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

Synchronous Removal of Small-Sized Antibiotics by a Bifunctional Photocatalytic Nanofiltration Membrane in a Continuous Flow-Through Process under Multiple Influent Matrices

Bifunctional photocatalytic nanofiltration (PNF) membranes are of increasing significance in removing micropollutants in the actual water environment, but there are still critical bottlenecks that greatly limit their practicality. In this work, a metal-free and visible light-responsive surface-anchored PNF membrane was fabricated for simultaneously and efficiently removing target antibiotics from real river water in a continuous flow-through process. The results exhibited that the optimal PNF-3 membrane was expectedly consisted of an inside tight sub-nanopore structured separation layer and an outside thinner, super hydrophilic mesoporous degradation layer. Consequently, the PNF-3 membrane irradiated via visible light exhibited outstanding removal rates of sulfamethoxazole, trimethoprim, and chloramphenicol (between 99.0 and 99.9%), accompanied with almost constant high water permeability. In addition, after repeating the fouling–physical rinsing process three times that lasted for 60 h, only sporadic adherent contaminants remained on the top surface, together with minimal total and irreversible fouling ratios (only 7.9 and 1.2%), strongly proving that the PNF-3 membrane displayed good self-cleaning performance. In addition, the acute and chronic biotoxicities of its permeate to Virbrio qinghaiensis sp. -67 were also reduced significantly to 11.4 and 10.1%, respectively. This study might provide valuable insights into the continuous enhancement of the practicality and effectiveness of PNF membranes in micro-polluted water purification scenarios

Schematic diagrams of the organization of RHDV luciferase replicon and the derived RHDV deletion mutants.

<p>(A) In bold, a schematic representations of RHDV luciferase replicon constructs; the unique <i>Cla</i>I site was introduced at 7381 nt. Fluc replaced most of the viral structural protein coding region by fusion PCR. White boxes denote RHDV nonstructural protein coding sequence. Gray boxes indicate a structural protein coding sequence. Lines indicate the 5′ and 3′ NCRs. Arrows point to the positions of the cleavage sites at the N and C termini of the proteins. (B) In-frame deletions of RHDV plasmids were generated by fusion PCR. The deleted sequence and positions are indicated for each mutant. Arrows point to the positions of the restriction site used to construct deletion mutants.</p

Oligonucleotides used for construction of RHDV luciferase replicons, VPg deletion mutant, 3D deletion mutant, 5′NCR deletion mutant, and detection of replicon.

*<p>Underlined nucleotides were required for cloning.</p

Time kinetics of the replicon in RK 13 cells.

<p>During time kinetics with the pRHDV-luc experiments, RK13 cells (200000 per well of a 6-well plate) were transfected with 1 µg of pRHDV-luc and pGL4.75. The cells were then lysed at different times post-transfection, and the Fluc activity was measured in RLU and normalized with respect to a cotransfected plasmid encoding a Renilla luciferase. Similar results were obtained in two independent experiments. pRHDV was used as negative control. In most cases, the variations are very small and therefore the error bars are not visible.</p

Luciferase activity in cells transfected with the RHDV luciferase replicon and several deletion mutant derivatives and qRT-PCR detection of viral mRNA levels.

<p>(A) Relative Luciferase activities in RK13 cell of mutants with deletions in 5'NCR,VPg, 3D, and the parental genotype pRHDV-luc. (B) Relative Luciferase activities levels in RK-13 cells of the replication-deficient plasmid (pRHDV-luc/Δ3D) and its derived deletion mutants (pRHDV-luc/Δ5’NCR/3D, pRHDV-luc/ΔVPg/3D) at 24 h post-transfection.The luciferase activity in RK13 cells was measured by determining the firefly luciferase activity at 24 h post-transfection, and normalization for transfection efficiency was performed by using the Renilla luciferase activity measured at the same time. The differences in luciferase activities produced by the pRHDV-luc and their mutant derivatives were compared by one-way ANOVA and Tukey’s multiple comparison test. Asterisks (*) indicate statistical differences compared to the parental genotype pRHDV-luc. RLU, relative light units.(C)qRT-PCR was used to evaluate the RNA level of viruses derived from pRHDV-luc and their mutant derivatives. The value determined with the parental genotype pRHDV-luc was set as 100% and used as a reference to normalize the replication of the other mutant replicons. Values are means and standard deviations for three independent experiments.</p

Detection of RNA replication with RT-PCR.

<p>Cytoplasmic RNA isolated 24 h post-transfection from RK-13 cells transfected with pRHDV-luc was subjected to standard RT-PCR to detect the accumulation of plus(+) and minus (−) strand. RT-PCR products separated by agarose gel electrophoresis show two PCR products from the pRHDV-luc, Lane M of the gel contains the DNA marker, lanes 1and 2 show RT-PCR reactions of reporter gene <i>Fluc</i>, lanes 5 and 6 show RT-PCR reactions of virus gene, lane 3 and 7 are control demonstrating that RT-PCR reactions without reverse transcriptase did not result into amplification of <i>Fluc</i> and <i>NSP3</i>, lane 4 and 8 show RT-PCR reaction of total RNA from non-tranfected RK-13 cells. Primers are shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0060316#pone-0060316-t001" target="_blank">Table 1</a>.</p

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