bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of angiogenic growth factors in dural arteriovenous fistula
Authors: Uranishi Ryunosuke , Nakase Hiroyuki , Sakaki Toshisuke 
Published: May 2009

Object. Although various mechanisms of the development of dural arteriovenous fistula (AVF) have been described, the exact course of its pathogenesis, including molecular processes mediating its genesis, is still unknown. Recently, the importance of sinus thrombosis and venous hypertension has been reported in experimental and clinical studies. Additionally, a role of angiogenic growth factors in the pathogenesis of vascular malformations of the central nervous system has been reported. In this study, the authors investigated the existence of sinus thrombosis in dural AVF and the expression of angiogenic growth factors (basic fibroblast growth factor [bFGF] and vascular endothelial growth factor [VEGF]) in nine patients with dural AVFs that were surgically resected.Methods. The authors examined histological features of dural AVFs that involved the transverse/sigmoid sinus in seven patients and the superior sagittal sinus in two. Sinus thrombosis was verified angiographically in seven cases and histologically in all cases. In surgically resected specimens the angiogenic growth factors bFGF and VEGF were examined immunohistochemically in nine patients with dural AVFs, with five dural sinuses from cadavers with unrelated central nervous system diseases serving as a normal control group. The media and perivascular connective tissues of the arteries in the wall of the normal dural sinuses stained faintly for bFGF; on the other hand, the expression of VEGF was not detected. In all patients with dural AVFs, the thick wall of the dural sinus stained strongly for bFGF, mainly in the subendothelial layer and media of the strongly proliferative vessels in the sinus wall, in addition to the perivascular connective tissues. In all nine cases VEGF was expressed in the endothelium of the sinus and perivascular connective tissues. In two cases, VEGF was expressed in many capillaries proliferating in the granulation-like tissues in sinuses that were obliterated by organized thrombi.Conclusions. It is concluded that the pathogenesis of dural AVF is still unknown, but that angiogenic growth factors, which might be produced by the healing process due to sinus thrombosis, may participate in the genesis of dural AVF. Understanding the mechanism of molecular pathogenesis in the development of dural AVF might aid in the establishment of a new therapeutic strategy for this dynamic vascular disease.
Functional brain mapping using positron emission tomography scanning in preoperative neurosurgical planning for pediatric brain tumors
Authors: Kaplan Allen M. , Bandy Daniel J. , Manwaring Kim H. , Chen Kewei , Lawson Michael A. , Moss S. David , Duncan Johnny D. , Wodrich David L. , Schnur James A. , Reiman Eric M. 
Published: May 2009

Object. The purpose of this report is to demonstrate the value of functional brain mapping using the positron emission tomography (PET) method for preoperative neurosurgical planning in children with brain tumors. Brain maps were used to characterize the relationship between potentially resectable tumors and functionally eloquent brain areas.Methods. Five children, ranging in age from 3 to 13 years, with hemispheric brain tumors adjacent to eloquent cortex were studied. Magnetic resonance (MR) imaging was used to identify the brain tumors; PET imaging after injection of [18F]fluorodeoxyglucose (FDG), [11C]l-methionine (CMET), or a combination of the two was performed to grade the tumors; and a [15O] H2O uptake study was used to characterize the anatomical relationships of the tumors to functional cortex. The cortical activation maps were obtained during control periods and during behavioral tasks and were used to document motor, visual, and speech and language organizational areas. Wada tests were performed in two patients. Language and speech activation was concordant with the results of Wada testing.Conclusions. Functional brain mapping using PET scans and coregistered MR images provided the neurosurgeon with precise definitions of structural and functional cortical areas; this altered surgical management in some cases and/or was used to predict outcome. The combination of PET imaging with FDG and/or CMET and measurements of [15O] water uptake was useful in characterizing and grading tumors and instrumental in achieving effective neurosurgical planning. Postoperative results in the five cases suggest that preoperative functional brain mapping has the potential to improve outcome by defining a surgical plan to maximize resection and minimize the risk of neurological sequelae.
Cell cycle arrest and astrocytic differentiation resulting from PTEN expression in glioma cells
Authors: Adachi Jun-ichi , Ohbayashi Katsumi , Suzuki Tomonari , Sasaki Tomio 
Published: May 2009

Object. Genetic alterations of the PTEN gene (also known as MMAC1 or TEP1) have frequently been identified in high-grade gliomas, indicating that inactivation of PTEN plays a crucial role in human glioma progression. The aim of this study was to assess the biological significance of PTEN inactivation in the development of glioma.Methods. The authors introduced wild-type PTEN complementary DNA into four human glioma cell lines (T98G, U-251MG, U-87MG, and A172) containing endogenous aberrant PTEN alleles. The number of colonies transfected with the wild-type PTEN was reduced to 15 to 32% of those found after transfection of a control vector, suggesting growth suppression by the exogenous PTEN. To analyze phenotypic alterations produced by PTEN expression, T98G-derived clones with inducible PTEN expression were further established using a tetracycline-regulated inducible gene expression system. Induction of PTEN expression suppressed the in vitro growth of T98G cells with accumulation of G1 phase cells. Furthermore, when cells were cultured in the presence of the extracellular matrix (ECM), PTEN expression caused distinct morphological changes, with multiple and elongated cytoplasmic processes similar to those of normal astrocytes. The level of glial fibrillary acidic protein, an intermediate protein specifically expressed in differentiated astrocytes, was upregulated concomitantly.Conclusions. These findings strongly indicate that exogenous PTEN expression inhibits the proliferation of glioma cells by inducing G1 arrest and elicits astrocytic differentiation in the presence of the ECM. Inactivation of PTEN would play an important role in the enhancement of unregulated growth of undifferentiated glioma cells.
Induction of heat shock protein 70 in the rat brain following intracisternal infusion of autologous blood: evaluation of acute neuronal damage
Authors: Klinge Petra M. , Beck Heike , Brinker Thomas , Walter Gerhard F. , Samii Madjid 
Published: May 2009

Object. Investigation into a potential treatment for the acute period following onset of spontaneous subarachnoid hemorrhage (SAH) is hampered by the lack of a standardized experimental model. For that purpose the authors elaborated on a small-animal model in which computer-controlled intracisternal blood infusion is used and investigated whether this model can reliably reproduce acute neuronal injury after SAH.Methods. Whole autologous blood (blood-infused group) or isotonic saline (control group) was infused into the cisterna magna or olfactory cistern of rats. The infusions decreased exponentially during a 5-minute period. Throughout the infusion period, intracranial pressure (ICP) was monitored. Neuronal injury was quantified by observing tissue immunoreactivity to a 70-kD heat shock protein (HSP70) and comparing this with the tissue's reaction to hematoxylin and eosin staining. On Days 1, 3, and 5, the CA1, CA3, and dentate gyrus regions of the hippocampus were analyzed, respectively.During saline infusion ICP increased within seconds beyond 80 mm Hg and afterward decreased in accordance with the infusion rate. During the infusion of blood, the same initial pressure peak was found, but the ICP remained increased beyond this pressure level throughout the 5-minute infusion period. The HSP70 immunoreactivity in the saline-infused group was found only on Day 1 in the CA1 region and the dentate gyrus, but not in the CA3. After injection of whole blood, there was HSP70-positive staining in the CA1, CA3, and dentate gyrus regions throughout the observation period.Conclusions. The controlled cisternal infusion of blood caused neuronal injury that resembled that of previous experimental models that produce SAH by rupture of intracranial vessels with endovascular techniques. Unlike those experiments, the intracisternal infusion technique presented by the authors provides more standardized bleeding with regard to ICP, the volume of subarachnoid blood, and the extent of acute cellular injury.
Skull bone regeneration in primates in response to basic fibroblast growth factor
Authors: Tabata Yasuhiko , Yamada Keisuke , Hong Liu , Miyamoto Susumu , Hashimoto Nobuo , Ikada Yoshito 
Published: May 2009

Object. The feasibility of using a biodegradable hydrogel incorporating basic fibroblast growth factor (bFGF) to induce bone regeneration at the site of a skull defect in monkeys was investigated.Methods. Basic fibroblast growth factor was incorporated into a bioabsorbable hydrogel, which was prepared through glutaraldehyde crosslinking of gelatin. Following treatment of monkey skull defects measuring 6 mm in diameter (six defects/experimental group) with gelatin hydrogel incorporating bFGF, skull bone regeneration was evaluated using soft x-ray studies, dual x-ray absorptometry, and histological examinations.The water content of the hydrogels varied according to the glutaraldehyde concentration in the hydrogel preparation. Gelatin hydrogels incorporating 100 µg of bFGF significantly promoted bone regeneration and the skull defect was completely closed 21 weeks after implantation. This is in marked contrast with the effect of the same dose of bFGF in solution form. Bone mineral density (BMD) measured at the sites of skull defect was enhanced by the bFGF-incorporating hydrogels. The BMD enhancement was more prominent at lower water contents of hydrogel. Empty gelatin hydrogels neither induced nor interfered with skull bone regeneration.Conclusions. The findings of this study indicate that bFGF coupled with bioabsorbable hydrogel is a very promising tool to assist in the regrowth of bone at the site of a skull defect, which clinically has been recognized as almost impossible.
Recovery of cutaneous pain sensitivity after end-to-side nerve repair in the rat
Authors: Kovačič Uroš , Bajrović Fajko , Sketelj Janez 
Published: May 2009

Object. The hypothesis that collaterally sprouting axons from an uninjured donor nerve may provide recovery of pain sensitivity in the skin after end-to-side nerve repair was investigated in rats. In addition, the effect of this technique on the donor nerve was examined.Methods. The distal stump of the transected peroneal nerve was sutured end to side to the intact sural nerve. No epineurial window or perineurial slit was made in the sural nerve at the site of coaptation. Other nerves in the leg were transected and ligated. Eighteen weeks later, the sural nerve was transected at a site distal from the coaptation site. The residual pain sensitivity in the peroneal innervation field in the instep was documented using the skin pinch test in three of 11 animals. The area of sensitivity encompassed 19 to 40% of the maximum nociceptive innervation area of the normal peroneal nerve. The nerve pinch test revealed functional sensory axons in all communicating peroneal nerves, in which 277 ± 119 myelinated axons (mean ± standard deviation) were found by histological investigation.Conclusions. The authors conclude that at least partial recovery of sensory function due to collateral sprouting of axons after end-to-side nerve repair is possible in principle. However, the presence of functional sensory axons in the peroneal nerve stumps did not guarantee the recovery of skin sensitivity to pain in all animals. No functional or morphological evidence of an untoward effect of collateral sprouting into the end-to-side communicating nerve was detected in the axons of the donor nerve itself.
Fatal secondary increase in serum S-100B protein after severe head injury
Authors: Raabe Andreas , Seifert Volker 
Published: May 2009

✓ The S-100B protein is a small cytosolic protein that is found in astroglial or Schwann cells. It is highly specific for brain tissue and is increasingly being investigated as a diagnostic tool to assess the neurological damage after head injury, stroke, subarachnoid hemorrhage, and cardiopulmonary bypass.The authors report on three patients with severe head injury with otherwise normal cerebral perfusion pressure, SaO2, PaCO2, and controlled intracranial pressure (ICP), in whom a secondary excessive increase in serum S-100B was observed. In all cases, the S-100B increase was followed by an increase in ICP. All three patients died within 72 hours after the excessive increase in S-100B. These findings indicate that major secondary brain damage may occur at a cellular level without being identified by current neuromonitoring techniques.
Stereotactic radiofrequency ablation for the treatment of gelastic seizures associated with hypothalamic hamartoma
Authors: Parrent Andrew G. 
Published: May 2009

✓ The author presents the case of a patient with gelastic seizures associated with a hypothalamic hamartoma, in whom partial resection of the hamartoma followed by temporal lobectomy and orbitofrontal corticectomy failed to reduce the seizures. Subsequent stereotactic radiofrequency ablation of the hamartoma resulted in progressive improvement in the seizure disorder during a 28-month follow-up period.There is support in the literature for the concept that gelastic seizures originate directly from the hamartoma; however, direct surgical approaches to these lesions pose significant risks. It is proposed that the technique of radiofrequency ablation provides a minimally invasive, low-risk approach for the treatment of hypothalamic hamartomas.
Localization of hand motor activation in Broca's pli de passage moyen
Authors: Boling Warren , Olivier André , Bittar Richard G. , Reutens David 
Published: May 2009

Object. The object of this study was to identify a reliable surface landmark for the hand motor area and to demonstrate that it corresponds to a specific structural component of the precentral gyrus.Methods. Positron emission tomography (PET) activation studies for hand motor function were reviewed in 12 patients in whom magnetic resonance imaging results were normal. Each patient performed a hand opening and closing task. Using a computer-assisted three-dimensional reconstruction of the surface of each hemisphere studied, the relationship of the hand motor area with cortical surface landmarks was evaluated.Conclusions. The region of hand motor activation can be reliably identified on the surface of the brain by assessing anatomical relationships to nearby structures. After identification of the central sulcus, the superior and middle frontal gyrus can be seen to arise from the precentral gyrus at a perpendicular angle. A bend or genu in the precentral gyrus is constantly seen between the superior and middle frontal gyrus, which points posteriorly (posteriorly convex). The location of hand motor function, identified using PET activation studies, is within the central sulcus at the apex of this posteriorly pointing genu. The apex of the genu of the precentral gyrus leads to a deep cortical fold connecting the pre- and postcentral gyri and elevating the floor of the central sulcus. This deep fold was described by Paul Broca as the pli de passage fronto-pariétal moyen, and the precentral bank of the pli de passage represents the anatomical substratum of hand motor function. Observers blinded to the results of the activation studies were able to identify the hand motor area reliably after instruction in using these surface landmarks.
Noninvasive evaluation of the malignant potential of intracranial meningiomas performed using proton magnetic resonance spectroscopy
Authors: Shiino Akihiko , Nakasu Satoshi , Matsuda Masayuki , Handa Jyoji , Morikawa Shigehiro , Inubushi Toshiro 
Published: May 2009

Object. Controversy exists about correlations between histological tumor grade and magnetic resonance (MR) spectroscopy data. The authors studied single-voxel proton MR spectroscopy as a noninvasive way to evaluate grade of malignancy in intracranial meningiomas.Methods. The authors compared the results of MR spectroscopy with those derived by the MIB-1 staining index (SI) in 29 meningiomas. Proton MR spectroscopy was performed using stimulated echo acquisition and volume-localized solvent-attenuated proton nuclear MR sequences before surgery or other therapy.Twenty-four tumors were histologically benign (13 meningothelial, three fibrous, four transitional, three angiomatous, and one chordoid); four were atypical (Grade II), and one was papillary (Grade III). The mean MIB-1 SI in the benign group was significantly lower than those in the other groups (p = 0.0041). The mean choline-containing compound (Cho)/creatine and phosphocreatine (Cr) ratios in the benign and nonbenign groups were 2.56 ± 1.26 and 7.85 ± 3.23, respectively (p = 0.0002). A significant linear correlation was observed between the Cho/Cr ratio and the MIB-1 SI (r0.05 = 0.74, p < 0.001). Necrosis was present histologically in four of the five meningiomas classified either as atypical or papillary. Magnetic resonance spectroscopy revealed a methylene signal in these meningiomas that was not detected in benign meningiomas. Of the five meningiomas in which only a lactate signal was observed, two were benign and the MIB-1 SI in these two benign meningiomas was higher than the mean value for the benign group. Alanine, detected in 12 of 30 meningiomas, did not correlate with either tumor grade or Cho/Cr ratio.Conclusions. Proton MR spectroscopy is a useful diagnostic method for determining the proliferative or malignant potential of meningiomas according to the Cho/Cr ratio. A lactate and/or methylene signal suggests a high-grade tumor.
Apoptotic elimination of peripheral T lymphocytes in patients with primary intracranial tumors
Authors: Morford Lorri A. , Dix Amy R. , Brooks William H. , Roszman Thomas L. 
Published: May 2009

Object. Patients with gliomas exhibit severe T lymphopenia during the course of the disease. This study was conducted to determine the mechanism(s) responsible for the lymphopenia.Methods. Using two-color fluorescent staining techniques, the authors show that significant numbers of T cells undergo apoptosis in the peripheral blood of patients with gliomas. To determine whether a glioma-derived factor(s) induces this apoptosis, rosette-purified T cells obtained from healthy donors were treated with glioma cell culture supernatant (GCCS) and examined for apoptosis. It is demonstrated that treatment of normal T cells with GCCS induced apoptosis only with concurrent stimulation of the T-cell receptor/CD3 complex. The addition of neutralizing antibodies to interleukin (IL)-10, IL-4, transforming growth factor-α, or tumor necrosis factor-β (lymphotoxin) did not rescue these T cells from apoptosis. Experiments were also conducted in which the degree of monocyte involvement in the induction of T-cell apoptosis was explored. The U937 cells were pretreated for 20 hours with a 1:20 dilution of GCCS. After the removal of GCCS, the U937 cells were cultured in transwell assays with stimulated T cells. Although control U937 cells did not induce apoptosis of the activated T cells, GCCS-pretreated U937 cells induced appreciable apoptosis in normal, stimulated T-cell cultures.Conclusions. These data indicate that one mechanism by which gliomas cause immunosuppressive effects is the induction of monocytes to release soluble factors that promote activated T-cell apoptosis. The loss of activated T cells leads to T lymphopenia and contributes to the deficiencies in cell-mediated immunity that have been observed during testing of glioma patients' immune function.
Improved efficiency of hypervolemic therapy with inhibition of natriuresis by fludrocortisone in patients with aneurysmal subarachnoid hemorrhage
Authors: Mori Tatsuro , Katayama Yoichi , Kawamata Tatsuro , Hirayama Teruyasu 
Published: May 2009

Object. To reduce the risk of ischemic complications in patients with subarachnoid hemorrhage (SAH), hypervolemic therapy is generally advocated. However, such conventional treatment cannot always ensure the maintenance of an effective intravascular volume expansion, because excessive natriuresis and osmotic diuresis occur after SAH. In this prospective study the authors examined the effects of inhibition of natriuresis with fludrocortisone acetate on intravascular volume expansion during hypervolemic therapy.Methods. Thirty patients with SAH were randomized and divided into two groups: controls (Group 1, 15 patients) and patients treated with 0.3 mg/day of fludrocortisone (Group 2, 15 patients). In all patients sodium and fluid intake levels were in excess of maintenance requirements in an attempt to maintain a positive water balance and a central venous pressure (CVP) of 8 to 12 cm H2O. The mean sodium and water intake levels for 14 days after SAH were significantly reduced by fludrocortisone in Group 2 (487 ± 34.52 mEq/day and 5159.2 ± 249.29 ml/day, respectively; p < 0.01) compared with Group 1 (634.2 ± 42.86 mEq/day and 6611.7 ± 365.67 ml/day). Fludrocortisone significantly reduced the urinary sodium excretion (p < 0.01) and urine volume (p < 0.01) in parallel, and effectively prevented a negative shift in the sodium as well as water balance (p < 0.01). The serum sodium level tended to decrease in Group 1, reaching 135 mEq/L on average, but not in Group 2 (p < 0.01). Hyponatremia in Group 1 was always observed at the optimal range of CVP values. A decrease in serum potassium level within the range of 2.8 to 3.5 mEq/L was transiently noted in 11 patients (73.3%) of Group 2, but was easily corrected. Possible side effects of fludrocortisone, such as pulmonary edema, were not encountered.Conclusions. Intravascular volume expansion in the presence of excessive natriuresis requires a large sodium and water intake and is often associated with hyponatremia. Inhibition of natriuresis with fludrocortisone can effectively reduce the sodium and water intake required for hypervolemia and prevent hyponatremia at the same time.