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Perairan barat Provinsi Lampung merupakan salah satu lokasi yang diperkirakan memiliki potensi energi gelombang yang cukup besar. Namun, minimnya informasi tentang titik potensial energi gelombang laut yang lebih rinci membuat kawasan ini belum dapat dieksplorasi dengan baik. Penelitian ini bertujuan untuk mendapatkan tinggi gelombang signifikan (Hs) yang merupakan salah satu variabel utama dalam menentukan energi gelombang laut di perairan barat Provinsi Lampung. Studi ini dilakukan melalui pemodelan numerik menggunakan model SWAN pada software Delft3D-WAVE dengan input model gelombang yang bersumber dari data ECMWF-Era 5 di laut lepas. Hasil pemodelan numerik menunjukkan gelombang signifikan terbesar terjadi pada musim barat dengan nilai 1,25-2,975 m. Sedangkan tinggi gelombang signifikan terkecil terjadi pada musim timur dengan nilai 0,941-2,079 m. Verifikasi hasil tersebut terhadap data AVISO menghasilkan nilai MAPE sebesar 16,355%, koefisien korelasi sebesar 0,8691, RMSE berkisar 0,277 m yang menunjukkan validasi yang baik dan memuaskan.

Background Chemoresistance is a major factor involved in a poor response and reduced overall survival in patients with advanced breast cancer. Although extensive studies have been carried out to understand the mechanisms of chemoresistance, many questions remain unanswered. Methods In this research, we used two isogenic MCF-7 breast cancer cell lines selected for resistance to doxorubicin (MCF-7DOX) or docetaxel (MCF-7TXT) and the wild type parental cell line (MCF-7CC) to study mechanisms underlying acquired resistance to taxanes in MCF-7TXT cells. Cytotoxicity assay, immunoblotting, indirect immunofluorescence and live imaging were used to study the drug resistance, the expression levels of drug transporters and various tubulin isoforms, apoptosis, microtubule formation, and microtubule dynamics. Results MCF-7TXT cells were cross resistant to paclitaxel, but not to doxorubicin. MCF-7DOX cells were not cross-resistant to taxanes. We also showed that multiple mechanisms are involved in the resistance to taxanes in MCF-7TXT cells. Firstly, MCF-7TXT cells express higher level of ABCB1. Secondly, the microtubule dynamics of MCF-7TXT cells are weak and insensitive to the docetaxel treatment, which may partially explain why docetaxel is less effective in inducing M-phase arrest and apoptosis in MCF-7TXT cells in comparison with MCF-7CC cells. Moreover, MCF-7TXT cells express relatively higher levels of β2- and β4-tubulin and relatively lower levels of β3-tubulin than both MCF-7CC and MCF-7DOX cells. The subcellular localization of various β-tubulin isoforms in MCF-7TXT cells is also different from that in MCF-7CC and MCF-7DOX cells. Conclusion Multiple mechanisms are involved in the resistance to taxanes in MCF-7TXT cells. The high expression level of ABCB1, the specific composition and localization of β-tubulin isoforms, the weak microtubule dynamics and its insensitivity to docetaxel may all contribute to the acquired resistance of MCF-7TXT cells to taxanes.