Blow-up for Semilinear Wave Equations with a Data of the Critical Decay having a Small Loss

It is known that we have a global existence for wave equations with super-critical nonlinearities when the data has a critical decay of powers. In this paper, we will see that a blow-up result can be established if the data decays like the critical power with a small loss such as any logarithmic power. This means that there is no relation between the critical decay of the initial data and the integrability of the weight, while the critical power of the nonlinearity is closely related to the integrability. The critical decay of the initial data is determined only by scaling invariance of the equation. We also discuss a nonexistence of local in time solutions for the initial data increasing at infinity

Critical Curve for p-q Systems of Nonlinear Wave Equations in Three Space Dimensions

AbstractThe existence of the critical curve for p-q systems for nonlinear wave equations was already established by D. Del Santo, V. Georgiev, and E. Mitidieri [1997, Global existence of the solutions and formation of singularities for a class of hyperbolic systems, in “Geometric Optics and Related Topics” (F. Colombini and N. Lerner, Eds.), Progress in Nonlinear Differential Equations and Their Applications, Vol. 32, pp. 117–139, Birkhäuser, Basel] except for the critical case. Our main purpose is to prove a blow-up theorem for which the nonlinearity (p, q) is just on the critical curve in three space dimensions. Moreover, the lower and upper bounds of the lifespan of solutions are precisely estimated, including the sub-critical case

距骨壊死に対するアルミナセラミック性人工距骨置換術のSAFE-Qを用いた臨床成績

Background: The purpose of this retrospective review was to evaluate the clinical outcomes of patients who underwent total talar replacement for talar necrosis using the SAFE-Q score, which was hypothesized to improve postoperatively. Methods: The study included 24 ankles of 22 patients who underwent total talar replacement from 2012 to 2018 and were evaluated using SAFE-Q preoperatively and postoperatively. Statistical analysis was performed using the mean values of the SAFE-Q and JSSF scale scores, and the range of ankle motion was compared before and 3 years after the surgery using the Wilcoxon signed-rank test. Results: The SAFE-Q scores improved postoperatively in the all the subcategories. “Pain and Pain-Related” changed from a mean value of 42.2±23.9 points preoperatively to a mean value of 84.6±12.6 points postoperatively (p<.01); “Physical Functioning and Daily Living” changed from 36.3±25.2 points to 73.4±20.5 points (p<.01); “Social Functioning” changed from 34.1±34.8 points to 81.0±25.3 points (p<.01); “Shoe-Related” changed from 41.3±28.9 points to 75.4±22.3 points (p<.01); “General Health and Well-Being” changed from 36.7±32.1 to 76.9±29.3 points (p<.01). Conclusion: Twenty-four osteonecrotic tali of 22 patients treated with alumina ceramic total talar replacement achieved good clinical results, as evaluated using the JSSF ankle/hindfoot score and SAFE-Q. Alumina ceramic total talar replacement is the mainstream treatment for talar osteonecrosis.博士（医学）・甲第856号・令和4年12月22

センタクテキ スプライシング ハンノウ ニヨル イデンシ ハツゲン セイギョ

The human genome sequence has been decoded, and the more complicated regulation of gene function is revealed in the post-genome era. In the various mechanisms of epigenome, RNA dramatically controls gene expression through the various post-transcriptional processing including transcription, splicing, cap addition, polyadenylation, nuclear export, translation. Especially, the alternative splicing is involved in all of those post-transcriptional regulations, as well as splicing of pre-mRNA. However, there were few reports, how the alternative splicing contributes to the regulations of cellular functions because of its difficulty of the analysis. This review discusses the molecular mechanism of alternative splicing and its regulator ; Serine/arginine-rich splicing factor （SRSF）. We also discuss how the SRSF genes sustain their own proper expressions and functions

Nectin-2 is a potential target for antibody therapy of breast and ovarian cancers

BACKGROUND: Nectin-2 is a Ca(2+)-independent cell-cell adhesion molecule that is one of the plasma membrane components of adherens junctions. However, little has been reported about the involvement of Nectin-2 in cancer. METHODS: To determine the expression of Nectin-2 in cancer tissues and cancer cell lines, we performed gene expression profile analysis, immunohistochemistry studies, and flow cytometry analysis. We also investigated the potential of this molecule as a target for antibody therapeutics to treat cancers by generating and characterizing an anti-Nectin-2 rabbit polyclonal antibody (poAb) and 256 fully human anti-Nectin-2 monoclonal antibodies (mAbs). In addition, we tested anti-Nectin-2 mAbs in several in vivo tumor growth inhibition models to investigate the primary mechanisms of action of the mAbs. RESULTS: In the present study, we found that Nectin-2 was over-expressed in clinical breast and ovarian cancer tissues by using gene expression profile analysis and immunohistochemistry studies. Nectin-2 was over-expressed in various cancer cell lines as well. Furthermore, the polyclonal antibody specific to Nectin-2 suppressed the in vitro proliferation of OV-90 ovarian cancer cells, which express endogenous Nectin-2 on the cell surface. The anti-Nectin-2 mAbs we generated were classified into 7 epitope bins. The anti-Nectin-2 mAbs demonstrated antibody-dependent cellular cytotoxicity (ADCC) and epitope bin-dependent features such as the inhibition of Nectin-2-Nectin-2 interaction, Nectin-2-Nectin-3 interaction, and in vitro cancer cell proliferation. A representative anti-Nectin-2 mAb in epitope bin VII, Y-443, showed anti-tumor effects against OV-90 cells and MDA-MB-231 breast cancer cells in mouse therapeutic models, and its main mechanism of action appeared to be ADCC. CONCLUSIONS: We observed the over-expression of Nectin-2 in breast and ovarian cancers and anti-tumor activity of anti-Nectin-2 mAbs via strong ADCC. These findings suggest that Nectin-2 is a potential target for antibody therapy against breast and ovarian cancers

Homeodomain-Interacting Protein Kinase-2 : A Critical Regulator of the DNA Damage Response and the Epigenome

Homeodomain-interacting protein kinase 2 (HIPK2) is a serine/threonine kinase that phosphorylates and activates the apoptotic program through interaction with diverse downstream targets including tumor suppressor p53. HIPK2 is activated by genotoxic stimuli and modulates cell fate following DNA damage. The DNA damage response (DDR) is triggered by DNA lesions or chromatin alterations. The DDR regulates DNA repair, cell cycle checkpoint activation, and apoptosis to restore genome integrity and cellular homeostasis. Maintenance of the DDR is essential to prevent development of diseases caused by genomic instability, including cancer, defects of development, and neurodegenerative disorders. Recent studies reveal a novel HIPK2-mediated pathway for DDR through interaction with chromatin remodeling factor homeodomain protein 1γ. In this review, we will highlight the molecular mechanisms of HIPK2 and show its functions as a crucial DDR regulator