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Biomedical subjects

Junichi Takada

Publications and source records attributed to Junichi Takada.

28 records · Page 2Linked to original sources

[QOL in osteoporotic patients with vertebral fractures].

Vertebral fractures leading to low back pain, spinal deformity, gastroesophageal reflux disease, and cardiopulmonary dysfunctions decrease the quality of life (QOL) in patients with osteoporosis. We had investigated the change of QOL in osteoporosis patients with back pain for 6 months. The relief of the pain improved "activities of daily living" , but did not "leisure, social activities" , "health perception" , "posture, figure" , and "fall, mental factors" . The control of pain and social approach such as fall prevention program are necessary to improve the QOL in patients with vertebral fractures.

Aged↗

Photothrombotic middle cerebral artery occlusion and reperfusion laser system in spontaneously hypertensive rats.

BACKGROUND AND PURPOSE: To establish a less invasive and reproducible focal ischemia model in the rat, we adopted a 2-laser system (ie, photothrombosis and YAG laser-induced reperfusion). METHODS: The distal middle cerebral artery (MCA) of spontaneously hypertensive rats was occluded by 568-nm krypton laser and intravenous infusion of the photosensitizing dye rose bengal and was recanalized by 355-nm ultraviolet laser irradiation. Cerebral blood flow was determined by laser-Doppler flowmetry at the penumbral cortex. Infarct volume was determined at 3 days after distal MCA occlusion. RESULTS: Brain temperature determined with infrared thermography was maintained within an acceptable range of approximately 1 degrees C upper shift of the center of brain temperature distribution during krypton or YAG laser irradiation. The average of the values (23 experiments; n=163) of coefficient of variation of infarct volume was 21+/-6%, indicating high reproducibility of this model. After distal MCA occlusion, cerebral blood flow was decreased to 32+/-16% of the control values and was increased to 98+/-21% after YAG laser-induced reperfusion. Infarct volume in these rats was 61+/-18 mm3 (coefficient of variation=30%; n=6). CONCLUSIONS: We have characterized a highly reproducible focal ischemia model utilizing a 2-laser system, one to induce thrombotic MCA occlusion and the other to facilitate reperfusion.

Animals↗

Vertebral body ischemia in the posterior spinal artery syndrome: case report and review of the literature.

STUDY DESIGN: A case of posterior spinal cord syndrome in which magnetic resonance images showed predominant T2 hyperintense signal in the adjacent vertebral body is reported. OBJECTIVES: To present the case for abnormal bone marrow magnetic resonance signal in the radiologic diagnosis of posterior spinal cord syndrome and to review its significance. SUMMARY OF BACKGROUND DATA: Infarction in the region of posterior spinal arteries has been rarely described. This is attributable not only to the infrequent occurrence of infarction of posterior spinal arteries, but also to a lack of well-established diagnostic procedures. It is of clinical value to define diagnostic images of posterior spinal cord syndrome, especially early in the course of the disease. METHODS: The subject was a 52-year-old man who was presented with acute nontraumatic myelopathy. Magnetic resonance imaging, performed serially after onset of the disorder from 5 hours to 11 months, was evaluated in comparison with neurologic findings. The literature was reviewed to discuss the magnetic resonance images of spinal cord infarction. RESULTS: The neurologic findings were consistent with posterior spinal cord syndrome. A magnetic resonance image taken at 5 hours after onset of the syndrome showed T2 hyperintense signal in the T12 vertebral body. At 3 days after onset, T2 hyperintense signal became obvious in the posterior portion of the spinal cord at T9-T12 vertebral levels. Follow-up magnetic resonance imaging at 41 days, 8 months, and 11 months showed a decrease in the size and intensity of the T2 signal change in the spinal cord and T12 vertebral body. In the literature, T2 hyperintense bone marrow signal was defined in one case of posterior spinal cord syndrome and seven cases of anterior spinal cord syndrome. CONCLUSIONS: Associated bone marrow abnormalities likely reflect the underlying pathology of the blood supply to the vertebral body, and may be an additional key sign for radiologic diagnosis of posterior spinal cord syndrome.

Acute Disease↗

Multiple insufficiency fractures with severe osteoporosis.

Multiple insufficiency fracture is a rare injury. We report a 63-year-old woman who spontaneously developed insufficiency fractures at multiple sites including ribs, sacrum, pubis, ischium, acetabulum, metatarsal bone, and femoral neck. The patient had severe osteoporosis with a bone mineral density of 0.267 g/cm(2), although there was no evidence of bone metabolic disease or metastatic bone tumor. Risk factors for osteoporosis in this case were her postmenopausal state and a history of gastrectomy. Interestingly, the serum level of insulin-like growth factor I, recognized as a growth factor that stimulates bone formation, was markedly decreased, and the patient had had viral hepatitis C. It was speculated that the synergistic effects of these disorders might have produced the osteoporosis, leading ultimately to the multiple insufficiency fractures.

Comorbidity↗

Brain ischemia augments exo-focal transgene expression of adenovirus-mediated gene transfer to ependyma in hypertensive rats.

The ependyma is one of the feasible targets for gene transfer to the brain. Using two different replication-deficient recombinant adenoviral vectors, AdCMVbetaGal or AdRSVIL10, we examined effects of cortical brain ischemia on transgene expression in the ependyma after administration of the vector into the lateral ventricle of spontaneously hypertensive rats (SHR). Expression of the reporter gene lacZ at the lateral ventricle was detected by histochemistry for semiquantitative scoring or by biochemical assay for quantitative analysis. Ependymal cells in the ventricles expressed the transgene as early as 6 h after gene transfer in both sham treatment and ischemia treatment. In the sham treatment, the expression peaked at 12 h and slowly decreased toward day 4 and day 7. However, transgene expressions in the ischemic brain on day 4 and day 7 were significantly higher than sham treatment. In the biochemical assay, beta-galactosidase activity detected on day 4 at the periventricular area of the ischemic group (37 +/- 9 mU/mg protein) was significantly greater than that of the sham group (12 +/- 4, P < 0.01). In the enzyme-linked immunosorbent assay for gene transfer of interleukin-10 (IL-10), IL-10 in the cerebrospinal fluid (CSF) of the ischemic group (11,633 +/- 4322 pg/ml) was significantly greater than that in the sham group (2460 +/- 1486, P < 0.05) on day 5. These results suggest that transgene expression in the exo-focal remote area of ependyma is augmented by cortical ischemia, and the ependyma may be a promising target of gene transfer of brain ischemia.

Adenoviridae↗

Adenovirus-mediated gene transfer to ischemic brain is augmented in aged rats.

Gene therapy may be a promising approach for the treatment of brain ischemia. Because older populations are susceptible to ischemic stroke, we examined the effects of aging on adenovirus-mediated gene transfer to the ischemic brain of rats. Brain ischemia was produced by photochemical occlusion of the distal middle cerebral artery of aged and adult spontaneously hypertensive rats. Ninety minutes after ischemia, an adenoviral vector encoding beta-galactosidase was injected into the contralateral (C) and ipsilateral [peri-ischemic (I-p) and ischemic core (I-c)] parietal cortices. Cerebral blood flow (CBF) was measured by laser Doppler flowmetry. Transgene expression was scored semiquantitatively as an expression score by histochemistry and also quantitatively analyzed by chemiluminescence assay. Changes in CBF after ischemia in aged rats were not significantly different from those in adult rats, although the infarct rim in the older rats tended to be closer to the midline than in the younger rats. beta-galactosidase was detected in both neurons and non-neuronal cells at C and I-p, and was primarily present in non-neuronal cells at I-c. The expression scores 1 and 4 days after ischemia in the aged rats were similar to those in the adult rats. However, the score for the I-c at 7 days after injection was significantly greater in the older rats than in the younger adult rats. beta-galactosidase activity at I-c 7 days after ischemia in the aged rats (8.0+/-1.7mU/mg protein) was significantly greater than that in the adult rats (1.3+/-0.4, p<0.01). Adenovirus-mediated gene transfer to the ischemic brain may thus be more effective in aged rats than in adult rats.

Adenoviridae↗

Osteoporosis in 5 elderly women with pubic osteolysis.

5 elderly women developed pubic osteolysis after spontaneous fracture of the pubic bone. Radiographs showed gradual progression of the osteolysis, followed by callus formation, and bone union after 4-5 months. Bone mineral density was low in all patients. White blood cell count, erythrocyte sedimentation rate, and C-reactive protein were normal. Urine deoxypyridinoline was high, but serum osteocalcin normal. Elderly women with spontaneous fractures and osteolysis of the pubic bone should be considered for evaluation of osteoporosis and treatment.

Aged↗

Long-term effects of benidipine on cerebral vasoreactivity in hypertensive rats.

We tested the hypothesis that long-term application of a Ca2+ channel blocker would ameliorate the functional and morphological deterioration of the cerebral arteries during hypertension. Male spontaneously hypertensive rats (SHR) were fed a standard rat chow, containing a low (3 mg/kg/day) or high dose (6 mg/kg/day) of benidipine, a Ca2+ channel blocker, for 2 months. Using a cranial window, we examined responses of the basilar artery to acetylcholine, sodium nitroprusside, (-)-(3S,4R)-4-(N-acetyl-N-hydroxyamino)-6-cyano-3,4-dihydro-2,2-dimethyl-2H-1-benzopyran-3-ol (Y-26763; an opener of ATP-sensitive K+ channels), and (R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide (Y-27632; an inhibitor of Rho-associated kinase). Mean arterial pressure of the control group was 193+/-5 mm Hg (mean+/-S.E.M.), while that of the low-dose benidipine group was 183+/-5 mm Hg and that of the high-dose group was 159+/-4 mm Hg. Dilator responses of the basilar artery to acetylcholine and Y-26763 were impaired in SHR compared with those of normotensive Wistar-Kyoto (WKY) rats and treatment with benidipine enhanced the vasodilator responses to acetylcholine and Y-26763 in SHR. Y-27632-induced dilatation of the basilar artery was enhanced in SHR compared to that in WKY rats and the vasodilatation was reduced by benidipine in SHR. Sodium nitroprusside caused similar dilatation of the basilar artery, in both WKY rats and the SHR control group, and benidipine did not affect nitroprusside-induced dilatation of the artery in SHR. The wall of the basilar artery was significantly thicker in SHR than in WKY rats and benidipine treatment reduced the wall thickness of the artery in SHR. These findings suggest that chronic treatment with a Ca2+ channel blocker may enhance the dilator capacity and reduce contractility of the basilar artery during hypertension. Benidipine may also ameliorate the morphological changes of the basilar artery in hypertension.

Acetylcholine↗

Fatigue subcapital fracture of the femur after the removal of the hip plate in transtrochanteric rotational osteotomy.

We report two cases of fatigue subcapital fracture of the femur after the removal of the hip plate used for fixation in transtrochanteric rotational osteotomy for osteonecrosis. Two patients, a 42-year-old man and a 43-year-old man, underwent transtrochanteric rotational osteotomy, and bony union was achieved in both patients. However, fatigue subcapital fracture of the femur occurred in both patients 15 months after the removal of the hip plate. Transtrochanteric rotational osteotomy greatly changes the trabecular bone structure in the proximal femur, thus affecting the strength of the femoral neck. Therefore, for the trabecular bone to be remodeled and for the proximal femur to achieve sufficient strength, a sufficient period is necessary after complete bony union has occurred in the transtrochanteric lesion, before removal of the plate.

Adult↗

Brain ischemia as a potential target of gene therapy.

Brain infarction is one of the most important age-associated medical conditions, and the age-related neuronal vulnerability to brain ischemia is suggested to play an important role. Recent advancements in gene transfer techniques have provided promising approaches to the treatment of brain ischemia. In experimental studies, the ischemic penumbra area can be targeted by gene transfer even after ischemic insult, and post-ischemic gene therapy seems effective in attenuation of ischemic damage in both global and focal brain ischemia. Perivascular approaches of gene transfer to the cerebral blood vessels through the subarachnoid space may lead to prevention of brain ischemia caused by vasospasm after subarachnoid hemorrhage. Gene transfer to cerebral blood vessels and ischemic brain tissue may offer future therapeutic approaches to stroke.

Adenoviridae↗