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Biomedical subjects

T Kirino

Publications and source records attributed to T Kirino.

At least 19 recordsLinked to original sources
PubMed2005

Subfrontal schwannoma.

Subfrontal schwannoma is a rare disease, which can be mis-diagnosed as an olfactory meningioma or a neuroblastoma, because of similar clinical symptoms and signs and neuroradiological features. Especially for young subjects, olfactory neuroblastoma should be carefully differentiated, since the management strategies for those lesions are significantly different. The craniofacial approach is often needed for the resection of a neuroblastoma. We report a case of 14-year old boy in which olfactory neuroblastoma was suspected prior to surgery, but turned out to be a schwannoma histologically. Molecular genetic examination revealed neither NF2 gene mutation nor loss of heterozygosity of chromosome 22q, unlike common schwannomas.

Adolescent↗
PubMed2005

Spinal intramedullary ependymal cyst: a case report and review of the literature.

We report a rare case of spinal intramedullary ependymal cyst in a 44-year-old female and reviewed 12 cases reported in the literature. The patient presented with slowly progressive lower limb paresis. She underwent biopsy of the cyst wall and placement of a cysto-subarachnoid shunt with complete recovery at the follow-up examination 18 months after surgery. This is a benign lesion and appropriate management should be performed at an early stage of the disease.

Adult↗
PubMed2004

Resolution of spinal epidural haematoma without surgery in a haemophilic infant.

Non-traumatic spinal epidural haematoma is a rare complication of haemophilia. We report a seven-month-old boy who presented with symptomatic spinal epidural haematoma. He was found to have a hemophilia B trait, and after factor IX replacement, his neurological signs were stabilized and follow-up MRI demonstrated rapid resolution of the haematoma. This illustrative case suggests that surgical intervention can be deferred as the first step in treating spinal epidural haematoma in a haemophilic infant.

Factor IX↗
PubMed2003

Intradural spinal seeding of a clival chordoma.

BACKGROUND: Following recent progress in radiological and surgical techniques for treating skull base tumours, more attention should be paid to the relatively rare phenomenon of intradural spinal seeding in cases of clival chordoma. CASE PRESENTATION: A 53-year-old man harboured intradural spinal seeding from a clival chordoma 11 years after his initial surgical treatment. He had undergone skull base surgery five times with extra- and intradural approaches, and adjuvant radiotherapy. His complaints of lumbago, paraparesis, and sensory disturbance of the lower left extremity prompted us to carry out imaging studies of the spinal cord, which revealed multiple intradural, extramedullary mass lesions at the thoracic and lumbosacral spinal level. The tumours were histopathologically diagnosed as spinal seeding of the clival chordoma with high proliferative potential (Ki-67 labelling index of 8.4%). INTERPRETATION: As long-term local control of skull base chordoma appears to be improving by the introduction of skull base surgical techniques and adjuvant radiotherapy, spinal intradural seeding might emerge as a potential complication. Close observation and timely imaging studies for spinal seeding of skull base chordoma would be required in long-term postoperative follow-ups, particularly for those patients with highly proliferative tumours.

Chordoma↗
PubMed2002

Co-transduction of Apaf-1 and caspase-9 highly enhances p53-mediated apoptosis in gliomas.

Mutation of the p53 gene plays a critical role in the development of cancer and response to cancer therapy. To analyze the mechanism of cancer development and to improve cancer therapy, it is important to assess which genes are downstream components of p53 in cancers, and whether the expression levels of these genes affect p53-mediated apoptosis. In this study, we transduced the wild type p53 gene along with the Apaf-1 and caspase-9 genes via adenovirus vectors into U251 and U-373MG glioma cells harbouring a mutated p53, and evaluated the degree of apoptosis. Co-induction of Apaf-1 and caspase-9 genes highly enhanced p53-mediated apoptosis in glioma cells. Induction of wild type p53 enhanced the expression levels of Bax, p21/WAF1, and Fas protein. To determine which gene is activated by wild type p53 induction and, in turn, activates Apaf-1 and caspase-9, we transduced the Bax, p21/WAF1 or Fas gene via adenovirus vector to U251 cells to achieve a similar expression level as that induced by the Adv for p53 in U251 cells. U251 cells transduced with Fas concomitant with the Apaf-1 and caspase-9 genes underwent drastic apoptosis. This suggests that induction of wild type p53 upregulates Fas, which in turn may play a role in the activation of Apaf-1 and caspase-9. These results are important for analyzing the mechanism of tumour development and for predicting the therapeutic effect of p53 replacement gene therapy in a particular patient.

Adenoviridae↗
PubMed2001

Over-expression of APAF-1 and caspase-9 augments radiation-induced apoptosis in U-373MG glioma cells.

The p53 tumor-suppressor gene plays a critical role in radiation-induced apoptosis. Several genes, including Bax and Fas, are involved in p53-mediated apoptosis, and their over-expression enhances the degree of radiation-induced apoptosis. Apaf-1 and caspase-9 have been reported to be downstream components of p53-mediated apoptosis, suggesting that these genes play a role in radiation-induced apoptosis. In this study, we transduced U-373MG cells harboring mutant p53 with the Apaf-1 and/or caspase-9 genes via adenoviral (Adv) vectors concomitant with X-ray irradiation and evaluated the degree of apoptosis. The percentage of apoptotic cells in U-373MG cells co-infected with the Adv for Apaf-1 (Adv-APAF-1) and that for caspase-9 (Adv-Casp9) and treated with irradiation (24%) was much higher than that in cells co-infected with Adv-APAF-1 and Adv-Casp9 and not treated with irradiation (0.86%) and that in cells infected with either Adv-APAF-1 or Adv-Casp9 and treated with irradiation (2.0% or 2.6%, respectively). The apoptosis induced by co-transduction of Apaf-1 and caspase-9 and irradiation was repressed in cells that were co-infected with the Adv for Bcl-X(L) but not in cells co-infected with the Adv for Bcl-2. These results indicate that Apaf-1 and caspase-9 play a role in radiation-induced apoptosis in cancer cells harboring mutant p53. Bcl-X(L) may be critically involved in the radioresistance of cancer cells by repressing Apaf-1- and caspase-9-mediated apoptosis. Expression of Apaf-1 and caspase-9 in tumors may be an important determinant of the therapeutic effect of irradiation in cancer treatment.

Adenoviridae↗
PubMed2001

Adenovirus-mediated transfer of p53 augments hyperthermia-induced apoptosis in U251 glioma cells.

PURPOSE: Hyperthermia kills glioma cells by inducing apoptosis and is thereby an effective therapeutic modality for the treatment of malignant gliomas. However, cells harboring mutated p53 are refractory to hyperthermia-induced apoptosis. In this study, we assessed whether or not adenovirus (Adv)-mediated transduction of p53 overrides this resistant mechanism. METHODS AND MATERIALS: We transduced the p53 wild-type tumor suppressor gene into U251 glioma cells harboring mutated p53 using Adv vectors in combination with hyperthermia (43, 44.5 degrees C), and evaluated the degree of cell death and apoptosis. RESULTS: The percentage of cells that had died, as measured by trypan blue staining, among U251 cells infected with the Adv for p53 (Adv-p53) and treated with hyperthermia, was significantly higher than the percentage of cells that had died among U251 cells infected with Adv-p53 and not treated with hyperthermia, or those infected with the control Adv for dE (Adv-dE) and treated with hyperthermia. The degree of apoptosis, measured at 24 h after treatment, in hyperthermia-treated U251 cells infected with Adv-p53 (43 degrees C, 73%; 44.5 degrees C, 92%) was much higher than that infected with Adv-p53 (41%), or that infected with control Adv-dE and treated with hyperthermia (43 degrees C, 1.3%; 44.5 degrees C, 19%). Treatment with combined hyperthermia and Adv-p53 infection induced cleavage of caspase-3 in U251 cells. CONCLUSION: These results indicate that Adv-mediated transduction of p53 would render glioma cells highly sensitive to hyperthermia.

Adenoviridae↗
PubMed2001

Expression of smooth muscle proteins in cavernous and arteriovenous malformations.

Cavernous malformations (CVMs) and arteriovenous malformations (AVMs) were immunostained for three smooth muscle cell (SMC)-specific protein markers (smooth muscle alpha-actin, SM1 and SM2). Smooth muscle alpha-actin, a widely used marker of SMCs, is reportedly one of the earliest proteins expressed during differentiation of SMCs and expressed in some kinds of mesoderm-derived cells. In contrast, SM1, an isoform of myosin heavy chain (MHC), is detected only in SMCs. SM2 is another MHC isoform and expressed in the contractile phenotype of SMC. All 14 intraaxial CVMs were positive for smooth muscle alpha-actin, but SM1 was detected in only three of them and SM2 was not found. Their staining pattern resembled that of normal intraparenchymal and pial veins. All 15 cerebral AVMs and 5 out of 6 extraaxial CVMs from the cavernous sinus, orbit and scalp were positive for all three markers, as were the normal cerebral arteries. The venous components of AVMs, as well as the arterial components, expressed SM2, and were different from normal veins in the brain and intraaxial CVMs. This study shows that the histological analysis using the three markers for SMC is useful to differentiate intraaxial CVM from AVM and extraaxial CVMs.

Actins↗
PubMed2001

Incidence of von Hippel-Lindau disease in hemangioblastoma patients: the University of Tokyo Hospital experience from 1954-1998.

BACKGROUND: Incidence of von Hippel-Lindau disease among hemangioblastomas is important clinical information affecting the management of hemangioblastomas. Studies from Western countries reported 36-40% for the incidence, but no report has been made on the Japanese population. METHOD: To investigate the incidence in Japan, we retrospectively analyzed all hemangioblastoma patients treated at The University of Tokyo Hospital from 1954 to 1998. By reviewing medical records and imaging studies, von Hippel-Lindau disease was diagnosed clinically following the currently suggested diagnostic criteria. FINDINGS: There were 82 hemangioblastoma patients recorded during the period, and 14 cases (17%) were compatible with von Hippel-Lindau disease. However, when the incidence was calculated for each of the three 15-year periods, which are 1954-1968 (first), 1969-1984 (second), and 1985-1998 (third), the number increased dramatically in the later periods: 2 of 33 (6%) during the first, 4 of 26 (15%) during the second, and 8 of 22 (36%) during the third period. Such increase occurred after the introduction of whole body CT to our institution in 1981, suggesting that improvement of imaging techniques contributed to the sensitivity of diagnosis. In addition, one recent patient with multiple hemangioblastomas was found to harbor germline mutation of the VHL, thereby being diagnosed as von Hippel-Lindau disease on the basis of molecular genetics. INTERPRETATION: The 40% incidence of von Hippel-Lindau disease in hemangioblastomas suggests that extensive screening for von Hippel-Lindau disease associated neoplasms, and probably molecular genetic examination, is indicated for all patients with hemangioblastomas, which should aim for earlier diagnosis and better management of this devastating hereditary disease.

Adolescent↗
PubMed2001

Clinical features and medical treatment of male prolactinomas.

BACKGROUND: Prolactinomas found in male patients show distinct clinical features compared to those in female patients, which may warrant a different treatment strategy. METHOD: To clarify their clinical features and to evaluate the treatment results, specifically the results of surgical treatment and non-surgical treatment solely with oral bromocriptine, we retrospectively reviewed our experience in male prolactinoma cases. FINDINGS: From 1988 to 1998, we had 184 pituitary adenoma patients, and thirteen of those were male patients with a pure prolactinoma. Of the thirteen patients, eight underwent transsphenoidal surgery followed by oral bromocriptine (surgical group), and five were treated solely with bromocriptine or terguride (non-surgical group). In both groups, the visual symptoms and signs resolved after the treatment, and the serum prolactin levels were normalised with minimal maintenance dose of bromocriptine. Notably, improvement of the visual symptom in the three non-surgically treated patients was observed within a week following the bromocriptine administration. INTERPRETATION: Although surgery would continue to play an important part of treatment in some cases with a large tumour, our experience suggests that drug treatment without surgery can be a safe and effective option in the management of male prolactinoma patients.

Adult↗
PubMed2001

Congestive brain oedema associated with a pial arteriovenous malformation with impaired venous drainage.

We describe two patients with an unruptured pial AVM accompanied by significant brain oedema at initial presentation. In both cases, the primary drainer was a cortical vein showing varicose dilatation. in which venous congestion was indicated by magnetic resonance imaging (MRI). The restriction of venous drainage presumably caused venous hypertension in the surrounding brain, leading to the brain oedema and neurological symptoms. Brain oedema can develop in patients with an unruptured AVM by venous congestion following spontaneous thrombosis of venous components. Varicosity in a major cortical draining vein and a small nidus are the possible lesions predisposing this fairly rare condition for unruptured AVMs.

Adolescent↗
PubMed2001

Tumour suppressor activity of human imprinted gene PEG3 in a glioma cell line.

BACKGROUND: Mouse imprinted gene Peg3 encodes a large C2H2 type zinc finger protein with unique characteristics. Peg3 knockout mice were found to show an impairment in maternal behaviour of the adult female. Mouse Peg3 is located on the proximal region of chromosome 7 which is syntenic to the long arm of human chromosome 19. It has been reported that a loss of heterozygosity (LOH) of chromosome 19q occurs frequently in several glioma types. RESULTS: We isolated human PEG3 cDNA. Both human and mouse PEG3 were strongly expressed in the adult brain and the Peg3 protein was localized in the nuclei of both neurones and glial cells. A significant decrease in PEG3 expression was more commonly observed in glioma cell lines as compared with that in primary cultures of astrocytes. Transfection of PEG3 cDNA in a glioma cell line resulted in a loss of tumorigenicity in nude mice. CONCLUSIONS: The human PEG3 gene is a paternally expressed imprinted gene. Introduction of PEG3 cDNA into the glioma cells suggests that human PEG3 protein functions as a tumour suppressor. Human PEG3 is located on 19q13.4 and is one of the candidates for tumour suppressor genes that are predicted to be sited in gliomas.

5' Untranslated Regions↗
PubMed2001

Successful radiosurgical treatment of lesional epilepsy of mesial temporal origin.

We report a case of successful radiosurgical treatment of lesional epilepsy of mesial temporal origin. A patient presented with a 2-year history of medically intractable complex partial seizures associated with a mesial temporal angioma. Interictal scalp EEG and MEG showed focal epileptiform activity around the lesion. 99mTc-HMPAO-SPECT and 18F-FDG-PET demonstrated depressed blood flow and glucose metabolism in the corresponding temporal lobe. The patient underwent gamma knife radiosurgery for the causative lesion with a low marginal dose of 18 Gy. After treatment, the partial attack ceased without shrinkage of the lesion or peri-lesional parenchymal radiation injury.

Adult↗
PubMed2001

Dendritic cells activate antitumor immunity for malignant intracranial germ cell tumor: a case report.

We report a 22-year-old male patient with a history of intracranial malignant germ cell tumor (GCT) who had undergone tumor resection twice, followed by radiation and chemotherapy. The tumor had rapidly recurred along the entire ventricular wall with extensive invasion into the brain parenchyma. The serum level of human beta-chorionic gonadotropin (beta-hCG) was 232.3 ng/ml on admission. Although tissue samples of the recurrent tumor could not be obtained, the previous histological diagnosis of germinoma and elevated serum beta-hCG levels suggested recurrence of malignant GCT. The patient declined chemotherapy but accepted dendritic cell (DC)-based immunotherapy. DC inoculation five times resulted in rapid tumor shrinkage and a significant decrease in the serum level of beta-hCG. Here we discuss the effectiveness of immunotherapy using DCs for recurrent intracranial malignant GCTs.

Adult↗
PubMed2001

Caspase-9 transduction overrides the resistance mechanism against p53-mediated apoptosis in U-87MG glioma cells.

OBJECTIVE: Conflicting reports have been published with regard to the relationship between the efficacy of p53 gene therapy and the p53 status of gliomas. In this study, we evaluated whether U-87MG glioma cells harboring wild-type p53 and U251 and U-373MG glioma cells harboring mutated p53 demonstrate different sensitivities to p53-induced apoptosis. In addition, we tested whether transduction of Bax or caspase-9, which are downstream components of p53-induced apoptosis, can override the resistance mechanism of U-87MG cells to apoptosis. METHODS: We transduced U-87MG, U251, and U-373MG glioma cells with p53, Bax, or caspase-9 genes via adenovirus (Adv) vectors, to induce the same level of respective proteins, and evaluated the degree of apoptosis. RESULTS: U-87MG cells were highly resistant to Adv for p53 (Adv-p53)-mediated apoptosis, whereas U251 and U-373 cells underwent extensive apoptosis after Adv-p53 infection. In U-87MG cells, the elevation of Bax and Fas was not as marked as that observed in U251 and U-373MG cells after Adv-p53 infection. Endogenous expression of Bcl-XL and Bcl-2 in U-87MG cells was greater than that in U251 and U-373MG cells. U-87MG cells were more resistant to Bax-mediated apoptosis than were U251 or U-373MG cells. In contrast, U-87MG cells were more sensitive to caspase-9-mediated apoptosis than were U251 or U-373MG cells, suggesting that transduction of caspase-9 may override the resistance mechanism of U-87MG to p53-mediated apoptosis. CONCLUSION: These results demonstrate that proapoptotic function induced by p53 transduction in U-87MG cells was repressed at several steps and that induction of caspase-9 may circumvent this resistance mechanism.

Apoptosis↗
PubMed2001

Co-transduction of Apaf-1 and caspase-9 augments etoposide-induced apoptosis in U-373MG glioma cells.

Several apoptosis-related genes have been reported to be involved in chemotherapy-induced apoptosis in cancers. An assessment of the relationship between expression of those genes and the degree of chemotherapy-induced apoptosis may be useful in improving the efficacy of cancer therapy. We transduced Apaf-1 (apoptotic protease-activating factor-1) and caspase-9 into U-373MG glioma cells using adenovirus (Adv) vectors in the presence of etoposide and evaluated the degree of apoptosis. The degree of apoptosis in etoposide-treated U-373MG cells infected with Adv for Apaf-1 (Adv-APAF1) was higher (27%) than that in cells infected with control Adv (14%), that in cells infected with Adv for caspase-9 (Adv-Casp9) was higher (34%) than that in cells infected with Adv-APAF1, and that in cells infected with both Adv-APAF1 and Adv-Casp9 was the highest (41%). Treatment with etoposide increased expression of p53 and decreased expression of Bcl-X(L) in U-373MG cells which harbored mutant p53. These results indicate that the expression of Apaf-1 and caspase-9 may be important determinants in predicting the sensitivity of cancers to chemotherapy. Adv-mediated co-transduction of Apaf-1 and caspase-9 should render cancer cells highly sensitive to chemotherapy.

Adenoviridae↗
PubMed2001

Risk of aneurysm recurrence in patients with clipped cerebral aneurysms: results of long-term follow-up angiography.

BACKGROUND AND PURPOSE: With many patients living long after microsurgical aneurysm clipping for subarachnoid hemorrhage (SAH) and with the evolution of intravascular procedures as less invasive alternatives, knowledge of the long-term results of clipping is becoming important. METHODS: Of 412 patients who underwent clipping of ruptured or unruptured cerebral aneurysms at our institution between 1976 and 1994 and who survived >3 years after surgery, 225 patients who were in good general condition and younger than 80 years were offered follow-up angiography to detect newly formed aneurysms. Of the 225, 80 patients (35.6%) agreed to undergo angiography. In addition, 32 patients underwent angiography for new medical indications other than SAH. Therefore, 112 patients underwent angiography, representing a total of 140 clipped aneurysms. RESULTS: The mean interval from surgery was 9.3 years for all patients and 9.0 years for the clipped aneurysms (range 3 to 21 years). Four aneurysm regrowths were detected of the 140 (2.9%) clipped aneurysms, representing 3 of 125 completely clipped aneurysms, 1 of 14 incompletely clipped aneurysms, and 0 of 1 aneurysm not studied with postoperative angiography. De novo aneurysms were detected in 9 of 112 (8.0%) patients. The annual rate of de novo aneurysm formation was 0.89%. CONCLUSIONS: This study shows that the annual rate of de novo aneurysm formation is relatively high (0.89%) and that the cumulative risk becomes significant after 9 years. In consideration of the fatality rate of SAH, follow-up angiography may be indicated for patients with clipped aneurysms 9 to 10 years after surgery.

Angiography, Digital Subtraction↗