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The aim of this study was to investigate the changes of brain electric field induced by symptom provocation in patients with obsessive-compulsive disorder (OCD) in comparison to healthy controls in the resting state. For this purpose, EEG recordings in conditions of initial rest, clean control, symptom provocation by imaginal exposure, and final rest were used for computing spatiotemporal activity characteristics based on microstate segmentation. Within-group comparisons were significant for the symptom provocation condition: OCD showed high global field power (GFP) and transition rates into a medial frontal microstate, whereas healthy controls showed high frequency of occurrence and high percent of dwelling time for a medial occipitoparietal microstate. Between-group comparisons demonstrated significantly lower GFP and dwelling time for the medial occipitoparietal microstate in OCD in several conditions including initial rest and symptom provocation. In addition, OCD compared to healthy controls showed significant instability of the medial occipitoparietal microstate, with high preference for transitions into the medial frontal microstate. In conclusion, during rest and symptom provocation, OCD patients make preferential use of a medial frontal brain network, with concomitant reduction of use of a medial occipitoparietal network, as shown by dwelling times, explained variance, and dynamic transition rates. These findings support the idea of a possible biological marker for OCD, which might correspond to pathological hyperactivation of the frontal control network.

Objectives: eLORETA (exact low-resolution brain electromagnetic tomography) is a technique created by Pascual-Marqui et al. [Int J Psychophysiol. 1994 Oct; 18(1): 49–65] for the 3-dimensional representation of current source density in the brain by electroencephalography (EEG) data. Kurtosis analysis allows for the identification of spiky activity in the brain. In this study, we focused on the evaluation of the reliability of eLORETA kurtosis analysis. For this purpose, the results of eLORETA kurtosis source localization of paroxysmal activity in EEG were compared with those of eLORETA current source density (CSD) analysis of EEG data in 3 epilepsy patients with partial seizures. Methods: EEG was measured using a digital EEG system with 19 channels. We set the bandpass filter at traditional frequency band settings (1–4, 4–8, 8–15, 15–30, and 30–60 Hz) and 5–10 and 20–70 Hz and performed eLORETA kurtosis to compare the source localization of paroxysmal activity with that of visual interpretation of EEG data and CSD analysis of eLORETA in focal epilepsy patients. Results: The eLORETA kurtosis analysis of EEG data preprocessed by bandpass filtering from 20 to 70 Hz and traditional frequency band settings did not show any discrete paroxysmal source activity compatible with the results of CSD analysis of eLORETA. In all 3 cases, eLORETA kurtosis analysis filtered at 5–10 Hz showed paroxysmal activities in the theta band, which were all consistent with the visual inspection results and the CSD analysis results. Discussion: Our findings suggested that eLORETA kurtosis analysis of EEG data might be useful for the identification of spiky paroxysmal activity sources in epilepsy patients. Since EEG is widely used in the clinical practice of epilepsy, eLORETA kurtosis analysis is a promising method that can be applied to epileptic activity mapping.

Aims Although increased digitalis-like immunoreactive substances have been found in cases of hypertension and heart failure, no information is available about digitalis-like immunoreactive substances in patients with hypertrophic cardiomyopathy. We investigated digitalis-like immunoreactive substances in the plasma and biopsied specimens of patients with hypertrophic cardiomyopathy. Methods and Results In 40 patients with hypertrophic cardiomyopathy (27 with the non-obstructive type and 13 with the obstructive type), the plasma concentration of digitalis-like immunoreactive substances was studied by fluorescence polarization immunoassay. Right ventricular endomyocardial biopsy specimens were analysed immunohistochemically, using a monoclonal antibody against digoxin. An increase in digitalis-like immunoreactive substances of more than 0·2ng.ml−1in plasma was found in six of 27 patients with non-obstructive hypertrophic cardiomyopathy (22·2%) and five of 13 with obstructive hypertrophic cardiomyopathy (38·4%). Under light microscopy, positive staining against the antibody was observed heterogeneously on some cardiocytes. In non-obstructive hypertrophic cardiomyopathy, digitalis-like immunoreactive substances in the plasma correlated with the left atrial dimension and inversely with the cardiac index. In obstructive hypertrophic cardiomyopathy, plasma and myocardial digitalis-like immunoreactive substances were positively correlated; they also correlated with left ventricular end-diastolic pressures. Under electron microscopy, digitalis-like immunoreactive substances were detected at the sarcolemma in the free wall, T-tubules, intercalated discs and Z-bands of cardiocytes. Conclusions Increased digitalis-like immunoreactive substances in plasma and cardiocytes, which may have been caused by pressure and/or volume overload, were found in patients with hypertrophic cardiomyopathy. Digitalis-like immunoreactive substances may act on the sarcolemma of cardiocytes and be transported into the cytoplasm.

highlights A comparative study of frontotemporal dementia (FTD), Alzheimer's disease (AD), and healthy control subjects (NC) was carried out in terms of the cortical localization of oscillatory EEG activity. As compared to NC, FTD had significantly reduced alpha generators in fronto-temporal cortices, while AD showed significantly stronger delta generators that included the frontal lobes. ROC curves demonstrate a moderate separation of FTD, AD, and NC groups. abstract Objective: To determine the electrophysiological characteristics of frontotemporal dementia (FTD) and the distinction with Alzheimer's disease (AD). Methods: We performed analyses of global field power (GFP) which is a measure of whole brain electric field strength, and EEG neuroimaging analyses with sLORETA (standardized low resolution electromag- netic tomography), in the mild stages of FTD (n = 19; mean age = 68.11 ± 7.77) and AD (n = 19; mean age = 69.42 ± 9.57) patients, and normal control (NC) subjects (n = 22; mean age = 66.13 ± 6.02). Results: In the GFP analysis, significant group effects were observed in the delta (1.5-6.0 Hz), alpha1 (8.5- 10.0 Hz), and beta1 (12.5-18.0 Hz) bands. In sLORETA analysis, differences in activity were observed in the alpha1 band (NC > FTD) in the orbital frontal and temporal lobe, in the delta band (AD > NC) in wide- spread areas including the frontal lobe, and in the beta1 band (FTD > AD) in the parietal lobe and senso- rimotor area. Conclusions: Differential patterns of brain regions and EEG frequency bands were observed between the FTD and AD groups in terms of pathological activity. Significance: FTD and AD patients in the early stages displayed different patterns in the cortical localiza- tion of oscillatory activity across different frequency bands.

The left atrial (LA) appendage is the most common site of thrombus formation in patients with atrial fibrillation, and integrated backscatter allows the quantiative assessment of LA spontaneous echo contrast (SEC). Integrated backscatter was used to examine the significance of measuring appendage SEC, specifically in relation to echocardiographic variables implying thromboembolism, in patients with chronic nonvalvular atrial fibrillation.Fifty-two patients with chronic nonvalvular atrial fibrillation and no prior anticoagulant therapy (35 men, 17 women, mean age 66 +/- 7 years) underwent transesophageal echocardiography with integrated backscatter analysis. The LA and LA appendage integrated backscatter intensity were measured with the regions of interest placed in the LA cavity and the appendage, respectively. The integrated backscatter intensity values for these two chambers (corrected "LA" and "LA appendage" integrated backscatter intensity, respectively) were corrected using values from the left ventricular cavity.The LA appendage integrated backscatter intensity values were available in 44 patients (85%). Overall, the corrected LA appendage integrated backscatter intensity was significantly increased compared with the corrected LA integrated backscatter intensity (2.8 +/- 2.2 vs 2.0 +/- 1.8 dB, p0.001). The corrected LA appendage integrated backscatter intensity was inversely correlated with the LA appendage velocity (r = -0.37, p0.05), but not with the LA dimension, appendage size, or left ventricular function. The corrected appendage integrated backscatter intensity (4.5 +/- 2.3 vs 2.4 +/- 1.9 dB, p0.01) and LA integrated backscatter intensity (3.2 +/- 2.1 vs 1.7 +/- 1.7 dB, p0.05) were higher in patients who had LA appendage thrombus (n = 8) than those who did not. With the corrected appendage integrated backscatter intensity set ator = 2.5 dB, the sensitivity for the presence of appendage thrombus was 88% and the specificity was 64%.Patients with chronic nonvalvular atrial fibrillation had a denser SEC in the LA appendage compared with SEC in the main LA cavity. The severity of the appendage SEC was influenced by the LA appendage function rather than its size. Quantification of SEC in the appendage, rather than main LA cavity, was more valuable for assessing embolic potential.

Long-chain fatty acids (LCFA) are the major energy substrate for heart and their oxidation is important for achieving maximal cardiac work. However, the mechanism of uptake of LCFA by myocardium has not been clarified. We previously reported that bovine myocardial LCFA transporter has a sequence homology to human CD36. Clinically, total defect of myocardial uptake of radiolabeled long-chain fatty acid analog [123I-BMIPP: Iodine-123 15-(p-iodophenyl)-(R,S)-methylpentadecanoic acid] has been reported in some restricted cases, but the etiology has not been clarified. In the present study, we analyzed CD36 expression and CD36 gene in subjects who showed total lack of myocardial 123I-BMIPP accumulation, and, vice versa, evaluated myocardial 123I-BMIPP uptake in subjects with CD36 deficiency. Four unrelated subjects were evaluated, Two were found to have negative myocardial LCFA accumulation by 123I-BMIPP scintigraphy, after which the expression of CD36 on their platelets and monocytes was analyzed. Remaining two subjects were identified as CD36 deficiency by screening, then 123I-BMIPP scintigraphy was performed. Expression of CD36 on platelets and monocytes was measured by flow cytometric analysis. The molecular defects responsible for CD36 deficiency was detected by allele-specific restriction enzyme analysis. CD36 expression was totally deficient in all 4 subjects on both platelets and monocytes. Two subjects were homozygous for a 478C--T mutation. One was heterozygous for the dinucleotide deletion of exon V and single nucleotide insertion of exon X, and remaining one was considered to be heterozygous for the dinucleotide deletion of exon V and an unknown gene abnormality. All cases demonstrated a completely negative accumulation of myocardial LCFA despite of normal myocardial perfusion, which was evaluated by thallium scintigraphy. In addition, all cases demonstrated apparently normal hepatic LCFA accumulation Thus, these findings suggested that CD36 acts as a major myocardial specific LCFA transporter in humans.

To elucidate the heart involvement associated with influenza virus infection, the authors studied the hearts of influenza A/PR/8/34 virus-inoculated ICR mice by light and electron microscopy, cardiac catheterization, virus assay, and indirect immunofluorescence. Light microscopy showed small necrotic foci with inflammatory cell infiltration spreading in the myocardium on days 3 to 7 and evidence of healing by day 9 after inoculation. Electron microscopy demonstrated that necrotic cell debris was phagocytosed by macrophages, and that degenerating cardiocytes, macrophages, and lymphocytes were often in close contact, suggesting immunologic interactions, and that platelet thrombi were present in some capillaries on days 3 to 5. Both systolic and diastolic functions of the left ventricle (LV) were impaired on days 3 to 9 and recovered almost to normal by day 14. The virus could be isolated from the heart on days 3 to 7. Immunofluorescent preparations showed virus antigens in the vascular walls and cardiocytes until day 7. These results suggest that the acute cardiac injury was related to cytotoxic immunologic interactions, virus-induced cytolysis and, at least in part, to ischemia due to intracapillary thrombosis. Compared with coxsackie B3 myocarditis in mice, the influenza myocarditis was mild in degree and short in duration, but the influenza infection is a most common and repetitive disease in humans. The clinical implications of this animal model with myocarditis are discussed.

1) Thirty-eight cases of idiopathic pericarditis in our institutes were analyzed and were classified into 3; group A: clinical picture of pericarditis, group B: clinical picture of peri-myocarditis and group C: dominant clinical picture of chronic pericardial effusion. 2) All cases of group A showed a good clinical course. 3) In group B cases with complete A--V block continued to have heart block with significant myocardial changes, and the prognosis may not be good. 4) Many cases of group C belonged to elderly female and the etiology was unclear. 5) Viral pericarditis was proven in only one case.

A result of mass-screening for uterine cervical cancer conducted by Hyogo Cancer Hospital performed using mobilunit from 1965 to 1978 was analyzed and presented in this paper. The total number of women taking our initial screening examination was 188, 183.5% women screened or 9,447 were transferred for the further accurate examination. The rate of participants for this 2nd examination was 93.8% on the average. In this initial screening examination, a result of cytological examination on Papanicolaou's classification was as follows; 94.87% for class I and II, 4.81% for class III, and 0.21% for class IV and V. In the 2nd examination, the rate of the negative, suspected positive were 70.6%, 22.5% and 6.9% respectively. 759 cervical cancers were detected in our screening. The detecting rate of cervical cancer was 0.4% among initially screened women and 8.6% among women who appeared for the accurate examination. As the detecting rate among women for the 2nd examination became higher year by year (20% increase during recent 3 years), the accuracy of our screening methodology appeared to be improving. The incidence rate of cervical cancer in our screening was classified as stage 0; 49.0%, Ia; 36.4%, Ib; 9.1%, II; 3.9% an III; 1.6%. The most of detected cancer was occupied by cancer in situ and early invasive cancer. Annual review showed there is a gradual and steady increase in incidence rate to stage 0 in our screening.

In an attempt to prove the hypothesis that virus myocarditis may be a cause of idiopathic cardiomyopathy, clinical and experimental studies were performed. Eleven patients with a presumptive or proven diagnosis of virus myocarditis were followed for one and a half to 13 years after the acute illness. One patient died in the acute stage, six recovered completely and one continued to have bifascicular block without subjective symptoms. Three patients had exertional dyspnea, cardiomegaly and an abnormal ECG three to 13 years after the onset, and two of them had an enlarged LV cavity with reduced EF and histological changes in myocardial biopsies. The clinical picture in these three cases was similar to that seen in congestive cardiomyopathy. Clinical observations of the heart in an epidemic of coxsackie B 3 virus infection among school children revealed that 49 (19%) of 263 infected children had abnormal chest-X ray, electrocardiographic or echocardiographic findings one to 10 months after the onset, however none of them developed cardiomyopathy. In experimental infection of weanling golden hamsters with coxsackie B 3 virus (Nancy strain), all animals developed acute and severe myocarditis, and the virus was detected in the myocardium. Hemodynamic data suggested decreased contractility of the left ventricle in the acute stage. Histologically the heart showed focal myocardial necrosis and cellular infiltration without calcification, findings which resemble those in human doxsackie B virus myocarditi. Thus, the golden hamster is a better animal model than the mouse in studies on virus myocarditis and postcarditic cardiomyopathy.