Biomedical subjects

K Taki

Publications and source records attributed to K Taki.

At least 19 recordsLinked to original sources

PubMed2006

Oxidative stress, advanced glycation end product, and coronary artery calcification in hemodialysis patients.

Coronary artery calcification is an index of the severity of atherosclerotic vascular disease, and may predict future adverse cardiovascular events in uremic patients undergoing hemodialysis (HD). HD patients are exposed to oxidative stress, and show high plasma levels of advanced glycation end products (AGEs). The association between oxidative stress, AGEs, established cardiovascular risk factors, and coronary artery calcification score (CACS) was studied in 225 HD patients (123 male, 102 female patients). CACS was measured by using multi-detector row computed tomography. Age, systolic blood pressure, calcium, calcium x phosphate, malondialdehyde, lipid peroxides, and pentosidine were significantly and positively correlated with CACS. Duration on HD tended to be positively correlated with CACS. From the independent variables included in the forward stepwise multiple linear regression analysis, only age, systolic blood pressure, lipid peroxides, calcium, and pentosidine were independently associated with CACS. The odds ratios for past history of coronary artery disease and the presence of diabetes mellitus for high CACS (> or =100) were 6.25 (95% confidence interval; 1.83-21.4) and 2.03 (95% confidence interval; 1.02-4.05), respectively. The plasma pentosidine was significantly and positively correlated with indoxyl sulfate. In conclusion, in addition to such traditional cardiovascular risk factors as past history, diabetes mellitus, aging, systolic blood pressure and calcium overload, oxidative stress (lipid peroxides), and AGE (pentosidine) are associated with extensive coronary artery calcification in HD patients. Lipid peroxidation and glycoxidation may be involved in the pathogenesis of coronary artery calcification.

Aged↗

PubMed2006

Enhancement of sodium/iodide symporter expression in thyroid and breast cancer.

The sodium/iodide symporter (NIS) mediates iodide uptake in the thyroid gland and lactating breast. NIS mRNA and protein expression are detected in most thyroid cancer specimens, although functional iodide uptake is usually reduced resulting in the characteristic finding of a 'cold' or non-functioning lesion on a radioiodine image. Iodide uptake after thyroid stimulating hormone (TSH) stimulation, however, is sufficient in most differentiated thyroid cancer to utilize beta-emitting radioactive iodide for the treatment of residual and metastatic disease. Elevated serum TSH, achieved by thyroid hormone withdrawal in athyreotic patients or after recombinant human thyrotropin administration, directly stimulates NIS gene expression and/or NIS trafficking to the plasma membrane, increasing radioiodide uptake. Approximately 10-20% differentiated thyroid cancers, however, do not express the NIS gene despite TSH stimulation. These tumors are generally associated with a poor prognosis. Reduced NIS gene expression in thyroid cancer is likely due in part, to impaired trans-activation at the proximal promoter and/or the upstream enhancer. Basal NIS gene expression is detected in about 80% breast cancer specimens, but the fraction with functional iodide transport is relatively low. Lactogenic hormones and various nuclear hormone receptor ligands increase iodide uptake in breast cancer cells in vitro, but TSH has no effect. A wide range of 'differentiation' agents have been utilized to stimulate NIS expression in thyroid and breast cancer using in vitro and in vivo models, and a few have been used in clinical studies. Retinoic acid has been used to stimulate NIS expression in both thyroid and breast cancer. There are similarities and differences in NIS gene regulation and expression in thyroid and breast cancer. The various agents used to enhance NIS expression in thyroid and breast cancer will be reviewed with a focus on the mechanism of action. Agents that promote tumor differentiation, or directly stimulate NIS gene expression, may result in iodine concentration in 'scan-negative' thyroid cancer and some breast cancer.

Base Sequence↗

PubMed2004

Evidence for an oscillatory signature in atmospheric neutrino oscillations.

Muon neutrino disappearance probability as a function of neutrino flight length L over neutrino energy E was studied. A dip in the L/E distribution was observed in the data, as predicted from the sinusoidal flavor transition probability of neutrino oscillation. The observed L/E distribution constrained nu(micro)<-->nu(tau) neutrino oscillation parameters; 1.9x10(-3) 0.90 at 90% confidence level.

Journal Article↗

PubMed2004

Hereditary paroxysmal ataxia with mental retardation: a clinicopathological study in relation to episodic ataxia type 2.

A case of hereditary acetazolamide-responsive paroxysmal ataxia with mild mental retardation in an autopsied Japanese man is described. His ataxic attacks had occurred for approximately 65 years since the age of 6. One of his daughters had severe mental retardation and epilepsy, and the other had paroxysmal ataxic attacks and mild mental retardation. Analysis of the subject's CACNA1A gene and that in his daughter revealed neither mutations nor CAG expansion. Neuropathologically, cortical degeneration consisting of the marked loss of Purkinje and granule cells was found exclusively in the cerebellar vermis. This was consistent with findings at autopsy for cases reported as spinocerebellar ataxia 6. In addition, there were minor anomalies, such as hypoplastic cerebellum and brainstem, heterotopic Purkinje cells, and cortical microdysgenesis of the temporal lobe. It is considered that the cerebellar cortical degeneration and the minor malformations found in the brain are closely related to one another, rather than having occurred independently.

Adult↗

PubMed2003

Differential distribution of vesicular glutamate transporters in the rat cerebellar cortex.

The chemical organization of excitatory axon terminals in the rat cerebellar cortex was examined by immunocytochemistry and in situ hybridization histochemistry of vesicular glutamate transporters 1 and 2 (VGluT1 and VGluT2). Chemical depletion of the inferior olivary complex neurons by 3-acetylpyridine treatment almost completely removed VGluT2 immunoreactivity from the molecular layer, leaving VGluT1 immunoreactivity apparently intact. On the other hand, neuronal deprivation of the cerebellar cortex by kainic acid injection induced a large loss of VGluT1 immunoreactivity in the molecular layer. In the cerebellar granular layer, both VGluT1 and VGluT2 immunoreactivities were found in mossy fiber terminals, and the two immunoreactivities were mostly colocalized in single-axon terminals. Signals for mRNA encoding VGluT2 were found in the inferior olivary complex, and those for VGluT1 and VGluT2 mRNAs were observed in most brainstem precerebellar nuclei sending mossy fibers, such as the pontine, pontine tegmental reticular, lateral reticular and external cuneate nuclei. These results indicate that climbing and parallel fibers selectively use VGluT2 and VGluT1, respectively, whereas mossy fibers apply both VGluT1 and VGluT2 together to accumulate glutamate into synaptic vesicles. Since climbing-fiber and parallel-fiber terminals are known to make depressing and facilitating synapses, respectively, VGluT1 and VGluT2 might have distinct properties associated with those synaptic characteristics. Thus, it would be the next interesting issue to determine whether mossy-fiber terminals co-expressing VGluT1 and VGluT2 show synaptic facilitation or depression.

Animals↗

PubMed2002

Sediment remediation for ecosystem in eutrophic lakes.

The remediation method--namely, a hybrid system combined with DAF and CRM--is studied in this paper for the size reduction of aqua-ecological circulation and for the elution control in lakes. Results show that two effects on water quality purification, the sediment washout effect and the elution control effect, can be induced by this system, and the biota inhabiting the lake is therefore shifted into an oligotrophic aspect, from blue algae to green algae and/or diatoms.

Ecology↗

PubMed2001

Lethal form of chondrodysplasia punctata with normal plasmalogen and cholesterol biosynthesis.

We present a male autopsied case of chondrodysplasia punctata with abnormal face, symmetrical proximal limb shortness, severe psychomotor developmental delay, respiratory muscle weakness, and death at the age of 2 years. Although his clinical manifestations were similar to those of rhizomelic chondrodysplasia punctata (RCDP), biochemical studies using skin fibroblasts did not document the peroxisomal dysfunction described in RCDP. In addition, the sterol profile, for which abnormalities have recently been reported in cases of X-linked dominant form chondrodysplasia punctata (CDPX2), was normal both in the liver and in the fibroblasts. This patient may represent a new lethal form of chondrodysplasia punctata.

Calcinosis↗

PubMed2001

Preferential acetazolamide-induced vasodilation based on vessel size and organ: confirmation of peripheral vasodilation with use of colored microspheres.

When carbonic anhydrase activity decreases, the regional blood flow (rBF) in organs increases as hypercapnia develops. However, the effects of acetazolamide (AZ)-induced vasodilation have not been estimated with respect to vessel size and organs. The aim of this study was to determine the diameter of the capillaries in various organs that respond to inhibition of carbonic anhydrase activity by AZ. White rabbits were anesthetized with urethane and ketamine and infused with AZ. While the systolic blood pressure (SBP), pH, hemoglobin concentration, and base excess did not change, the partial pressure of arterial oxygen (PaO2) increased significantly and the partial pressure of arterial carbon dioxide (PaCO2) decreased significantly with AZ. The rBF was calculated by using 3 different sizes (15, 25, and 50 microm) of colored microspheres (CM). The rBF measured with 15 microm CM in the brain, kidneys, and liver increased in response to AZ, and the rBF in these organs was different with the different sizes of CM. However, the rBF calculated by using the different sizes of CM in the stomach and abdominal muscle did not change after the administration of AZ. The AZ-induced vasodilation occurred in all sizes of vessels in the liver, in the small and medium-sized vessels in kidneys, and in the larger capillaries in the brain.

Abdominal Muscles↗

PubMed2001

In vivo transduction of central neurons using recombinant Sindbis virus: Golgi-like labeling of dendrites and axons with membrane-targeted fluorescent proteins.

A new recombinant virus which labeled the infected neurons in a Golgi stain-like fashion was developed. The virus was based on a replication-defective Sindbis virus and was designed to express green fluorescent protein with a palmitoylation signal (palGFP). When the virus was injected into the ventrobasal thalamic nuclei, many neurons were visualized with the fluorescence of palGFP in the injection site. The labeling was enhanced by immunocytochemical staining with an antibody to green fluorescent protein to show the entire configuration of the dendrites. Thalamocortical axons of the infected neurons were also intensely immunostained in the somatosensory cortex. In contrast to palGFP, when DsRed with the same palmitoylation signal (palDsRed) was introduced into neurons with the Sindbis virus, palDsRed neither visualized the infected neurons in a Golgi stain-like manner nor stained projecting axons in the cerebral cortex. The palDsRed appeared to be aggregated or accumulated in some organelles in the infected neurons. Anterograde labeling with palGFP Sindbis virus was very intense, not only in thalamocortical neurons but also in callosal, striatonigral, and nigrostriatal neurons. Occasionally there were retrogradely labeled neurons that showed Golgi stain-like images. These results indicate that palGFP Sindbis virus can be used as an excellent anterograde tracer in the central nervous system.

Acylation↗

PubMed2000

Antinociceptive effect induced by intraperitoneal administration of vitamin K2 (menatetrenone) in ICR mice.

The antinociceptive effect of vitamin K2 (menatetrenone) in mice was examined using tail-flick and formalin test. Menatetrenone at doses of 10, 50 and 100 mg/kg, i.p. produced a dose-dependent and significant inhibition of the tail-flick response in mice. Menatetrenone (50 and 100 mg/kg, i.p.) had no significant effect on the duration of the first phase of the formalin-induced flinching. However, menatetrenone (100 mg/kg, i.p.) significantly inhibited the second phase of the formalin-induced flinching. I.p. administration of menatetrenone (100 mg/kg) significantly reduced the duration of nociceptive responses induced by i.t. injection of bradykinin, but not of substance P, prostaglandin E2 or N-methyl-D-aspartate (NMDA). These present data suggest that i.p. pretreatment with menatetrenone produced dose-dependent antinociceptive effect in mice. This effect may be, at least in part, mediated by the inhibition of bradykinin dependent nociceptive transmission in the spinal cord.

Analgesics↗

PubMed2000

Modulation of the formalin-induced nociceptive response by diabetes: possible involvement of intracellular calcium.

We examined the involvement of cytosolic calcium in the modulation of the formalin-induced nociceptive response by diabetes. Injection of formalin into the hindpaw of mice produced a biphasic nociceptive response consisting of immediate (first phase) and tonic (second phase) components. Although the duration of the first-phase response was significantly longer in diabetic mice than in non-diabetic mice, the second phase was significantly shorter in diabetic mice. The first-phase response was dose-dependently and significantly reduced by pretreatment with ryanodine, which blocks Ca(2+) release from Ca(2+)/caffeine-sensitive microsomal pools. The second-phase response was also significantly increased when diabetic mice were pretreated with ryanodine. However, ryanodine had no significant effect on either the first-phase or second-phase response in non-diabetic mice. On the other hand, pretreatment with thapsigargin, which inhibits Ca(2+) uptake into the inositol-1,4, 5-trisphosphate-sensitive microsomal Ca(2+) pool, significantly enhanced the first-phase response in non-diabetic mice. Furthermore, thapsigargin significantly and dose-dependently reduced the second phase of the formalin-induced nociceptive response in non-diabetic mice. Thapsigargin administered i.t. did not significantly affect either the first- or the second-phase response in diabetic mice. These results suggest that the change in the formalin-induced nociceptive response in diabetic mice may be due, at least in part, to the modification of nociceptive transmission in the spinal cord by intracellular calcium.

Animals↗

PubMed2000

Constant involvement of the Betz cells and pyramidal tract in multiple system atrophy: a clinicopathological study of seven autopsy cases.

We investigated clinicopathologically the pyramidal signs, including spasticity, hyperreflexia, and Babinski's sign, and the involvement of the pyramidal tract and primary motor cortex, in seven Japanese autopsy cases of multiple system atrophy (MSA). Pyramidal signs were observed in six (86%) of the seven autopsy cases. Hyperreflexia and Babinski's sign were each evident in five patients, but spasticity was observed in only one patient. Loss of Betz cells and presence of glial cytoplasmic inclusions in the primary motor cortex were noticed in all seven cases. Astrocytosis in the fifth layer of the primary motor cortex was noticed in five cases, but its presence was not related to the duration of the disease. Involvement of the pyramidal tract in the spinal cord, particularly of the small myelinated fibers, was observed in all seven cases, but no involvement of the pyramidal tract in the midbrain was evident in any of the six cases in which this structure was examined. In MSA, pyramidal signs were shown to be present more frequently than believed before, and the clinicopathological correlation between pyramidal signs and involvement of the pyramidal tract was obvious. Constant involvement of Betz cells in MSA has not been reported. Our clinicopathological findings may also make a contribution to the understanding of the clinicopathological hallmarks of MSA.

Female↗

PubMed2000

Tumor necrosis factor-alpha and tumor necrosis factor receptor I, II levels in patients with severe burns.

Tumor necrosis factor alpha (TNF-alpha) and tumor necrosis factor receptor I and II (TNFRI and TNFRII) were studied in 24 burn patients who had a total burn surface area (TBSA) of 50.2 +/- 20.4%. Immediately after the injury, both the TNFRI and TNFRII levels correlated significantly with TBSA (r = 0.7344, P < 0.0001; r = 0.6074, P = 0.0012). The TNFRI and TNFRII levels immediately after the injury were significantly higher in the 11 patients who later died of their burns than in the 13 patients who survived (0.8 +/- 0.4 ng/ml vs. 1.8 +/- 0.7 ng/ml, P = 0.0002; 2.3 +/- 1.1 ng/ml vs. 4.5 +/- 1.6 ng/ml, P = 0.0009). The TNF-alpha levels immediately after the injury did not differ significantly between the group that survived and the group that died. The TNFRI and TNFRII values for the entire follow-up period also correlated significantly with TBSA. Peak TNFRI and TNFRII levels were significantly higher in the group that died than in the group that survived (6.0 +/- 4.7 ng/ml vs. 14.1 +/- 7.8 ng/ml, P = 0.0009; 7.0 +/- 5.1 ng/ml vs. 16.7 +/- 5.2 ng/ml, P = 0.0003). The TNF-alpha levels correlated significantly with both the TNFRI and the TNFRII levels. The TNFRI and TNFRII levels thus closely reflected the severity of the burns in both the acute postburn period and the subsequent follow-up period. In other words, these parameters well reflected the severity and outcome of the burns, irrespective of the presence or absence of accompanying infection.

Adult↗

PubMed2000

A group of cortical interneurons expressing mu-opioid receptor-like immunoreactivity: a double immunofluorescence study in the rat cerebral cortex.

mu-Opioid receptor-expressing neurons in the rat cerebral neocortex were characterized by an immunolabeling method with an antibody to a carboxyl terminal portion of the receptor. They were small, bipolar, vertically elongated, non-pyramidal neurons, and scattered mainly in layers II-IV. We examined chemical characteristics of mu-opioid receptor-expressing neocortical neurons by the double immunofluorescence method. Almost all neuronal cell bodies expressing mu-opioid receptor-like immunoreactivity showed immunoreactivity for GABA, suggesting that they were cortical inhibitory interneurons. mu-Opioid receptor-immunoreactive neurons were further studied by the double staining method with markers for the subgroups of cortical GABAergic neurons. Immunoreactivities for vasoactive intestinal polypeptide, corticotropin releasing factor, choline acetyltransferase, calretinin and cholecystokinin were found in 92, 79, 67, 35 and 35% of mu-opioid receptor-immunoreactive cortical neurons, respectively. In contrast, less than 10% of mu-opioid receptor-immunoreactive neurons showed immunoreactivity for parvalbumin, calbindin, somatostatin, neuropeptide Y or nitric oxide synthase. Moreover, mu-opioid receptor-immunoreactive neurons very frequently exhibited preproenkephalin immunoreactivity, but not preprodynorphin immunoreactivity. The present results indicate that mu-opioid receptor-expressing neurons belong to a distinct subgroup of neocortical GABAergic neurons, because vasoactive intestinal polypeptide, corticotropin releasing factor, choline acetyltransferase, calretinin and cholecystokinin have often been reported to coexist with one another in single neocortical neurons. Methionine-enkephalin, which is a major product of the preproenkephalin gene, is known to be one of the most potent endogenous ligands for mu-opioid receptor. Thus, the expression of mu-opioid receptor in preproenkephalin-producing neurons suggested that mu-opioid receptor serves as an autoreceptor for the subpopulation of GABAergic interneurons at a single-neuron or population level.

Animals↗

PubMed2000

Gastrotonometry represents dramatic increase in PcO2 after acetazolamide administration.

BACKGROUND: We sought to evaluate the parameters of CO2 transport during the administration of acetazolamide in order to assess the role of carbonic anhydrase in CO2 transport. MATERIALS AND METHODS: The partial pressure of carbon dioxide in tissue (PtCO2), arterial blood (PaCO2) and end-tidal gas (PETCO2) were monitored to study the correlation between PaCO2, PtCO2 and PETCO2 in spontaneously breathing healthy volunteers after the intravenous administration of acetazolamide 6 mg kg-1. RESULTS: At 60 min after the administration of acetazolamide, the PtCO2 peaked at more than 60 mmHg, and although it decreased by 90 min, it then remained stable above the baseline value. The PaCO2 did not change and the PETCO2 decreased significantly. The changes in PtCO2 were greater than those of either PaCO2 or PETCO2. The minute ventilation increased progressively throughout the study. CONCLUSIONS: We concluded that gastrotonometry represents a new method for monitoring the dramatic increase in PtCO2 induced by drugs such as acetazolamide clinically, and that it could be a warning against acetazolamide administration in severe patients without keeping a ventilation and circulation reserve.

Acetazolamide↗

PubMed2000

An evaluation of neurobehavioural problems as perceived by family members and levels of family stress 1-3 years following traumatic brain injury in Japan.

OBJECTIVE: To ascertain the proportion of patients with traumatic brain injury (TBI) admitted to a Japanese district hospital and to evaluate the levels of stress and anxiety in fami ies living with those TBI patients. DESIGN: A retrospective study of patients admitted to hospital from April 1995 to March 1997 and a questionnaire study of family members of survivors. SETTING AND SUBJECTS: All patients referred or transferred to the Emergency Department at the Saga Medical School Hospital, Japan with a primary diagnosis of TBI were studied. Family members living with TBI patients were sent questionnaires. MAIN OUTCOME MEASURES: The Barthel Index, the Patient Competency Rating Scale, the modified Caregiver Strain Index and the Hospital Anxiety and Depression Scale. RESULTS: There were 34 patients who required hospitalization for care relating to TBI. Of these, nine family members took part in the questionnaire study. Three carers reported fairly high levels of stress and another three carers were considered to be at risk of anxiety and depression. There was a tendency for family members who reported that patients had difficulties in performing behavioural tasks to have higher levels of stress themselves. CONCLUSION: These preliminary results showed that family members experienced certain levels of stress and were also at risk of anxiety and depression. The impact of TBI on families as well as patients should receive more attention.

Adolescent↗

PubMed1999

Algogenic mediator-induced nociceptive response in diabetic mice.

The duration of the somatostatin-, bradykinin- or prostaglandin F2alpha-induced nociceptive response was significantly less in diabetic mice than in non-diabetic mice. Subcutaneous injection of 7-benzylidenenaltrexone (0.1, 0.3 and 1 mg/kg), an antagonist of delta1-opioid receptors, had no significant effect on either somatostatin-, bradykinin- or prostaglandin F2alpha-induced nociceptive responses in non-diabetic mice. 7-Benzylidenenaltrexone (0.1 and 0.3 mg/kg, s.c.) also had no significant effect on somatostatin- or prostaglandin F2alpha-induced nociceptive responses in diabetic mice. However, the bradykinin-induced nociceptive response in diabetic mice was dose-dependently and significantly increased when 7-benzylidenenaltrexone (0.1, 0.3 and 1 mg/kg, s.c.) was injected 10 min before the injection of bradykinin. These results suggest that a spinal delta1-opioid receptor-mediated endogenous antinociceptive system may inhibit the bradykinin-mediated nociceptive responses in the second phase of the formalin-induced nociceptive response in diabetic mice.

Animals↗

PubMed1999

Efficacy of blood purification therapy for heat stroke presenting rapid progress of multiple organ dysfunction syndrome: a comparison of five cases.

Five patients were admitted to our hospital because of classical heat stroke during the heat waves which attacked our country in the summers 1994 and 1995. The clinical and laboratory findings of all patients suggested the rapid progress of multiple organ dysfunction syndrome (MODS). Blood purification (BP) therapy, in addition to conventional treatment, was performed in three of the patients. Despite their disastrous general condition, all completely recovered or recovered sufficiently to be transferred to a rehabilitation hospital. Two additional patients were treated with conventional treatment only and both died in 1-3 days after admission. Clinical characteristics and laboratory findings on admission showed no differences between the cases receiving BP therapy and those not receiving BP therapy. These findings suggest that, in heat stroke patients, additional BP therapy may provide a better prognosis than conventional therapy only. These beneficial effects of BP may have been due mainly to the removal of proinflammatory cytokines related to heat stroke.

APACHE↗