巻号一覧
215 巻 (2008)
- 4 号 p. 295-
- 3 号 p. 199-
- 2 号 p. 119-
- 1 号 p. 1-
215 巻, 2 号
June
選択された号の論文の9件中1～9を表示しています
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Reviews
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Tetsuya Suhara, Makoto Higuchi, Michie Miyoshi2008 年 215 巻 2 号 p. 119-124
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーDementia, a progressive cognitive decline, leads to a gradually increasing restriction of daily activities. Alzheimer's disease (AD) is the most common form of dementia. The pathological features of AD include plaques and tangles which are constituted by amyloid β peptide (Aβ) and tau protein. These amyloidogenic molecules have been mechanistically implicated in the pathogenesis of AD and related neurodegenerative dementias. The key strategy for establishment of diagnostic and therapeutic approaches to AD is sensitive and specific detection of the incipient neuropathology characteristics of AD, combined with emerging treatments that counteract molecular processes in AD pathogenesis. Recent advances in molecular imaging research have enabled visualization of brain amyloidosis. The rapid development of different compounds suitable for visualizing amyloid would permit pathology-specific diagnosis of AD at an asymptomatic stage in a noninvasive manner, and could also allow early immunotherapeutic intervention without causing an excessive neuroinflammatory response.抄録全体を表示PDF形式でダウンロード (626K) -
Kenichi Meguro2008 年 215 巻 2 号 p. 125-131
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーThe borderline condition between normal aging and dementia is a major issue of concern for health policy planning because of an early intervention for possible prevention of dementia. Since 1988, the author has been involved in a community-based program on stroke, dementia, and bed-confinement prevention in Tajiri, northern Japan (the Osaki-Tajiri Project). As a part of the project, a cross-sectional study of aged patients with mild cognitive impairment in Tajiri was undertaken to investigate the clinical features of the condition, in addition to a longitudinal study to research its progression to dementia with possible risk factors. Impairment of the basic functions of attention and executive function was noted, as opposed to impairment in the cognitive domain itself. Magnetic resonance imaging (MRI) findings showed a pattern close to that of healthy persons in their 80s, rather than that of patients with cognitive deficit. The results of the longitudinal study showed more progression to dementia when the Clinical Dementia Rating (CDR) was 0.5 in domains other than memory. No effects of lifestyle, internal diseases or psychosocial intervention were confirmed. In progression to Alzheimer's disease, generally low cognitive function and general atrophy were involved, whereas frontal lobe function, atrophy of the frontal and temporal lobes, white matter changes and cerebral infarction were related to progression to vascular dementia. For health policy planning for dementia prevention, we consider that excessive dependence on primary prevention should be avoided; rather, secondary prevention, using the CDR, psychological testing and MRI are desirable.抄録全体を表示PDF形式でダウンロード (295K) -
Masaru Mimura2008 年 215 巻 2 号 p. 133-140
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーIn addition to their memory impairment, individuals with Alzheimer's disease (AD) often suffer from deficits in self-awareness. Awareness of memory deficits or metamemory is a multifaceted function, comprising on-line self-monitoring, generalized self-beliefs of memory efficacy, and generalized knowledge about memory functions. Awareness of memory problems in early-stage AD is a matter of clinical importance from a humanistic point of view, because higher levels of awareness may be associated with better future outcomes. Current methods of measuring awareness tend to fall into two categories, i.e., to introduce a questionnaire assessing patient/caregiver discrepancies; or to ask a patient to prospectively predict or retrospectively postdict their own memory performances. Characteristics of each measure as well as relationship between the two measures were discussed. For the performance prediction/postdiction paradigm, we used recognition memory of auditory verbal learning tests and awareness of memory deficits were examined in 24 individuals with early-stage AD. In addition to their significantly impaired recognition memory, individuals with AD displayed underawareness of memory deficits even at this early stage. They retrospectively overestimated memory performance after actual performance, but appeared to benefit from feedback and displayed intact on-line awareness of memory dysfunction, leading to normal prediction of the second session. However, individuals with AD again failed to retrospectively incorporate incidents of memory failure into generalized self-belief systems. Brain/behavior correlational analyses suggest that the prefrontal cortex and posterior dorsomedial regions including the precuneus may be involved in self-awareness.抄録全体を表示PDF形式でダウンロード (785K)
Review and Hypothesis
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Atsushi Yamadori2008 年 215 巻 2 号 p. 141-147
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーDementia is a clinical syndrome characterized by a loss of intelligence once possessed by an individual. Clinically intelligence can be defined as an ability of an individual to get involved in social life as a responsible and independent member by employing his/her own cognitive resources in the most effective way. This ability has been attributed either to a unique faculty called g-factor or to the sum of several slave mental faculties such as memory, language, spatio-manual capacity and so on. Dementia is thus thought to be caused either by a loss of g-factor, or by the simultaneous loss of two or three slave faculties. Based on a long term observation of a couple of cases of senile degenerative dementia and many cases of Korsakoff amnesic syndrome, the author refutes both interpretation and proposes a qualitatively different hypothesis that senile degenerative dementia is a manifestation of the disorganization of the structure of consciousness, one of whose function is to bring up the stored mental contents to the state of awareness and make them available to the conscious manipulation. In degenerative dementia, slowly progressive dissolution of the structure of consciousness causes the breakdown of the integrity of social activity as well as personality. It is hard to confirm whether the mental resources themselves are destroyed or not in this process.抄録全体を表示PDF形式でダウンロード (359K)
Regular Contributions
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Xuan-Fu Xu, Chuan-Gao Xie, Xing-Peng Wang, Jun Liu, Yong-Chun Yu, Hong ...2008 年 215 巻 2 号 p. 149-157
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーCyclooxygenase-2 (COX-2), a prostaglandin synthetase, is involved in development of certain tumors. We therefore analyzed COX-2 expression in pancreatic cancer tissues (53 samples) and Panc-1 human pancreatic cancer cells by immunohistochemistry, RT-PCR and western-blotting analyses. Also, immunohistochemistry of proliferating cell nuclear antigen (PCNA) was performed. We found expression of COX-2 was dramatically upregulated in 36 of 53 cases (67.9%) and the expression of COX-2 was associated with the diameter (> 3 cm) of the tumors (p < 0.05), but not with the age, gender, tumor location, differentiation, lymph-node metastases and TNM stage. The positivity rate of PCNA expression in the pancreatic cancer cells of the COX-2 positive group (32.88 ± 13.26%) was significantly higher than that in the COX-2 negative group (24.56 ± 11.51%) (p < 0.05). Then we investigated the effect of selective inhibitors of COX-2 (NS398 and celecoxib) on proliferation of Panc-1 cells by 3-(4,5 dimethyl-2-thiazolyl)-2.5-diphenyl-2H-tetrazolium bromide (MTT) assay. Either NS398 or celecoxib suppressed proliferation of Panc-1 cells dose-dependently in vitro. Furthermore, Panc-1 cells were implanted into nude mice, and celecoxib was administrated orally with feed. The volume of the tumor xenografted into nude mice was decreased by 51.6% in the celecoxib group (p < 0.01). In conclusion, the increased expression of COX-2 may be responsible for rapid proliferation of pancreatic cancer, and specific inhibition of COX-2 suppresses proliferation of Panc-1 cells in vitro and in nude mice. The selective inhibitor of COX-2 may be an effectual agent for pancreatic cancer chemoprevention.抄録全体を表示PDF形式でダウンロード (792K) -
Hisashi Masugata, Shoichi Senda, Fuminori Goda, Ayumu Yamagami, Hiroyu ...2008 年 215 巻 2 号 p. 159-165
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーLeft ventricular (LV) hypertrophy and dysfunction due to hypertension have been established as risk markers for stroke in hypertensive patients. The purpose of this study was to examine the differences in LV hypertrophy and dysfunction between patients with cerebral hemorrhage and those with cerebral infarction. The study enrolled 23 hypertensive patients with cerebral infarction, 25 hypertensive patients with cerebral hemorrhage, and 24 normotensive controls (controls). Standard echocardiography was performed; LV mass index was measured to evaluate LV hypertrophy, and conventional diastolic transmitral flow velocities were measured to assess LV diastolic function, which was also evaluated by measuring mitral annular velocities using tissue Doppler echocardiography. The Tei index, which reflects both the diastolic and systolic function of LV, was also calculated. The LV mass index and Tei index were significantly higher in cerebral hemorrhage (116 ± 38 g/m2 and 0.57 ± 0.13) than those in controls (92 ± 20 g/m2 and 0.46 ± 0.10) (p < 0.05). In contrast, the LV mass index and Tei index in cerebral infarction (100 ± 27 g/m2 and 0.46 ± 0.12) were not different from those in controls. Thus, the Tei index was significantly worse in the patients with cerebral hemorrhage than in those with cerebral infarction (p < 0.05). On the other hand, the parameters, which reflect diastolic function, showed no significant differences between cerebral hemorrhage and cerebral infarction. These results indicate that LV hypertrophy and dysfunction due to hypertension are more apparent in patients with cerebral hemorrhage than in those with cerebral infarction.抄録全体を表示PDF形式でダウンロード (334K) -
Kazuyoshi Kohu, Eiji Yamabe, Ayako Matsuzawa, Daisuke Onda, Hiroshi Su ...2008 年 215 巻 2 号 p. 167-180
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーIn the evolution of primates, the common marmoset belongs to the new world monkey family and is distinct from the great ape family (which includes humans). In this study, we predicted the amino acid sequences of 30 immunity-related genes from the common marmoset and compared them with those from human and mouse. The domain composition of each orthologous protein was analyzed by the SMART tool and was found to be the same among the three species. A BLAST search revealed that the common marmoset and human proteins were 86% identical on average, whereas the conservation between the common marmoset and mouse or between the human and mouse was only 60%. This indicates that the common marmoset and human proteins are closely related and are similarly divergent from the mouse. We divided the 30 proteins into two categories based on the degree of conservation between the common marmoset and mouse amino acid sequences. One group included 19 proteins and had a relatively high level of conservation (68% identical), whereas the other 11 proteins were less conserved (45% identical). This suggests that these immunity-related genes do not evolve at a uniform rate. Interestingly, however, ligand/receptor pairs such as interleukin-6 and interleukin-6 receptor appear to have evolved simultaneously.抄録全体を表示PDF形式でダウンロード (1433K) -
Saeko Okutsu, Hiroyasu Hatakeyama, Makoto Kanazaki, Hiroshi Tsubokawa, ...2008 年 215 巻 2 号 p. 181-187
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーExcess glutamate and Ca2+ influx into neurons exacerbate brain damage such as ischemia. Astrocytes at the site of damage proliferate and attenuate the glutamate- and Ca2+-induced neuronal damage by removing excess glutamate and Ca2+ through the N-methyl-D-aspartate (NMDA) glutamate receptor and the L-type Ca2+ channel, respectively. Fibroblasts are commonly mobilized to the site of damage, probably supporting the restoration process. Notably, fibroblasts express the L-type voltage-sensitive Ca2+ channel, but not central nervous system-specific NMDA glutamate receptor. We examined if electric pulse stimulation (EPS) was capable of inducing NMDA receptor on fibroblasts by way of Ca2+ channel activation, so that they could potentially have a neuroprotective role. To activate L-type Ca2+ channel, we delivered electric pulse to cultured NIH3T3 mouse fibroblasts. EPS of 20 V with a pulse duration of 2 msec at a frequency of 1 Hz for more than 1 h up to 24 h successfully introduced Ca2+ into NIH3T3 fibroblasts as detected by Fluo-4AM calcium imaging, which was totally inhibited by a L-type Ca2+ channel inhibitor, verapamil. Remarkable expression of NMDA receptor mRNA in the fibroblasts after 24-h EPS was demonstrated by RT-PCR. Verapamil treatment during EPS totally abrogated the EPS-induced NMDA receptor mRNA expression. To the best of our knowledge, this is the first report showing that electric pulse is able to induce sustained Ca2+ influx via L-type Ca2+ channel in a non-excitatory fibroblast, which leads to the expression CNS-specific NMDA receptor mRNA. Neuroprotective role of NMDA receptor induced in fibroblasts needs to be further examined.抄録全体を表示PDF形式でダウンロード (342K) -
Keiya Fujimori, Astuhiro Takanashi, Chikara Endo, Akira Sato2008 年 215 巻 2 号 p. 189-197
発行日: 2008年
公開日: 2008/06/25
ジャーナル フリーFetal endocrinological responses to chronic hypoxemia are useful in elucidating the process of growth restriction at earlier stages of fetal development. The purpose of this study was to observe endocrinological responses to prolonged (24-h) non-acidemic hypoxemia in preterm goat fetuses. Fetal hormonal changes were examined in chronically instrumented goat fetuses at gestational day 96-102 (0.7 gestation) during continuous nitrogen infusion into the maternal trachea to create prolonged fetal hypoxemia. Plasma levels of arginine vasopressin (AVP), epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH) and cortisol were measured, along with fetal heart rate (FHR) and fetal blood pressure (FBP). Fetal arterial pO2 declined significantly from 25.0 ± 1.0 mmHg at baseline to 15.3 ± 1.0 mmHg after 2 h of hypoxemia, then remained at this level. FHR increased significantly throughout the experiment, but FBP remained unchanged. AVP and ACTH levels rose significantly after 2 h of hypoxemia, and declined to the control values after 12 h. There was no significant increase in the epinephrine level during 24-hr hypoxemia. In contrast, norepinephrine significantly increased after 2 h of hypoxemia and remained at the elevated levels throughout the remainder of the experiment. Thus, preterm fetuses could respond to acute hypoxic stress by increasing the plasma levels of AVP, norepinephrine and ACTH. However, despite the rapid increase in ACTH, the level of cortisol in the fetal plasma was significantly elevated only after 18 h of hypoxemia. The chemoreceptors of preterm fetuses, which regulate the release of cortisol or epinephrine, may be less sensitive to hypoxic insults.抄録全体を表示PDF形式でダウンロード (344K)
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