Hypofractionated stereotactic radiosurgery for aggressive vertebral haemangioma and useful follow-up imaging modality: case report and review of the literature.

We report the use of an advanced magnetic resonance image (MRI) sequence to detect the treatment response after SRS for aggressive vertebral haemangioma (VH). A 63-year-old female patient presented with back pain, bilateral lower extremity weakness (grade IV), and sensory change in the saddle area. MRI revealed a vertebral body mass compressing the spinal cord at T10, which had high T2 and low T1 signal intensity. Three-dimensional volumetric sagittal time-resolved imaging of contrast kinetics (TRICKS) abdominal magnetic resonance angiography (MRA) showed it to be hypervascular. SRS with the Novalis beam shaping system (BrainLAB; Heimstetten®, Germany) was performed on the gross tumor volume of 14.954 mL. 30 Gy was given to the 90% isodose line in 5 fractions. Seven days later, the patient underwent decompressive laminectomy for weakness. Seven months later, the patient's motor weakness was improved to allow for unassisted gait, and back pain and sensory changes resolved. Follow-up MRI revealed no significant change on T1 and T2 signal intensity images. However, TRICKS abdominal MRA demonstrated disapprearance of the hypervascularity. Seven years after SRS, the same signal intensity images showed shrinkage of the mass and resolution of compression of the spinal cord, and the signal intensity of the T1 image was changed to iso- and high signal intensity.

Treatment pulse application for magnetic stimulation.

Treatment and diagnosis can be made in difficult areas simply by changing the output pulse form of the magnetic stimulation device. However, there is a limitation in the range of treatments and diagnoses of a conventional sinusoidal stimulation treatment pulse because the intensity, width, and form of the pulse must be changed according to the lesion type. This paper reports a multidischarge method, where the stimulation coils were driven in sequence via multiple switching control. The limitation of the existing simple sinusoidal pulse form could be overcome by changing the intensity, width, and form of the pulse. In this study, a new sequential discharge method was proposed to freely alter the pulse width. The output characteristics of the stimulation treatment pulse were examined according to the trigger signal delay applied to the switch at each stage by applying a range of superposition pulses to the magnetic simulation device, which is widely used in industry and medicine.

Benign submucosal lesions of the stomach and duodenum: imaging characteristics with endoscopic and pathologic correlation.

Benign submucosal lesions of the stomach and duodenum are occasionally encountered during endoscopy. But endoscopy has its limitations in the diagnosis and differentiation of these lesions, because submucosal lesions are often difficult to visualize at endoscopy due to minimal change of the overlying mucosa. Furthermore, endoscopic biopsy may not always yield adequate tissue for diagnosis due to the submucosal location of the lesions. For this reason, the role of radiologic imaging is important in the diagnosis of submucosal lesions of the stomach and duodenum. Recent advances in computed tomography (CT) and sonographic technology are helpful in narrowing the differential diagnosis of gastroduodenal submucosal lesions. In contrast to endoscopy and barium studies, CT or ultrasonography (US) provides information about both the gastric wall and the extragastric extent of the disease. Arterial phase contrast enhanced CT enables us to discriminate a mass of submucosal from that of a mucosal origin in the differential diagnosis of gastric or duodenal lesions. Although endoscopic sonography has been considered the better modality in the diagnosis of gastroduodenal submucosal lesions, transabdominal sonography can still be an alternative method to endoscopic sonography in assessing of the origin and character of the submucosal lesions. Some gastroduodenal submucosal lesions have similar radiologic findings that make differentiation difficult. But despite overlaps in radiologic findings, some lesions have characteristic radiologic features that may suggest a specific diagnosis. Knowledge of the differential diagnosis of benign submucosal lesions in the stomach and duodenum may promote correct diagnosis and appropriate treatment.

Loss of mitochondrial membrane potential and caspase activation enhance apoptosis in irradiated K562 cells treated with herbimycin A.

PURPOSE: We previously reported that herbimycin A (HMA) alters the mode of cell death of K562 cells induced by radiation and enhanced their radiosensitivity. In the present study, we explored the apoptosis-inducing activity of HMA and the fundamental mechanism via which it regulates radiation-induced cell death. MATERIALS AND METHODS: Chronic myelogenous leukemia (CML) cell line K562 was used. For X-irradiation and drug treatment, cells were plated at approximately 2x10(5) cells/ml. Exponentially growing cells were treated with 10 Gy of X-ray using a 6-MeV X-ray machine at a dose rate of 200-300 cGy/min. The cells were treated with 0.25 microM HMA immediately after irradiation and HMA remained for the entire culture period. The modes of cell death were discriminated by morphological changes, analysis of cell cycle, analysis of the mitochondrial events, and the expression of apoptosis-related proteins. RESULTS: Our data demonstrates that radiation induced a significant time-dependent increase of cell death and failed to sustain a prolonged G2 arrest in K562 cells. Radiation-induced cell death caused the accumulation of cyclinB1 and weak nuclear fragmentation, suggesting a mitotic catastrophe. This mitotic catastrophe was dependent upon the mitochondrial permeability transition pore (PTP) opening and was independent of caspase-3. In contrast, K562 cells treated with radiation and HMA had an accelerated cell death and induced a p53-independent apoptosis. This apoptotic pathway was dependent upon an initial hyperpolarization of the mitochondrial inner membrane, following the release of cytochrome c and subsequent caspase-3 activation. CONCLUSIONS: Two mechanisms of radiation-induced cell death in K562 cells, mitotic catastrophe and apoptosis, are regulated through distinct pathways, mitochondria and caspase-independent and -dependent, respectively. The findings of this study may provide new insights into improving the efficiency of radiotherapy in CML patients.

Epidermal growth factor receptor is related to poor survival in glioblastomas: single-institution experience.

PURPOSE: There are conflicting results surrounding the prognostic significance of epidermal growth factor receptor (EGFR) status in glioblastoma (GBM) patients. Accordingly, we attempted to assess the influence of EGFR expression on the survival of GBM patients receiving postoperative radiotherapy. MATERIALS AND METHODS: Thirty three GBM patients who had received surgery and postoperative radiotherapy at our institute, between March 1997 and February 2006, were included. The evaluation of EGFR expression with immunohistochemistry was available for 30 patients. Kaplan-Meier survival analysis and Cox regression were used for statistical analysis. RESULTS: EGFR was expressed in 23 patients (76.7%), and not expressed in seven (23.3%). Survival in EGFR expressing GBM patients was significantly less than that in non-expressing patients (median survival: 12.5 versus 17.5 months, p=0.013). Patients who received more than 60 Gy showed improved survival over those who received up to 60 Gy (median survival: 17.0 versus 9.0 months, p=0.000). Negative EGFR expression and a higher radiation dose were significantly correlated with improved survival on multivariate analysis. Survival rates showed no differences according to age, sex, and surgical extent. CONCLUSION: The expression of EGFR demonstrated a significantly deleterious effect on the survival of GBM patients. Therefore, approaches targeting EGFR should be considered in potential treatment methods for GBM patients, in addition to current management strategies.

A case of gerstmann-sträussler-scheinker disease.

BACKGROUND: Gerstmann-Sträussler-Scheinker disease (GSS) is a type of human transmissible spongiform encephalopathy (TSE) that is determined genetically. CASE REPORT: A 46-year-old woman presented with a slowly progressive ataxic gait and cognitive decline. She was alert but did not cooperate well due to severe dementia and dysarthria. High signal intensities in the cerebral cortices were evident in MRI, especially in diffusion-weighted images (DWI). A prion protein gene (PRNP) analysis revealed a P102L (proline-to-leucine) mutation in codon 102. CONCLUSIONS: This is the first reported case of GSS (confirmed by PRNP analysis) in Korea. Distinctive MRI findings are also presented.

Pituitary hemorrhage : classification and related factors.

OBJECTIVE: Clinical features of pituitary hemorrhage vary from asymptomatic to catastrophic. The purpose of this study was to evaluate the factors related to severity of hemorrhage of pituitary adenoma. METHODS: Pituitary hemorrhage was noted in 32 of 88 patients who underwent operations between January 2000 and December 2007. Clinical status was classified into group I (no hemorrhage symptoms), II (mild to moderate symptoms without neurological deficit), and III (with neurological deficit), and was compared to radiological, pathological, and operative findings. All patients were operated by transsphenoidal approach, and hemorrhage-related symptoms were relieved. RESULTS: Groups I, II, and III comprised 15, 10 and 7 patients, respectively. In group I, hemorrhage volume was under 1 mL in 11 (73.3%), but, it was above 1 mL in 7 (70%) of group II and in all cases of group III. Hemorrhage stage based on MRI findings was chronic or subacute in 11 (73.3%) of group I, acute in 6 (60%) of group II, and acute or hyperacute in 6 (85.7%) of group III. Pathological examination revealed chronic-stage hematomas in 5 (50%) group II patients. Functioning adenomas were found in 5 (33.3%) group I patients but none in group II or III patients. Silent adenomas were found in 4 (26.7%), 8 (80%), and 3 (42.9%) in groups I, II, and III, respectively. CONCLUSION: Clinical features of pituitary hemorrhage may differ with the radiological and immunohistopathlogical findings. Persistent symptoms are related to the chronic stage of hematoma requiring surgery for symptom relief. Neurological deficits are caused by large amount of acute hemorrhage requiring emergency operation. Silent adenoma is related to the severity of pituitary hemorrhage.

Spontaneous intraorbital hemorrhage: a case report.

Intraorbital hemorrhage is a rare clinical condition caused by orbital trauma, surgery around the orbit, intraorbital vascular abnormalities, and neoplasm. It was reported to occur spontaneously without any known causes and in association with orbital pseudotumor in a very few cases. A 59-year-old, female patient admitted with sudden onset of severe exophthalmos and pain on the left eye. Orbital CT and MR imaging suggested hemorrhage in the upper part of retrobulbar area of the left orbit. Cerebral angiography was taken to rule out any possible vascular abnormalities. On the left carotid cerebral angiography, the run-off of the distal ophthalmic artery was not seen and the engorgement of the supraophthalmic artery was noted. Systemic administration of corticosteroid did not improve the clinical status and craniectomy was done and retrobulbar hematoma was removed, and the clinical symptoms and signs were improved. Authors report a case of spontaneous intraorbital hemorrhage with the clinical features similar to those of orbital pseudotumor, requiring surgical decompression.

Prediction of enophthalmos by computer-based volume measurement of orbital fractures in a Korean population.

PURPOSE: To estimate posttraumatic enophthalmos using computer-based volume measurement of the orbital fracture to provide information on surgical guidelines. METHODS: The fracture volume of orbital wall fractures in 35 patients who did not undergo surgery was measured using a Rapidia work station system. Hertel ophthalmometry, diplopia, and ocular motility were investigated. The fracture volume measurements relative to the intact contralateral orbit were correlated with enophthalmos, diplopia, and ocular motility. Patients were examined at the initial visit, then at 1 week, 1 month, and 3 months. RESULTS: There was a correlation between the fracture volume and enophthalmos. Late enophthalmos increased in size in proportion to the volume of the fractured site. The predicted orbital fracture volume with an enophthalmos measurement of 2 mm or more was 2.30 ml. CONCLUSIONS: Computer-based measurements of orbital fracture volume can be used to predict overall enophthalmos and provide useful information to surgeons.

The increase in hepatic uncoupling by fenofibrate contributes to a decrease in adipose tissue in obese rats.

Fenofibrate is a drug that has been suggested to inhibit weight gain by increasing the catabolism of fatty acid in the hepatic mitochondria. We hypothesized that fenofibrate induces an increase in energy expenditure in the hepatic mitochondria, which results in the reduction of adipose tissue. In this study we measured hepatic uncoupling protein (UCP)-2, -3, core temperatures and abdominal fat composition with MRI in Otsuka Long-Evans Tokushima Fatty rats. The fenofibrate group (n=7) was fed fenofibrate (320 mg/kg) mixed chow. The control group (n=7) was fed chow only. The body weight (531.6+/-7.6 g) of the fenofibrate group was significantly lower than that (744.3+/-14.9 g) of the control group (p<0.005). The areas of visceral and subcutaneous fat in the fenofibrate group (11.0+/-0.9 cm(2), 4.2+/-0.3 cm(2)) were significantly less than those in the control group (21.0+/-0.7 cm(2), 7.4+/-0.4 cm(2)) (p=0.046, respectively). The esophageal and rectal temperatures of the fenofibrate group (37.7+/-0.1 degrees C, 33.1+/-0.2 degrees C) were significantly higher than those of the control group (37.3+/-0.1 degrees C, 32.2+/-0.1 degrees C) (p=0.025, p=0.005). There was de novo expression of UCP-3 in the liver of the fenofibrate group. These data suggest that increased energy dissipation, via hepatic UCP-3 by fenofibrate, contribute to decreased weight gain in obese rats.

Antitumor activity of TRAIL recombinant adenovirus in human malignant glioma cells.

Tumor necrosis factor-Related Apoptosis-Inducing Ligand (TRAIL) has been reported to specifically kill malignant cells but to be relatively nontoxic to normal cells. One of disadvantages to previous in vivo protocols was the need for large quantities of TRAIL recombinant protein to suppress tumor growth. To evaluate the antitumor activity and therapeutic value of the TRAIL gene, we constructed adenoviral vectors expressing the human TRAIL gene (Ad.hTRAIL) and transferred them into malignant glioma cells in vitro and tumors in vivo, as an alternative to recombinant soluble TRAIL protein. The results show that TRAIL-sensitive glioma cells infected Ad.hTRAIL undergo apoptosis through the production and expression of TRAIL protein. The in vitro transfer elicited apoptosis, as demonstrated by the quantification of viable or apoptotic cells and by the analysis of cleavage of poly (ADP-ribose) polymerase. Furthermore, in vivo administration of Ad.hTRAIL at the site of tumor implantation suppressed the outgrowth of human glioma xenografts in SCID mice. These results further define Ad.hTRAIL as an anti-tumor therapeutic and demonstrate its potential use as an alternative approach to treatment for malignant glioma.

Expression of Cell Surface Receptors on Human Glioblastoma Xenograft Model in NOD/SCID Mouse.

PURPOSE: To obtain basic data for development of a glioblastoma-specific immunotoxin, the expression of variable cell surface receptors on a human glioblastoma xenograft model was evaluated, using NOD/SCID mice. MATERIALS AND METHODS: We developed a xenograft model in NOD/SCID mice implanted with a human glioblastoma cell line (U-87MG). Immunohistochemical studies were performed on implanted tumor nodules (n=8) using antibodies against CD71, EGFR, IGF-IRalpha, CXCR4 and IL-4Ralpha. RESULTS: Expression of IL-4Ralpha, in implanted tumornodules, was the highest of the cell surface receptors evaluated in this study. However, the endothelial cells in, and around, the tumor nodules also revealed immunopositivity against IL-4Ralpha. The immunoreactivity of IL-4Ralpha, and other surface receptors such as CD71, IGF-IRalpha and EGFR, was prominent in tumor nodules associated with tumor necrosis. CONCLUSION: IL-4Ralpha would be a possible target for the development of glioblastoma-specific immunotoxin, although there are limitations due to its endothelial expression.