ANALISIS BANJIR RANCANGAN DENGAN METODE HSS NAKAYASU PADA BENDUNGAN GINTUNG

Jebolnya Situ Gintung merupakan akibat dari perubahan debit banjir yang terus bertambah. Hal tersebut perlu diana/isis terhadap debit banjir rancangan yang selanjutnya dapat digunakan untuk merencanakan Bendungan Gintung yang baru. Berdasarkan permasalahan di atas, maka perlu dikembangkan perhitungan banjir rancangan dengan metode HSS Nakayasu. Perhitungan dengan menggunaan data hujan. Pada penelitian ini digunakan 18 Pos stasiun penangkar hujan yang diseleksi menurut kelayakan data menjadi 9 pos stasiun hujan dengan memasukan nilai hujan harian maksimum tahunan. Data curah hujan yang disaring memilki tingkat kepercayaan yang rendah, namun masih masuk ke dalam data aman. Dalam penentuan debit banjir rencana terlebih dahulu dilakukan ana/isa frekuensi dan penetapan sebaran data curah hujan kemudian diuji dengan chi-kuadrat. Distribusi yang sesuai adalah distribusi Log Pearson Type III. Dari hasil ana/isa debit banjir rancangan, untuk merencanakan bendungan digunakan debit banjir kala ulang Ql000 = 289,348 m3/dt

T-cadherin loss promotes experimental metastasis of squamous cell carcinoma

T-cadherin is gaining recognition as a determinant for the development of incipient invasive squamous cell carcinoma (SCC). However, effects of T-cadherin expression on the metastatic potential of SCC have not been studied. Here, using a murine model of experimental metastasis following tail vein injection of A431 SCC cells we report that loss of T-cadherin increased both the incidence and rate of appearance of lung metastases. T-cadherin-silenced SCC metastases were highly disordered with evidence of single cell dissemination away from main foci whereas SCC metastases overexpressing T-cadherin developed as compact, tightly organised sheets. SCC cell adhesion to vascular endothelial cells (EC) in culture was increased for T-cadherin-silenced SCC and decreased for T-cadherin-overexpressing SCC. Confocal microscopy showed that T-cadherin-silenced SCC adherent on EC display an elongated morphology with long thin extensions and a high degree of intercalation within the EC monolayer, whereas SCC overexpressing T-cadherin formed poorly-spread multicellular aggregates that remain on the outer surface of the EC monolayer. T-cadherin-deficient SCC or human keratinocyte cells exhibited increased transendothelial migration in vitro which could be attenuated in the presence of EGFR inhibitor gefitinib. Our data suggest that loss of T-cadherin can increase metastatic potential and aggressiveness of SCC, possibly due to facilitating arrest and extravasation through the vascular wall and/or more efficient establishment of metastases in the new microenvironment

FGF2 induces RANKL gene expression as well as IL1beta regulated MHC class II in human bone marrow-derived mesenchymal progenitor stromal cells

OBJECTIVE: Human bone marrow mesenchymal stromal cells (hBM-MSC) are being applied in tissue regeneration and treatment of autoimmune diseases (AD). Their cellular and immunophenotype depend on isolation and culture conditions which may influence their therapeutic application and reflect their in vivo biological functions. We have further characterised the phenotype induced by fibroblast growth factor 2 (FGF2) on healthy donor hBM-MSC focusing on the osteoimmunological markers osteoprotegerin (OPG), receptor activator of nuclear factor kB (RANK), RANK ligand (RANKL) and HLA-DR and their regulation of expression by the inflammatory cytokines IL1beta and IFNgamma. METHODS: RANK, RANKL, OPG and HLA-DR expression in hBM-MSC expanded under specific culture conditions, were measured by RT-PCR and flow cytometry. MAPKs induction by FGF2, IL1beta and IFNgamma in hBM-MSC was analysed by immunoblotting and RT-PCR. RESULTS: In hBM-MSC, OPG expression is constitutive and FGF2 independent. RANKL expression depends on FGF2 and ERK1/2 activation. IL1beta and IFNgamma activate ERK1/2 but fail to induce RANKL. Only IL1beta induces P38MAPK. The previously described HLA-DR induced by FGF2 through ERK1/2 on hBM-MSC, is suppressed by IL1beta through inhibition of CIITA transcription. HLA-DR induced by IFNgamma is not affected by IL1beta in hBM-MSC, but is suppressed in articular chondrocytes and lung fibroblasts. CONCLUSIONS: RANKL expression and IL1beta regulated MHC-class II, both induced via activation of the ERK1/2 signalling pathway, are specific for progenitor hBM-MSC expanded in the presence of FGF2. HLA-DR regulated by IL1beta and ERK1/2 is observed on hBM-MSC during early expansion without FGF2 suggesting previous in vivo acquisition. Stromal progenitor cells with this phenotype could have an osteoimmunological role during bone regeneration