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Objective. The aim of this study was to clarify the effect of a stable concentration of propofol on interictal high‐frequency oscillations (HFOs), which may contribute to identifying the epileptogenic zone intraoperatively for resection surgery. Methods. Nine patients with drug‐resistant focal epilepsy who underwent invasive pre‐surgical evaluation with chronic subdural electrodes were recruited. Five‐minute electrocorticograms during wakefulness, slow‐wave sleep, and under a stable brain concentration of propofol were recorded with the same electrodes. In each patient, 1–10 pairs of electrodes were selected for both electrodes with EEG changes within 5 seconds from the ictal onset (ictal pattern for 5 seconds [IP5]) and those outside the area of IP5 with no interictal epileptiform discharges (non‐epileptiform [nEPI]). The numbers of ripples (80‐250 Hz) and fast ripples (>250 Hz) were measured semi‐automatically using an established algorithm. Statistical testing was performed with a mixed effect model. Results. Thirty‐seven pairs of electrodes from nine patients were analysed for IP5 and 29 pairs from seven patients were analysed for nEPI. The numbers of HFOs differed between the areas (IP5 and nEPI) and among the conditions (wakefulness, slow‐wave sleep, propofol anaesthesia) (all p <0.01). The HFO occurrence rates were significantly higher for IP5 than those for nEPI in all conditions (for both ripples and fast ripples in all conditions; p <0.01). Significance. The occurrence rates of HFOs for IP5 were significantly higher than those for nEPI under propofol anaesthesia. These are fundamental findings for intraoperative HFO analysis, however, the following limitations should be considered: physiological HFOs could not be completely differentiated from pathological HFOs; in order to apply an HFO detector, an appropriate cut‐off threshold is needed; an artefact of the impulse response filter appears as an HFO; and the series was comprised of a small number of heterogeneous patients.

Background. Brain dysfunction in Japanese benign adult familial myoclonus epilepsy (BAFME) has not been elucidated. Aim. To clarify diffuse brain dysfunction as indicated by posterior dominant rhythm (PDR) slowing in patients with BAFME. Methods. The frequency of PDR on EEG was studied in 19 BAFME patients (50.6±15.7 years) and 38 age‐matched control subjects (50.1±14.5 years). We investigated the relationship between age and PDR in both groups. Results. PDR frequency in the patient group (9.1±0.7 Hz) was significantly slower than that of age‐matched control subjects (10.4±1.1 Hz; p<0.0001), regardless of the use of anticonvulsants. There was no significant difference in PDR slowing with age between groups. Conclusion. These findings suggest that Japanese patients with BAFME have mild diffuse brain dysfunction with minimal progression.

We recently reported clinical anticipation in Japanese families with benign adult familial myoclonus epilepsy (BAFME). However, it remains unknown whether clinical anticipation is predominantly associated with paternal or maternal transmission. We investigated the relationship between gender of the transmitting parent and clinical anticipation in nine BAFME families. Clinical anticipation regarding either cortical tremor or generalised seizures was observed in all 12 parent/child pairs (8 mother/child pairs and 4 father/child pairs). Moreover, a higher degree of clinical anticipation was associated with maternal transmission than with paternal transmission (p=0.03). Although a causative gene for BAFME still remains unknown, our finding suggests that BAFME and diseases with unstable expanding repeats, including those in non-coding regions, might share a similar molecular mechanism because such diseases often show clinical anticipation with maternal transmission.

We recently reported clinical anticipation in Japanese families with benign adult familial myoclonus epilepsy (BAFME). However, it remains unknown whether clinical anticipation is predominantly associated with paternal or maternal transmission. We investigated the relationship between gender of the transmitting parent and clinical anticipation in nine BAFME families. Clinical anticipation regarding either cortical tremor or generalised seizures was observed in all 12 parent/child pairs (8 mother/child pairs and 4 father/child pairs). Moreover, a higher degree of clinical anticipation was associated with maternal transmission than with paternal transmission (p=0.03). Although a causative gene for BAFME still remains unknown, our finding suggests that BAFME and diseases with unstable expanding repeats, including those in non‐coding regions, might share a similar molecular mechanism because such diseases often show clinical anticipation with maternal transmission.

Argon plasma coagulation (APC) is considered to be a safe thermocoagulation technique, but some reports show perforation and deformity during and after APC. In this study, we investigated the usefulness of prior submucosal injection for APC. APC over the mucosa was performed on fresh resected porcine esophagus, stomach, and colon with prior submucosal injection of normal saline (injection group) and without it (control group). The depth of tissue damage increased linearly with pulse duration up to the shallower submucosal layer in both groups. After that, tissue damage in the injection group remained confined to the shallower submucosal layer under any condition, whereas that in the control group continued to extend. The tissue damages of the injection groups were significantly (P<0.05) shallower than those of the control groups that reached the deeper submucosal layer in all the organs. Submucosal injection of normal saline before the application of APC may limit tissue damage and prevent perforation and deformity.

Showing the safety of argon plasma coagulation (APC) over mucosal defects duringafter endoscopic mucosal resection (EMR), 2 studies using resected pig (ex vivo) and living minipig (in vivo) stomachs were performed. As an ex vivo study, APC was applied over mucosal defects in 2 groups; with prior submucosal saline injection and without injection. Only subtle tissue damage was observed in the injection group, whereas apparent damage was observed in the noninjection group. The damaged distances in depth significantly increased as the pulse duration increased and those at the pulse duration of 4 seconds, which might be maximal in clinical practice, were approximately 1 mm. As an in vivo study, APC was applied over mucosal defects immediately after EMR. Only subtle tissue damage was observed even at the pulse duration of 20 seconds as shown in the ex vivo study. APC can be performed safely over the mucosal defects duringafter EMR.

We compared the phagocytosis of immune complexes (IC) and iC3b-opsonized derivatives (iC3b-IC) by human neutrophils. The phagocytosis of iC3b-IC via FcγR and CR3 was much greater than that of IC via FcγR alone. Adding ethanol to the cells decreased iC3b-IC phagocytosis to that of IC, which was not affected by these reagents, suggesting that the enhanced phagocytosis is attributable to CR3-mediated phospholipase D activation. The IC phagocytosis was inhibited more effectively by anti-FcγIIIB, whereas the iC3b-IC phagocytosis was partly inhibited only by anti-FcγRII. The main FcγR might differ in IC and iC3b-IC phagocytosis.

The paper presents an autopsy case of mixed connective tissue disease (MCTD) with pulmonary hypertension (PH) and a review of literature. A 33-year-old woman with Raynaud's phenomenon and dyspnea of one year duration was diagnosed as having MCTD on the basis of a higher titer (1:163,840) of serum antibodies to the ribonucleoprotein (RNP). Cardiac catheterization showed complicating PH, confirmed an autopsy by the findings of concentric intimal cellular proliferation and typical plexiform lesions in the small arteries and arterioles of the lung, suggesting primary PH. Fatal PH with MCTD has been reported only 6 cases in literature including our case. All were young females, with histopathological findings consistent with plexogenic pulmonary arteriopathy in 5 cases and with recurrent pulmonary thromboembolism in the other. The aetiology of PH is still unknown, but it may be due to vasoconstriction evoked by the hyper-reactivity of the vessels.

In 12 normal subjects, use of ear densitography permitted measurement of systolic time intervals (STI) during uninterrupted treadmill exercise to over 90 percent maximal heart rate on a modified Bruce protocol. Results for control (sitting → standing) → end-exercise at 18 minutes → 10 minutes' sitting recovery were—heart rate (HR): (77→86)→171→98 beats per minute; preejection period (PEP): (106→111)→49→110 msec; ejection time index (ETI) (351→330)→380→366 msec; PEP/LVET (0.42→0.49)→0.29→0.45. Heart rate increased steadily to 18 minutes. In contrast, the PEP/LVET decrease was almost complete by three minutes and both ETI and PEP responses were bimodal with respective plateaus between three and six minutes and three and nine minutes. All STI and HR curves showed rapid restitution during early recovery. The changes during treadmill exercise were numerically comparable to those during bicycle exercise at a common heart rate. The results indicate that it is technically feasible to measure systolic time intervals with precision during uninterrupted treadmill exercise; responses to treadmill exercise were in the direction expected and quantitatively comparable to bicycle exercise at comparable stress level. These observations provide the technical and physiologic bases for applying this method in clinical treadmill exercise testing.

We compared the phagocytosis of immune complexes (IC) and iC3b‐opsonized derivatives (iC3b‐IC) by human neutrophils. The phagocytosis of iC3b‐IC via FcγR and CR3 was much greater than that of IC via FcγR alone. Adding ethanol to the cells decreased iC3b‐IC phagocytosis to that of IC, which was not affected by these reagents, suggesting that the enhanced phagocytosis is attributable to CR3‐mediated phospholipase D activation. The IC phagocytosis was inhibited more effectively by anti‐FcγIIIB, whereas the iC3b‐IC phagocytosis was partly inhibited only by anti‐FcγRII. The main FcγR might differ in IC and iC3b‐IC phagocytosis.

ABSTRACTCapsule-forming Klebsiella pneumoniaeK1 caused primary liver abscess in two household members of a family. The causative isolates had identical pulsed-field gel electrophoresis patterns and were determined to be sequence type 23. An additional member of the family was found to carry the same strain without clinical manifestation.

Wakefulness and sleep arise from global changes in brain physiology that may also govern the flow of neural activity between cortical regions responsible for perceptual processing versus planning and action. To test whether and how the sleep/wake cycle affects the overall propagation of neural activity in large-scale brain networks, we applied single-pulse electrical stimulation (SPES) in patients implanted with intracranial EEG electrodes for epilepsy surgery. SPES elicited cortico-cortical spectral responses at high-gamma frequencies (CCSRHG, 80-150 Hz), which indexes changes in neuronal population firing rates. Using event-related causality (ERC) analysis, we found that the overall patterns of neural propagation among sites with CCSRHG were different during wakefulness and different sleep stages. For example, stimulation of frontal lobe elicited greater propagation toward parietal lobe during slow-wave sleep than during wakefulness. During REM sleep, we observed a decrease in propagation within frontal lobe, and an increase in propagation within parietal lobe, elicited by frontal and parietal stimulation, respectively. These biases in the directionality of large-scale cortical network dynamics during REM sleep could potentially account for some of the unique experiential aspects of this sleep stage. Together these findings suggest that the regulation of conscious awareness and sleep is associated with differences in the balance of neural propagation across large-scale frontal-parietal networks.