Tafsir Ideologis Dalam Khazanah Intelektual Islam

One of the causes is not the end of the study the Koran is the Koran contains many possible meanings (Wujûh al-Ma‘ânî) continuous potential can be explored and interpreted in accordance with the methods and tendencies interpreter. Therefore, no wonder the result was rich in meaning and interpretation is different, so lure the attention of others to re-refine and refuse to offer a different perspective. This viewpoint difference is attributed to the possibility of the many meanings of the Koran, also due to socio-cultural and areas of specialization of each interpreter. Ideology and political upheaval Muslims initial period stimulate the birth of the leaders of rival political and theological thinking bolder and varied. As evidence, if at the time of the Prophet and the Companions interpretation of verses mutashâbih tend to be avoided, the interpretation of later generations of the same paragraph as the focus of their attention and more wide open. So also with the interpretation of the Koran political interests and ideological bias increasingly widesprea

Faktor-Faktor Yang Mempengaruhi Kinerja Lembaga Keuangan Mikro Syari\u27ah Dengan Menggunakan Metode Indonesia Zakat Development Report (IZDR)

This research aims to measure the performance of BMT Hudatama and UJKSAl-Hidayat as two Islamic Microfinance Institutions in Semarang, Central Java. Research method used in this study is performance measurement tools issued by Indonesia Magnificence of Zakat (IMZ) in Indonesia Zakat and Development Report (IZDR) in 2011. This method includes five measurement indicators; 1) Islamic compliance, legality, and institutional performances;2) Management performance; 3) Financial performance; 4) Economic efficiency; and 5) Social legitimacy performance. This study used primary and secondary data. Primary data were taken from interview and BMT Hudatama and Islamic Financial Service Unit of Al-Hidayaat\u27s annual report. Secondary data were obtained from review of related literature. The comparison between the two institutions indicates that BMT Hudatama is better than UJKS AL-Hidayat in terms of its performance. However, the comparison with U test or Mann whitney U Test indicates that there is no significant difference between the performace of the two institutionsPenelitian ini bertujuan untuk mengukur kinerja Lembaga Keuangan Mikro Syari\u27ah (LKMS) yaitu BMT Hudatama dan UJKS Al-Hidayaat di Kab/KotaSemarang Jawa Tengah. Metode yang digunakan adalah metode pengukurankinerja prima yang dikeluarkan oleh Indonesia Magnificence of Zakat (IMZ)dalam Indonesia Zakat and Development Report (IZDR) 2011 mencakuplima indikator pengukuran yaitu: 1) Kinerja kepatuhan syari\u27ah, legalitasdan kelembagaan, 2) Kinerja Manajemen, 3) Kinerja Keuangan, 4) KinerjaPendayagunaan Ekonomi, dan 5) Kinerja Legitimasi Sosial. Penelitian inimenggunakan data primer dan data sekunder. Data primer diperoleh dariwawancara dan laporan tahunan dari BMT Hudatama dan Unit Jasa KeuanganSyari\u27ah Al Hidayaat. Sedangkan data sekunder diperoleh dengan melakukanstudi literatur yang berkaitan dengan penelitian.Dalam perbandingan kinerjaprima BMT Hudatama lebih baik dari UJKS Al-Hidayaat. Namun dalamperbandingan dengan menggunakan uji U atau Mann whitney U Test untukmelihat signifikansi perbedaannya, didapatkan tidak ada perbedaan yangsignfikan kinerja prima BMT Hudatama dan UJKS Al-Hidayaa

Perlakuan Agens Hayati untuk Mengendalikan Hawar Daun Bakteri dan Meningkatkan Produksi Benih Padi Sehat

The research objectives were to evaluate biological agent treatments in controlling bacterial leaf blight (BLB) and increasing plant growth and seed production of rice. The experiment was conducted in the greenhouse and field using the same experimental design (randomized block design with two factors) and three replications. The first factor was seed treatments, i.e. negative control, positive control, streptomycin sulphate 0.2%, Pseudomonas diminuta + Bacillus subtilis, matriconditioning + streptomycin sulphate 0.2%, and matriconditioning + P. diminuta + B. subtilis. Spraying plants (second factor): untreated control, streptomycin sulphate 0.2%, biological agent F112, biological agent F198, and biological agent F57. In the greenhouse, matriconditioning + P. diminuta + B. subtilis improved seed germination, plant height, and plant dry weight. Spraying plants with biological agent F112 increased plant dry weight. Meanwhile, matriconditioning + P. diminuta + B. subtilis followed by spraying plants with biological agent F112 reduced the BLB severity. In the field, matriconditioning + P. diminuta + B. subtilis improved seedling dry weight. Matriconditioning + P. diminuta + B. subtilis and spraying plants with biological agents F112 controlled BLB and increased plant growth. However, all treatments were not able to increase healthy seed production

Mitochondrial permeability transition is a central coordinating event of apoptosis.

In a number of experimental systems, the early stage o the apoptotic process, i.e. the stage that precedes nuclear disintegration, is characterized by the breakdown of the inner mitochondrial transmembrane potential (ΔΨ(m)). This ΔΨ(m) disruption is mediated by the opening of permeability transition (PT) pores and appears to be critical for the apoptotic cascade, since it is directly regulated by Bcl-2 and since mitochondria induced to undergo PT in vitro become capable of inducing nuclear chromatinolysis in a cell-free system of apoptosis. Here, we addressed the question of which apoptotic events are secondary to mitochondrial PT. We tested the effect of a specific inhibitor of PT, bongkrekic acid (BA), a ligand of the mitochondrial academic nucleotide translocator, on a prototypic model of apoptosis; glucocorticoid-induced thymocyte death. In addition to abolishing the apoptotic ΔΨ(m) disruption, BA prevents a number of phenomena linked to apoptosis: depletion of nonoxidized glutathione, genetic generation of reactive oxygen species, translocation of NFκB, exposure of phosphatidylserine residues on the outer plasma membrane, cytoplasmic vacuolization, chromatin condensation, and oligonucleosomal DNA fragmentation. BA is also an efficient inhibitor of p53- dependent thymocyte apoptosis induced by DNA damaged. These data suggest that a number of apoptotic phenomona are secondary to PT. In addition, we present data indicating that apoptotic ΔΨ(m) disruption is secondary to transcriptional events. These data connect the PT control point to the p53- and ICE/Ced 3-regulated control points of apoptosis and place PT upstream of nuclear and plasma membrane features of PCD.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

MAVS-Mediated Apoptosis and Its Inhibition by Viral Proteins

BACKGROUND: Host responses to viral infection include both immune activation and programmed cell death. The mitochondrial antiviral signaling adaptor, MAVS (IPS-1, VISA or Cardif) is critical for host defenses to viral infection by inducing type-1 interferons (IFN-I), however its role in virus-induced apoptotic responses has not been elucidated. PRINCIPAL FINDINGS: We show that MAVS causes apoptosis independent of its function in initiating IFN-I production. MAVS-induced cell death requires mitochondrial localization, is caspase dependent, and displays hallmarks of apoptosis. Furthermore, MAVS(-/-) fibroblasts are resistant to Sendai virus-induced apoptosis. A functional screen identifies the hepatitis C virus NS3/4A and the Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) nonstructural protein (NSP15) as inhibitors of MAVS-induced apoptosis, possibly as a method of immune evasion. SIGNIFICANCE: This study describes a novel role for MAVS in controlling viral infections through the induction of apoptosis, and identifies viral proteins which inhibit this host response

Protection of pancreatic INS-1 β-cells from glucose- and fructose-induced cell death by inhibiting mitochondrial permeability transition with cyclosporin A or metformin

Hyperglycemia is detrimental to β-cell viability, playing a major role in the progression of β-cell loss in diabetes mellitus. The permeability transition pore (PTP) is a mitochondrial channel involved in cell death. Recent evidence suggests that PTP inhibitors prevent hyperglycemia-induced cell death in human endothelial cells. In this work, we have examined the involvement of PTP opening in INS-1 cell death induced by high levels of glucose or fructose. PTP regulation was studied by measuring the calcium retention capacity in permeabilized INS-1 cells and by confocal microscopy in intact INS-1 cells. Cell death was analyzed by flow cytometry. We first reported that metformin and cyclosporin A (CsA) prevented Ca2+-induced PTP opening in permeabilized and intact INS-1 cells. We then showed that incubation of INS-1 cells in the presence of 30 mM glucose or 2.5 mM fructose induced PTP opening and led to cell death. As both metformin and CsA prevented glucose- and fructose- induced PTP opening, and hampered glucose- and fructose- induced cell death, we conclude that PTP opening is involved in high glucose- and high fructose- induced INS-1 cell death. We therefore suggest that preventing PTP opening might be a new approach to preserve β-cell viability

Bax Function in the Absence of Mitochondria in the Primitive Protozoan Giardia lamblia

Bax-induced permeabilization of the mitochondrial outer membrane and release of cytochrome c are key events in apoptosis. Although Bax can compromise mitochondria in primitive unicellular organisms that lack a classical apoptotic machinery, it is still unclear if Bax alone is sufficient for this, or whether additional mitochondrial components are required. The protozoan parasite Giardia lamblia is one of the earliest branching eukaryotes and harbors highly degenerated mitochondrial remnant organelles (mitosomes) that lack a genome. Here we tested whether human Bax expressed in Giardia can be used to ablate mitosomes. We demonstrate that these organelles are neither targeted, nor compromised, by Bax. However, specialized compartments of the regulated secretory pathway are completely ablated by Bax. As a consequence, maturing cyst wall proteins that are sorted into these organelles are released into the cytoplasm, causing a developmental arrest and cell death. Interestingly, this ectopic cargo release is dependent on the carboxy-terminal 22 amino acids of Bax, and can be prevented by the Bax-inhibiting peptide Ku70. A C-terminally truncated Bax variant still localizes to secretory organelles, but is unable to permeabilize these membranes, uncoupling membrane targeting and cargo release. Even though mitosomes are too diverged to be recognized by Bax, off-target membrane permeabilization appears to be conserved and leads to cell death completely independently of mitochondria

Mitochondrial Dysfunction Links Ceramide Activated HRK Expression and Cell Death

Cell death is an essential process in normal development and homeostasis. In eyes, corneal epithelial injury leads to the death of cells in underlying stroma, an event believed to initiate corneal wound healing. The molecular basis of wound induced corneal stromal cell death is not understood in detail. Studies of others have indicated that ceramide may play significant role in stromal cell death following LASIK surgery. We have undertaken the present study to investigate the mechanism of death induced by C6 ceramide in cultures of human corneal stromal (HCSF) fibroblasts.Cultures of HCSF were established from freshly excised corneas. Cell death was induced in low passage (p<4) cultures of HCSF by treating the cells with C6 ceramide or C6 dihydroceramide as a control. Cell death was assessed by Live/Dead cell staining with calcein AM and ethidium homodimer-1 as well as Annexin V staining, caspase activation and TUNEL staining Mitochondrial dysfunction was assessed by Mito Sox Red, JC-1 and cytochrome C release Gene expression was examined by qPCR and western blotting.Our data demonstrate ceramide caused mitochondrial dysfunction as evident from reduced MTT staining, cyto c release from mitochondria, enhanced generation of ROS, and loss in mitochondrial membrane potential (ΔΨm). Cell death was evident from Live -Dead Cell staining and the inability to reestablish cultures from detached cells. Ceramide induced the expression of the harikari gene(HRK) and up-regulated JNK phosphorylation. In ceramide treated cells HRK was translocated to mitochondria, where it was found to interact with mitochondrial protein p32. The data also demonstrated HRK, p32 and BAD interaction. Ceramide-induced expression of HRK, mitochondrial dysfunction and cell death were reduced by HRK knockdown with HRK siRNA.Our data document that ceramide is capable of inducing death of corneal stromal fibroblasts through the induction of HRK mediated mitochondria dysfunction