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

Graphene Oxides Decorated with Carnosine as an Adjuvant To Modulate Innate Immune and Improve Adaptive Immunity <i>in Vivo</i>

Current studies have revealed the immune effects of graphene oxide (GO) and have utilized them as vaccine carriers and adjuvants. However, GO easily induces strong oxidative stress and inflammatory reaction at the site of injection. It is very necessary to develop an alternative adjuvant based on graphene oxide derivatives for improving immune responses and decreasing side effects. Carnosine (Car) is an outstanding and safe antioxidant. Herein, the feasibility and efficiency of ultrasmall graphene oxide decorated with carnosine as an alternative immune adjuvant were explored. OVA@GO-Car was prepared by simply mixing ovalbumin (OVA, a model antigen) with ultrasmall GO covalently modified with carnosine (GO-Car). We investigated the immunological properties of the GO-Car adjuvant in model mice. Results show that OVA@GO-Car can promote robust and durable OVA-specific antibody response, increase lymphocyte proliferation efficiency, and enhance CD4⁺ T and CD8⁺ T cell activation. The presence of Car in GO also probably contributes to enhancing the antigen-specific adaptive immune response through modulating the expression of some cytokines, including IL-6, CXCL1, CCL2, and CSF3. In addition, the safety of GO-Car as an adjuvant was evaluated comprehensively. No symptoms such as allergic response, inflammatory redness swelling, raised surface temperatures, physiological anomalies of blood, and remarkable weight changes were observed. Besides, after modification with carnosine, histological damages caused by GO-Car in lung, muscle, kidney, and spleen became weaken significantly. This study sufficiently suggest that GO-Car as a safe adjuvant can effectively enhance humoral and innate immune responses against antigens <i>in vivo</i>

The expression levels of IFN-β and IFN-responsive genes in NDV-infected A549 and DF1 cells.

<p>(A) The IFN-β protein levels in A549 cells stimulated by NDV were assayed by ELISA so as to determine its effect to IFN signaling. (B) The IFN-responsive genes IFIT1, ISG15, Mx1, and IFN-β were further quantified by Real-time PCR in V-deficient rZJ1-VS and <i>wt</i> ZJ-1-infected A549 cells. (C) IFN-responsive genes in rZJ1-VS or ZJ1 infected DF1 cells. Gene expression was compared between DF1 cells infected with rZJ1-VS and <i>wt</i> virus ZJ1 at a MOI 3. *Gene expressions were enhanced significantly in rZJ1-VS-infected cells than those in rZJ1-infected cells (P < 0.01). (D) The V protein expression levels in NDV-infected A549 and DF1 cells. The P and V protein were detected in WB assay at different time points post infection with NDV strain ZJ1.</p

Recovery of V-deficient recombinant NDV from an infectious clone.

<p>(A) Schematic representation of a V-deficient gene mutation in a full-length cDNA clone. To selectively block expression of V, modification was performed after the RNA-editing site of the full-length cDNA clone pTVT-ZJ1 to introduce a stop codon in the ORF with +1 frameshift. (B) Mutation in the genome of recovered rZJ1-VS was confirmed by sequencing. Total viral RNA was extracted and RT-PCR-amplified for sequencing. The genome of rZJ1-VS was identical to the <i>wt</i> ZJ1 except for AT for TA after the RNA editing-site. (C) Expression of V protein was examined in DF-1 cells infected with rZJ1-VS or ZJ1 at MOI 3. The V protein was undetectable in the rZJ1-VS infected cells; by contrast, ZJ1 expressed V protein in the infected cells at the same point. (D) Growth curves of rZJ1-VS and the <i>wt</i> ZJ1 in DF1 and Vero cells. Replication of rZJ1-VS was compared to ZJ1 in early infection. (E) Cytopathic effect (CPE) caused by rZJ1-VS or ZJ1 in DF1 cells infected with rZJ1-VS or ZJ1 at MOI 0.01.</p

STAT1 expression in NDV infected or V-expressing plasmids transfected cells.

<p>(A) No STAT1 reduction was observed in Vero cells infected with NDV ZJ1, 9a5b or LaSota at MOI 3 at 6, 12 or 24 hpi. (B) Over-expression of ZJ1, 9a5b and LaSota V protein did not effect on STAT1 expression in Vero cells transfected with V-expressing plasmids. (C) STAT1 was reduced at 48 h post-transfection in NDV-infected Vero cells (MOI = 3) transfected in advance with V-expressing plasmids. (D) STAT1 expression in A549 cells transfected with V expressing plasmids or infected with ZJ1 or LaSota was detected at 48 h post-transfection or 12 h post-infection by indirect fluorescence assay. These infected A549 cells were fixed and detected for P/V/W proteins with a mixture of anti-serum Pab-V1 and Pab-V2; while the presence of STAT1 was determined by anti-STAT1 antibody (ab31369). Cellular nuclei were stained with 4,6-diamidino-2-phenylindole (DAPI).</p

Newcastle disease virus infection impaired IFN-α-induced STAT1 phosphorylation.

<p>(A) IFN-α-induced phosphorylated STAT1 degradation in NDV-infected A549 and Vero cells. A549 or Vero cells were infected with NDV strains ZJ1 at MOI 3. At indicated time points post infection, A549 and Vero cells were stimulated with 500 U/ml human IFN-α or IFN-γ in 1 ml DMEM at 37°C for 15 min. Uninfected cells were stimulated with IFN as negative controls (IFNα+/infection-). IFN-α-induced phospho-STAT1 was observed (IFNα+/infection+) for reduction in total STAT1 proteins. IFN-γ-induced phospho-STAT1 proteins were not reduced. (B) Phospho-STAT1 in A549 cells transfected with V-expressing plasmids after stimulation with IFN-α. (C) Expression level of STAT1 and phospho-STAT1 decreased in V-expressing Vero cells after IFN-α stimulation. Vero cells were mock transfected with pCI-neo plasmids. Cells on glass coverlips were transfected with pCI-V/ZJ1 plasmids. At 48 h post-transfection, cells were treated with IFN-α for 15 min prior to fixation as in “Material and methods”. V protein was detected by a mixture of anti-serum Pab-V1 and Pab-V2; STAT1 and phosphorylation were determined by anti-STAT1 antibody (ab31369) and anti-phospho-STAT1 antibody (ab30645). Cellular nuclei were stained with DAPI.</p

The reduction of total and phosphorylated STAT1 in NDV-infected cells was inhibited after treatment with Ub E1 inhibitor PYR-41 at different time points.

<p>(A) STAT1 and phospho-STAT1 expression levels in PYR-41 treated Vero cells at 6 hpi. (B) Phospho-STAT1 levels in PYR-41 treated Vero cells at 4, 6, 8 hpi. (C) Exogenous mutant STAT1 lacking 701aa phosphorylation site were not degraded in the course of NDV infection. One microgram pFlag-STAT1 or pFlag-Y701F was transfected into A549 cells cultured in 6-well plates. At 12 h post transfection, the cells were subsequently infected with NDVs at a MOI of 3. The cells were harvested at 24 hpi. (D) The expression levels of IFN-responsive genes in V-expressing A549 cells after stimulation of IFN-α. A549 cells in 6-well plates were transfected with 3 μg pCI-V or pCI-neo for each well as above-described. At 4 h and 8 h post-transfection, the cells were harvested following the treatment with 500 U/ml IFN-α for 30 min.</p

Identification of a Susceptibility Locus for Severe Adolescent Idiopathic Scoliosis on Chromosome 17q24.3

<div><p>Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity, affecting around 2% of adolescents worldwide. Genetic factors play an important role in its etiology. Using a genome-wide association study (GWAS), we recently identified novel AIS susceptibility loci on chromosomes 10q24.31 and 6q24.1. To identify more AIS susceptibility loci relating to its severity and progression, we performed GWAS by limiting the case subjects to those with severe AIS. Through a two-stage association study using a total of ∼12,000 Japanese subjects, we identified a common variant, rs12946942 that showed a significant association with severe AIS in the recessive model (<i>P</i> = 4.00×10⁻⁸, odds ratio [OR] = 2.05). Its association was replicated in a Chinese population (combined <i>P</i> = 6.43×10⁻¹², OR = 2.21). rs12946942 is on chromosome 17q24.3 near the genes <i>SOX9</i> and <i>KCNJ2</i>, which when mutated cause scoliosis phenotypes. Our findings will offer new insight into the etiology and progression of AIS.</p></div

Association of the 27 SNPs in the two-stage association study for AIS in Japanese.

<p>Combined results of GWAS and the replication study. RAF: risk allele frequency. CI: confidence interval.</p>a<p>calculated by <i>x</i>² test. <i>P</i> values below the genome-wide significance level (P<5×10⁻⁸) are in bold.</p

Association of rs12946942 with severe AIS in Japanese and Chinese populations.

<p>RAF: risk allele (T allele) frequency. CI: confidence interval.</p><p>Data of <i>P</i> value, odds ratio (95% CI) and P_BD are for the recessive model (G/G and G/T vs T/T).</p>a<p>by <i>x</i>² test.</p>b<p>homogeneity of odds ratios by the Breslow-Day test.</p>c<p>by the Mantel-Haenszel method.</p