This study systematically compared the mechanical performances and polymerization shrinkage of two novel dual-cured resin composites (DCRC) with one conventional packable light-cured resin composite (LCRC) for their application as core build-up material by micro-hardness test, flexural strength test, push-out test, and digital image correlation analysis. The LCRC had a significantly higher micro-hardness (p less then 0.05) whereas the bond strength demonstrated no difference. The mean values of three materials ranged from 35.16 and 64.82 for the Vickers hardness and from 4.66 MPa to 11.53 MPa for the bond strength. The flexure strength of the three materials was not statistically different from each other. LCRC demonstrated 1.88% of volumetric shrinkage while the two DCRC showed 5.06% and 4.91%, respectively. In general, the DCRC demonstrated a comparable flexural strength and bond strength as the LCRC, however, the significant polymerization shrinkage of DCRC should be emphasized.Acquired hemophilia A (AHA) is a bleeding disorder caused by the acquired appearance of inhibitor for factor VIII. Approximately half of all patients with AHA have some type of underlying disease. We herein report the case of a 72-year-old Japanese man with AHA who presented with infectious aortic aneurysms due to an underlying Helicobacter cinaedi infection. To our knowledge, this is the first report of AHA triggered by a bacterial infection; however, there may be similar cases that remain undiagnosed because this pathogen is difficult to identify. Clinicians should consider the possibility of H. cinaedi as a causative pathogen in patients presenting with a fever of unknown origin.We herein describe a Charcot-Marie-Tooth disease (CMT) family with a MFN2 mutation with atypical ocular manifestations. The proband, his mother, his third daughter, and his deceased maternal grandfather all had symptoms of CMT and a visual impairment (either cataracts or severe astigmatism). On whole-exome sequencing for the proband having CMT and congenital cataracts, we identified a c.314C>T (p.Thr105Met) mutation in MFN2, but no mutation in the causative genes associated with cataracts. This missense mutation in MFN2 co-segregated with CMT and the atypical ocular manifestations in this family. The findings of this study might help to expand the clinical phenotype of heterogeneous MFN2-related CMT.Acquired coagulation factor V (FV) inhibitors are rare disorders in which antibodies against FV develop under various conditions. We herein report the case of a 71-year-old woman with FV inhibitor during radiochemotherapy for pancreatic cancer. Multiple purpuras suddenly appeared on her bilateral upper limbs with prolonged coagulation data (APTT 97.3 seconds). The FV activity was less than 3% and the FV inhibitor was positive (1.7 B.U./mL). Oral prednisolone induced a rapid normalization of the coagulation data and FV activity and a rapid disappearance of FV inhibitor within 7 days. Early diagnosis and treatment may therefore be important in cases of factor V inhibitor.A 23-year-old woman was transferred to our hospital due to exacerbating dyspnea with wheeze. After admission, we started mechanical ventilation immediately, and she was diagnosed with status asthmatics. On the following day, she was able to be weaned from the ventilator. However, she required re-intubation because of an unstable respiratory condition just after extubation. Detailed neurological investigations identified blepharoptosis and muscle weakness with easy fatigability. An edrophonium test was positive. Anti-acetylcholine receptor antibody was detected in her serum. She was finally diagnosed with myasthenia gravis and successfully treated with neostigmine and a low-dose corticosteroid.Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a rare progressive neurodegenerative disease caused by either homozygous or compound heterozygous mutations in the SACS gene. The original ARSACS cases found in Quebec showed very homogenous phenotypes characterized by cerebellar ataxia, spasticity, and polyneuropathy. However, many cases with atypical phenotypes have been found in other regions and ethnic groups. We herein present a Japanese patient with atypical ARSACS who showed cerebellar ataxia and polyneuropathy, but no spasticity. She carried novel compound heterozygous mutations (p.Lys4326Glu and p.Leu1412Lysfs*16) in the SACS gene. The brain MRI findings were useful for making a diagnosis of ARSACS.We herein report a case of fatal pancreatitis induced by an immune checkpoint inhibitor. A 62-year-old man with cancer of unknown primary was treated with pembrolizumab. After 12 cycles, immune-related pneumonitis developed and was treated with prednisolone. Selleck TAK-981 Three months later, pancreatitis developed, which was successfully treated with hydration and protease inhibitors. Eight months later, another attack of pancreatitis occurred, which did not respond to therapy, including high-dose corticosteroids, and he eventually died. This is the first report describing fatal immune checkpoint inhibitor-related pancreatitis. Despite the rarity of this complication, attention should be paid to its potential severity and treatment.We herein report a case of myelin oligodendrocyte glycoprotein-antibody-associated disorder (MOG-AD) presenting with corticomeningeal encephalitis. The patient exhibited oral ulceration, a mild impairment of consciousness, fever, nausea, nuchal rigidity, positivity for human leukocyte antigen type B51, and neutrophil-dominant pleocytosis and interleukin-6 level in cerebrospinal fluid (CSF). Magnetic resonance imaging (MRI) revealed a right temporal lesion with leptomeningeal gadolinium enhancement. The initial diagnosis was neuro-Behçet's disease presenting with meningoencephalitis; however, a cell-based assay detected anti-MOG antibody in the serum and CSF and the patient also experienced bilateral optic neuritis. After administering steroid therapy, his neurologic symptoms and CSF abnormalities improved along with the disappearance of gadolinium enhancement and the lesion on MRI. This case suggests that MOG-AD may present with corticomeningeal encephalitis prior to the onset of optic neuritis.