腰椎无砂粒体型色素性神经鞘瘤一例

本文报道1例53岁女性腰椎无沙粒体型色素性神经鞘瘤患者的临床资料,患者主要临床表现为腰背部持续性钝痛。CT显示腰3、4椎体水平椎管及左侧椎间孔区不均质实性病灶,呈哑铃状,左侧椎间孔扩大;MRI显示病灶T1WI呈混杂稍高信号,T2WI呈混杂略低信号,DWI呈团块状扩散受限,增强扫描呈轻度不均匀强化信号。经病理诊断为腰椎非沙粒体型色素性神经鞘瘤。     

Characteristics and Treatment Outcomes of Small-bowel Angioectasia in Systemic Sclerosis Patients: A Retrospective Observational Study

Objective Systemic sclerosis (SSc) is defined as an autoimmune disease presenting with fibrosis of various organs and vascular endothelial damage. Vascular lesions, including small-bowel angioectasias, are also frequently detected in SSc patients. Polidocanol injection (PDI) is a safe and effective hemostatic treatment for gastrointestinal bleeding. We evaluated the outcomes of PDI for small-bowel angioectasia in SSc patients. Methods We retrospectively evaluated 65 consecutive SSc patients (61 women; mean age, 64.3 years old) who underwent capsule endoscopy (CE) and/or double-balloon endoscopy at Hiroshima University Hospital between April 2012 and December 2019. Patients Patients were stratified according to the presence of small-bowel angioectasia. Among patients who underwent CE during the same period, those with small-bowel angioectasia without concomitant diseases were compared with SSc patients with small-bowel angioectasia. Clinical and endoscopic characteristics, treatment outcomes, and the incidence of metachronous small-bowel angioectasia after PDI were evaluated. Results SSc patients with small-bowel angioectasia exhibited significantly lower hemoglobin levels and a significantly higher incidence of skin telangiectasia than those without small-bowel angioectasia. On a multivariate analysis of the presence of small-bowel angioectasia, anemia and skin telangiectasia were significant independent factors. SSc patients with small-bowel angioectasia included a higher proportion of women and exhibited a significantly higher incidence of metachronous small-bowel angioectasia than X. The characteristics of small-bowel angioectasia and outcomes of PDI were not significantly different between the two groups. No post-treatment rebleeding cases or adverse events were noted. Conclusion CE should be performed for SSc patients with anemia and/or skin telangiectasia. PDI is effective for SSc patients with small-bowel angioectasia.     

Inhibition of enamel demineralization by buffering effect of S‐PRG filler‐containing dental sealant

The buffering capacity and inhibitory effects on enamel demineralization of two commercially available dental sealants were evaluated in this study. The effects of filler particles were also examined. Disks of enamel and cured sealant materials of BeautiSealant (silica or S‐PRG filler) or Teethmate F‐1 were incubated in lactic acid solutions (pH 4.0) for 1–6 d. The pH changes and amounts of ions released in the solutions were assessed, and enamel surfaces were observed using a scanning electron microscope. The pH of the solution with BeautiSealant (S‐PRG filler) was neutralized from pH 4.0 to pH 6.1 (after incubation for 1 d) and from pH 4.0 to pH 6.7 (after incubation for 6 d). In addition, no release of calcium ions was detected and the enamel surface was morphologically intact in scanning electron microscopy images. However, the pH of the solution with Teethmate F‐1 remained below pH 4.0 during incubation from days 1 to 6. Calcium release was increased in solutions up to and after 6 d of incubation. Scanning electron microscopy images showed that the structures of hydroxyapatite rods were exposed at the specimen surfaces as a result of demineralization. Ions released from S‐PRG filler‐containing dental sealant rapidly buffered the lactic acid solution and inhibited enamel demineralization.     

In vivo degradation of resin-dentin bonds produced by a self-etch and an etch-and-rinse adhesive

Resin-dentin bonds are known to degrade in the relatively aggressive oral environment. In order to obtain greater insight into the interfacial degradation process, we examined, by using transmission electron microscopy (TEM), the interfacial ultrastructure of two adhesives bonded to dentin after 1 yr in vivo. Class V cavities were prepared on the buccal surfaces of 14 intact teeth of two monkeys and then restored by using either the two-step self-etch adhesive, Unifil Bond, or the two-step etch-and-rinse adhesive, Single Bond, in combination with the restorative microhybrid composite, Z250. After 1 yr, 10 other teeth were restored by using the same materials (controls). One day later, the monkeys were killed, following which the microtensile bond strength to dentin was determined and the interfacial ultrastructure was examined by TEM. Whereas no noticeable changes in the morphology of the resin-dentin interface were observed between the 1-d and 1-yr specimens for Unifil Bond, Single Bond exhibited signs of interfacial degradation, in particular at the bottom of the 3 microm-deep hybrid layer. In conclusion, the adhesive interface produced by the etch-and-rinse adhesive was less resistant to degradation than that produced by the self-etch system.     

HMGA2 as a potential molecular target in KMT2A‐AFF1‐positive infant acute lymphoblastic leukaemia

Acute lymphoblastic leukaemia (ALL) in infants is an intractable cancer in childhood. Although recent intensive chemotherapy progress has considerably improved ALL treatment outcome, disease cure is often accompanied by undesirable long‐term side effects, and efficient, less toxic molecular targeting therapies have been anticipated. In infant ALL cells with KMT2A (MLL) fusion, the microRNA let‐7b (MIRLET7B) is significantly downregulated by DNA hypermethylation of its promoter region. We show here that the expression of HMGA2, one of the oncogenes repressed by MIRLET7B, is reversely upregulated in infant ALL leukaemic cells, particularly in KMT2A‐AFF1 (MLL‐AF4) positive ALL. In addition to the suppression of MIRLET7B, KMT2A fusion proteins positively regulate the expression of HMGA2. HMGA2 is one of the negative regulators of CDKN2A gene, which encodes the cyclin‐dependent kinase inhibitor p16^INK4A. The HMGA2 inhibitor netropsin, when combined with demethylating agent 5‐azacytidine, upregulated and sustained the expression of CDKN2A, which resulted in growth suppression of KMT2A‐AFF1‐expressing cell lines. This effect was more apparent compared to treatment with 5‐azacytidine alone. These results indicate that the MIRLET7B‐HMGA2‐CDKN2A axis plays an important role in cell proliferation of leukaemic cells and could be a possible molecular target for the therapy of infant ALL with KMT2A‐AFF1.