Morenkov AV, Seledtsova GV, Kozlov VA.
Antiproliferative effect of bone marrow cells on leukemic cells.
Immunobiology 1995;192:205–17.
[17] Seledtsov VI, Rabinovich SS, Kaschenko EA, Felde MA, Banul NV,
Poveschenko OV, Astrakov SV, Savchenko SA, Kafanova M,
Seledtsova GV, kozlov VA. Immunologocal and clinical aspects of
applying cellular therapy in treating consequences of head injury. Cell
Technol Biol Med 2005; (in press).
[18] Smith GM, Miller RH. Immature type-1 astrocytes suppress glial scar
formation, are motile and interact with blood vessels. Brain Res
1991;543:111–2.
[19] Wu S, Suzuki Y, Kitada M, Kataoka K, Kitaura M, Chou H, et al. New
method for transplantation of neurosphere cells into injured spinal
cord through cerebrospinal fluid in rat. Neurosci Lett 2002;318:81–4.