Digital subtraction technique for evaluation of peri-implant bone change in digital dental imaging

The purpose of this study was to investigate digital subtraction technique in digital dental imaging for implant performance, used to quantitatively evaluate bone change around dental implants. For longitudinal assessment of peri-implant bone change, we applied subtraction technique to digital peri-apical radiographs using a digital dental imaging system in two cases at the upper canine and premolar regions. In both cases, we found two peaks of bone change at the crestal region; we also quantitatively demonstrated a marked change over the first one-month period and approximately three-month period spanning the fourth month to the end of the sixth month following implantation. Digital peri-apical radiography accommodating the digital subtraction program should be re-acknowledged as a reliable modality for assessing amount of bone change at local implantation sites.     

Gross hematuria after SARS-CoV-2 vaccination: questionnaire survey in Japan

Clinical and Experimental Nephrology - Recent clinical reports indicate a correlation between gross hematuria after the coronavirus 2019 (COVID-19) vaccination in patients with glomerulonephritis,...     

Vascular endothelial growth factor receptor 1 (VEGFR1) tyrosine kinase signaling facilitates granulation tissue formation with recruitment of VEGFR1<Superscript>+</Superscript> cells from bone marrow

Vascular endothelial growth factor (VEGF)-A facilitates wound healing. VEGF-A binds to VEGF receptor 1 (VEGFR1) and VEGFR2 and induces wound healing through the receptor’s tyrosine kinase (TK) domain. During blood flow recovery and lung regeneration, expression of VEGFR1 is elevated. However, the precise mechanism of wound healing, especially granulation formation on VEGFR1, is not well understood. We hypothesized that VEGFR1-TK signaling induces wound healing by promoting granulation tissue formation. A surgical sponge implantation model was made by implanting a sponge disk into dorsal subcutaneous tissue of mice. Granulation formation was estimated from the weight of the sponge and the granulation area from the immunohistochemical analysis of collagen I. The expression of fibroblast markers was estimated from the expression of transforming growth factor-beta (TGF-β) and cellular fibroblast growth factor-2 (FGF-2) using real-time PCR (polymerase chain reaction) and from the immunohistochemical analysis of S100A4. VEGFR1 TK knockout (TK^?/?) mice exhibited suppressed granulation tissue formation compared to that in wild-type (WT) mice. Expression of FGF-2, TGF-β, and VEGF-A was significantly suppressed in VEGFR1 TK^?/? mice, and the accumulation of VEGFR1⁺ cells in granulation tissue was reduced in VEGFR1 TK^?/? mice compared to that in WT mice. The numbers of VEGFR1⁺ cells and S100A4⁺ cells derived from bone marrow (BM) were higher in WT mice transplanted with green fluorescent protein (GFP) transgenic WT BM than in VEGFR1 TK^?/? mice transplanted with GFP transgenic VEGFR1 TK^?/? BM. These results indicated that VEGFR1-TK signaling induced the accumulation of BM-derived VEGFR1⁺ cells expressing F4/80 and S100A4 and contributed to granulation formation around the surgically implanted sponge area in a mouse model.     

Antigen‐specific airway IL‐33 production depends on FcγR‐mediated incorporation of the antigen by alveolar macrophages in sensitized mice

Although interleukin (IL)‐33 is a candidate for the aggravation of asthma, the mechanisms underlying antigen‐specific IL‐33 production in the lung are unclear. Therefore, we analysed the mechanisms in mice. Intra‐tracheal administration of ovalbumin (OVA) evoked increases in IL‐33 and IL‐33 mRNA in the lungs of both non‐sensitized and OVA‐sensitized mice, and the increases in the sensitized mice were significantly higher than in the non‐sensitized mice. However, intra‐tracheal administration of bovine serum albumin did not increase the IL‐33 level in the OVA‐sensitized mice. Depletion of neither mast cells/basophils nor CD4⁺ cells abolished the OVA‐induced IL‐33 production in sensitized mice, suggesting that the antigen recognition leading to the IL‐33 production was not related with either antigen‐specific IgE‐bearing mast cells/basophils or memory CD4⁺ Th2 cells. When a fluorogenic substrate‐labelled OVA (DQ‐OVA) was intra‐tracheally administered, the lung cells of sensitized mice incorporated more DQ‐OVA than those of non‐sensitized mice. The lung cells incorporating DQ‐OVA included B‐cells and alveolar macrophages. The allergic IL‐33 production was significantly reduced by treatment with anti‐FcγRII/III mAb. Depletion of alveolar macrophages by clodronate liposomes significantly suppressed the allergic IL‐33 production, whereas depletion of B‐cells by anti‐CD20 mAb did not. These results suggest that the administered OVA in the lung bound antigen‐specific IgG Ab, and then alveolar macrophages incorporated the immune complex through FcγRII/III on the cell surface, resulting in IL‐33 production in sensitized mice. The mechanisms underlying the antigen‐specific IL‐33 production may aid in development of new pharmacotherapies.     

Novel types of staphylococcal cassette chromosome mec elements identified in clonal complex 398 methicillin-resistant Staphylococcus aureus strains

The structures of staphylococcal cassette chromosome mec (SCCmec) elements carried by 31 clonal complex 398 (CC398) methicillin-resistant Staphylococcus aureus (MRSA) strains isolated from the participants at a conference were analyzed. The SCCmecs were classified into novel types, namely, IX, X, V(5C2&5) subtype c, and IVa. Type V(5C2&5) subtype c, IX, and X SCCmecs carried genes conferring resistance to metals. The structures of SCCmecs from CC398 strains were distinct from those normally found in humans, adding to the evidence that humans are not the original host for CC398.     

Impact of optical coherence tomography- and coronary angioscopy-assessed neointimal tissue characteristics on occurrence of periprocedural myonecrosis in patients with in-stent restenosis

Several characteristics of neointimal tissues, including neoatherosclerotic progression, have been reported in lesions with in-stent restenosis (ISR). However, the effects of these characteristics on outcomes after percutaneous coronary intervention (PCI) for ISR lesions remain unclear. We assessed the relationships between neointimal tissue characteristics and the occurrence of periprocedural myonecrosis (PMN) after PCI in ISR lesions. We investigated 72 ISR lesions in 72 patients with stable angina pectoris (SAP) who underwent pre- and post-revascularization optical coherence tomography (OCT) and coronary angioscopy (CAS). All lesions were classified as with PMN, defined by an elevated peak high-sensitivity cardiac troponin-T level during the 24-h post-PCI period, and without PMN. PMN was observed in 23 (31.9?%) lesions. PMN lesions had higher frequencies of OCT-derived thin-cap fibroatheroma (26.1 vs. 6.1?%, P?=?0.03), CAS-derived intensive yellow neointima (30.4 vs. 10.2?%, P?=?0.04), neointima with complex surface (60.9 vs. 28.6?%, P?=?0.01), and CAS-derived atheromatous appearance (CAS-AAP), defined as yellow plaque including complex thrombi underneath disrupted neointimal coverage after ballooning (47.8 vs. 16.3?%, P?=?0.008) at the most stenotic sites inside stents, compared to lesions without PMN. Multivariate logistic regression analysis identified CAS-AAP (odds ratio: 3.568, 95?% confidence interval: 1.109–11.475, P?=?0.033) as an independent predictor of PMN. For ISR lesions in SAP patients, an OCT- and CAS-based assessment of neointimal tissue characteristics might help to predict the occurrence of PMN.