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Biomedical subjects

Nobuo Araki

Publications and source records attributed to Nobuo Araki.

13 recordsLinked to original sources
PubMed2007

Feasibility study of a pilot-scale sewage treatment system combining an up-flow anaerobic sludge blanket (UASB) and an aerated fixed bed (AFB) reactor at ambient temperature.

A feasibility test of a 17 m3-pilot-scale sewage treatment system was carried out by continuous feeding of raw municipal sewage under ambient temperature conditions. The system consisted of a UASB and an aerated fixed bed reactor. Some of the effluent from the fixed bed reactor was returned to the UASB influent in order to provide a sulfate source. The total BOD of 148-162 mg l(-1) in the influent was reduced to a more desirable 11-25 mg l(-1) in the final effluent. The levels of methane-producing activity from acetate and H2/CO2 gas at 10 degrees C were only 2% and 0% of those at 35 degrees C, respectively. On the other hand, the sulfate-reducing activity levels of the UASB sludge were relatively high at 10 degrees C, for example, 18% for acetate and 9% for H2/CO2 gas, compared to the activity levels at 35 degrees C. Therefore, BOD oxidization by sulfate reduction in the UASB was greater than that by methane production under low temperature conditions. This sulfate-reducing activity tended to be proportional to the copy number of adenosine-5'-phosphosulfate (APS) reductase genes in DNA extracted from the sludge.

Aerobiosis↗
PubMed2006

Subventricular zone-derived neuroblasts migrate and differentiate into mature neurons in the post-stroke adult striatum.

Recent studies have revealed that the adult mammalian brain has the capacity to regenerate some neurons after various insults. However, the precise mechanism of insult-induced neurogenesis has not been demonstrated. In the normal brain, GFAP-expressing cells in the subventricular zone (SVZ) of the lateral ventricles include a neurogenic cell population that gives rise to olfactory bulb neurons only. Herein, we report evidence that, after a stroke, these cells are capable of producing new neurons outside the olfactory bulbs. SVZ GFAP-expressing cells labeled by a cell-type-specific viral infection method were found to generate neuroblasts that migrated toward the injured striatum after middle cerebral artery occlusion. These neuroblasts in the striatum formed elongated chain-like cell aggregates similar to those in the normal SVZ, and these chains were observed to be closely associated with thin astrocytic processes and blood vessels. Finally, long-term tracing of the green fluorescent-labeled cells with a Cre-loxP system revealed that the SVZ-derived neuroblasts differentiated into mature neurons in the striatum, in which they expressed neuronal-specific nuclear protein and formed synapses with neighboring striatal cells. These results highlight the role of the SVZ in neuronal regeneration after a stroke and its potential as an important therapeutic target for various neurological disorders.

Animals↗
PubMed2006

Enhanced neurogenesis in the ischemic striatum following EGF-induced expansion of transit-amplifying cells in the subventricular zone.

In the subventricular zone (SVZ) of the adult mammalian brain, neural stem cells continually produce transit-amplifying precursors, which generate neuroblasts migrating into the olfactory bulb. Previous studies have suggested that SVZ cells also have the capacity to generate some striatal neurons after cerebral ischemia. The infusion of epidermal growth factor (EGF) has been demonstrated to increase the number of these regenerated neurons. However, which cell types in the SVZ are stimulated to proliferate or differentiate after EGF infusion remains unknown. In this paper, we demonstrated that cerebral ischemia results in an increase in the number of EGF receptor (EGFR)-positive transit-amplifying cells in the SVZ. EGF infusion into the ischemic brain caused the number of transit-amplifying cells to increase and the number of neuroblasts to decrease. On the other hand, after an interval of 6 days after the discontinuation of EGF infusion, a significant increase in the number of neuroblasts was found, both in the striatum and the SVZ. These results suggest that the replacement of neurons in injured striatum can be enhanced by an EGF-induced expansion of transit-amplifying cells in the SVZ.

Animals↗
PubMed2006

Effect of L-DOPA on nitric oxide production in striatum of freely mobile mice.

In Parkinson's disease, nitric oxide (NO) and other free radicals are thought to be involved in neuronal degeneration. Furthermore, L-DOPA is suggested to have a cytotoxic action on dopaminergic neurons. We studied 24-h NO production and the effect of L-DOPA on this in freely mobile mice using in vivo microdialysis. A microdialysis probe was implanted into the right striatum 12 h before the experiment. This dialysis probe was perfused with Ringer solution for 100 min, then with 20, 50, or 100 nM L-DOPA for 20 min, and finally with Ringer solution. Dialysate fractions were collected every 20 min for 4 h. Production of nitrite and total NO were significantly higher during daytime than during nighttime. Nitrate production was increased significantly by L-DOPA. NO production in the striatum appears to exhibit a diurnal rhythm and to increase with exposure to L-DOPA.

Analysis of Variance↗
PubMed2005

Albumin attenuates neutrophil activation induced by stimulators including antibodies against neutrophil-specific antigens.

As neutrophil activation is related to several adverse transfusion reactions, we studied about the activation induced by anti-neutrophil antibodies and the stabilizing effects of albumin pretreatment by means of flow cytometry. Anti-neutrophil monoclonal antibody (anti-HNA-1a, 1b, 2a) alone induced CD11b expression and shedding of L-selectin, and anti-HNA-1a reinforced reactive oxygen species (ROS) production. Albumin pretreatment significantly reduced CD11b expression and L-selectin shedding induced by fMLP and ROS production induced by PMA, G-CSF combined with PMA or LPS-fMLP, or anti-HNA-1a combined with PMA. These findings suggest that anti-HNA-1a is related to adverse reactions and albumin has a regulating effect on neutrophil activation.

Antibodies, Monoclonal↗
PubMed2005

[Tension-type headache].

Tension-type headache is the most common type of primary headache. Life time prevalence of tension-type headache in general population ranges from 30 to 78%. It is the least studied of the primary headache disorders, despite the fact that it has the highest socio-economic impact. In the new 'The International Classification of Headache Disorders', tension-type headache is divided into episodic and chronic subtypes. The exact mechanisms of tension -type headache are not known. Peripheral pain mechanisms are most likely to play a role in episodic headache, whereas central pain mechanisms play a more important role in chronic tension-type headache. Treatments of tension-type headache include not only medication but also the physical therapy. In many uncertain cases there is overuse of medication. Two months after medication overuse has ceased, chronic tension-type should be diagnosed.

Humans↗
PubMed2004

A peroxisome proliferator-activated receptor-gamma agonist reduces infarct size in transient but not in permanent ischemia.

BACKGROUND AND PURPOSE: Activators of peroxisome proliferator-activated receptor-gamma (PPARgamma), a member of the PPAR family, increase levels of CuZn-superoxide dismutase (SOD) in cultured endothelium, suggesting a mechanism by which it may exert its protective effect within the brain. These properties raise the question of whether a PPARgamma agonist may be neuroprotective in models of ischemia without reperfusion, in which oxidative injury is less prevalent. METHODS: In 2 groups of rats, 90 minutes of middle cerebral artery (MCA) occlusion was followed by 1 day of reperfusion, with 1 group receiving pioglitazone (a PPARgamma agonist) starting 72 hours before MCA occlusion (MCAO) and continuing through the day of occlusion, whereas the other group received vehicle only. In 2 comparable groups, the MCA was occluded permanently. One day after occlusion, the animals were tested neurologically and infarct volumes were calculated. In a separate group, rats were treated with pioglitazone or vehicle for 4 days. Tissue was obtained from the cortex and the striatum 2 hours into reperfusion after 90 minutes of MCAO, and the tissue was examined for CuZn-SOD by Western blot. RESULTS: Results show a significant reduction in infarct size in the treated rats, with transient MCAO but not permanent MCAO. There was also an improvement in neurological score in the treated animals after transient MCAO. The level of CuZn-SOD was increased in the cortex in treated animals. CONCLUSIONS: These data, which show that a PPARgamma agonist reduces infarct size in transient but not permanent MCAO, suggest that the role of PPARgamma is specific to events occurring during reperfusion. Our data point to CuZn-SOD as the mediator of this neuroprotection.

Animals↗
PubMed2004

FK506 abrogates delayed neuronal death via suppression of nitric oxide production in rats.

BACKGROUND AND PURPOSE: The mechanism of the neuroprotective effect of FK506 in relation to nitric oxide (NO) production has not been clarified in vivo. We have investigated the effect of FK506 on ischemia-induced NO production in association with the pathogenesis of delayed neuronal death (DND) in rats. METHODS: In vivo microdialysis was performed in the hippocampus of male Sprague-Dawley rats (250-350 g). Dialysate samples were collected every 3 min. In the ischemia group (n=16), global ischemia was induced for 21 min and reperfusion was achieved. In the FK506 treatment group (n=25), FK506 (1 mg/kg, i.v.) was administered 21 min prior to the onset of global ischemia. Sham operations were done (n=15). The levels of NO(2)(-) in the dialysate samples were determined by the Griess reaction. The animals were decapitated 7 days after ischemia. Coronal brain sections were stained with hematoxylin and eosin. RESULTS: In the ischemia group, the NO(2)(-) level significantly increased during ischemia. In the FK506 treatment group, there was no significant change in the NO(2)(-) level during ischemia. In histological examinations, FK506 treatment showed a neuroprotective effect against DND. CONCLUSIONS: The effect of FK506 inhibiting NO production contributes to the neuro-protective effect of FK506 on DND in the hippocampus.

Analysis of Variance↗
PubMed2004

Mechanisms responsible for delayed and immediate hemolytic transfusion reactions in a patient with anti-E + Jk(b)+ Di(b) and anti-HLA alloantibodies.

Immediate hemolytic transfusion reactions (IHTR) occurred in the course of delayed hemolytic transfusion reactions (DHTR). An 84-year-old man had received a blood transfusion 20 years ago. Progressive anemia developed, because of continuous bleeding from a bladder tumor. He was transfused with concentrated red blood cells (CRC) which were Rh-E antigen negative, because he had anti-E antibodies (day 0). He received CRC on day 3, and underwent resection of bladder tumor on day 6. Although crossmatch-compatible CRCs were prepared for the operation, those were not required and were kept in a refrigerator in the ward. On day 9, when a CRC kept in the ward was transfused, he suddenly had a IHTR. In order to analyze a mechanism of IHTR, the anti-Jk(b) and anti-Di(b) antibodies, anti-HLA antibodies and the concentrations of inflammatory cytokines were measured in serum samples. The anti-Jk(b) and anti-Di(b) antibodies increased prior to IHTR experienced on day 9. The concentrations of IL-6 and IL-1beta increased from day 2, while the concentration of IL-8 increased from day 7. The anti-HLA class I antibody could be detected 2 days before IHTR. Thus, the anti-Jk(b) and anti-Di(b) antibodies induced the production of inflammatory cytokines and symptoms of DHTR and IHTR. The anti-HLA class I antibody could be produced in spite of using the filer for removing leukocytes, and may take part in the induction of IHTR. Further, blood products should be transfused soon after completing a crossmatch test in patients with anti-RBC alloantibodies.

Aged↗
PubMed2004

[Diplopia in Wallenberg's syndrome].

The incidence and mechanism of diplopia were investigated in 31 patients with Wallenberg's syndrome resulting from acute dorsolateral medullary infarction. Diplopia was found in 10 of 31 patients (32%), with 5 patients reporting vertical diplopia alone and 5 reporting vertical and horizontal diplopia. Diplopia in Wallenberg's syndrome is considered to be caused by a lesion involving the otolith-ocular system. Vertical diplopia is simply explained by ocular skew deviation due to a lesion involving the vestibular nucleus; in which the affected eye becomes deviated inferiorly. In this situation, rotation of the eye due to ocular tilt reaction also occurs. Concomitant horizontal diplopia may require involvement of the medial longitudinal fasciculus (MLF), which produces skew deviation in mirror image; the unaffected eye becomes deviated inferiorly. When downward deviation of the eye affected by dysfunction of the vestibular nucleus and that due to MLF dysfunction affecting the other eye are comparable, only horizontal diplopia becomes apparent. MLF syndrome may be accompanied by paralytic pontine exotropia (PPE) or non-paralytic pontine exotropia (NPPE), both of which may also participate in the appearance of horizontal diplopia.

Adult↗
PubMed2004

[Central post-stroke pain in Wallenberg syndrome].

We analyzed clinical characteristics of central post-stroke pain (CPSP), constant and burning pain, in 32 patients with Wallenberg syndrome due to infarction. CPSP developed in 44% (14/32) of the patients; 8 in acute stage (within 4 days after the stroke) and 8 in chronic stage(10-120 days after the stroke). Apart from one exceptional case, CPSP was present in the hypalgesic side of face and extremities. In 9 cases of typical type (Currier's distribution of sensory disturbance), CPSP occurred in the ipsilateral face to the lesion during acute stage. Among them, 2 cases developed severe lancinating pain in chronic stage. In 5 cases of ventral type, it occurred in the contralateral extremities during chronic stage. Spino- and trigemino-thalamic tract are injured but medullary reticular formation is intact in Wallenberg syndrome. It is, therefore, considered that CPSP in Wallenberg syndrome is caused by denervation sensitivity of "paleo-reticulothalamic" tract within the reticular formation.

Adult↗
PubMed2003

[Pitfall in migraine treatment].

Migraine is a very common disorder. In Japan, an estimated 8.4% of population experience migraine, but most of them go undiagnosed and undertreated. Recent advances in basic and applied clinical neuroscience have led to the development of sumatriptan, a new class of selective serotonin (5-hydroxytryptamine (5-HT)) receptor agonists that activate 5-HT 1B/1D receptors. Following sumatriptan several other triptans were produced. They have three main mechanism of action: cranial vasoconstriction, peripheral trigeminal inhibition, and inhibition of transmission through second order neurons of the trigeminocervical complex. Even in our country, we can now use three kinds of triptans, which are very effective medicine against acute migraine with a well-developed scientific rationale. Despite the higher price, triptans were preferred over ergots in most patients. Recently Limmroth et al reported a prospective study for medication overuse headache (MOH) in 98 patients. The mean critical duration until onset of MOH was shortest for triptans (1.7 years), longer for ergots (2.7 years), and longest for analgesics (4.8 years). The mean critical monthly intake frequencies was lowest for triptans (18 single doses per month), higher for ergots (37), and highest for analgesics (114). We should keep in mind that overuse of triptans leads to MOH faster and with lower dosages compared with ergots and analgesics.

Contraindications↗