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Biomedical subjects

Y Terayama

Publications and source records attributed to Y Terayama.

At least 19 recordsLinked to original sources

Cabergoline scavenges peroxynitrite enhanced by L-DOPA therapy in patients with Parkinson's disease.

Long-term or high-dose L-DOPA therapy in patients with Parkinson's disease (PD) may accelerate degeneration of dopaminergic neurons, possibly by increasing oxidative stress. To investigate the effects of cabergoline on peroxynitrite-mediated oxidative damage caused by L-DOPA, the concentration of 3-nitrotyrosine in cerebrospinal fluid (CSF) of 18 PD patients was compared with that in 20 normal controls. The concentration of 3-nitrotyrosine in patients following L-DOPA therapy was significantly higher than in untreated PD patients and controls. On the other hand, the concentration in PD patients after cabergoline therapy was significantly lower than in PD patients after L-DOPA therapy alone. These data suggest that cabergoline scavenges peroxynitrite induced by L-DOPA in patients with PD.

Aged↗

Perivascular infiltrate of memory lymphocytes and mature dendritic cells in MG thymomas.

In thymomas associated with myasthenia gravis (MG), the authors found that perivascular infiltrates of memory lymphocytes and mature dendritic cells (DCs) were more frequent in patients with early improvement after thymectomy than in patients without response to thymectomy. Although these findings may be limited to particular types of thymoma, thymectomy may interrupt the recruitment of mature DCs in thymus and export of activated T cells to extra-thymic tissues, thereby improving the disease.

Aged↗

Expression of cholesteryl ester transfer protein (CETP) in germinal centre B cells and their neoplastic counterparts.

AIMS: Cholesteryl ester transfer protein (CETP) is known to facilitate the transfer of lipids between plasma lipoproteins. Previous studies on human tissues have determined that the spleen contains large amounts of CETP mRNA, while the exact location of CETP in such organs remains unknown. In the present study, our aim was to locate CETP protein expression at the cellular level in human normal and neoplastic lymphoid organs. METHODS AND RESULTS: In-situ hybridization (ISH) and immunohistochemistry were applied to pathology specimens. A specific rabbit anti-CETP antibody was used for immunohistochemical analysis, together with another CETP-specific monoclonal antibody. A riboprobe for ISH was derived from CETP cDNA. Immunohistochemically, CETP was localized in germinal centre B cells and a proportion of marginal zone B cells. ISH showed that CETP mRNA was located mostly in the same areas. When 141 malignant lymphomas of various subtypes were studied, high expression of CETP, equivalent to that found in normal germinal centre B cells, was demonstrated in lymphoma subtypes that are currently regarded as the neoplastic counterparts of primarily germinal centre B cells. CONCLUSION: CETP localizes B cells in germinal centres, a proportion of post-germinal centre B cells and their neoplastic counterparts.

Animals↗

Myeloperoxidase-antineutrophil cytoplasmic antibody-associated sensorineural hearing loss.

A 36-year-old female with hyperthyroidism that had been treated with propilthiouracil (PTU) complained of tinnitus and hearing loss in both ears. She was treated with steroid administration by an otolaryngologist; however, hearing continued to fluctuate when the steroids were tapered. Laboratory evaluation revealed a decreased complement level and elevated levels of immunoglobulin M (IgM) and myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA). With the withdrawal of PTU and high-dose methylprednisolone, she had excellent return of right-sided hearing. In recent years, there have been many reports about MPO-ANCA-associated small vessel vasculitis. Although any organ may be affected by this disease, there are no reports about MPO-ANCA-associated progressive hearing loss without any other organ involvement. The present case suggests the possibility that inner ear blood flow impairment due to ANCA-associated small vessel vasculitis induces the so-called autoimmune sensorineural hearing loss.

Adult↗

Springtime pollinosis and oral allergy syndrome in Sapporo.

OBJECTIVE: The purpose of this present study was to investigate pollinosis in the spring and oral allergy syndrome (OAS) in Sapporo to utilize it for future treatment. MATERIALS AND METHODS: Of the patients referred to our out-patient clinic during April and May in 1999. all those that were suspected to have pollinosis were asked to fill in a questionnaire. A 101 patients (30 males and 71 females) with a mean age of 33 years (range 7-74 years) answered the questionnaire. In all, the patients specific IgE tests were performed. RESULTS: The most common allergen was birch, affecting 54 of 87 patients (62%). In 61% of patients with birch allergy, we observed fruit and vegetable allergy. Among them, apple was the most prevalent allergen (97%), followed by peach (67%), cherry (58%), pear (40%), plum (40%) and melon (33%). The sensitivity of skin prick test with commercial extract to apple was low (11%). CONCLUSION: Patients with birch pollen allergy had OAS much more frequently than ever reported in Japan, although OAS has not widely been known in Japan. Patients with birch pollen allergy should be informed about the possibility of hypersensitivity to certain fruits.

Adolescent↗

Development of a novel, weighted, quantifiable stroke scale: Japan stroke scale.

BACKGROUND AND PURPOSE: Several stroke scales are available for estimation of the severity of stroke, but none of them provides information regarding the relative weights of the observed variables. To define an integrated severity of stroke, we developed a quantifiable stroke scale with weighted variables that apply conjoint analysis to calculate the relative weight of each item. METHODS: We selected 10 variables (consciousness, language, neglect, hemianopsia, gaze, pupillary abnormality, facial palsy, plantar reflex, sensation, and weakness) based on the multivariate analysis of the Keio Stroke Patient Database Battery. The variables were categorized and evaluated for their distribution and sensitivity. The categorizations were then modified and rechecked. The procedure was repeated until the appropriate categorization was obtained from 198 patients. A temporary stroke scale without weight was then formulated, and the reliability of the scale was examined and revised with 80 new stroke patients. As a next step, 150 neurologists were asked to rank a set of 27 virtual patients, each with a different combination of variables, according to severity. From these rankings, conjoint analysis was used to derive utility scores (weights) for each factor level. RESULTS: The relative weights of each of the factors were as follows: consciousness 49.8%, language 9.9%, weakness of lower extremity 7.3%, pupillary abnormality 6.8%, gaze palsy 5.6%, weakness of arm 4.3%, weakness of hand 3.7%, neglect 3.7%, facial palsy 2.4%, plantar reflex 2.2%, hemianopsia 2.2%, and sensory impairment 2.1%. The total score for a patient could be calculated from the sum of the scores for each of the variables ranging from -0.38 to 27.86. Scoring of 100 patients with acute stroke was carried out, and the changes in scores were followed for validation. Longitudinal clinical monitoring of the patients correlated well with the scores in each patient. The interrater and intrarater reliabilities of the scale were excellent (weighted kappa 0.83; Cronbach's alpha 0.998). CONCLUSIONS: The Japan Stroke Scale is a parametric stroke scale that provides a quantitative measure of the severity of stroke. Each of the variables of the scale has a relative weight according to the severity of stroke. Reliability and responsiveness were proved to be excellent. The present data revealed a potentiality for the Japan Stroke Scale to be a universally accepted and reliable standardized system from the clinimetrical point of view.

Acute Disease↗

P-ANCA-positive Wegener's granulomatosis presenting with hypertrophic pachymeningitis and multiple cranial neuropathies: case report and review of literature.

An autopsy case of hypertrophic pachymeningitis and multiple cranial neuropathies is reported. A 53-year-old woman with paraplegia and various neurological signs which developed over a 2 year period was diagnosed as having an epidural mass with thickened dura mater extending from the lower cervical to the thoracic spinal cord. In addition, bilateral episcleritis, blephaloptosis, and blindness of the right eye with various cranial nerve deficits were found to be caused by the mass lesions involving the paranasal sinuses, orbit, and the cavernous sinus. Perinuclear antineutrophil cytoplasmic antibody (p-ANCA) was positive, but cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) was negative by enzyme-linked immunosorbent assay. The partially removed epidural mass with hypertrophied dura mater and biopsy of the paranasal lesions showed chronic granulomatous inflammation with vasculitis. The remaining lesions resolved with steroid therapy with remarkable neurological improvement. The positive p-ANCA test, paranasal involvement, the report of a similar histopathological case and a review of the literature on granulomatous pachymeningitis suggest the presence of p-ANCA-positive Wegener's granulomatosis with central nervous system involvement characterized by hypertrophic pachymeningitis and/or multiple cranial neuropathies.

Antibodies, Antineutrophil Cytoplasmic↗

Risk factors accelerating cerebral degenerative changes, cognitive decline and dementia.

OBJECTIVES: Factors accelerating cerebral degenerative changes represent potentially modifiable risks for cognitive decline. Putative risk factors accelerating subtle cognitive decline and dementia were correlated with repeated measures of cerebral atrophy, CT densitometry, perfusions and cognitive testing among neurologically and cognitively normative ageing volunteers. METHODS: Two hundred and twenty-four normative subjects at increased risk for cognitive decline were admitted to the study. Mean entry age was 59. 5+/-15.8 years. Mean follow-up is 4.3+/-3.1 years. At follow-up, 22 developed subtle cognitive decline (deltaCCSE>/=-3), 19 became demented, eight with vascular type (VAD) and 11 with Alzheimer's type (DAT) and 183 remain cognitively unchanged. Standardized questionnaires, medical, neuropsychological, neurological and blood work examinations were obtained. Cerebral atrophy, tissue densities and perfusions were measured by xenon-enhanced CT. RESULTS: After age 60, cerebral atrophy, ventricular enlargement, polio- and leuko-araiosis geometrically increased as perfusions declined. Risk factors accelerating perfusional decline, cerebral atrophy, polio-araiosis and leuko-araiosis (thinning of grey-white matter densities) were: transient ischaemic attacks (TIAs), hypertension, smoking, hyperlipidemia, male gender. At age 71.5+/-11.9, subtle cognitive decline began, accelerated by TIAs, hypertension and heart disease. Leuko-araiosis began before cognitive decline. TIAs, hypertension and hyperlipidemia correlated with VAD. Excessive cortical perfusional decreases and cerebral atrophy correlated with cognitive decline. Family history of neurodegenerative disease correlated with DAT. CONCLUSION: TIAs, hypertension, hyperlipidemia, smoking and male gender accelerate cerebral degenerative changes, cognitive decline and dementia.

Adult↗

[Short interval change of 99mTc-ethyl cysteinate dimer single photon emission computed tomography in Wilson's disease].

We studied short interval change of cranial computed tomography (CT), magnetic resonance imaging (MRI) and 99mTc-ethyl cysteinate dimer single photon emission computed tomography (99mTc-ECD SPECT) in a case of Wilson's disease. Before treatment, CT scan showed low density changes in the bilateral thalamus and basal ganglia, and MRI demonstrated high intensity in same lesions. 99mTc-ECD SPECT study revealed a hypoperfusion in bilateral thalamus. After 2 months under D-penicillamine therapy, neurological findings had improvement. Hypoperfusion in the thalamus with 99mTc-ECD SPECT significantly improved, whereas abnormal findings of CT scan and MRI persisted. 99mTc-ECD SPECT study may be useful for the planning of the treatment of Wilson's disease.

Adolescent↗

Age-related cerebrovascular disease alters the symptomatic course of migraine.

Migraine headaches usually decrease in frequency and severity and often cease during advancing age. Occasionally, migraineurs report late-life migrainous accompaniments, i.e., auras without headache, particularly when typical migraine attacks terminate or diminish following major or minor strokes, at which time the auras may become atypical. Clinical observations such as these suggest that degenerative cerebrovascular changes accompanying aging may modify the course of migraine headaches particularly those with aura. To test this hypothesis, we quantitated age-related changes in cerebral vasodilator capacitance by measuring local cerebral blood flow utilizing xenon contrast computed tomography (CT) scanning before and after oral administration of the pharmacological cerebral vasodilator, acetazolamide (Diamox). Measurements were compared among 27 normal volunteers without headache (aged 24-94 years; mean age 61.1 +/- 17.6) and 37 carefully categorized groups of migraine patients (aged 27-83 years; mean age 59.4 +/- 12.4). The normals comprised Group A. Migraineurs were divided into two subgroups: Group B consisted of 27 migraineurs with and without aura who continued to suffer from incapacitating and frequent headaches and Group C consisted of 10 migraineurs who no longer suffered from severe and frequent headaches, two of whom still complained of atypical auras of the "late-life migrainous accompaniments" type. Cerebral vasodilator capacitance significantly declined with advancing age among normals and the two groups of migraineurs, confirming the development of age-related cerebrovascular diseases. Global CBF increases after Diamox in Group B (with persistent and severe migraine), were significantly greater compared with normals without headache, and with Group C consisting of migraineurs whose headaches had decreased, subsided, or become replaced by late-life migrainous accompaniments (Group C). Results establish that cerebrovasodilator capacitance declines with advancing age, probably due to progressive cerebral atherosclerosis, since these declines were accentuated by risk factors for stroke, particularly TIAs or documented lacunar infarcts by CT. Progressive impairments of cerebral vasodilator capacitance among migraineurs were associated with: (i) reductions in frequency and severity of migrainous cephalalgia and (ii) appearance of late-life migrainous accompaniments.

Adult↗

Risk factors for cerebral degenerative changes and dementia.

It is concluded that the most important determinants for cerebral neurodegenerative changes and cognitive decline during aging are neuronal shrinkage and/or loss, which are accelerated by certain risk factors: e.g. TIAs, hypertension, heart disease, hyperlipidemia, smoking, heavy alcohol consumption, male gender, low educational status, family history of cerebrovascular disease and absence of estrogen replacement therapy among women. Some of these risk factors are remediable by therapeutic interventions, including prevention of TIAs and medications that control hypertension, heart disease, hyperlipidemia and estrogen replacement in postmenopausal women, as well as abstention from abuse of tobacco and alcohol. Cerebral neurodegenerative changes measured by neuroimaging appear to be premorbid markers for depleted neuronal and synaptic reserves which predispose to the onset of dementias of both VAD and DAT types. Normal subjects at risk for cognitive decline include those with TIAs, hypertension and heart disease since these risk factors measurably accelerate cerebral atrophy, ventricular enlargement, leukoaraiosis, and decline in cortical perfusion.

Adult↗

[Clinicopathological investigation of malignant alteration in nasal and paranasal sinus papilloma using flow cytometric DNA ploidy].

Among tumors of the head and neck, nasal and paranasal sinus papilloma is a relatively rare benign tumor. However, it is different from other benign nasal and paranasal tumors, in histological morphology, and in higher probabilities of recurrence, complication with malignant tumor, and malignant alteration. In this study, we examined clinically and pathologically 30 patients with nasal and paranasal sinus papilloma who underwent operations in our department between 1975 and 1994. The tumor occurred in the opening of the maxillary sinus in 19 patients and in the nasal septum in 7 patients. Destruction of bone was observed in 12 patients. Pathological examination revealed inverted papilloma in 17 patients, exophytic papilloma in 13 patients, and atypia in 4 patients. Recurrence was observed in 9 patients, and malignant alteration was observed in 5 patients. Using paraffin sections, aneuploidy was assessed by flow cytometric DNA ploidy. Diploid in 25 cases (83.3%) and aneuploid in 5 cases (16.7%) were observed. Risk factors of malignant alteration in nasal and paranasal papilloma are considered to be 1) developmental morphology, 2) destruction of bones, 3) atypia in pathology, 4) recurrence before progression to malignancy, and 5) the presence of aneuploidy. The 5 patients in whom malignant alteration was observed each showed 4 of the 5 risk factors, suggesting that malignant alteration is most likely to occur in nasal and paranasal papilloma that show 4 or 5 risk factors. The period up to malignant alteration varies; in one patient, it was more than 10 years. Therefore, follow-up observation over a long period is required.

Adult↗

Normal human aging: factors contributing to cerebral atrophy.

Factors that accelerate rates of 'normal' age-related cerebral atrophic and degenerative changes are important because they may predispose to cognitive declines. To determine characteristic patterns of normal aging, risk factors were correlated with serial neurological-neuropsychological examinations, CT measures of progressive cerebral atrophy, local tissue hypodensities, or perfusional declines. Both cross-sectional and longitudinal designs were utilized. Ninety-four cognitively and neurologically normal aging volunteers, 15 with a history of transient ischemic attacks (TIAs), were followed for mean intervals of 3.0+/-2.1 years. Results indicated that: (1) after age 60, cerebral atrophy, polio- and leuko-araiosis doubled and cerebral perfusion decreased, with marked individual variations; (2) risk factors independently accelerating cerebral atrophy and cortico-subcortical perfusional declines included TIAs, hypertension, smoking, hyperlipidemia, excessive alcohol consumption and male gender; (3) progressive leuko-araiosis correlated directly with cortical atrophy and cortical perfusional declines. We posit that: (1) cerebral atrophy and degenerative changes result from neuronal shrinkage and/or loss, which are accelerated by TIAs, hypertension, smoking, hyperlipidemia, excessive alcohol consumption and male gender; (2) accelerated cerebral atrophic and degenerative changes identified by neuroimaging should be considered as markers for depleted neuronal synaptic reserves, which predispose to cognitive declines. Interventions available for controlling some of these risk factors include control of TIAs, hypertension, and hyperlipidemia, as well as tobacco and alcohol withdrawal.

Adult↗

Prognostic value of admission blood pressure in patients with intracerebral hemorrhage. Keio Cooperative Stroke Study.

BACKGROUND AND PURPOSE: Patients with acute stroke on admission to the hospital are often found to have high blood pressure. The purpose of the present study was to investigate the prognostic value of admission blood pressure in patients with acute intracerebral hemorrhage, including putaminal, thalamic, subcortical, cerebellar, and pontine hemorrhage. METHODS: A total of 1701 patients with intracerebral hemorrhage of the putamen (n = 776; mean +/- SD age, 58 +/- 14 years) thalamus (n = 538; 63 +/- 12 years), subcortex (n = 153; 61 +/- 16 years), cerebellum (n = 110; 64 +/- 11 years), and pons (n = 124; 59 +/- 13 years) were examined. The mean blood pressure on admission in patients with a fatal outcome was compared with that in patients who survived. RESULTS: The mean age in each patient group (putaminal, thalamic, subcortical, cerebellar, and pontine hemorrhage) with fatal outcome was older than that with nonfatal outcome, while ANCOVA indicated no correlation between age and blood pressure on admission or age and volume of hematoma. The mean arterial blood pressure on hospital admission was 126.9 +/- 25.8 mm Hg (+/-SD) in cases of putaminal. 127.4 +/- 22.6 mm Hg in thalamic, 116.4 +/- 20.6 mm Hg in subcortical, 123.5 +/- 23.9 mm Hg in cerebellar, and 133.0 +/- 26.0 mm Hg in pontine hemorrhage. The mean blood pressure on admission in patients with a fatal outcome among those with putaminal (136.0 +/- 36.3 mm Hg) and thalamic (133.2 +/- 22.1 mm Hg) hemorrhage was significantly higher than that in those with a nonfatal outcome (123.8 +/- 20.6 mm Hg for putaminal, 101.6 +/- 22.5 mm Hg for thalamic) (P < .01). No correlation between mean blood pressure and outcome was observed in the patients with subcortical (116.5 +/- 22.2 mm Hg for nonfatal, 114.9 +/- 22.0 mm Hg for fatal outcome), cerebellar (125.2 +/- 22.2 mm Hg, 116.9 +/- 28.8 mm Hg), and pontine (129.9 +/- 23.8 mm Hg, 136.0 +/- 27.7 mm Hg) hemorrhage. The volume of hematoma on admission in patients with fatal outcome with putaminal (58.2 +/- 24.4 mL), thalamic (27.0 +/- 13.1 mL), subcortical (32.9 +/- 14.4 mL), and cerebellar (31.4 +/- 28.6 mL) hemorrhage was greater than that in those with nonfatal outcome (20.8 +/- 11.4 mL, 7.1 +/- 4.8 mL, 18.3 +/- 10.6 mL, and 8.1 +/- 4.2 mL, respectively; P < .01), while no correlation between volume of hematoma and outcome was observed in patients with pontine hemorrhage. CONCLUSIONS: The above data suggest that an increased mean blood pressure and volume of hematoma on admission in putaminal and thalamic hemorrhage were related to increased mortality, while in patients with subcortical, cerebellar, and pontine hemorrhage, the mean blood pressure was not related to the clinical outcome.

Age Factors↗

Classification, diagnosis and treatment of vascular dementia.

Vascular dementia (VAD) is considered to be the second most common cause of dementia in Europe and the US. In Asia and many developing countries, it is more common than dementia of the Alzheimer's type (DAT). VAD is the most preventable form of dementia associated with later life. The pathogenesis of VAD is multifactorial, and it represents a heterogeneous, not a homogeneous, clinical entity. Classification of VAD by pathogenesis is important for its prevention and treatment. Control of the risk factors for VAD reduces its incidence and stabilises or improves cognitive performance following stroke. Proper diagnostic evaluation of VAD requires: (i) a well defined quantitative assessment of the cognitive deficits present; (ii) assessment of risk factors for stroke; (iii) identification of cerebral vascular lesions by history, neurological examination and neuroimaging; (iv) exclusion of other causes of dementia; (v) establishment of a positive diagnosis of possible, probable or definite VAD versus DAT or mixed VAD/DAT; and (vi) identification of the temporal relationship between cognitive deficits and cerebral vascular lesions. VAD can be subdivided into 8 major types, as follows: (i) multi-infarct dementia secondary to large cerebral emboli [type 1]; (ii) strategically placed infarctions causing dementia [type 2]; (iii) multiple subcortical lacunar lesions secondary to atherosclerosis or degenerative arteriolar changes [type 3]; (iv) Binswanger's disease (arteriosclerotic subcortical leukoencephalopathy) [type 4]; (v) mixtures of types 1, 2 and 3 [type 5]; (vi) haemorrhagic lesions causing dementia [type 6]; (vii) subcortical dementia secondary to hereditary factors (type 7); and (viii) mixtures of DAT and VAD (type 8). Treatment is dictated by the pathogenetic subtype of VAD that is present.

Dementia, Vascular↗

[A case of Guillain-Barré syndrome treated with plasma exchange and intravenous high-dose immune globulin].

We describe a 69-year-old female with Guillain-Barré syndrome (GBS) whose paresthesia and weakness improved after plasma exchange (PE) and intravenous high-dose immune globulin (i.v.I.G.). She felt a paresthesia in her right arm, and 7 days later she noticed right arm weakness followed by gait disturbance within 2 days. She received a series of 6 PEs, but paresthesia and weakness did not improve. Following the last PE trial of this series, she was treated by i.v.I.G. (0.4 g/kg) for 5 days. After i.v.I.G., paresthesia and weakness improved in a few days. After 2nd series of 6 PEs, she was able to walk. In this clinical course, the treatment of i.v.I.G. after PE seemed to be effective. This case raises the possibility that i.v.I.G. might be the treatment in GBS patients with insufficient effect of PE.

Aged↗

Surgical results of tympanoplasty with hokudai-shaped partial and total ossicular replacement prostheses.

The surgical results of tympanoplasty using a ceramic partial ossicular replacement prosthesis (PORP) or a ceramic total ossicular replacement prosthesis (TORP) were analyzed. The present study included 25 ears in 22 patients who underwent tympanoplasty between December 1986 and September 1994 and were followed up for more than 6 months postoperatively. Because the ceramic prosthesis was extruded from 2 of the 25 ears, the surgical results in the other 23 ears were analyzed, Surgical results were assessed according to a criterion that permits comparison with data from around the world. The criterion considers a postoperative airbone gap within 20 dB as a success. According to this criterion, the success rate was 90.9% for PORP, 50.0% for TORP, and 69.6% in total. These results are comparable with those found at other centers.

Adolescent↗