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Junko Hara

Publications and source records attributed to Junko Hara.

13 recordsLinked to original sources
PubMed2006

QEEG monitoring of Alzheimer's disease treatment: a preliminary report of three case studies.

Previous research has shown that quantitative electroencephalography (qEEG) can monitor treatment of Alzheimer's Disease (AD). This study investigated the ability of a qEEG measure based on EEG variance, combined with a delayed recognition memory task, to measure treatment effects on patients with AD. Three AD patients with very mild AD (CDR=0.5, FAST stage 3) were monitored with task specific EEG at multiple time points before and after medication treatment. Patients had their EEG recorded while performing a recognition memory task. A measure of (normalized) variance was applied to the EEG data. To the extent possible, the subjects received this treatment monitoring multiple times. These patients were monitored a total of 14 times, which yielded 11 measurements of qEEG change during the course of treatment. The direction of change in patients' qEEG values agreed with patients' medication treatment on 10 out of 11 occasions, p < 0.006 (binomial test) and was more accurate than monitoring with the relative theta power, p < 0.05. The results of this monitoring also showed that the qEEG measure accurately reflected treatment in a dose dependent manner. These results were independent of the specific medication monitored; Galantamine, Memantine, Nicotine, and Rivastigmine. In conclusion, this qEEG method may be useful for measuring AD treatment responses.

Aged↗
PubMed2005

Methods to improve the detection of mild cognitive impairment.

We examined whether the performance of the National Institute of Aging's Consortium to Establish a Registry for Alzheimer's Disease's 10-word list (CWL), part of the consortium's neuropsychological battery, can be improved for detecting Alzheimer's disease and related disorders early. We focused on mild cognitive impairment (MCI) and mild dementia because these stages often go undetected, and their detection is important for treatment. Using standardized diagnostic criteria combined with history, physical examination, and cognitive, laboratory, and neuroimaging studies, we staged 471 community-dwelling subjects for dementia severity by using the Clinical Dementia Rating Scale. We then used correspondence analysis (CA) to derive a weighted score for each subject from their item responses over the three immediate- and one delayed-recall trials of the CWL. These CA-weighted scores were used with logistic regression to predict each subject's probability of impairment, and receiver operating characteristic analysis was used to measure accuracy. For MCI vs. normal, accuracy was 97% [confidence interval (C.I.) 97-98%], sensitivity was 94% (C.I. 93-95%), and specificity was 89% (C.I. 88-91%). For MCI/mild dementia vs. normal, accuracy was 98% (C.I. 98-99%), sensitivity was 96% (C.I. 95-97%), and specificity was 91% (C.I. 89-93%). MCI sensitivity was 12% higher (without lowering specificity) than that obtained with the delayed-recall total score (the standard method for CWL interpretation). Optimal positive and negative predictive values were 100% and at least 96.6%. These results show that CA-weighted scores can significantly improve early detection of Alzheimer's disease and related disorders.

Aged↗
PubMed2005

Difference in obesity phenotype between orexin-knockout mice and orexin neuron-deficient mice with same genetic background and environmental conditions.

Orexins are a pair of neuropeptides expressed by a population of neurons located in the lateral hypothalamic area (LHA). Prepro-orexin- or orexin receptor type 2-deficient animals exhibit a phenotype remarkably similar to the human sleep disorder, narcolepsy, which is characterized by sleep/wakefulness fragmentation. Human narcolepsy is known to be associated with metabolic abnormalities, including an increased frequency of obesity and non-insulin-dependent diabetes mellitus. Complex disruption of energy homeostasis in orexin neuron-deficient transgenic mice (orexin/ataxin-3 mice) is also manifested as late-onset obesity despite eating less. Here, we report that the development of obesity in orexin neuron-ablated narcoleptic mice is critically dependent on their genetic background and environmental factors, and the phenotype is different from that of prepro-orexin knockout mice even under the same genetic background and environmental factors, suggesting that factors that co-localize in orexin neurons might have important roles in the regulation of energy homeostasis. Our observation also suggests that the obesity observed in orexin neuron-deficient narcolepsy is dependent on the genetic background and environmental factors.

Animals↗
PubMed2005

Kinetics of trichloroethene dechlorination with iron powder.

The dechlorination of trichloroethene (TCE) with metallic iron is an advantageous method for the remediation of contaminated groundwater and soil. The toxic reaction intermediates such as dichloroethenes (DCEs) and vinyl chloride (VC), however, occasionally accumulate in the pathway of the reaction. We have been trying to suppress these intermediates by using metallic iron powder containing impurities. In order to investigate the reaction pathways, we measured the production rates of the intermediates and the final products of the dechlorination of TCE such as DCEs, VC, ethyne or ethene. Ethyne, ethene, ethane and cis-DCE were observed as the major products, and trans-DCE, 1,1-DCE, VC, C3-hydrocarbons (such as propane, propylene), C4-hydrocarbons (such as n-butane) and methane were observed as the minors. Also the rate constants of TCE to ethyne and ethyne to ethene were larger than any other constants. These fact show the production of ethene/ethane via ethyne is the main pathway of the dechlorination of TCE using the metallic iron powder.

Alkynes↗
PubMed2005

EEG detection of early Alzheimer's disease using psychophysical tasks.

In this study, we hypothesized that a quantitative EEG (qEEG) method for measuring EEG variability combined with specific psychophysical tasks could improve the classification accuracy of subjects with normal aging vs. mild cognitive impairment (MCI) or mild dementia due to Alzheimer's Disease and Related Disorders (ADRD). The cross-sectional sample consisted of 48 subjects (32 normal aging and 16 ADRD: n = 3 mild dementia, n = 13 MCI FAST stage 3). During EEG recording, subjects performed two visual, delayed recognition memory tasks as well as a task that tested their ability to perceive structure-from-motion (SFM). These EEG data were used to compute qEEG measures of the (normalized) variance of posterior cortical activity during the first 150 milliseconds (ms) after stimulus onset and the variance of anterior cortical activity during the second 150 ms epoch. The ratio, anterior/posterior cerebral qEEG value, was then computed for each subject, and the optimal cutoff value identified to discriminate normal from impaired subjects. An optimal qEEG cutoff value for the delayed recognition memory tasks correctly discriminated 30 of the 32 normal aging subjects (94% specificity) and 14 of 16 MCI-to-mild ADRD subjects (88% sensitivity). On the other hand, the application of this qEEG measure to EEG data recorded while subjects performed a SFM task did not distinguish between ADRD and normal aging any better than chance. In conclusion, this qEEG measure is specific to the psychophysical task being performed by the subject. When it was combined with delayed recognition memory tasks, it yielded results that are comparable to the accuracies reported by PET scan studies of normal aging vs. AD with mild cognitive impairment. These results warrant further evaluation.

Aged↗
PubMed2004

Orexin peptides prevent cataplexy and improve wakefulness in an orexin neuron-ablated model of narcolepsy in mice.

Narcolepsy-cataplexy is a neurological disorder associated with the inability to maintain wakefulness and abnormal intrusions of rapid eye movement sleep-related phenomena into wakefulness such as cataplexy. The vast majority of narcoleptic-cataplectic individuals have low or undetectable levels of orexin (hypocretin) neuropeptides in the cerebrospinal fluid, likely due to specific loss of the hypothalamic orexin-producing neurons. Currently available treatments for narcolepsy are only palliative, symptom-oriented pharmacotherapies. Here, we demonstrate rescue of the narcolepsy-cataplexy phenotype of orexin neuron-ablated mice by genetic and pharmacological means. Ectopic expression of a prepro-orexin transgene in the brain completely prevented cataplectic arrests and other abnormalities of rapid eye movement sleep in the absence of endogenous orexin neurons. Central administration of orexin-A acutely suppressed cataplectic behavioral arrests and increased wakefulness for 3 h. These results indicate that orexin neuron-ablated mice retain the ability to respond to orexin neuropeptides and that a temporally regulated and spatially targeted secretion of orexins is not necessary to prevent narcoleptic symptoms. Orexin receptor agonists would be of potential value for treating human narcolepsy.

Animals↗
PubMed2003

Hypothalamic orexin neurons regulate arousal according to energy balance in mice.

Mammals respond to reduced food availability by becoming more wakeful and active, yet the central pathways regulating arousal and instinctual motor programs (such as food seeking) according to homeostatic need are not well understood. We demonstrate that hypothalamic orexin neurons monitor indicators of energy balance and mediate adaptive augmentation of arousal in response to fasting. Activity of isolated orexin neurons is inhibited by glucose and leptin and stimulated by ghrelin. Orexin expression of normal and ob/ob mice correlates negatively with changes in blood glucose, leptin, and food intake. Transgenic mice, in which orexin neurons are ablated, fail to respond to fasting with increased wakefulness and activity. These findings indicate that orexin neurons provide a crucial link between energy balance and arousal.

Animals↗
PubMed2003

A possible mechanism for improvement by a cognition-enhancer nefiracetam of spatial memory function and cAMP-mediated signal transduction system in sustained cerebral ischaemia in rats.

1. Accumulated evidence indicates that the adenylyl cyclase (AC)/cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-responsive element binding protein (CREB) signal transduction system may be linked to learning and memory function. 2. The effects of nefiracetam, which has been developed as a cognition enhancer, on spatial memory function and the AC/cAMP/PKA/CREB signal transduction system in rats with sustained cerebral ischaemia were examined. 3. Microsphere embolism (ME)-induced sustained cerebral ischaemia was produced by injection of 700 microspheres (48 micro m in diameter) into the right hemisphere of rats. Daily oral administration of nefiracetam (10 mg kg(-1) day(-1)) was started from 15 h after the operation. 4. The delayed treatment with nefiracetam attenuated the ME-induced prolongation of the escape latency in the water maze task that was examined on day 7 to 9 after ME, but it did not reduce the infarct size. 5. ME decreased Ca(2+)/calmodulin (CaM)-stimulated AC (AC-I) activity, cAMP content, cytosolic PKA Cbeta level, nuclear PKA Calpha and Cbeta levels, and reduced the phosphorylation and DNA-binding activity of CREB in the nucleus in the right parietal cortex and hippocampus on day 3 after ME. The ME-induced changes in these variables did not occur by the delayed treatment with nefiracetam. 6. These results suggest that nefiracetam preserved cognitive function, or prevented cognitive dysfunction, after sustained cerebral ischaemia and that the effect is, in part, attributable to the prevention of the ischaemia-induced impairment of the AC/cAMP/PKA/CREB signal transduction pathway.

Animals↗
PubMed2002

Pheochromocytoma presenting as an abdominal emergency: association with perforation of the colon.

A pheochromocytoma is a rare tumor derived from the adrenal medulla (or from chromaffin cells of sympathetic ganglia). Its symptoms derive mostly from the excessive release of catecholamines (adrenaline and noradrenaline). Hypertension is the most recognized feature of this disease, but gastrointestinal manifestations can on rare occasions be just as serious and life threatening. This report describes a rare case of a 70-year-old woman with pheochromocytoma who developed an acute abdominal emergency with shock and panperitonitis as a result of perforation of the descending colon which was effectively treated by surgical removal of the tumor and the perforated colon. There have been 2 such cases in the English literature in whom a pheochromocytoma was associated with perforation of the colon. Successful surgical removal of such a pheochromocytoma has been not reported previously. Our case demonstrates the importance of recognizing that a pheochromocytoma presents with a wide spectrum of manifestations, and rapid treatment brings improvement to the patient.

Abdomen, Acute↗