La fundación de la Madrasa al-Adāb por la Asociación de ulemas musulmanes argelinos en la ciudad de Hennaya (Tremecén) en 1950

A biphenyl-fused BODIPY was synthesized through a facile oxidative cyclization of peripheral aryl-substituents at the β-position of the BODIPY unit. The extended π-system of the fused BODIPY induces near-infrared (NIR) absorption and strong π–π interactions in the solid state. These features are beneficial for the application of the dye as a functional material. The biphenyl-fused BODIPY dye was demonstrated to exhibit photocurrent conversion ability on the basis of its <i>n</i>-type semiconducting property

Summary of the cases of altered diagnosis.

<p>AA: anaplastic astrocytoma, AO: anaplastic oligodendroglioma, AOA: anaplastic oligoastrocytoma, GBM: glioblastoma, GBMO: glioblastoma with oligodendroglioma component.</p

Overall survival (OS) analysis based on the histological subclassifications.

<p>a: Conventional Grade III gliomas (AA, AO and AOA) show significantly better prognosis than Grade IV gliomas (GBM, GBMO). b: GBMO presented longer survival compared to GBM, although it is statistically not significant (p = 0.068). c: Oligodendroglial tumor (“oligo”; AO, AOA, GBMO) shows significantly better prognosis compared to pure astrocytic tumor (“pure astro”; AA, GBM). d: The survival curve of AA patients is almost identical to that of GBM patients.</p

Final diagnosis of the 111 cases.

<p>AA: anaplastic astrocytoma, AO: anaplastic oligodendroglioma,</p><p>AOA: anaplastic oligoastrocytoma, GBM: glioblastoma,</p><p>GBMO: glioblastoma with oligodendroglioma component.</p

Characteristics of 111 Patients.

<p>ACNU: Nimustine hydrochloride, TMZ: Temozolomide, CDDP: Cisplatin, CBDCA: Carboplatin, KPS: Karnofsky performance status.</p

Cellular Functions and Gene and Protein Expression Profiles in Endothelial Cells Derived from Moyamoya Disease-Specific iPS Cells

<div><p>Background and purpose</p><p>Moyamoya disease (MMD) is a slow, progressive steno-occlusive disease, arising in the terminal portions of the cerebral internal carotid artery. However, the functions and characteristics of the endothelial cells (ECs) in MMD are unknown. We analyzed these features using induced pluripotent stem cell (iPSC)-derived ECs.</p><p>Methods</p><p>iPSC lines were established from the peripheral blood of three patients with MMD carrying the variant <i>RNF213 R4810K</i>, and three healthy persons used as controls. After the endothelial differentiation of iPSCs, CD31⁺CD144⁺ cells were purified as ECs using a cell sorter. We analyzed their proliferation, angiogenesis, and responses to some angiogenic factors, namely VEGF, bFGF, TGF-β, and BMP4. The ECs were also analyzed using DNA microarray and proteomics to perform comprehensive gene and protein expression analysis.</p><p>Results</p><p>Angiogenesis was significantly impaired in MMD regardless of the presence of any angiogenic factor. On the contrary, endothelial proliferation was not significant between control- and MMD-derived cells. Regarding DNA microarray, pathway analysis illustrated that extracellular matrix (ECM) receptor-related genes, including integrin β3, were significantly downregulated in MMD. Proteomic analysis revealed that cytoskeleton-related proteins were downregulated and splicing regulation-related proteins were upregulated in MMD.</p><p>Conclusions</p><p>Downregulation of ECM receptor-related genes may be associated with impaired angiogenic activity in ECs derived from iPSCs from patients with MMD. Upregulation of splicing regulation-related proteins implied differences in splicing patterns between control and MMD ECs.</p></div

Overall survival analysis of AA and GBM according to the treatment variations.

<p>The graph shows comparison of OS between AA and GBM patients who underwent Nimustine hydrochloride (ACNU) - based chemotherapy (a), Temozolomide (TMZ) - based chemotherapy (b), and 60 Gy of radiation therapy (c). There is no statistical siginificance.</p

The result of DNA microarray analysis.

<p>Panel A shows unsupervised clustering analysis of moyamoya disease (MMD)—and control—iPSECs. Panel B shows the volcano plot of all probes. The broken blue line and continuous red line denote significantly downregulated and upregulated genes in MMD-iPSECs, respectively (fold change >3, <i>P</i> < 0.01). Panels C and D show the significantly downregulated and upregulated genes in pathway analyses of MMD-iPSECs, respectively. Dotted line indicates the significance level (<i>P</i> < 0.05).</p

The results of RT-PCR analysis and Western blotting in iPSECs.

<p>Panel A shows the photographs of RT-PCR for integrin β3 (<i>ITG-β3</i>) and <i>ITG-β8</i> in MMD-iPSECs (<i>upper</i>) and the quantitative data (<i>middle</i>: <i>ITG-β3</i> and <i>lower</i>: <i>ITG-β8</i>, *<i>P</i> < 0.05, †<i>P</i> < 0.02). β-actin was used to normalize loading variations. Panel B shows the photographs of Western blotting for interin β3 in MMD-iPSECs (<i>upper</i>) and the quantitative data (<i>lower</i>, †<i>P</i> < 0.02). α-tubulin was used to normalize loading variations.</p

Characterization of human-induced pluripotent stem cells (iPSCs) from patients with moyamoya disease (MMD) and control subjects.

<p>Panel A shows the results of RT-PCR analysis of the Sendai virus and human embryonic stem (ES) cell markers in each iPSC line. Panel B shows the immunoreaction of ES cell markers <i>OCT3/4</i>, <i>NANOG</i>, <i>SSEA1</i>, and <i>TRA-1-60</i> and the reaction for alkaline phosphatase staining in all iPSC colonies. Scale bars: 100 μm. Panel C shows the representative photomicrographs of karyotype analysis in each MMD-iPSC line. Panel D shows the representative photomicrographs of the formation of teratoma in each MMD-iPSC line. “G”: Glandular structure (endoderm), “C”: Cartilage (mesoderm), and “MP”: Melanin pigment (ectoderm). Scale bars: 100 μm.</p