Biomedical subjects
Publications and source records attributed to T Kitahara.
A patient who lost consciousness and had a convulsion caused by brain ischemia during balloon inflation in connection with percutaneous transluminal angioplasty was successfully treated with a continuous-perfusion dilatation catheter without complications.
A 39-year-old Japanese woman had been receiving propylthiouracil for 5 years for hyperthyroidism when she developed myalgia, scleritis, proteinuria, fever, and inflammation of the nose. Examination of a renal biopsy specimen showed focal segmental necrotizing glomerulonephritis. Indirect immunofluorescent staining showed a highly positive perinuclear pattern of anti-neutrophil cytoplasmic antibody (ANCA) in her serum. Enzyme-linked immunosorbent assay (ELISA) of the ANCA showed positivity for anti-proteinase 3, anti-myeloperoxidase, anti-leukocyte elastase, and anti-lactoferrin, but anti-cathepsin G and anti-lysozyme were negative. Because ELISA showed the titer of anti-leukocyte elastase antibody to be markedly elevated, we challenged this data by performing dot blot analysis. The patient's serum reacted with the native form, but not with denatured leukocyte elastase. Propylthiouracil-induced vasculitis was suspected. Symptoms abated within 2 weeks and all values of ANCA were reduced after the drug was withdrawn. Vasculitis is a rare side-effect of propylthiouracil therapy. Recently it was reported in association with ANCA. We present the findings of this patient and compare them with those described in 19 published cases of propylthiouracil-induced vasculitis associated with ANCA.
Stereotactic radiosurgery, a rapidly evolving technology, provides precise high-dose irradiation to brain lesions and tumors. A new method using digital subtraction angiographic images of a personal computer-image display terminal interfaced to our picture archiving and communication system (PACS) performs measurements and calculations of the coordinates of the location of the center of the lesion to be treated. The time required to calculate the coordinates was performed by three methods: hand calculation, digitizer method, and PACS method. These three coordinates were compared in 10 cases. The hand calculation method required approximately 50 minutes, the digitizer method required approximately 10 minutes, and the PACS method approximately 3 minutes. The difference is statistically significant (P < .001). The three methods were equally accurate. This type of PACS application using inexpensive personal computers interfaced more directly to a PACS is an emerging trend that facilitates wider access to images and to manipulating them for specialized applications.
The differential display method was applied to identify gene expression which is especially up-regulated in the rat denervated skeletal muscle. Total RNA from normal and denervated facial muscles was isolated, amplified by PCR using certain primers, and separated by electrophoresis on polyacrylamide gel. PCR products which were apparently higher in the operated than in the control side were cut out from the gel and subsequently sequenced. One of the cDNA fragments obtained in the present study showed about 80% identity in nucleotide sequence and about 84% identity in amino acid sequence to one of the NADH: ubiquinone oxidoreductase (complex I) subunits from the bovine heart mitochondria (813). Complex I, the first and largest enzyme of the mitochondrial respiratory chain, transfers electrons from NADH to ubiquinone-10 (UQ-10). B13 is a 13 kDa subunit; deficiency of which causes incomplete or incorrect assembly of a functional complex I, resulting in one of the types of human mitochondrial myopathy. Northern blot analysis and in situ hybridization histochemistry confirmed that rat B13 mRNA expression was up-regulated after denervation and was distributed throughout whole muscle cell body. These findings suggest that up-regulation of the rat B13 mRNA expression after denervation plays an important role in the effective electron transfer from NADH to UQ-10 in skeletal muscle cells, resulting in restriction of lipid peroxidation and biological tissue damage.
The purpose of the present study was to obtain quantitative values for human skull structures in a cross-sectional analysis of offspring and their parents. The offspring were classified into three groups according to age. For each of 11 maxillo-facial and nine dento-alveolar structural angular measurements, the mean and SD were calculated for each set of paternal, maternal, midparent and offspring. The standard deviation unit (SDU) values were calculated from the disparity between the measured value in a given individual, i.e. father, mother, midparent, offspring, and their corresponding group mean value. Three disparity values (D.v.), expressed by the difference between the SDU values in each pair (father-offspring, mother-offspring and midparent-offspring), were developed to evaluate the degree of familial resemblance for each of 20 morphometric measurements, and the differences among these values in three age groups were then investigated. The similarity ratio (S.r.), expressing the degree of correlation to the father and mother, was derived by processing the D.v. The relationship between the maxillo-facial S.r. and the dento-alveolar S.r. was analysed in each age group. There were significant differences between the D.v. in families and those in unrelated control groups. Consistency between the S.r. for maxillo-facial and that for dento-alveolar measurements was found in the older age groups. It is concluded that individual growth of skull morphology might be more predictable using the present method.
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The purpose of this study was to evaluate hemodynamic compromise in terms of baseline CBF and CRC in patients with chronic cerebral occlusive lesions and its modulation by a superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis. The study subjects were 10 healthy volunteers and 49 chronic ischemic patients with stenosis or occlusion of the internal carotid artery (ICA) or middle cerebral artery (MCA). The hemodynamics were measured using stable xenon enhanced computed tomographic CBF measurement with the acetazolamide challenge. The compromised hemodynamics in patients with chronic steno-occlusive lesions did not improve during their natural course after two months. STA-MCA bypass modulated hemodynamic compromise in the ischemic patients. We recommend STA-MCA bypass for patients with reduced CRC, regardless of whether baseline CBF is reduced or normal. Hemodynamic classification using a combination of baseline CBF values and CRC values is useful for evaluating cerebral hemodynamics and for choosing the best treatment for cerebral ischemia with occlusive lesions.
The purpose of this study was to evaluate hemodynamic compromise in the patients with moyamoya disease and surgical modulation of the hemodynamics using stable xenon enhanced computed tomographic CBF measurement with the acetazolamide challenge. The study group consisted of 15 preoperative cases and 17 postoperative cases. In the preoperative group, regional resting cerebral blood flow (rCBF) and regional cerebrovascular reserve capacity (rCRC) were reduced. The reduction was more prominent in the anterior circulation than in the posterior circulation. In the postoperative group, rCBF and rCRC were still low in the anterior circulation. Revascularization increased the resting CBF but did not change the CRC. Postoperative CBF did not increase in adults but increased in children. These findings suggest that the misery perfusion state may be present only in the child's brain. Measurement of CBF and CRC is useful to evaluate the hemodynamics of moyamoya disease.
Successful revascularization improves ischemic symptoms in the pediatric patients with moyamoya disease. However, it is not clear whether the revascularization prevents future intracranial hemorrhage from the residual moyamoya vessels. The purpose of this study is to investigate perioperative morphological and hemodynamic changes in the moyamoya vessels. Four pediatric patients (age < 15 years old) with bilateral moyamoya disease were selected for this study. To quantify the number of moyamoya vessels, T1-weighted transverse images at the level of the basal ganglia and the thalamus were selected and characteristic flow voids in the lentiform nucleus were counted. Resting CBF and cerebrovascular reserve capacity (CRC) were measured pre- and 1 year after surgery using Xenon-CT CBF method with acetazolamide test. The ratio of deep CBF/cortical CBF was calculated as an index of hemodynamic stress distribution. The one-year follow-up studies showed that 1) the number of moyamoya vessels decreased on the operative side, but did not change on the non-operative sides in all cases; 2) the ratio of deep CBF/cortical CBF decreased on the operative sides, but did not change in the non-operative sides; and 3) the CRC increased on both sides. This observation suggests the possibility that revascularization surgery may be effective for preventing the future risk intracranial hemorrhage.
Most of patients with cerebrovascular disease are associated with hypertension. Hypertension induces progressive atheromatous changes in cerebral arteries, and often causes steno-occlusive lesions of cerebral arteries. Angiotensin converting enzyme (ACE) inhibitor cilazapril is one of the antihypertensive drugs. It was reported that cilazapril improved resting cerebral blood flow (CBF) and cerebrovascular reserve capacity (CRC) in experimental studies. In this clinical study, the authors investigated whether long-term treatment with cilazapril could improve CBF and CRC in patients with steno-occlusive lesions of the major cerebral arterial trunk, measured by stable xenon computerized tomography (Xe-CT) with acetazolamide challenge. On the other hand, CBF and CRC in the calcium blocker-treated patients were measured in the same way. CBF did not change after long-term treatment with both cilazapril and calcium blocker. In the cilazapril-treated group, CRC was increased significantly (p < 0.05). However, CRC did not change in the calcium blocker-treated group. It was recognized that long-term treatment with cilazapril did not decrease CBF and improved CRC in patients with occlusive lesions of the major cerebral arterial trunk.
The effects of sodium bicarbonate on cerebral blood flow (CBF) and intracellular pH were studied in five normal volunteers. CBF and intracellular pH were measured by stable xenon computed tomography and phosphorus-31 magnetic resonance spectroscopy (31P-MRS) respectively. Each patient received 7% sodium bicarbonate (3.5 ml/kg body weight) infused intravenously for 15 minutes. Before and after this injection, CBF intracellular pH and physiological parameters were measured. CBF and PaCO2 were significantly increased. On the other hand, hematocrit and intracellular pH were decreased. These result suggests that three factors are thought to contribute to increase CBF during administration of sodium bicarbonate in humans: 1) arterial dilatation in response to carbon dioxide 2) an decrease of hematocrit 3) intracellular acidosis.
Cerebral blood flow (CBF) is usually decreased in patients with hypertensive putaminal hemorrhage (HPH). However, there are few reports concerning cerebrovascular reserve capacity (CRC) in these cases. This study evaluated cerebral hemodynamics in patients with HPH by measuring CBF and CRC. CBF and CRC were measured by stable xenon enhanced computed tomography (Xe-CT) in 11 patients with HPH (HPH group) and 11 patients with essential hypertension without intracerebral hematoma (non-HPH group). CBFs of the hemisphere and thalamus in the HPH group were lower than those in the non-HPH group. And the CBF of the hemisphere was increased transiently after the surgical evacuation of the hematoma. Thereafter, it fell gradually. The CRCs were also lower in acute stage of the HPH group. The CRC recovered during the chronic stage. Hemodynamics in patients with HPH can be modulated by surgical removal of hematoma. However, some adjunct therapies are necessary to prevent delayed neuronal inactivity, Stable Xe-CT with acetazolamide test is useful to evaluate hemodynamics in the HPH patients.
Two cases of bilateral Lermoyez's syndrome and one case of unilateral Lermoyez's syndrome are reported. The patients had recurrent episodes of vertigo with improvement of hearing or tinnitus, which is characteristic is Lermoyez's syndrome. In case 1, a 48-year-old female, dehydration with glycerol or furosemide induced nystagmus and improved bilateral hearing and the gain of the vestibulo-ocular reflex, while overhydration with drinking water impaired bilateral hearing with disappearance of nystagmus. These findings indicate that she had endolymphatic hydrops in both ears, suggesting that simultaneous changes in bilateral cochlear and vestibular function induce Lermoyez's syndrome. In case 3, a 52-year-old female, which we already reported, endolymphatic collapse in both ears may have changed bilateral inner ear function, resulting in Lermoyez's syndrome. On the other hand, patients 2, a 47-year-old male, experienced a vertigo attack with improvement of unilateral hearing after defibrinogenation therapy. In this case, slowly developing insufficiency of the inner ear blood supply may have caused the gradual hearing loss. It seemed that decreasing blood viscosity by defibrinogenation allowed blood to rush into the labyrinth, causing vertigo but at the same time improving hearing. We proposed that there are two types of Lermoyez's syndrome, bilateral (cases 1 and 3) and unilateral (case 2).
Unilateral labyrinthectomy (UL) causes ocular and postural asymmetries, which disappear over time in the processes of equilibrium recovery known as vestibular compensation. It has been reported that N-methyl-D-aspartate (NMDA) receptors are involved in vestibular compensation. In the present study, in order to elucidate the NMDA receptor-mediated neural circuit responsible for the development of vestibular compensation, we used Fos expression as a marker of neural activation and examined the effects of MK801, a specific antagonist of NMDA receptors, on UL-induced Fos expression in the rat brainstem. After UL, Fos-like immunoreactive (-LIR) neurons were observed in the ipsilateral medial vestibular nucleus (ipsi-MVe), the contralateral prepositus hypoglossal nucleus (contra-PrH) and the contralateral inferior olive beta subnucleus (contra-IOb). Fos-LIR neurons gradually disappeared in the processes of vestibular compensation. It is suggested that the activation of the ipsi-MVe, the contra-PrH and the contra-IOb neurons after UL are the initial event of vestibular compensation. Intraperitoneal injection of MK801 in the processes of vestibular compensation caused reappearance of UL-induced behavioral deficits. During the decompensation induced by MK801, Fos-LIR neurons appeared in the contra-MVe, the ipsi-PrH and the bilateral-IOB. It is suggested that the contra-MVe, the ipsi-PrH and the bilateral-IOb neurons are inhibited by glutamatergic synapses driving inhibitory neurons via NMDA receptors in the processes of vestibular compensation and that disinhibition of these nuclei induced by MK801 causes decompensation. However, MK801 caused neither Fos expression nor behavioral decompensation after vestibular compensation is accomplished. All these findings that the NMDA receptor-mediated inhibitory modulation in the central vestibular system plays an important role for the initial processes of the development of vestibular compensation.
There has been controversy regarding the best treatment for acute intracerebral hemorrhage. Early surgical evacuation alone seems to provide only limited amelioration of this condition, and additional therapeutic strategies should be investigated to obtain a better outcome. To test the feasibility of post-evacuation treatment, basic fibroblast growth factor (b-FGF) was administered into the evacuated cavity and its effect was evaluated in terms of the pathological changes around the lesion. A transient (10 min) intracerebral mass lesion was created by inflation of a microballoon in the caudate nucleus in rats. Basic-FGF (500 or 1000 ng) was injected into the evacuated cavity after deflation and removal of the balloon, and then histological changes were evaluated in the CA1 subfield of the hippocampus and cavity wall. The results demonstrate a protective effect against the neuronal damage in CA1 pyramidal cells and an increase of angiogenesis in the evacuated cavity wall after b-FGF administration. These observations suggest that local administration of b-FGF after evacuation may prevent secondary neuronal damage in the area surrounding an acute mass lesion and facilitate more rapid repair of the damaged brain.
BACKGROUND: Neuron-specific enolase (NSE) and myelin basic protein (MBP) in the peripheral venous blood (PVB) have been reported to be sensitive markers for judging the prognosis of patients with head injury. However, to our knowledge, the levels of NSE and MBP in the internal jugular venous blood (IJVB) have never been studied. METHODS: In 25 patients with acute head injury, blood samples were taken from the internal jugular vein and the peripheral vein at the same time before any medical or surgical procedure was performed. The levels of NSE and MBP in the both venous blood samples were measured. The time interval between injury and sampling was 1.5-8.0 hours (mean 4.3 hours). The levels of NSE and MBP in the IJVB were compared to those in the PVB. The relationship between the clinical outcome and the serum levels of those was evaluated. RESULTS: The levels of NSE and MBP in the IJVB were almost equal to those in the PVB. The levels of NSE and MBP were significantly higher in the patients who died than in those who survived. In the survivors, the levels of NSE and MBP in the IJVB were 17.6 +/- 11.4 ng/ml and 1.4 +/- 1.5 ng/ml, whereas in the patients who died, both levels were elevated to 51.3 +/- 27.3 ng/ml (p < 0.005) and to 11.3 +/- 9.5 ng/ml (p < 0.01), respectively. CONCLUSIONS: The assay of serum NSE and MBP levels provides a reliable laboratory indicator of the degree of brain damage and allows early prediction of the prognosis in patients with acute head injury.
The efficacy and cost/performance benefit of radionuclide bone scintigraphy in monitoring metastatic bone activity remain controversial. Recently developed bone metabolic markers are expected to play an additional role in the diagnosis of bone metastasis. We measured osteoclastic and osteoblastic markers in 267 patients with breast cancer (100 with bone metastasis), 38 patients with prostatic cancer (25 with bone metastasis), 50 patients with lung cancer (12 with bone metastasis) and 33 patients with miscellaneous cancers (13 with bone metastasis) and compared the values in the presence and absence of bone metastasis. Bone metabolic markers, both osteoclastic and osteoblastic, increased significantly in patients with bone metastasis. In breast cancer (bone metastasis is mostly of the mixed type), osteoclastic markers were good in detecting bone metastasis. In prostatic cancer (bone metastasis is mostly osteoblastic), osteoclastic and osteoblastic markers were equally effective in detecting bone metastasis. In lung cancer (bone metastasis is mostly osteolytic), osteoclastic markers were elevated preferentially in bone metastasis. Over all, osteoclastic markers were more sensitive in the diagnosis of bone metastasis, and among osteoclastic markers, serum pyridionoline-cross-linked carboxyterminal telopeptide was the most efficient in both specificity (91.0%) and sensitivity (48.6%) for detecting bone metastasis.