Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “brain”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,315 records · Page 73Linked to original sources
PubMed1987

Optical properties of human brain tissue, meninges, and brain tumors in the spectral range of 200 to 900 nm.

Considering the increasing use of lasers in neurosurgery and the increasing number of wavelengths of laser light becoming available, we evaluated optical properties between 200 and 900 nm of meninges, normal human brain tissue, and brain tumors. We used a two-beam spectral photometer with an integrating sphere as the measuring instrument. The material consisted of 13 brains and 1 specimen each of dura mater, falx, and arachnoid obtained at autopsy and 30 samples of brain tumors removed during operation. In tissue samples more than 5 mm thick, the relative levels of absorption and scattering were estimated from the relative level of reflection measured according to the Kubelka-Munk theory. In thin tissue slices, penetration depth was calculated according to Beer's law from measurements of reflection and transmission. Generally, in all tissues there was an increase of reflection, scattering, and penetration depth and a decrease of absorption from the ultraviolet up to the near infrared spectral range interrupted by the absorption bands of hemoglobin. Within the ultraviolet spectral range, no major differences of optical properties were observed. Within the visible and near infrared spectral range, white matter reflected most of the incident power and showed the lowest level of absorption and the shortest penetration depth. Low grade gliomas revealed optical properties similar to those of gray matter. In comparison with normal brain tissue, meningiomas and glioblastomas showed significantly higher levels of absorption calculated according to the Kubelka-Munk theory from reflection measurements in thick tissue samples, but also deeper penetration obtained from measurements of reflection and transmission in thin slices, especially within the near infrared spectral range.

Aged↗
PubMed2005

Sequential visualization of brain and fiber tract deformation during intracranial surgery with three-dimensional ultrasound: an approach to evaluate the effect of brain shift.

OBJECTIVE: We present a technique that allows intraoperative display of brain shift and its effects on fiber tracts. METHODS: Three patients had intracranial lesions (one malignant glioma, one metastasis, and one cavernoma) in contact with either the corticospinal or the geniculostriate tract that were removed microneurosurgically. Preoperatively, magnetic resonance diffusion-weighted imaging (DWI) was performed to visualize the fiber tract at risk. DWI data were fused with those obtained from anatomic T1-weighted magnetic resonance imaging. A single-rack three-dimensional ultrasound neuronavigation system, which simultaneously displays the MRI scan and the corresponding ultrasound image, was used intraoperatively for 1) navigation; 2) definition of fixed and potentially shifting ultrasound landmarks near the fiber tract; and 3) sequential image updating at different steps of resection. The result was time-dependent brain deformation data. With a standard personal computer equipped with standard image software, the brain shift-associated fiber tract deformation was assessed by use of sequential landmark registration. After surgery, DWI was performed to confirm the predicted fiber tract deformation. RESULTS: The lesions were removed without morbidity. Comparison of three-dimensional ultrasound with DWI and T1-weighted magnetic resonance imaging data allowed us to define fixed and potentially shifting landmarks close to the respective fiber tract. Postoperative DWI confirmed that the actual fiber tract position at the conclusion of surgery corresponded to the sonographically predicted fiber tract position. CONCLUSION: By definition and sequential intraoperative registration of ultrasound landmarks near the fiber tract, brain shift-associated deformation of a tract that is not visible sonographically can be assessed correctly. This approach seems to help identify and avoid eloquent brain areas during intracranial surgery.

Adolescent↗
PubMed1995

[The findings indicate that HSP70 expression is closely related to ischemic brain injury, and that HSP70 expression is not related to either breakdown of the blood-brain barrier or reactive axonal changes].

The relationship between the 70-kilodalton hear shock protein (HSP70), morphological changes in neurons, protein extravasation, and reactive axonal changes was evaluated in rats with fluid percussion injuries to the right side of the brain. (4.8-5.6 atm, 20 ms). From 1 hour to 2 weeks after injury (or sham injury), serial sections of the brains were immunostained with antibodies to HSP70, rat IgG, and 68-kilodalton neurofilament. Ischemic changes in neurons in the injured cortex were noted in samples taken from 6 to 48 hours after injury, and macroscopic hemorrhages were noted in the corpus callosum and external capsule. Reactive axonal swelling was observed in the brain stem in samples taken from 6 to 48 hours after injury. Immunostaining of HSP70 was positive in the injured cortex from 6 hours to 1 week after injury. Maximal immunostaining was observed by 48 hours after injury in the injured cortical layers II and III. The region of HSP70 expression at 24 and 48 hours postinjury was the same as the region of ischemic cell changes. There were discrepancies between the region of HSP70 expression and the regions of IgG immunoreactivity and reactive axonal changes. These findings indicate that HSP70 expression is closely related to ischemic brain injury, and that HSP70 expression is not related to either breakdown of the blood-brain barrier or reactive axonal changes.

Animals↗
PubMed2004

Brain insulin impairs amyloid-beta(1-40) clearance from the brain.

Cerebral amyloid-beta peptide (Abeta) clearance plays a key role in determining the brain level of Abeta; however, its mechanism remains unclear. In this study, we investigated cerebral Abeta clearance across the blood-brain barrier (BBB) by using the Brain Efflux Index method. [125I]Abeta(1-40) was eliminated from rat brain to circulating blood with a half-life of 48.8 min and a half-saturation concentration of 8.15 nm. The Abeta(1-40) elimination rate was reduced by 30.5% in 23-month-old rats compared with 7-week-old rats. The intact form of Abeta(1-40) was detected in plasma after intracerebral administration, indicating the occurrence of efflux transport of intact Abeta(1-40). The Abeta(1-40) elimination rate was significantly inhibited by coadministration of 100 microg/ml insulin and 1 mm thiorphan by 44.6 and 34.0%, respectively. The level of intact [125I]Abeta(1-40) in the brain was increased by coadministration of insulin. Among insulin-degrading enzyme inhibitors, bacitracin inhibited the elimination rate, whereas N-ethylmaleimide and metal chelators had no effect. Receptor-associated protein, fucoidan, 3-bromo-5-t-butyl-4-hydroxy-benzylidenemalonitrile, anti-IGF-I receptor antibody, and l-tyrosine did not affect the Abeta(1-40) elimination rate, suggesting that the relevant receptors or transporters are not likely to be involved in the clearance. In conclusion, the present study has demonstrated the involvement of a proteolytic degradation process and an insulin-sensitive process in cerebral Abeta(1-40) clearance in the rat.

Aging↗
PubMed2001

Application of an in vivo brain microdialysis technique to studies of drug transport across the blood-brain barrier.

There is a wide range of methods available for studying the transport of drugs across the blood-brain barrier (BBB) which is equipped with several systems to transport drugs as well as endogenous nutrients and waste products. The in vivo brain microdialysis technique, which allows direct sampling of the brain interstitial fluid (ISF), is a powerful means of characterizing influx and efflux transport across the BBB. In this paper, we review our results from the successful application of this technique to BBB drug transport studies. The drugs investigated include novel and CNS-active peptides, some agents that are actively removed from the brain ISF across the BBB, and a brain-directed prodrug.

Biological Transport↗
PubMed2005

The role of blood-brain barrier permeability in brain tumor imaging and therapeutics.

OBJECTIVE: Our purpose is to describe methods of assessing leakiness of the blood-brain barrier and explain mechanisms for exploiting the blood-brain barrier for therapeutic purposes. CONCLUSION: Knowledge of the workings of the blood-brain barrier is important for an understanding of the ways in which blood-brain barrier permeability may be used as a surrogate marker for drug therapeutic response. Manipulation of the blood-brain barrier may provide a means for selectively targeting tumors for drug delivery.

Animals↗
PubMed2000

Drug targeting to the brain using avidin-biotin technology in the mouse; (blood-brain barrier, monoclonal antibody, transferrin receptor, Alzheimer's disease).

A beta1-40 peptide radiopharmaceuticals could be used to image A beta brain amyloid in transgenic mouse models of Alzheimer's disease should the A beta peptide radiopharmaceutical be made transportable through the blood-brain barrier (BBB) in vivo. The present studies used the RI7-217 rat monoclonal antibody to the mouse transferrin receptor as a BBB drug targeting vector for the delivery to brain of A beta1-40 radiolabeled with either 125-Iodine or 111-Indium. The A beta peptide radiopharmaceutical is conjugated to the RI7 MAb using avidin biotin technology, wherein the A beta1-40 peptide radiopharmaceutical is monobiotinylated (bio) and bound to a conjugate of the RI7 MAb and streptavidin (SA). The [125 I]-bio-A beta1-40 or the [111 In]-bio-A beta1-40 either free or bound to the RI7/SA conjugate was injected intravenously into anesthetized adult mice and plasma pharmacokinetics and organ uptake were measured over the next 60 minutes. The A beta1-40 peptide radiopharmaceutical radiolabeled with 111-Indium was the preferred formulation, compared to peptide labeled with 125-Iodine, because there was a greater metabolic stability and reduced artifactual organ uptake of metabolites associated with the use of the 111-Indium nuclide. However, biotinylated A beta1-40 peptide radiopharmaceuticals conjugated to the RI7/SA brain drug targeting system were metabolically unstable in mice in vivo owing to active biotinidase activity. Future work involving brain drug targeting in mice that utilizes avidin biotin technology will need to incorporate biotin analogues that are resistant to biotinidase.

Amidohydrolases↗
PubMed1999

Chronic systemic administration of tumor necrosis factor alpha and HIV gp120: effects on adult rodent brain and blood-brain barrier.

Since tumor necrosis factor alpha (TNF-alpha) and HIV gpl20 glycoprotein are both neurotoxic, the possibility that systemic sources of these two agents mediate AIDS-associated blood-brain barrier (BBB) breakdown and brain damage was tested in two murine models: (1) intramuscular implantation of a TNF-alpha-transfected tumor in nu/nu mice and (2) daily subcutaneous injections of HIV gpl20 in BALB/c mice. The BBB remained intact; brain damage was not found, and apoptotic cell numbers did not increase. These results show that normal adult brain and BBB is unaffected by exposure to TNF-alpha or HIV gpl20 and suggest that severity of brain disease is not directly affected by systemic levels of these compounds.

Animals↗
PubMed1989

Brain kininogen following experimental brain injury: evidence for a secondary event.

Previous studies have shown that following experimental brain injury cerebral arterioles dilate and display endothelial lesions and reduced responsiveness to hypocapnia. These abnormalities are caused by cyclo-oxygenase-dependent free radical generation. There is evidence that the kallikrein-kinin system may in part stimulate the cyclooxygenase-dependent damage since bradykinin is a powerful stimulator of prostaglandin formation and it has recently been shown that a specific kinin receptor blocker decreases the arteriolar abnormalities caused by injury. In order to further examine the hypothesis that the kallikrein-kinin system is important in inducing damage, rat brain tissue was examined for kininogen, the precursor of kinins, at 10 minutes and 1, 3, 6, 15, 24, 48, and 72 hours after injury. A fluid-percussion brain injury device was attached over the right cerebral cortex of rats and a 1.6-atmosphere pressure injury was administered. The kininogen content was determined by a radioimmunoassay procedure in tissues which were free of intravascular blood. After injury, bleeding was confined mainly to the right hemisphere. The kininogen content in the right hemisphere was significantly elevated by one hour after injury, continued to rise until 15 hours after injury, then was significantly decreased by 2 days after injury. In the left hemisphere, kininogen was significantly elevated at 1 hour postinjury, returned toward control levels over the 3- to 6-hour period after injury, then was again elevated at 15 hours after injury. These studies also show that brain water and cerebrovascular permeability were greater at 15 hours postinjury than at earlier time points. The data further support a role for the kallikrein-kinin system in brain injury and, when considered with the results of other studies, suggest that a secondary event is occurring in the 12- to 24-hour period after neural injury. The authors hypothesize that this secondary event is related to endothelial and vascular repair and may be important for the return of normal cerebrovascular function.

Animals↗
PubMed1993

Therapeutic effects of local delivery of dexamethasone on experimental brain tumors and peritumoral brain edema.

To determine if dexamethasone administered by osmotic pump directly to brain tumors would control peritumoral edema and at the same time suppress tumor growth and prolong survival, the authors studied experimental brain tumors produced in 102 rabbits by implanting VX2 carcinoma cells. Of these, 58 animals were separated into three treatment groups: Group 1 included 15 untreated rabbits; Group 2 included 18 rabbits treated with systemic dexamethasone (4 mg/kg/day); and Group 3 included 25 rabbits treated with local dexamethasone (0.24 mg/day) delivered by osmotic pump. Systemic or local dexamethasone was administered from Day 3 or Day 7 after tumor implantation, and animals were sacrificed on Day 13. A survival study was performed with 44 rabbits separated into the same treatment groups, beginning drug delivery on Day 7. Brain water content in the white matter of sacrificed animals was measured by the specific gravity method. The length and width of the brain tumors in all animals were measured and the tumor volume estimated. Findings showed that systemic and local dexamethasone administered from Day 3 or Day 7 was associated with a significant (5% level) inhibition of tumor volume as well as a mean reduction of brain edema in most tested sites. Systemic and local dexamethasone therapy also resulted in a significant (5% level) increase in survival time relative to the untreated group. These short-term results suggest that locally delivered dexamethasone may constitute a clinically important therapeutic modality.

Animals↗
PubMed1994

Blood-brain barrier permeability in staphylococcal cerebritis and early brain abscess.

The pattern of radiographic enhancement in cases of brain abscess has been extensively studied, but the magnitude of blood-brain barrier (BBB) damage that accompanies enhancement has not. The question of whether BBB permeability increases continuously as a cerebritis evolves into an abscess was studied. The tracers 3H-labeled aminoisobutyric acid and 14C-labeled butanol were used in a rat Staphylococcus aureus cerebritis model to measure simultaneously BBB permeability and blood flow. The rats were examined at 1, 2, 3, 5, or 7 days after inoculation, and tissue samples were collected from the cerebritis site and uninoculated regions. Permeability of the BBB in the cerebritis region increased to five times the normal values by 72 hours after inoculation, then reached a plateau. The plasma volume in the cerebritis region increased to six times greater than the normal value at 72 hours, then remained unchanged. Uninoculated brain in both ipsilateral and contralateral hemispheres showed no significant changes. Cerebral blood flow was not substantially altered at the inoculated or uninoculated sites. In this model, incidence of BBB damage rises rapidly, reaches a plateau, and does not continue to increase despite the ongoing evolution of a cerebritis into an abscess. The BBB damage is accompanied by an increase in the regional plasma volume, a novel finding that has not been previously reported in central nervous system inflammation. These results suggest that the vascular events contributing to brain edema formation become established early in the cerebritis phase and imply that control of the host's inflammatory response is important in the management of cerebritis-associated brain edema.

Animals↗
PubMed1994

Vascular permeability factor in brain metastases: correlation with vasogenic brain edema and tumor angiogenesis.

Metastatic brain tumors are almost always associated with vasogenic brain edema, which in turn plays a pivotal role in the evolution of neurological morbidity associated with these lesions. Attention has recently focused on a group of proteinaceous vascular permeability factors (VPF's) that are capable of inducing angiogenesis and promoting increased capillary permeability. To test the hypothesis that metastatic brain tumors expressing VPF's are associated with peritumoral cerebral edema, a rabbit polyclonal immunoglobulin (Ig) G anti-VPF was used to immunostain pathological specimens of metastatic cerebral tumors obtained from 22 patients who underwent surgery at Yale-New Haven Hospital. Magnetic resonance (MR) imaging was used to correlate VPF staining in tumor tissue with the occurrence of peritumoral brain edema. A histological study of the microvasculature was then conducted by immunostaining the specimens for endothelial cell factor VIII surface antigen, using two gliosis specimens as controls. Results revealed 21 of 22 tumors stained positively for VPF's; the negative-VPF tumor was a melanoma that exhibited no peritumoral edema. Twenty of 22 tumors had MR imaging-evident vasogenic edema. The presence and intensity of VPF immunostaining of microvascular features were noted and compared. Factor VIII staining demonstrated tumor vascularity to be most abundant in VPF-rich regions of tumor. The authors therefore report a high correlation between the presence of VPF's and the occurrence of peritumoral brain edema associated with cerebral metastases.

Brain Edema↗
PubMed1998

Na+,K(+)-ATPase isozymes in the bovine brain grey matter and brain stem.

Active preparations of Na+,K(+)-ATPase containing three types of catalytic isoforms were isolated from the bovine brain to study the structure and function of the sodium pump. Na+,K(+)-ATPase from the brain grey matter was found to have a biphasic kinetics with respect to ouabain inhibition and to consist of a set of isozymes with subunit composition of alpha 1 beta 1, alpha 2 beta m and alpha 3 beta m (where m = 1 and/or 2). The alpha 1 beta 1 form clearly dominated. For the first time, glycosylation of the beta 1-subunit of the alpha 1 beta 1-type isozymes isolated from the kidney and brain was shown to be different. Na+,K(+)-ATPase from the brain stem and axolemma consisted mainly of a mixture of alpha 2 beta 1 and alpha 3 beta 1 isozymes having identical ouabain inhibition constants. In epithelial and arterial smooth muscle cells, where the plasma membrane is divided into functionally and biochemically distinct domains, the polarized distribution of Na+,K(+)-ATPase is maintained through interactions with the membrane cytoskeleton proteins ankyrin and spectrin (Nelson and Hammerton, 1989; Lee et al., 1996). We were the first to show the presence of the cytoskeleton protein tubulin (beta 5-isoform) and glyceraldehyde-3-phosphate dehydrogenase in a high-molecular-weight complex with Na+,K(+)-ATPase in brain stem neuron cells containing alpha 2 beta 1 and alpha 3 beta 1 isozymes. Consequently, the influence of not only subunit composition, but also of glycan and cytoskeleton structures and other plasma membrane-associated proteins on the functional properties of Na+,K(+)-ATPase isozymes is evident.

Animals↗
PubMed1976

[Delayed radiation necrosis of the brain simulating a brain tumor--report of two cases (author's transl)].

Two cases of delayed radiation necrosis of the brain were reported. Case 1 was a 50-year-old man who had right hemiparesis and disorientation 26 months after Linac irradiation (5,000 rad), preceded by the operation for right maxillar carcinoma. A left carotid angiogram demonstrated a left temporal mass lesion, extending the frontal lobe. Case 2 was a 41-year-old man who had previously the operation for right intraorbital plasmocytoma, followed by two times Co irradiation (6,400 rad, and 5,000 rad). He had the signs and symptoms of intracranial hypertension 36 months after last irradiation. A left carotid angiogram demonstrated a left temporal mass lesion. Both cases were treated by administration of steroid hormone, which alleviated the signs and symptoms, followed by the temporal lobectomy. Microscopic examinations showed necrosis of the brain tissues associated with hyaline degeneration of blood vessel walls and perivascular cell infiltration. The signs and symptoms of intracranial hypertension subsided postoperatively. The other thirteen cases as same as ours were collected from literature, which showed the signs and symptoms simulating a brain tumor (like a metastic brain tumor) after the irradiation to extracranial malignant tumors, and the diagnosis of radiation necrosis were made by the operation or autopsy. A follow-up for a long time is necessary, because the pathological changes in the brain may be progressive and extending in some cases, although the decompressive operations for mass lesion are excellent in result.

Adult↗
PubMed2000

Interleukin-1beta -induced changes in blood-brain barrier permeability, apparent diffusion coefficient, and cerebral blood volume in the rat brain: a magnetic resonance study.

The cytokine interleukin-1beta (IL-1beta) is implicated in a broad spectrum of CNS pathologies, in which it is thought to exacerbate neuronal loss. Here, the effects of injecting recombinant rat IL-1beta into the striatum of 3-week-old rats were followed noninvasively from 2 to 123 hr using magnetic resonance imaging and spectroscopy. Four hours after injection of IL-1beta (1 ng in 1 microliter), cerebral blood volume was significantly increased, the blood-brain barrier (BBB) became permeable to intravenously administered contrast agent between 4.5 and 5 hr, and the apparent diffusion coefficient (ADC) of brain water fell by 6 hr (5.42 +/- 0. 35 x 10(-4) mm(2)/sec treated, 7.35 +/- 0.77 x 10(-)(4) mm(2)/sec control; p < 0.001). At 24 hr the BBB was again intact, but the ADC, although partially recovered, remained depressed at both 24 and 123 hr (p < 0.03). Depleting the animals of neutrophils before IL-1beta injection prevented the BBB permeability at all time points, but the ADC was still depressed at 6 hr (6.64 +/- 0.34 x 10(-4) mm(2)/sec treated, 7.49 +/- 0.38 x 10(-4) mm(2)/sec control; p < 0.005). No changes were seen in brain metabolites using proton spectroscopy at 6 hr after IL-1beta. Intraparenchymal injection of IL-1beta caused a neutrophil-dependent transient increase in BBB permeability. The presence of neutrophils within the brain parenchyma significantly contributed to the IL-1beta-induced changes in cerebral blood volume and the ADC of brain water. However, IL-1beta apparently had a direct effect on the resident cell populations, which persisted well after all recruited leukocytes had disappeared. Thus the action of IL-1beta alone can give rise to magnetic resonance imaging-visible changes that are normally attributed to alterations to cellular homeostasis.

Acute Disease↗
PubMed2000

Brain-derived neurotrophic factor and neurotrophin-3 levels in Alzheimer's disease brains.

In the present study, we investigated the levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in post-mortem brain tissue of Alzheimer's disease (AD) patients, and we observed a significant increase of BDNF concentration in hippocampus and parietal cortex of AD patients, as well as a negative correlation between NT-3 levels and age in hippocampus and putamen of control subjects, and for BDNF in frontal cortex. A defining feature of AD is the post-mortem identification of neuritic plaques and neurofibrillary tangles in the brain, however, a more significant neuropathological finding is the degeneration of cholinergic neurones of the basal forebrain, critically involved in memory and cognition. Neurotrophic factors are partly responsible for the maintenance of neuronal function and structural integrity in the adult brain. Our results provide, therefore, evidence that, under conditions of progressive neurodegeneration the brain stimulates the over expression of certain neurotrophic factors as a possible mechanisms of compensation, and that during senescence the expression of these molecules is regulated.

Age Factors↗
PubMed2003

Changes in the blood-brain barrier permeability and in the brain tissue trace element concentrations after single and repeated pentylenetetrazole-induced seizures in rats.

The behaviour of brain capillary endothelium to the passage of macromolecules in single and repeated seizures conditions and its relationship to the brain trace element concentrations are the main subject of this study. For this purpose, animals were treated with either single or repeated doses of pentylenetetrazole (PTZ). As a marker of blood-brain barrier (B-BB) permeability changes, Evans Blue (EB) dye was used. Seizure activity was observed and seizure patterns and convulsion times were recorded. PTZ treatment induced generalised tonic-clonic seizure in all animals, but seizures were found to be lasting longer in single seizure group than repeated seizures group. Seizures induced by single dose PTZ treatment resulted in bilateral EB leakage in the preoptic area, caudate nucleus, putamen, thalamus, hypothalamus, midbrain, and the superior colliculus. However, repeated PTZ-induced seizures led to EB leakage in the brains of only few number of rats, and it was confined to hypothalamus, caudate nucleus, cerebellum, thalamus, and pons. On the other hand, while the levels of copper (Cu) and iron (Fe) in brain tissue were found to be decreased significantly in the repeated seizures group when compared with the other groups, the levels of zinc (Zn) did not show any differences between groups. These results indicate that the regional B-BB opening markedly differs between single and repeated PTZ-induced seizures group and this difference may be due to PTZ tolerance and changes in cerebral endothelial structure.

Animals↗
PubMed2005

Upregulated gene expression of local brain-derived neurotrophic factor and nerve growth factor after intracisternal administration of marrow stromal cells in rats with traumatic brain injury.

OBJECTIVE: To examine the effects of rat marrow stromal cells (rMSCs) on gene expression of local brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) after injection of rMSCs into Cistern Magnum of adult rats subjected to traumatic brain injury (TBI). METHODS: A modified Feeney's TBI model was created in 48 adult rats. rMSCs were harvested from 3-month-old rats, and injected into Cistern Magnum in 24 rats subjected to TBI (Group cell transplantation). Saline was given through Cistern Magnum to another 24 rats subjected to TBI (Group saline control). Animals were sacrificed 1, 2 and 3 weeks after intervention, and special brain tissue blocks were dissected for total RNA extraction from each block. BDNF and NGF mRNA were reverse-transcribed into cDNA and further expanded by polymerase chain reaction (PCR). The expression of target genes was evaluated using semi-quantitative methods. RESULTS: Group cell transplantation had higher BDNF and NGF gene expressions than Group saline control during a period of less than 3 weeks (P<0.05). CONCLUSIONS: rMSCs transplantation via Cistern Magnum in rats subjected to traumatic brain injury can enhance expressions of local brain NGF and BDNF to a certain extent.

Animals↗