Studi Potensi Jumlah Penumpang Bus Pemadu Moda Rute Malang – Bandar Udara Juanda Pp

Bandar Udara Malang yang belum melayani banyak tujuan penerbangan membuat pengguna moda pesawat memilih Bandar Udara Juanda. Disisi lain angkutan yang melayani rute Malang-Juanda PP hanya angkutan travel. Untuk itu dibutuhkan moda lain yang lebih ekonomis dan memiliki kapasitas lebih banyak dibandingkan angkutan travel. Bus pemadu moda adalah moda alternatif yang dapat memenuhi kebutuhan tersebut.Pengumpulan data dilakukan dengan penyebaran kuisioner karakteristik sosial-ekonomi, karakteristik perjalanan serta kuisioner dengan teknik penyusunan stated preference. Stated preference memiliki atribut biaya perjalanan, waktu tempuh dan frekuensi keberangkatan. Sedangkan untuk prediksi tarif bus pemadu moda yang direncanakan diperoleh dari perhitungan BOK. Tarif yang telah diperoleh dari perhitungan BOK dibandingkan dengan nilai ATP dan WTP yang diperoleh dari kuisioner yang telah disebarkan. Sehingga didapatkan tarif ideal yang akan diberlakukan apabila bus pemadu moda tersebut direalisasikan.Setelah melakukan perhitungan tarif berdasarkan BOK diperoleh tarif sebesar Rp 23.374,- serta berdasarkan ATP dan WTP diperoleh tarif sebesar Rp 43.675,-. Dengan demikian perkiraan awal tarif bus pemadu moda sebesar Rp 40.000,- dapat diberlakukan. Hasil dari pemodelan pemilihan moda dengan metode stated preference untuk selisih biaya perjalanan Malang-Juanda: dan Juanda-Malang : , untuk selisih waktu tempuh perjalanan () rute Malang-Juanda : dan rute Juanda-Malang : , sedangkan untuk selisih Frekuensi Keberangkatan () rute Malang-Juanda : dan rute Juanda-Malang : .Potensi perpindahan pengguna travel ke bus pemadu moda rute Malang-Juanda sebanyak 705 orang per hari (83,97%). Sedangkan untuk rute Juanda-Malang sebanyak 1516 orang per hari (90,24%)

Mutational Landscape of the primary tumors.

<p>(<b>A</b>) The cumulative distribution of the somatic mutations identified on the targeted exons of the four patients primary tumors is reported as a function of their class and predicted protein changes. (<b>B</b>) Circular diagram <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0056185#pone.0056185-Krzywinski1" target="_blank">[48]</a> representing all 23 chromosomes and their cytogenetic map (outer circle, grey scale bands and red centromeres). The logR tumor/normal coverage ratios (black dots) and the inferred CNA (red: amplification, blue: deletion, blue bars: Loss of Heterozygosity) identified in the 4 primary tumors (from outer to inner circle: SK01600, SK00115, SK00102, SK00072) using whole exome sequencing data are represented. (<b>C</b>) Chromosome-arm level copy number aberrations are observed in the 22 autosomes when >20% of a chromosome arm is reported as deleted (blue) or amplified (red). (<b>D</b>) A focal deletion of ∼10 Mb (set of blue segments) including a large (4.3 Mb) CNA segment affects <i>PIK3R1</i> gene in SK00115 primary tumor. The LogR ratio of tumor/normal coverage (x axis) at each exon capture probe (grey dots) allows the identification of DNA segments deleted (blue bars) or amplified (red bars). (<b>E</b>) Similar to (D), a focal amplification of <i>EFGR</i> containing segment (red) is identified in addition to the chromosome 7 trisomy in patient SK01600 primary tumor. Some segments may appear to overlap as a result of the plotting resolution.</p

Somatic non-synonymous mutations observed in the primary tumors and overlapping with known COSMIC (v55) entries.

1<p>Can includes normal DNA contamination and effect of copy number.</p>2<p>The same position but not the same mutation was found in Glioma.</p

Combined Genetic and Genealogic Studies Uncover a Large BAP1 Cancer Syndrome Kindred Tracing Back Nine Generations to a Common Ancestor from the 1700s

<div><p>We recently discovered an inherited cancer syndrome caused by BRCA1-Associated Protein 1 (<i>BAP1</i>) germline mutations, with high incidence of mesothelioma, uveal melanoma and other cancers and very high penetrance by age 55. To identify families with the BAP1 cancer syndrome, we screened patients with family histories of multiple mesotheliomas and melanomas and/or multiple cancers. We identified four families that shared an identical <i>BAP1</i> mutation: they lived across the US and did not appear to be related. By combining family histories, molecular genetics, and genealogical approaches, we uncovered a BAP1 cancer syndrome kindred of ~80,000 descendants with a core of 106 individuals, whose members descend from a couple born in Germany in the early 1700s who immigrated to North America. Their descendants spread throughout the country with mutation carriers affected by multiple malignancies. Our data show that, once a proband is identified, extended analyses of these kindreds, using genomic and genealogical studies to identify the most recent common ancestor, allow investigators to uncover additional branches of the family that may carry <i>BAP1</i> mutations. Using this knowledge, we have identified new branches of this family carrying BAP1 mutations. We have also implemented early-detection strategies that help identify cancers at early-stage, when they can be cured (melanomas) or are more susceptible to therapy (MM and other malignancies).</p></div

Core of the 106-member nine-generation pedigree, K4.

<p>Numbers above symbols represent year of birth; dates of death are not shown to maintain confidentiality. The founding couple was born in Germany in 1710 and 1712, respectively. We were able to trace the origin of the founder male to a Swiss couple, born in 1588 and in 1591, respectively. De-identified patient IDs are shown below the symbols (e.g.11-III-4). Slashed symbols represent deceased individuals. Obligate carriers are indicated with red symbols. All individuals who were tested for presence of germline <i>BAP1</i> mutations are indicated with a star: green stars indicate <i>BAP1</i> wild type status; red stars indicate <i>BAP1</i> mutant carriers. When available, types of malignancies are listed below symbols and ages of diagnoses are indicated in parentheses. Red arrows indicate the probands; blue symbols indicate individuals that we identified through our genealogy search and found to be affected with MM and/or other BAP1 associated malignancies; orange symbols indicate newly identified family branches, that we are actively recruiting into our study, with currently unknown medical history or <i>BAP1</i> status. MM, mesothelioma; UM, uveal melanoma; BCC, basal cell carcinoma; RCC, renal cell carcinoma; CM, cutaneous melanoma; SCC, squamous cell carcinoma; all other cancer types are indicated by their full name or anatomical location; “unknown”, the cause of death was cancer, but the histological type was not identified. “other cancers”, malignancies possibly associated with <i>BAP1</i> mutations.</p

BAP1 cytoplasmic staining and LOH in MM biopsies.

<p><b>(A)</b> Representative histology (Hematoxylin and Eosin staining) and BAP1 IHC. Controls: Panel a, normal strip of pleural mesothelial cells; d, MM biopsy containing wild-type BAP1. Note BAP1 nuclear staining and faint cytoplasmic staining; black arrows identify representative normal mesothelial cells in a and MM cells in d. Panels b, c, e and f, BAP1-mutant MM biopsies from MARF11-III-1 (b,e) and MARF18-III-1 (c,f). Note cytoplasmic BAP1 staining and absence of nuclear staining in MM cells; black arrows identify representative tumor cells indicating LOH for BAP1. Note that nearby infiltrating “normal” lymphocytes and endothelial cells show nuclear BAP1 staining (red arrows) as they retain one normal BAP1 allele. Original magnification, 400X. <b>(B)</b><i>BAP1</i> sequencing of germline and tumor DNAs from MARF11-III-1 and MARF18-III-1 reveals heterozygosity in germline DNA and LOH in tumor cell DNA. Top panels, germline DNA from both patients shows a ‘C’ deletion (grey shadowed area): the wild-type allele and the mutant allele show the same peak intensity indicating a heterozygous mutation. Bottom Panels, tumor cell DNA, from both patients, shows a homozygous C deletion. The electropherogram of tumor cell DNA shows that the allele with the C deletion has a higher peak, indicating that only the mutant allele is present in the tumor cells. The lower peak is likely generated by the wild type allele of some contaminating normal cells. DNA sequence of wild-type—AGTCCCCTGGC; DNA sequence of mutant—AGTCCCTGGCG.</p

Electropherogram of BAP1 c.1717_1717delC mutation and chromosome 3 IBD shared haplotypes in the 4 founder MARF patients studied.

<p><b>(A)</b> Representative electropherogram of germline <i>BAP1</i> MARF2-IV-2 founder mutation. The heterozygous C deletion at nucleotide position c.1717 of the <i>BAP1</i> gene is predicted to be a frame-shift mutation leading to a truncated protein of 573 amino acids in length. Nucleotide sequence is shown above the electropherogram and predicted amino acid changes are below. <b>(B)</b> Idiogram showing Identity By Descent (IBD) shared haplotypes of the DNA regions surrounding <i>BAP1</i> in the germline DNA of the 4 founder MARF patients studied. The p-arm of chromosome 3 depicts the position and extent of shared IBD haplotype segments (LOD>3) that overlap the <i>BAP1</i> gene. Red line: MARF11-III-1 + MARF40-III-1 (chr3:21.8–55.9, 34.2 Mbp, LOD = 176.6); green line: MARF2-IV-2 + MARF40-III-1 (chr3:25.55–55.12, 29.6 Mbp, LOD = 145.2); blue line: MARF2-IV-2 + MARF11-III-1 (chr3:25.55–55.12, 29.6 Mbp, LOD = 142.1); gray line: MARF2-IV-2 + MARF18-III-1 (chr3:45.40–54.5, 9.1 Mbp, LOD = 38.8); orange line: MARF18-III-1 + MARF40-III-1 (chr3:45.40–54.5, 9.1 Mbp, LOD = 38.1); purple line: MARF11-III-1 + MARF18-III-1 (chr3:45.40–54.5, 9.1 Mbp, LOD = 37.1). Gray oval represents the centromere.</p