Prosedur penyelesaian pembiayaan bermasalah pada akad mudharabah dalam rangka meminimalisir resiko di BMT Amanah Usaha Mulia Magelang

Permasalah kehidupan perekonomian yang sulit, membuat masyarakat berinisiatif untuk membuka usaha sendiri. Mereka membutuhkan suatu bantuan berupa dana untuk memperlancar usahanya, maka BMT Amanah Usaha Mulia Magelang ikut untuk mengembangkan produknya yaitu pembiayaan mudharabah sesuai perkembangan dunia perbankan dalam target peningkatan keuntungan dan menyejahterakan masyarakat. Dengan diberikanya pembiayaan tersebut, terkadang muncul adanya pembiayaan bermasalah dikarenakan ada beberapa faktor diantaranya ketidakmampuan anggota untuk membayar tepat waktu atau jatuh tempo pembayaran diakibatkan karena usaha anggota yang kurang lancar dan lain sebagaianya. Tugas Akhir ini berjudul “ Prosedur Penyelesaian Pembiayaan Bermasalah pada Akad Mudharabah Dalam Rangka Meminimalisir Risiko” Berdasarkan judul tersebut dapat diambil rumusan masalah yaitu apa penyebab terjadinya pembiayaan bermasalah pada BMT Amanah Usaha Mulia Magelang dan bagaimana prosedur penyelesaian pembiayaaan bermasalah pada akad mudharabah di BMT Amanah Usaha Mulia Magelang. Penelitian ini merupakan penelitian lapangan dimana sumber data yang digunakan berasal dari data primer dan sekunder yang diperoleh melalui metode wawancara dengan manajer, bagian pembiayaan dan dokumentasi. Metode yang digunakan dalam penelitian ini adalah deskriptif kualitatif yang bertujuan untuk menggambarkan secara sistematis dan akurat mengenai objek penelitian. Berdasarkan hasil penelitian dapat disimpulkan bahwa penyebab terjadinya pembiayaan bermasalah yaitu faktor internal meliputi kurang telitinya petugas BMT dalam menganalisi data calon anggota, kurang disiplinya dalam penagihan dan eksternal meliputi karakter anggota yang kurang baik, usahanya bangkrut dan terjadinya bencana alam yang tidak terduga. Adapun prosesdur yang digunakan BMT Amanah Usaha Mulia dalam menyelesaian pembiayaan bermasalah pada akad mudharabah dengan cara kekeluargaan atau musyawarah dengan anggota, penjadwalan kembali (rescheduling), persyaratan kembali (reconditioning), pengambilan jaminan (eksekusi), dan write off final. Di BMT Amanah Usaha Mulia dalam penyelesaian pembiayaan bermasalah jarang menngunakan jalur hukum, tetapi sering menggunakan cara kekeluargaan yang dianggap lebih efektif dan eksekusi jaminan apabila anggota tersebut sudah mengalami macet atau bermasalah

The effects of Mcl-1 and Bak over-expression in mammalian cells on IBV-induced PARP cleavage.

<p>H1299 (upper panel) and Huh7 cells (lower panel) were transfected with pxj40-myc-Mcl-1, pxj40-myc-Bak or pxj40-myc empty vector and either mock-infected (M) or infected with IBV at 16 hours post transfection. Cells were harvested 24 hours post infection and western blot analysis was performed using the indicated specific antibodies, with anti-tubulin as a loading control.</p

Affymetrix array analysis of the expression of BCL2-related genes in IBV-infected Vero cells at 24 hours post-infection.

<p>Affymetrix array analysis of the expression of BCL2-related genes in IBV-infected Vero cells at 24 hours post-infection.</p

Regulation of Mcl-1 expression by MEK-1, PI3K and GADD153.

<p>(A) Induction of Mcl-1 in IBV-infected cells in the presence or absence of either 20 mM of MEK-1 inhibitor U0126 or 40 mM of PI3K inhibitor LY294002. Vero, and H1299 cells were incubated with normal medium (DMSO-), LY294002 in DMSO, U0129 in DMSO and DMSO only (DMSO+) for 1 hour, and then infected with IBV at a multiplicity of infection of approximately 2 in the presence or absence of the inhibitors. Cells were harvested at 16 hours post-infection, and total RNA extracted. The relative amounts of Mcl-1 transcripts were determined by quantitative RT-PCR and normalized against GAPDH. The relative fold of Mcl-1 induction in IBV-infected cells was determined by comparing with mock-infected cells. (B) Induction of Mcl-1 in IBV-infected cells by the pro-apoptotic transcription factor GADD153. H1299 cells were transfected with either siGADD153 or a non-targeting control for 72 hours and subsequently infected with IBV. Cells were harvested at 16, 18 and 20 hours post infection for western blot analysis using specific antibodies against the indicated proteins, with anti-actin as a loading control. M, mock infection.</p

Analysis of the expression of BCL2-related proteins in IBV-infected Vero cells, chicken fibroblast DF1 cells and chicken embryos.

<p>(A) Vero cells were infected with IBV, harvested at 0, 8, 16 and 24 hours post-infection, and lysates prepared. Western blot analysis was performed with the indicated specific antibodies, and probed with anti-actin as a loading control. (B) Chicken fibroblast DF1 cells were either infected with IBV, harvested at 8 and 16 hours post-infection and RNA extracted. RT-PCR analysis was carried out using specific primers for the indicated genes, with GAPDH as a loading control. (C) 10-day-old chicken embryos were inoculated with either mock virus (M) or IBV (1000 plaque-forming units per egg) in a 37°C incubator for 48 hours. Total RNA was extracted from homogenized tissues and used for RT-PCR using specific primers as above (B).</p

The effects of manipulation of the expression of Bak and Mcl-1 on the replication and transcription of IBV RNA and the synthesis of IBV proteins in mammalian cells.

<p>(A) The effects of down-regulation of Bak and Mcl-1 by RNA interference on the synthesis of IBV proteins in mammalian cells. H1299 cells were transfected with siRNA duplexes targeting Mcl-1, Bak and EGFP, and infected with IBV at 72 hours post-transfection. The culture medium and cells were harvested separately for Western blot analysis, using specific antibodies for IBV-S and IBV-N and anti-tubulin as a loading control. M, mock infection. (B) The effects of down-regulation of Bak and Mcl-1 by RNA interference on the replication and transcription of IBV RNA in mammalian cells. Cells were harvested for Northern blot analysis, using specific probes for Bak, Mcl-1 and the 3′-UTR of IBV, with a GAPDH probe as loading control. (C) The effects of over-expression of Bak and Mcl-1 on the synthesis of IBV proteins in mammalian cells. H1299 (upper panel) and Huh7 cells (lower panel) were transfected with pxj40-myc-Mcl-1, pxj40-myc-Bak or pxj40-myc empty vector and either mock-infected (M) or infected with IBV at 16 hours post transfection. The culture medium and cells were harvested separately 24 hours post infection, and western blot analysis was performed using the indicated specific antibodies, with anti-tubulin as a loading control.</p

Analysis of Bak and Mcl-1 expression at the mRNA and protein levels in IBV-infected mammalian cells.

<p>(A) Northern blot analysis of Bak and Mcl-1 expression at the mRNA level in IBV-infected mammalian cells. Vero, H1299 and Huh7 cells infected with (A) IBV or (B) UV-IBV were harvested at 0, 8, 12, 16 and 24 hours post-infection, respectively, and total RNA was extracted. Northern blot analysis was carried out with specific probes for Bak and Mcl-1. The same membrane was also probed with a GAPDH probe as a loading control. (B). Western blot analysis of Bak and Mcl-1 expression at the protein level in mammalian cells. Vero, H1299 and Huh7 cells infected with IBV were harvested at 0, 8, 12, 16, 24 and 36 hours post-infection, respectively, and cell lysates prepared. Western blot analysis was performed using specific antibodies as indicated, with anti-actin as a loading control. M, mock infection.</p

Additional file 2 of Nutrition-related diseases and cardiovascular mortality in American society: national health and nutrition examination study, 1999–2006

Additional file 2:Supplementary Table 2. Sensitivity analyses for all-cause and cardiovascular mortality hazard ratios (HRs) for participants aged 20 years and older according to nutrition-related diseases: NHANES survey 1999–2006 with follow-up through 2015.

Identified SNPs in the genome of <i>S</i>. <i>mutans</i> C180-2 and C180-2FR.

<p>a nonsyn: non-synonymous coding SNP.</p><p>b This intergenic region is located upstream of a putative mutase and a putative permease chloride channel (<i>permease_A</i>).</p><p>c This intergenic region is located between the <i>pepX</i> and <i>glpF</i> genes.</p><p>Identified SNPs in the genome of <i>S</i>. <i>mutans</i> C180-2 and C180-2FR.</p

Gene organization at two intergenic regions in <i>S</i>. <i>mutans</i> C180-2 and C180-2FR.

<p>A. Orientation of the genes up- and down-stream of the intergenic region 1 (Inter-1). The sequences of Inter-1 in C180-2, C180-2FR, <i>S</i>. <i>mutans</i> UA159, <i>S</i>. <i>mutans</i> LJ23, <i>S</i>. <i>mutans</i> NN2025 and <i>S</i>. <i>mutans</i> GS5 are given in the blue bar. The red letter indicates the SNP; the purple box indicates the TATAAT box; the red box indicates the transcription start site of the operon; B. Orientation of the genes up- and down-stream of the intergenic region 2 (Inter-2). In both A and B, the red lines indicate the location of the SNPs.</p