Rapid extraction of emotional expression: evidence from evoked potential fields during brief presentation of face stimuli

Although the emotional expression of faces is believed to be accessed rapidly, previous ERP studies hardly found correlates of these processes. Here, we report findings from a study that investigated dichoptic binocular interaction using emotional face stimuli. Thirty-one subjects were briefly presented with schematic normal and scrambled faces (of neutral, positive, or negative expression) that occurred simultaneously in the left and right visual fields. Stimuli for both eyes could be congruent (control) or incongruent (dichoptic). Subjects decided which of the superimposed images in both hemi-fields appeared more "face-like" and during this task, the EEG was recorded from 30 channels. VEPs were analysed topographically according to the influence of the different experimental conditions (defined by presentation form, emotional expression, and location). Behavioural responses to the ambiguous dichoptic stimuli demonstrated a functional eye dominance not related to visual acuity and conventional eye preference. Electrophysiological data revealed three components with mean latencies of 85, 160, and 310 ms. Topography of the second component (equivalent to the face-related N170) differed in left-right and anterior-posterior direction compared with simple checkerboard stimuli. Dichoptic presentation caused reduced field strength of all three, and increased latency of the first component. Faces with negative expression yielded largest field strength of the second and third components. Besides that, emotional expression affected topography not only of late, but also the first component. This provides new evidence about the timing of perceptual processes related to facial expression, indicating that already VEP components occurring at 80-90 ms are sensitive to emotional content.     

An increase in body temperature during radiofrequency ablation of liver tumors

Radiofrequency ablation (RFA) therapy using an active needle electrode inserted into liver tumors has been used clinically. To avoid hyperthermia, we investigated the relationship between the total output energy of the applied radiofrequency wave and changes in body temperature (BT) in patients receiving RFA. Fifteen patients undergoing RFA of liver tumors with general anesthesia were enrolled. The total output energy of radiofrequency waves was calculated from the power and duration of RFA. Changes in rectal (T(rect)) and tympanic temperatures were measured throughout the study. The mean number of liver tumors per patient was 1.7 +/- 1.3. The mean RFA time was 30.0 +/- 26.3 min. The mean total output energy was 125,935 +/- 114,506 J. The mean value of T(rect) increased from 36.3 degrees C +/- 0.5 degrees C to 37.0 degrees C +/- 1.0 degrees C (P < 0.01). A linear correlation was obtained between the total output energy and the changes in T(rect), indicating that T(rect) increased approximately by 1 degrees C for every 3000 J/kg of total output energy. The increase in BT during RFA of liver tumors under general anesthesia is predictable. Close observation of total output energy delivered and BT are required, and preparation of cooling measures is important, in RFA of liver tumors. IMPLICATIONS: The increase in body temperature (BT) is predictable during radiofrequency ablation (RFA) of liver tumors under general anesthesia. Close observation of total output energy delivered and BT are required, and preparation of cooling measures is important, in RFA of liver tumors.     

Clinical, electrophysiological, and serological overlap between Miller Fisher syndrome and acute sensory ataxic neuropathy

We report a patient with severe sensory ataxia, areflexia, and ophthalmoplegia with preservation of limb muscle strength. Electrophysiological examinations revealed peripheral sensory nerve involvement. A serological examination showed the elevation of IgG antibodies to various b-series gangliosides as well as GT1a. These indicated that this case is an overlap between acute sensory ataxic neuropathy and Miller Fisher syndrome. Autoantibody is implicated as potential pathogenic agents in some cases of acute sensory ataxic neuropathy.     

Increased expression of manganese superoxide dismutase is associated with that of nitrotyrosine in myopathies with rimmed vacuoles

Oxidative stress has been suggested as one of the pathogenetic mechanisms of inclusion body myositis (IBM). To study the role of antioxidant enzymes in myopathies with rimmed vacuoles, we examined expressions of copper, zinc superoxide dismutase (Cu, Zn-SOD) and manganese superoxide dismutase (Mn-SOD), and the relationship between SODs and other proteins localized in rimmed vacuoles in muscle biopsy specimens from three cases of sporadic IBM and two of distal myopathy with rimmed vacuoles (DMRV) as well as eight control cases of myopathies without rimmed vacuoles. Immunoblot analysis showed distinct protein bands of both SODs in IBM and DMRV using subtype-specific antibodies. Intensities of immunoreactive bands for Mn-SOD in IBM and DMRV were stronger than those in the control cases. Immunohistochemistry disclosed accumulation of both SODs in vacuolated muscle fibers in all cases of IBM and DMRV. Immunoreactivity for Mn-SOD was often colocalized with that of nitrotyrosine, cytochrome oxidase, tau, and lysosome-associated membrane proteins 2 (LAMP-2) in vacuolated fibers. Some of the Cu, Zn-SOD-positive vacuolated fibers were associated with ubiquitin. The two SODs may have different roles for cell protection, and the expression of Mn-SOD is associated with nitric oxide-induced oxidative damage in myopathies with rimmed vacuoles.     

Increased clusterin (apolipoprotein J) expression in human and mouse brains infected with transmissible spongiform encephalopathies

Clusterin (apolipoprotein J), a multifunctional protein involved in amyloidogenesis in Alzheimer's disease, was studied immunohistochemically in both human transmissible spongiform encephalopathies (TSEs) and a mouse model of human TSE. Clusterin immunoreactivity was co-localized with plaque-type deposits but not with punctate-type prion protein (PrP) deposits in human TSEs. On the other hand, clusterin-positive astrocytes were readily demonstrated in the regions of punctate PrP deposits, but not around plaque PrP deposits despite the presence of surrounding astrocytes. Clusterin expression in astrocytes was not disease specific, but the punctate immunoreactivity for clusterin was more prominently demonstrated in TSEs with punctate PrP deposits. Serial analysis in the mouse model of human TSE revealed that clusterin expression in astrocytes was enhanced in the lesions with punctate-type PrP deposits during the disease progression. Thus, the induction of clusterin expression in astrocytes could be more enhanced by punctate-type PrP deposits than by plaque-type deposits. The clusterin molecules co-localized in plaque PrP deposits might be derived not from surrounding astrocytes but from other resources such as cerebrospinal fluid and blood plasma, both of which contain clusterin in significant amounts. Taken together with previously reported findings of the anti-amyloidogenic property in clusterin, our findings suggest that clusterin may be induced as one of the important molecules participating in the neurodegeneration caused by abnormally deposited PrP.     

Impairment of mitochondrial DNA repair enzymes against accumulation of 8-oxo-guanine in the spinal motor neurons of amyotrophic lateral sclerosis

Oxidative stress plays an important role in the pathogenesis of amyotrophic lateral sclerosis (ALS). In the present study, we investigated the expression of two major human enzymes that prevent errors caused by 8-oxoguanine (8-oxoG), a mitochondrial form of 8-oxoG DNA glycosylase (hOGG1) and oxidized purine nucleoside triphosphatase (hMTH1). We also investigated the relationship between their expression and the 8-oxoG accumulation observed in the large motor neurons of the lumbar spinal cord in seven cases of adult onset sporadic ALS, four cases of subarachnoid hemorrhage (SAH) and four control cases. 8-oxoG immunoreactivity increased in most large motor neurons in both the ALS and SAH cases. However, the large motor neurons in the control cases often lacked hOGG1 immunoreactivity, although some neurons expressed hOGG1 in either homogeneous or fine granular patterns. In SAH cases, most large motor neurons showed a fine granular pattern proportional to the increased 8-oxoG immunoreactivity. However, only half of the remaining motor neurons in ALS expressed hOGG1 in the fine granular pattern, and the rest did not show any immunoreactivity. In addition, small aggregates of hMTH1 in the nuclei of the anterior horn cells were present in several ALS cases. Our results indicate that the oxidative damage accumulates in the mitochondria of motor neurons in ALS, and that hOGG1 does not repair the damage efficiently, which may lead to a loss of motor neurons in ALS.     

Expression of 8-oxoguanine DNA glycosylase is reduced and associated with neurofibrillary tangles in Alzheimer's disease brain

Recent studies have confirmed the role of reactive oxygen species in the pathogenesis of Alzheimer's disease (AD). 8-Oxo-2'-deoxyguanosine accumulation in AD brain has been discussed, but few studies of DNA repair enzymes in AD brain have been done. Further, a relationship between mitochondrial function and oxidative stress has been noticed. In this study, to evaluate the repair mechanism for oxidative DNA damage in AD brain, we investigated brain tissues from autopsy cases of AD and control cases using an antibody against the mitochondrial form of 8-oxoguanine DNA glycosylase (hOGG1-2a), an enzyme that repairs 8-oxo-2'-deoxyguanosine. hOGGI-2a is expressed mainly in the neuronal cytoplasm in both AD and control cases in regionally different manners. Expression of hOGG1-2a is decreased in the orbitofrontal gyrus and entorhinal cortex in AD compared to that in control cases. Immunoreactivity to hOGG1-2a is associated with neurofibrillary tangles, dystrophic neurites and reactive astrocytes in AD. Our results indicate that the repair enzyme for oxidative damage in mitochondrial DNA may not function appropriately in AD, and thus oxidative DNA damage in mitochondria may be involved in the pathomechanism of AD.     

Dorsal root rupture injury induces extension of astrocytic processes into the peripheral nervous system and expression of GDNF in astrocytes

Preganglionic brachial plexus injuries fall into two categories according to the lesion site, root avulsion injury and root rupture injury. The latter type of injury involves part of the peripheral nervous system (PNS) component at the injured spinal cord surface. Previous investigators have used rhizotomy of experimental animals as a model for dorsal root rupture injury. However, the effect on the central nervous system (CNS)–PNS junction accompanied by the mechanical stress from traction force is hard to estimate in this model. The current study aimed to demonstrate temporal molecular alterations from the CNS–PNS junction to the ruptured dorsal root after traction injury by immunohistochemical procedures. At 28 days after dorsal rupture injury, GFAP-positive structures could be clearly identified showing rather straight lines from the centro–peripheral junction toward the peripheral stump in the ruptured dorsal root. Immunoelectron microscopy for GFAP verified GFAP IR within the astrocytic processes at the injured dorsal root at 28 days after dorsal rupture injury. Glial cell line-derived neurotrophic factor immunoreactivity (GDNF IR) was slightly upregulated within the Schwann cell bodies on the injured dorsal root at 24–48 h after rupture injury. However, GDNF IR had appeared showing a process-like profile on the ruptured dorsal root by 28 days, and it was closely related with GFAP-positive structures. In contrast, a small increase in GFAP IR was only detected on the proximal side on the rhizotomized dorsal root at 28 days after rhizotomy. A marked decrease in NF IR and S-100 IR was observed at the ruptured dorsal root from 7 days. On the other hand, laminin IR was strongly upregulated on the ruptured dorsal root from 48 h to 7 days, and was still evident at 28 days. We therefore conclude that the astrocytes show a unique ability to extend their processes toward the stump. This ability may provide a new medium for the study of axonal regeneration in future clinical experiments.     

A network system of medical and welfare information service for the patients,their families,hospitals, local governments,and commercial companies in a medical service area

A service information system using the Internet, which connected the various people who are related to medical treatment and nursing welfare, was constructed. An intractable neurological disease patient who lives in the Onga district, Fukuoka, Japan, and the people who are related to the service were chosen as test users in an experimental model. The communicated service information was divided into open-use data (electronic bulletin board, welfare service, medical care service, and link to private company service home page) and closed-use data (the individual patient's hysterics). The open data server was installed in an Internet service provider The open data could be accessed not only by the patient, but also by the family, information center, companies, hospitals, and nursing commodity store related to patient's nursing and medical treatment. Closed data server was installed in an information center (public health center). Only patient and information center staff can access the closed data. Patients should search and collect the service information of various medical and welfare services by themselves. Therefore, services prepared for the patient are difficult to know, and they cannot be sufficiently utilized. With the use of this information system, all usable service information became accessible, and patients could easily use it. The electronic bulletin board system (BBS) was used by patients for knowing each other or each others' family, and was used as a device for exchange of wisdom. Also, the questions for the specialist, such as doctor, dentist, teacher, physical therapist, care manager, welfare office staff member, and public health nurse, and the answers were shown on the BBS. By arranging data file, a reference of various patients in question and answer, which appeared in this BBS, was made as "advisory hints" and was added to the open data. The advisory hints became the new service information for the patients and their family. This BBS discovered the possibility of becoming an important information source for companies, hospital and, administration to know the requirements of patients and their families and the kind of services to be served. Although suppliers provide medical and welfare services for the patient, there is a tendency that the service information is sent by the suppliers at their own convenience. The information system in which various people participated was constructed in order to collect information for the patient, taking a patient-oriented approach. The result of the model test showed that this information system using Internet technology is a good system for both the service supplier and its receiver.     

MGMT和Ki-67在胶质母细胞瘤中的表达对ACNU化疗预后的影响

背景与目的:胶质母细胞瘤是预后极差的常见颅内恶性肿瘤,手术切除、放疗和化疗联合应用是常规治疗方法;Ki-67是肿瘤细胞生长活跃程度的标志,与胶质瘤的分级显著相关;O6-甲基鸟嘌呤DNA甲基转移酶(MGMT)是一种DNA修复蛋白,其表达影响肿瘤对化疗药的敏感性。本研究通过免疫组织化学方法对胶质母细胞瘤的Ki-67和MGMT进行检测,探讨其对胶质母细胞瘤化疗预后的影响。方法:总结39例脑胶质母细胞瘤患者的性别、年龄、术前Karnofsky评分、生存时间等;将患者手术切除标本石蜡切片进行Ki-67和MGMT的免疫组织化学染色,计算细胞核染色阳性率;多元逐步回归分析法判断Ki-67和MGMT的表达与患者生存时间的关系。结果:本组病例男22例,女17例;年龄21～75岁,平均54.0岁;生存时间6～38个月,平均19.3个月,中位生存期17.0个月。Ki-67在所有标本有不同程度的表达,表现为胞核明显染色,Ki-67阳性率4.0%～26.6%,平均10.5%。MGMT除2例外均有不同程度表达,胞浆染色较淡,胞核可见浓染,MGMT胞核阳性率0%～51.4%,平均21.2%。Ki-67阳性率与生存时间无相关性。MGMT胞核阳性率与生存时间呈负相关(P=0.002)。结论:Ki-67在胶质母细胞瘤表达与肿瘤的预后无关。MGMT在胶质母细胞瘤表达与肿瘤化疗后的预后有关,MGMT的检测对胶质母细胞瘤术后化疗可能有指导意义。