Self-similarity of low-frequency earthquakes.

Low-frequency earthquakes are a particular class of slow earthquakes that provide a unique source of information on the physical processes along a subduction zone during the preparation of large earthquakes. Despite increasing detection of these events in recent years, their source mechanisms are still poorly characterised, and the relation between their magnitude and size remains controversial. Here, we present the source characterisation of more than 10,000 low-frequency earthquakes that occurred during tremor sequences in 2012-2016 along the Nankai subduction zone in western Shikoku, Japan. We show that the scaling of seismic moment versus corner frequency for these events is compatible with an inverse of the cube law, as widely observed for regular earthquakes. Their radiation, however, appears depleted in high-frequency content when compared to regular earthquakes. The displacement spectrum decays beyond the corner frequency with an omega-cube power law. Our result is consistent with shear rupture as the source mechanism for low-frequency earthquakes, and suggests a self-similar rupture process and constant stress drop. When investigating the dependence of the stress drop value on the rupture speed, we found that low-frequency earthquakes might propagate at lower rupture velocity than regular earthquakes, releasing smaller stress drop.

Silent KEL alleles identified from Japanese individuals with the Ko phenotype.

BACKGROUND AND OBJECTIVE: The rare Ko phenotype lacks all 36 antigens in the Kell blood system. The molecular basis of the Ko phenotype has been investigated, and more than 40 silent KEL alleles are reported by many investigators. The majority of silent alleles are the KEL*02 background. Here, we report molecular genetic analysis of the KEL gene in Japanese individuals with the Ko phenotype. MATERIALS AND METHODS: The Ko phenotype was screened from Japanese blood donors for several years using monoclonal anti-Ku or anti-K14 by an automated blood grouping system PK7300. Kell-related antigens were typed by standard tube tests. Genomic DNA was extracted from the blood samples, and KEL gene was analysed by polymerase chain reaction (PCR) and Sanger sequencing. RESULTS: We collected 35 Ko blood samples with K-k-, Kp(a-b-), Js(a-b-) and K14-. PCR and sequence analysis revealed that 11 individuals were homozygous for a mutant KEL allele with a c.299G>C (p.Cys100Ser) mutation (rs. 200268316). Three individuals were homozygous for the KEL*02N.24 allele that is c.715G>T (p.Glu239*), and one individual was homozygous for the KEL*02N.40 allele that is c.1474C>T (p.Arg492*). Five individuals were homozygous for novel KEL alleles with single-nucleotide mutations, four individuals had a c.2175delC (p.Pro725 fs*43), and one individual had a c.328delA (p.Arg110 fs*79). The remaining 15 individuals were compound heterozygous, and eight new alleles were identified from them. CONCLUSIONS: We identified three known and ten new silent KEL alleles from Japanese individuals with the Ko phenotype. The KEL allele with the c.299G>C (p.Cys100Ser) mutation was the most frequent.

Control of the wetting properties of

To investigate whether it is possible to control the wetting of ^{4}He crystals on a wall in superfluid, the contact angles of ^{4}He crystals were measured on rough and smooth walls at very low temperatures. A rough wall was prepared in a simple manner in which a commercially available coating agent for car mirrors, which makes the glass surface superhydrophobic, was used to coat a glass plate. The contact angles of ^{4}He crystals were increased by approximately 10^{∘} on the rough wall coated with the agent. Therefore, the increase in the repellency of ^{4}He crystals in superfluid was demonstrated to be possible on a very rough surface. The enhancement of the contact angles and a scanning electron microscopy image of the coated surface both suggest that a Cassie-Baxter state of ^{4}He crystals was realized on the surface; the crystals did not have full contact with the wall, but entrapped superfluid was present beneath the crystals in the hollow parts of the rough wall.

Geophysics. Migrating tremor off southern Kyushu as evidence for slow slip of a shallow subduction interface.

Detection of shallow slow earthquakes offers insight into the near-trench part of the subduction interface, an important region in the development of great earthquake ruptures and tsunami generation. Ocean-bottom monitoring of offshore seismicity off southern Kyushu, Japan, recorded a complete episode of low-frequency tremor, lasting for 1 month, that was associated with very-low-frequency earthquake (VLFE) activity in the shallow plate interface. The shallow tremor episode exhibited two migration modes reminiscent of deep tremor down-dip of the seismogenic zone in some other subduction zones: a large-scale slower propagation mode and a rapid reversal mode. These similarities in migration properties and the association with VLFEs strongly suggest that both the shallow and deep tremor and VLFE may be triggered by the migration of episodic slow slip events.

Modulatory effects of the GABAergic basal ganglia neurons on the PPN and the muscle tone inhibitory system in cats.

Pedunculopontine tegmental nucleus (PPN) contributes to the control muscle tone by modulating the activities of pontomedullary reticulospinal systems during wakefulness and rapid eye movement (REM) sleep. The PPN receives GABAergic projection from the substantia nigra pars reticulata (SNr), an output nucleus of the basal ganglia. Here we examined how GABAergic SNr-PPN projection controls the activity of the pontomedullary reticulospinal tract that constitutes muscle tone inhibitory system. Intracellular recording was made from 121 motoneurons in the lumbosacral segments in decerebrate cats (n=14). Short train pulses of stimuli (3 pulses with 5 ms intervals, 10-40 mA) applied to the PPN, where cholinergic neurons were densely distributed, evoked eye movements toward to the contralateral direction and bilaterally suppressed extensor muscle activities. The identical PPN stimulation induced IPSPs, which had a peak latency of 40-50 ms with a duration of 40-50 ms, in extensor and flexor motoneurons. The late-latency IPSPs were mediated by chloride ions. Microinjection of atropine sulfate (20 mM, 0.25 ml) into the pontine reticular formation (PRF) reduced the amplitude of the IPSPs. Although conditioning stimuli applied to the SNr (40-60 mA and 100 Hz) alone did not induce any postsynaptic effects on motoneurons, it reduced the amplitude of the PPN-induced IPSPs. Subsequent injection of bicuculline (5 mM, 0.25 ml) into the PPN blocked the SNr effects. Microinjections of NMDA (5 mM, 0.25 ml) and muscimol (5 mM, 0.25 ml) into the SNr reduced and increased the amplitude of the PPN-induced IPSPs, respectively. These results suggest that GABAergic basal ganglia output controls postural muscle tone by modulating the activity of cholinergic PPN neurons which activate the muscle tone inhibitory system. The SNr-PPN projection may contribute to not only control of muscle tone during movements in wakefulness but also modulation of muscular atonia of REM sleep. Dysfunction of the SNr-PPN projection may therefore be involved in sleep disturbances in basal ganglia disorders.

Facial exercise therapy for facial palsy: systematic review and meta-analysis.

UNLABELLED: The effectiveness of facial exercises therapy for facial palsy has been debated in systematic reviews but its effects are still not totally explained. OBJECTIVE: To perform a systematic review with meta-analysis to evaluate the effects of facial exercise therapy for facial palsy. DATA SOURCES: A search was performed in the following databases: Cochrane Controlled Trials Register Library, Cochrane Disease Group Trials Register, MEDLINE, EMBASE, LILACS, PEDro, Scielo and DARE from 1966 to 2010; the following keywords were used: 'idiopathic facial palsy', 'facial paralysis', 'Bell's palsy', 'physical therapy', 'exercise movement techniques', 'facial exercises', 'mime therapy' 'facial expression', 'massage' and 'randomized controlled trials'. REVIEW METHODS: The inclusion criteria were studies with facial exercises, associated or not with mirror biofeedback, to treat facial palsy. RESULTS: One hundred and thirty-two studies were found but only six met the inclusion criteria. All the studies were evaluated by two independent reviewers, following the recommendations of Cochrane Collaboration Handbook for assessment of risk of bias (kappa coefficient = 0.8). Only one study presented sufficient data to perform the meta-analysis, and significant improvements in functionality was found for the experimental group (standardized mean difference (SMD) = 13.90; 95% confidence interval (CI) 4.31, 23.49; P = 0.005). CONCLUSION: Facial exercise therapy is effective for facial palsy for the outcome functionality.

[Advanced thymic carcinoma effectively treated by surgical resection and postoperative radiation therapy: report of a case].

Thymic carcinomas are rare neoplasms, and standard treatment has not yet been established. We reported a case of advanced thymic carcinoma effectively treated by surgical resection and postoperative radiation therapy. A 71-year-old man was pointed out an abnormal shadow on chest X-ray. Chest computed tomography (CT) scan demonstrated an anterior mediastinal tumor. The tumor was diagnosed as carcinoma by CT-guided tumor biopsy and was extirpated completely with combined partial resection of the left lung. Microscopically, the tumor was diagnosed as thymic carcinoma with direct invasion to the left lung. Following postoperative radiation therapy, the patient is doing well without apparent recurrence 5 years after surgery.

Promoter polymorphisms in the IRF3 gene confer protection against systemic lupus erythematosus.

In order to identify a novel candidate gene in systemic lupus erythematosus (SLE), we analysed a panel of six genes encoding molecules involved in the type I interferon (IFN) system. We first identified variants in the five genes related to type I IFN pathway by sequencing. Genotyping of a panel of eight selected single-nucleotide polymorphisms (SNPs) in six candidate genes (TLR9, MYD88, IRF3, IRF7, IFNB1, IFNA17) was performed in 137 patients with SLE and matched with 152 healthy controls using polymerase chain reaction-restriction fragment length polymorphism analysis. In functional assay, quantitative real-time polymerase chain reaction was performed to assess constitutive IRF3 mRNA expression in peripheral blood mononuclear cells from healthy subjects with different IRF3 promoter haplotypes. Among eight SNPs genotyped, an IRF3 SNP at -925 was found to be associated with SLE after correction for multiple tests (corrected P=0.016). Of total five IRF3 SNPs genotyped, the promoter IRF3 SNPs -925A/G and -776C/T showed the most significant association with SLE. With regard to -925A/G, the frequency of GG genotype was significantly decreased among SLE patients compared with the control group (1.5% vs. 9.9%; chi(2)=10.0, P=0.0015, odds ratio 0.12, 95% confidence interval 0.027-0.554). Our experimental data indicated that constitutive IRF3 mRNA expression was significantly lower in cells carrying the minor G-T/G-T haplotype pair compared with those carrying the major A-C haplotype. In conclusion, we showed that the promoter SNPs of the IRF3 gene were significantly associated with resistance against SLE.

Turbulence in boundary flow of superfluid 4He triggered by free vortex rings.

The transition to turbulence in the boundary flow of superfluid 4He is investigated using a vortex-free vibrating wire. At high wire vibration velocities, we found that stable alternating flow around the wire enters a turbulent phase triggered by free vortex rings. Numerical simulations of vortex dynamics demonstrate that vortex rings can attach to the surface of an oscillating obstacle and expand unstably due to the boundary flow of the superfluid, forming turbulence. Experimental investigations indicate that the turbulent phase continues even after stopping the injection of vortex rings, which is also confirmed by the simulations.

Cellular basis of verruciform xanthoma: immunohistochemical and ultrastructural characterization.

BACKGROUND: Verruciform xanthoma (VX) holds two basic pathogenic interests: (1) Why and how do macrophage foam cells accumulate exclusively in the sub-basal papillae? and (2) What underlies the disease chronicity? Moreover, an unsolved question is which came first - epithelial hyperplasia or foam cell collection? MATERIALS AND METHODS: We analyzed 36 oral mucosal lesions to dissect a series of linked cellular changes in VX using immunohistochemical and ultrastructural techniques. RESULTS: Macrophage scavenger receptor-1 (MSR-1), monocyte chemoattractant protein-1 (MCP-1), CCR2, and oxidized low-density lipoprotein (ox-LDL) were all expressed by foam cells. VX epithelium showed reactivity for MCP-1, HLA-DR and IL8 in varying degrees, and showed a nearly 40% reduction in Langerhans cell density. In sub-epithelial inflammatory infiltrates, CD8+ T cells preponderated (>70%), but only a minority were positive for granzyme B (<1%). Keratinocyte/basal lamina complex exhibited disruption of basal lamina, squamatization and cytolysis of basal cells, fragmentation of desmosomes, and intraepithelial migration of macrophages. In severely inflamed papillae, necrotic foam cells were scavenged by adjacent macrophages. CONCLUSIONS: Under synergistic regulation of T cells, MCP-1/CCR2-mediated macrophage recruitment in the sub-basal papillae and the lysosomal engulfment of epithelial lipids by MSR-1-bearing macrophages may be central in VX formation. Once developed, ox-LDL-induced foam cell necrosis and macrophage-dependent debris disposal may cyclically perpetuate VX.

Amelioration of lacrimal gland inflammation by oral administration of K-13182 in Sjögren's syndrome model mice.

Regulation of the adhesion of mononuclear cells to endothelial cells is considered to be a critical step for the treatment of inflammatory diseases, including autoimmune diseases. K-13182 was identified as a novel inhibitor for these adhesions. K-13182 inhibited the expression of vascular cell adhesion molecule-1 (VCAM-1, CD106) on human umbilical vein endothelial cells (HUVECs) and on mouse vascular endothelial cell line (MAECs) induced by tumour necrosis factor (TNF)-alpha. K-13182 also inhibited the adhesion of mononuclear cells to these HUVECs and MAECs, indicating that K-13182 suppressed these adhesions mediated by cellular adhesion molecules including VCAM-1. To evaluate the therapeutic effect in autoimmune disease model mice, K-13182 was orally administered to non-obese diabetic (NOD) mice as Sjögren's syndrome (SS) model mice. Severe destructive inflammatory lesions were observed in the lacrimal glands of vehicle-treated control mice; however, 8-week administration of K-13182 inhibited the mononuclear cell infiltration into the inflammatory lesions of the lacrimal glands. In K-13182-treated mice, the decrease in tear secretion was also prevented compared to the control mice. In addition, the apoptosis and the expression of FasL (CD178), perforin, and granzyme A was suppressed in the lacrimal glands of K-13182-treated mice. Therefore, K-13182 demonstrated the possibility of therapeutic efficacy for the inflammatory region of autoimmune disease model mice. These data reveal that VCAM-1 is a promising target molecule for the treatment of autoimmune diseases as a therapeutic strategy and that K-13182 has the potential as a new anti-inflammatory drug for SS.

Hamartomatous proliferations of odontogenic epithelium within the jaws: a potential histogenetic source of intraosseous epithelial odontogenic tumors.

BACKGROUND: The jawbone is replete with a vestige of odontogenesis. The overall consensus is that intraosseous remnants of the enamel organ and dental lamina are the only histogenetic option for central epithelial odontogenic tumors. Curiously, incipient tumors or possible precursor conditions of residual odontogenic epithelium have rarely been reported in the literature. METHODS: We microscopically evaluated 39,660 biopsy samples to determine the presence of a tumor-like odontogenic epithelial nodule in the maxilla and mandible. RESULTS: Seven intraosseous specimens that associated with a focal proliferation of odontogenic epithelium were retrieved. Six hamartomatous processes showed four different morphologic patterns comparable with the tumor nests comprising ameloblastoma (n = 1), squamous odontogenic tumor (n=1), calcifying epithelial odontogenic tumor (n=2) and calcifying cystic odontogenic tumor (n=2). Among six lesions, four were the intrafollicular development. The remaining case of interest was multiple hyperplastic clear rests of Malassez in association with an impacted tooth. CONCLUSION: Although it is impossible to predict the fate of these microscopic structures of hamartomatous character, the present case series indicates that any of the dormant embryonic residues of odontogenic epithelium can return to an active state, capable of non-reactive, probably neoplastic proliferation of pathological significance.

Association between ADAM33 polymorphisms and adult asthma in the Japanese population.

BACKGROUND: ADAM33, a member of the ADAM (a disintegrin and metalloprotease) family, is a putative asthma susceptibility gene recently identified by positional cloning. It is important to know whether the association exists in ethnically diverse populations. OBJECTIVE: To assess whether genetic functional variants of ADAM33 relate to the susceptibility or some phenotypes in adult patients with bronchial asthma in a Japanese population. METHODS: We searched for single nucleotide polymorphisms (SNPs) in ADAM33 by PCR-directed sequencing and identified 48 SNPs. Fourteen SNPs were selected with regard to the LD pattern, and genotyped by Taq-Man and PCR-RFLP methods. We conducted an association study of ADAM33 with 504 adult asthmatic patients and 651 controls, and haplotype analyses of related variants were performed. RESULTS: Significant associations with asthma were found for the SNPs T1 (Met764Thr), T2 (Pro774Ser), S2 and V-3 (with the lowest P-value for T1, P = 0.0015; OR 0.63). We analysed the haplotype using these four polymorphisms, and found a positive association with haplotype CCTG (P = 0.0024). CONCLUSION: Our results replicate associations reported recently in other ethnic populations, and suggest that the ADAM33 gene is involved in the development of asthma through genetic polymorphisms.

Intraparotid pseudoglandular schwannoma.

A unique intraparotid location of a rare pseudoglandular schwannoma is described. Although the diagnosis of schwannoma could readily be substantiated, accurate subtyping was initially mislabeled. The pitfall was in failing to acknowledge the presence of multiple well-formed gland-like structures, which is instantly thought to be cystically dilated salivary ducts. Immunohistochemically, epithelial-appearing cells lining the duct-like spaces proved to be schwannian in nature. Interpretation of an immediately recognizable gland-like architecture is more problematic when a pseudoglandular variant originates from a nerve coursing through the gland, as here.

Peripheral odontogenic tumor: a clinicopathologic study of 30 cases. General features and hamartomatous lesions.

BACKGROUND: Peripheral odontogenic tumors (POT), either neoplastic or hamartomatous, are rare. This study briefly summarizes the general features of POT and selectively reviews the histomorphologic spectrum of under-recognized hamartomatous lesions that we have designated peripheral odontogenic hamartomas (POH) in order to shed more light into the pathogenesis of POT. METHODS: Archival material accessioned at our institutions between 1970 and 2004 was systematically searched to identify examples of POT/POH. RESULTS: Among 39 660 biopsies, we retrieved 25 cases of 'classical' POT and five cases of 'unique' POH. Odontogenic fibroma and ameloblastoma were by far the most common. Of POH, two purely epithelial lesions showed multiple strands of basaloid rests [odontogenic gingival epithelial hamartoma (OGEH)] and a conglomerate of polyhedral epithelium, ghost cells and concentric calcifications (calcifying epithelial odontogenic tumor-like hamartoma), respectively. OGEH and peripheral squamous odontogenic tumor (PSOT) deserve to be a related entity. In two types of mixed POH, ectomesenchymal elements appeared juxtaposed to the squamous lining (gingival cyst-like organoid hamartoma) and ghost cells aggregated in the enamel organ of a microdont (peripheral odontoma). None of POH exhibited continuity with the surface epithelium. CONCLUSION: On the basis of this relatively limited series of cases, POH, to conceptualize a unified histogenetic source, are speculated to arise from the soft-tissue remnants of dental lamina. Gingival rests of Serres seem to retain the ability to pursue epithelial-ectomesenchymal interactions that are necessary leading to odontoma formation.

Ameloblastoma ex calcifying odontogenic cyst (dentinogenic ghost cell tumor).

Calcifying odontogenic cyst (COC) has shown to be of extensive diversity in its clinical and histopathological features, as well as in its biological behavior. In this report, a rare case is described of ameloblastoma ex COC (dentinogenic ghost cell tumor) and the relevant literature is briefly reviewed.

Sclerosing mucoepidermoid carcinoma of the oral cavity.

Sclerosing mucoepidermoid carcinoma (SMEC) with eosinophilia is a rare but distinctive tumor usually affecting the thyroid. SMEC involvement of salivary gland is exceptional, with only six cases in the literature. We present here the first case of an intermediate-grade SMEC, arising from the intraoral minor salivary glands. A particularly interesting finding is the cytoplasmic accumulation of eosinophilic hyaline granules in carcinoma cells, similar to aberrant zymogen-like granules previously described in salivary sclerosing polycystic adenosis.

Gallbladder perforation: color Doppler findings.

Gallbladder (GB) perforation is a life-threatening complication of acute cholecystitis, and early diagnosis prevents delay in patient management. We present two cases of GB perforation diagnosed by color Doppler ultrasonography. Each clearly showed a flow signal passing through the perforated site, leading to prompt and successful surgical treatment. This interesting observation suggests that color Doppler ultrasonography is useful in the diagnosis of GB perforation.