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Background Some adults suffer sudden cardiac death after previous surgical repair of tetralogy of Fallot (TOF), and in such cases, ventricular tachycardia is believed to be the most frequent cause of death. However, we report a case of cardiac arrest due to paroxysmal complete atrioventricular block in an adult with dextrocardia and repaired TOF. Case summary A 49-year-old woman with dextrocardia and a history of surgical treatment for TOF lost consciousness three times. A previously implanted loop recorder showed a 60-second cardiac arrest, and complete atrioventricular block was diagnosed. An electrophysiological study showed prolongation of the His-ventricular interval but no ventricular tachycardia. A dual chamber pacemaker was implanted, and there has been no recurrence of syncope in the 23 months since implantation. Discussion There is little evidence for paroxysmal complete atrioventricular block in patients with repaired TOF. This case suggests that paroxysmal complete atrioventricular block can occur late after surgical repair of TOF, and research needs to elucidate whether it is the cause of sudden cardiac death in some patients with TOF.

Synovitis, acne, pustulosis, hyperostosis and osteitis (SAPHO) syndrome has been proposed to describe a clinicoradiological entity manifesting in the joints, skin and bones. We describe a patient with SAPHO syndrome for whom bilateral tonsillectomy was effective for the treatment of arthralgia, which was quantified using multiple pain scales.

We demonstrate quantitative electron holographic tomography using a latex sphere as a simple example. Although a simple object is used, we believe that the observations made in this study will lead to further developments in electron holographic tomography. In particular, we make the quantitative interpretation of artifacts caused by incomplete angular information, i.e. a 'missing wedge'.

Background. Chronic low oxygen in the tubulointerstitial area is a crucial cause of renal degradation and tubulointerstitial damage. Previous reports have suggested that the maintenance of renal blood flow plays a role in the suppression of progressive renal damage. Neovascularization is important for the maintenance of blood flow. We studied the production of angiogenic factors by culturing renal proximal tubular epithelial cells (PTEC) under hypoxic conditions. Methods. Cultured PTEC were exposed to normal and low-oxygen conditions. The levels of angiogenin (ANG) and vascular endothelial growth factor (VEGF) in the cell supernatants were measured by enzyme-linked immunosorbent assay. The messenger RNAs (mRNAs) of ANG and VEGF in the PTEC were examined by real-time reverse transcriptase polymerase chain reaction (real-time RT–PCR). The presence of ANG, VEGF and hypoxia-inducible factor-1 (HIF-1) was studied by immunofluorescence techniques. The effect of cobalt chloride (CoCl2), which is an HIF-1 inducer, on the production of ANG and VEGF was also examined in order to elucidate the contribution of the HIF-1 pathway to the production of these cytokines. Results. ANG and VEGF were demonstrated to exist in the cell supernatants, and ANG and VEGF mRNAs were detected in the PTEC. Hypoxic conditions stimulated the secretion of ANG (2.5-fold vs normoxia, P

In this study, Cu and Fe single crystals are used to examine the change in secondary electron intensity associated with Ga(+) ion channelling in a focused ion beam (FIB) system. The single crystals having three different orientations are tilted with respect to the beam incidence and the resulting variation in the secondary electron intensity is measured through the variation in brightness of the crystals. It is shown that intensity minima appear at the beam directions normal to the lower indices of the crystal orientations. The appearance of the intensity minima including the magnitude of the minima is consistent with the prediction based on the event of ion channelling in the crystal and is affected by the crystal structure. The effect of background on the intensity minima is discussed in this study. It is suggested that the presence of the intensity minima may be used to identify a crystal orientation including a crystal structure.

Background Vestibular schwannoma (VS) is a tumor of the vestibular nerve that transmits balance information from the inner ear to the brain. Sensorineural hearing loss occurs in 95% of patients with these tumors, but the cause of this loss is not well understood. We posit a role of VS-secreted extracellular vesicles (EVs) as a major contributing factor in cochlear nerve damage. Methods Using differential centrifugation, we isolated EVs from VS cell line HEI-193 and primary cultured human VS cells from patients with good hearing or poor hearing. The EVs were characterized using a Nanosight device and transmission electron microscopy and by extracting their RNA content. The EVs' effects on cultured murine spiral ganglion cells and organotypic cochlear cultures were studied using a transwell dual-culture system and by direct labeling of EVs with PKH-67 dye. EV-induced changes in cochlear cells were quantified using confocal immunohistochemistry. Transfection of VS cells with a green fluorescent protein-containing plasmid was confirmed with reverse transcription PCR. Results Human VS cells, from patients with poor hearing, produced EVs that could damage both cultured murine cochlear sensory cells and neurons. In contrast, EVs derived from VS cells from patients with good hearing did not damage the cultured cochlear cells. Conclusions This is the first report on EVs derived from VSs and on the capacity of EVs from VSs from patients with hearing loss to selectively damage cochlear cells, thereby identifying a potential novel mechanism of VS-associated sensorineural hearing loss.

Serratia Mn-superoxide dismutase (SOD) was modified with dextran (Dx) of M.W. 80K and polyethyleneglycol (PEG) of M.W. 5K. SOD was modified at 34% of its free amino groups by Dx. DX-SOD retained 67% of the enzymatic activity of native SOD and had cross-reacted less with anti-SOD in vitro but higher immunogenicity against SOD in vivo. SOD was modified at 24% of the free amino groups by PEG. PEG-SOD retained 52% of the enzymatic activity, had lower antigenicity and immunogenicity, and induced immuno-tolerance to SOD. The half-life of PEG-SOD in the rat blood circulation was about ten times as long as that of SOD. PEG-modification of SOD enhanced its pharmacological activities as an anti-inflammatory and radioprotective agent.

A preparation containing formate dehydrogenase, cytochrome b1 and nitrate reductas_??_ was solubilized and partially purified from the particulate fraction of E. coli cells growr_??_ anaerobically under the conditions favorable for nitrate respiration. Some properties o_??_ formate dehydrogenase and cytochrome b1 in this purified preparation were investigated It was suggested that formate dehydrogenase is a metalloflavoprotein with essential sulf_??_ hydryl groups. Its activity was strongly bu_??_ reversibly inhibited by molecular oxyge_??_ The prosthetic group of cytochrome b1 was decisively identified as protoheme, and it was found that the cytochrome is autoxidizable. The reduction of cytochrome b1 by formate was shown to require, in addition to formate dehydrogenase, a lipid-soluble factor which could be replaced by vitamin K3 in the solubilized system.We are indefted to Drs. H. Maeno and S. Sakakibara for generous gifts of crude snake venonand crystalline protohemin, respectively.