Pengaruh Pembiayaan Modal Kerja Terhadap Keuntungan Nasabah Bank Syariah Berrdasarkan Prinsip Mudharabah (Studi Terhadap PT. Bank Sulselbar Syariah Cabang Makassar)

Pembiayaan modal kerja adalah pembiayaan yang diberikan kepada nasabah untuk membiayai kebutuhan modal kerja usaha para nasabah yang menggunakan akad Mudha>rabah. Mudha>rabah merupakan salah satu bentuk dari perkonsian, yang mana salah satu pihak disebut pemilik modal yang menyediakan sejumlah uang tertentu, sementara pihak lain disebut pengelola dana yaitu orang yang menjalankan usaha. Tujuan dilakukannya penelitian ini untuk mengetahui peningkatan pendapatan nasabah bank syariah setelah mendapatkan pembiayaan modal kerja dengan menggunakan prinsip Mudha>rabah pada PT. Bank Sulselbar cabang Makassar. Metode analisis yang digunakan adalah analisis regresi sederhana dengan melakukan uji-t untuk mengetahui pengaruhnya. Penelitian ini menggunakan metode kuesioner sebagai alat pengumpulan data. Populasi dalam penelitian ini adalah seluruh nasabah yang mendapatkan pembiayaan modal kerja pada PT. Bank Sulselbar cabang Makassar yang sampai saat ini berjumlah 65 nasabah. Penentuan jumlah sampel menggunakan teknik pengambilan sampel Non Probability Sampling yaitu teknik purposive sampling yang jumlah sampelnya sebanyak 29 orang. Data yang diperoleh melalui kuesioner yang diuji dengan uji validitas dan uji reliabilitas, serta analisis data menggunakan analisis regresi sederhana dan uji t. Hasil regresi sebagai berikut : Y = 3,705 + 0,749X + e Dari hasil analisis regresi di atas, menunjukkan bahwa keuntungan nasabah dipengaruhi oleh pembiayaan modal kerja. Hasil uji-t menunjukkan bahwa pembiayaan modal kerja memiliki nilai thitung (8,253) > ttabel (2,048) artinya variabel bebas (independent) yaitu pembiayaan modal kerja berpengaruh secara signifikan terhadap variabel terikat (dependent) yaitu keuntungan nasabah. Dengan demikian disimpulkan bahwa pembiayaan modal kerja dengan menggunakan prinsip Mudha>rabah mempengaruhi keuntungan nasabah pada PT. Bank Sulselbar Syariah cabang Makassar

Separation and recovery of organic acids from fermented kitchen waste by an integrated process

Organic acids produced from anaerobic digestion of kitchen waste were recovered using a new integrated method which consisted of freezing and thawing, centrifugation, filtration and evaporation. The main organic acid produced was lactic acid (98%). After the freezing and thawing process, 73% of the total suspended solids were removed and the organic acids were elevated from 59.0 to 70 g/L. The evaporation technique was used to further concentrate the organic acids up to 224 g/L. Using the integrated recovery method, the reduction of the total suspended solids in the solution achieved was about 93%. The material balance for the recovery process was also presented

Quercetin prevents progression of disease in elastase/LPS-exposed mice by negatively regulating MMP expression

Abstract Background Chronic obstructive pulmonary disease (COPD) is characterized by chronic bronchitis, emphysema and irreversible airflow limitation. These changes are thought to be due to oxidative stress and an imbalance of proteases and antiproteases. Quercetin, a plant flavonoid, is a potent antioxidant and anti-inflammatory agent. We hypothesized that quercetin reduces lung inflammation and improves lung function in elastase/lipopolysaccharide (LPS)-exposed mice which show typical features of COPD, including airways inflammation, goblet cell metaplasia, and emphysema. Methods Mice treated with elastase and LPS once a week for 4 weeks were subsequently administered 0.5 mg of quercetin dihydrate or 50% propylene glycol (vehicle) by gavage for 10 days. Lungs were examined for elastance, oxidative stress, inflammation, and matrix metalloproteinase (MMP) activity. Effects of quercetin on MMP transcription and activity were examined in LPS-exposed murine macrophages. Results Quercetin-treated, elastase/LPS-exposed mice showed improved elastic recoil and decreased alveolar chord length compared to vehicle-treated controls. Quercetin-treated mice showed decreased levels of thiobarbituric acid reactive substances, a measure of lipid peroxidation caused by oxidative stress. Quercetin also reduced lung inflammation, goblet cell metaplasia, and mRNA expression of pro-inflammatory cytokines and muc5AC. Quercetin treatment decreased the expression and activity of MMP9 and MMP12 in vivo and in vitro, while increasing expression of the histone deacetylase Sirt-1 and suppressing MMP promoter H4 acetylation. Finally, co-treatment with the Sirt-1 inhibitor sirtinol blocked the effects of quercetin on the lung phenotype. Conclusions Quercetin prevents progression of emphysema in elastase/LPS-treated mice by reducing oxidative stress, lung inflammation and expression of MMP9 and MMP12.http://deepblue.lib.umich.edu/bitstream/2027.42/78260/1/1465-9921-11-131.xmlhttp://deepblue.lib.umich.edu/bitstream/2027.42/78260/2/1465-9921-11-131.pdfPeer Reviewe

Analisis Morfometrik Daun Cabai Bergejala Kuning Keriting Menggunakan Pendekatan Pengolahan Citra Digital dan Algoritma Data Mining

Gejala kuning keriting pada daun cabai umumnya disebabkan oleh infeksi Begomovirus. Daun tanaman terinfeksi tidak hanya mengalami perubahan warna sebagai indikator rusaknya klorofil tetapi juga mengalami perubahan morfologi bentuk. Penelitian ini bertujuan menguantifikasi gejala infeksi Begomovirus berdasarkan perubahan morfologi bentuk daun menggunakan pengolahan citra digital dan algoritma data mining yang akan memudahkan dalam pemantauan dan analisis perkembangan penyakit tanaman. Total 33 citra daun cabai rawit bergejala kuning keriting maupun tidak bergejala menjadi dataset penelitian ini. Citra daun cabai tersebut diolah dan diekstrak karakteristik bentuknya berupa circularity, aspect ratio, roundness, dan solidity menggunakan aplikasi Fiji-ImageJ. Selanjutnya dilakukan uji beda (uji-t), pengelompokan citra menggunakan algoritma Simple K-Means, dan evaluasi ketepatan hasil pengelompokan berdasarkan indeks ARI dan NMI. Hasil penelitian menunjukkan bahwa secara umum ada perbedaan bentuk yang nyata antara daun bergejala dengan daun tidak bergejala. Daun cabai rawit bergejala kuning keriting memiliki rata-rata nilai aspect ratio dan solidity yang lebih kecil dibandingkan daun cabai tidak bergejala, sebaliknya memiliki rata-rata nilai circularity dan roundness yang lebih besar dibandingkan daun cabai tidak bergejala. Evaluasi ketepatan pengelompokan sampel daun cabai rawit bergejala maupun tidak bergejala berdasarkan indeks ARI dan NMI menghasilkan nilai terbaik untuk pengelompokkan ke dalam dua kelompok.Morphometric Analysis of Chili Leaves with Yellow Curly Symptom Using Digital Image Processing Approach and Data Mining Algorithm Yellow curling symptoms on chili leaves are generally caused by Begomovirus infection. The leaves of infected plants not only change color as an indicator of chlorophyll damage but also experience changes in morphological shape. This research aims to quantify the symptoms of Begomovirus infection based on morphological changes in leaf shape using digital image processing and data mining algorithms that will facilitate monitoring and analysis of plant disease development. A total of 33 images of cayenne pepper leaves with yellow curly symptoms and without symptoms became the dataset of this study. Using the Fiji-ImageJ application, the chili leaf images were processed and extracted in the shape characteristics, i.e., circularity, aspect ratio, roundness, and solidity. Furthermore, a t-test and image clustering using the Simple K-Means algorithm was conducted, followed by evaluation of the accuracy of the clustering results based on the ARI and NMI indexes. The results showed that, in general, there was a significant difference in shape between symptomatic and non-symptomatic leaves. The ratio and solidity value of leaves with yellow curly symptom was smaller than those of non-symptomatic chili leaves. In contrast, circularity and roundness value of symptomatic leaves was larger than those of non-symptomatic chili leaves. Evaluation of the accuracy of samples grouping for cayenne pepper leaves with and without symptoms based on the ARI and NMI indicated that grouping them into two groups gave the best value

VEGF, FGF1, FGF2 and EGF gene polymorphisms and psoriatic arthritis

BACKGROUND: Angiogenesis appears to be a first-order event in psoriatic arthritis (PsA). Among angiogenic factors, the cytokines vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), and fibroblast growth factors 1 and 2 (FGF1 and FGF2) play a central role in the initiation of angiogenesis. Most of these cytokines have been shown to be upregulated in or associated with psoriasis, rheumatoid arthritis (RA) or ankylosing spondylitis (AS). As these diseases share common susceptibility associations with PsA, investigation of these angiogenic factors is warranted. METHODS: Two hundred and fifty-eight patients with PsA and 154 ethnically matched controls were genotyped using a Sequenom chip-based MALDI-TOF mass spectrometry platform. Four SNPs in the VEGF gene, three SNPs in the EGF gene and one SNP each in FGF1 and FGF2 genes were evaluated. Statistical analysis was performed using Fisher's exact test, and the Cochrane-Armitage trend test. Associations with haplotypes were estimated by using weighted logistic models, where the individual haplotype estimates were obtained using Phase v2.1. RESULTS: We have observed an increased frequency in the T allele of VEGF +936 (rs3025039) in control subjects when compared to our PsA patients [Fisher's exact p-value = 0.042; OR 0.653 (95% CI: 0.434, 0.982)]. Haplotyping of markers revealed no significant associations. CONCLUSION: The T allele of VEGF in +936 may act as a protective allele in the development of PsA. Further studies regarding the role of pro-angiogenic markers in PsA are warranted

Aldose reductase deficiency in mice protects from ragweed pollen extract (RWE)-induced allergic asthma

<p>Abstract</p> <p>Background</p> <p>Childhood hospitalization related to asthma remains at historically high levels, and its incidence is on the rise world-wide. Previously, we have demonstrated that aldose reductase (AR), a regulatory enzyme of polyol pathway, is a major mediator of allergen-induced asthma pathogenesis in mouse models. Here, using AR null (AR^-/-) mice we have investigated the effect of AR deficiency on the pathogenesis of ragweed pollen extract (RWE)-induced allergic asthma in mice and also examined the efficacy of enteral administration of highly specific AR inhibitor, fidarestat.</p> <p>Methods</p> <p>The wild type (WT) and AR^-/-mice were sensitized and challenged with RWE to induce allergic asthma. AR inhibitor, fidarestat was administered orally. Airway hyper-responsiveness was measured in unrestrained animals using whole body plethysmography. Mucin levels and Th2 cytokine in broncho-alveolar lavage (BAL) were determined using mouse anti-Muc5A/C ELISA kit and multiplex cytokine array, respectively. Eosinophils infiltration and goblet cells were assessed by H&E and periodic acid Schiff (PAS)-staining of formalin-fixed, paraffin-embedded lung sections. T regulatory cells were assessed in spleen derived CD4⁺CD25⁺T cells population.</p> <p>Results</p> <p>Deficiency of AR in mice led to significantly decreased PENH, a marker of airway hyper-responsiveness, metaplasia of airway epithelial cells and mucus hyper-secretion following RWE-challenge. This was accompanied by a dramatic decrease in infiltration of eosinophils into sub-epithelium of lung as well as in BAL and release of Th2 cytokines in response to RWE-challenge of AR^-/-mice. Further, enteral administration of fidarestat significantly prevented eosinophils infiltration, airway hyper-responsiveness and also markedly increased population of T regulatory (CD4⁺CD25⁺FoxP3⁺) cells as compared to RWE-sensitized and challenged mice not treated with fidarestat.</p> <p>Conclusion</p> <p>Our results using AR^-/-mice strongly suggest the role of AR in allergic asthma pathogenesis and effectiveness of oral administration of AR inhibitor in RWE-induced asthma in mice supports the use of AR inhibitors in the treatment of allergic asthma.</p

Effects of cigarette smoke condensate on proliferation and wound closure of bronchial epithelial cells in vitro: role of glutathione

BACKGROUND: Increased airway epithelial proliferation is frequently observed in smokers. To elucidate the molecular mechanisms leading to these epithelial changes, we studied the effect of cigarette smoke condensate (CSC) on cell proliferation, wound closure and mitogen activated protein kinase (MAPK) activation. We also studied whether modulation of intracellular glutathione/thiol levels could attenuate CSC-induced cell proliferation. METHODS: Cells of the bronchial epithelial cell line NCI-H292 and subcultures of primary bronchial epithelial cells were used for the present study. The effect of CSC on epithelial proliferation was assessed using 5-bromo-2-deoxyuridine (BrdU) incorporation. Modulation of epithelial wound repair was studied by analysis of closure of 3 mm circular scrape wounds during 72 hours of culture. Wound closure was calculated from digital images obtained at 24 h intervals. Activation of mitogen-activated protein kinases was assessed by Western blotting using phospho-specific antibodies. RESULTS: At low concentrations CSC increased proliferation of NCI-H292 cells, whereas high concentrations were inhibitory as a result of cytotoxicity. Low concentrations of CSC also increased epithelial wound closure of both NCI-H292 and PBEC, whereas at high concentrations closure was inhibited. At low, mitogenic concentrations, CSC caused persistent activation of ERK1/2, a MAPK involved in cell proliferation. Inhibition of cell proliferation by high concentrations of CSC was associated with activation of the pro-apoptotic MAP kinases p38 and JNK. Modulation of intracellular glutathione (GSH)/thiol levels using N-acetyl-L-cysteine, GSH or buthionine sulphoximine (BSO), demonstrated that both the stimulatory and the inhibitory effects of CSC were regulated in part by intracellular GSH levels. CONCLUSION: These results indicate that CSC may increase cell proliferation and wound closure dependent on the local concentration of cigarette smoke and the anti-oxidant status. These findings are consistent with increased epithelial proliferation in smokers, and may provide further insight in the development of lung cancer

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015

SummaryBackground The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding Bill & Melinda Gates Foundation

Characterization of a new full length TMPRSS3 isoform and identification of mutant alleles responsible for nonsyndromic recessive deafness in Newfoundland and Pakistan

BACKGROUND: Mutant alleles of TMPRSS3 are associated with nonsyndromic recessive deafness (DFNB8/B10). TMPRSS3 encodes a predicted secreted serine protease, although the deduced amino acid sequence has no signal peptide. In this study, we searched for mutant alleles of TMPRSS3 in families from Pakistan and Newfoundland with recessive deafness co-segregating with DFNB8/B10 linked haplotypes and also more thoroughly characterized the genomic structure of TMPRSS3. METHODS: We enrolled families segregating recessive hearing loss from Pakistan and Newfoundland. Microsatellite markers flanking the TMPRSS3 locus were used for linkage analysis. DNA samples from participating individuals were sequenced for TMPRSS3. The structure of TMPRSS3 was characterized bioinformatically and experimentally by sequencing novel cDNA clones of TMPRSS3. RESULTS: We identified mutations in TMPRSS3 in four Pakistani families with recessive, nonsyndromic congenital deafness. We also identified two recessive mutations, one of which is novel, of TMPRSS3 segregating in a six-generation extended family from Newfoundland. The spectrum of TMPRSS3 mutations is reviewed in the context of a genotype-phenotype correlation. Our study also revealed a longer isoform of TMPRSS3 with a hitherto unidentified exon encoding a signal peptide, which is expressed in several tissues. CONCLUSION: Mutations of TMPRSS3 contribute to hearing loss in many communities worldwide and account for 1.8% (8 of 449) of Pakistani families segregating congenital deafness as an autosomal recessive trait. The newly identified TMPRSS3 isoform e will be helpful in the functional characterization of the full length protein

Prosiding Seminar Hasil Penelitian Kebahasaan Dan Kesastraan

Buku Prosiding Seminar Hasil Penelitian Kebahassaan dan Kesastraan ini adalah salah satu dari sekian banyak buku yang dimaksudkan sebagai pendukung program literasi. Buku ini berisi delapan belas makalah hasil penelitian bahasa dan enam belas makalah hasil penelitian sastra yang berasal dari berbagai instansi di empat kementerian, yaitu Kementerian Pendidikan dan Kebudayaan, Kementerian Agama, Kementerian Informasi dan Komunikasi, dan Kementerian Riset, Teknologi, dan Pendidikan Tinggi. Makalah-makalah tersebut telah diseminarkan di Balai Bahasa Daerah Istimewa Yogyakarta pada 24—25 Agustus 2016 dan telah direvisi serta disunting oleh tim penyunting. Buku ini diharapkan bermanfaat bagi pembaca, khususnya para dosen, peneliti,dan pemerhati bahasa dan sastra