Pengaruh Jumlah Tanaman Per Polibag Dan Pemangkasan Terhadap Pertumbuhan Dan Hasil Tanaman Mentimun Kyuri (Cucumis Sativus L.)

Mentimun merupakan salah satu tanaman sayuran buah yang banyak dikonsumsi segar maupun olahan. Sebagai komoditas yang memiliki nilai ekonomis tinggi maka diperlukan budidaya yang tepat untuk mendapatkan produksi tinggi dan kualitas mutu yang baik. Di dalam USAha peningkatan hasil panen, kepadatan tanaman (populasi) merupakan salah satu faktor penting. Kegiatan pemeliharaan dan USAha peningkatan produksi buah mentimun yang penting adalah pemangkasan. Pemangkasan pucuk batang bertujuan untuk menghambat pertumbuhan vegetatif tanaman yang terus menerus, sehingga asimilat yang dihasilkan tanaman akan lebih terkonsentrasikan kepada perkembangan generatif tanaman. Tujuan dari penelitian ini adalah untuk mempelajari pengaruh jumlah tanaman per polibag dan pemangkasan terhadap pertumbuhan dan hasil pada tanaman mentimun Kyuri. Penelitian ini dilaksanakan di Green House Balai Latihan Kerja Singosari-Malang, yang berlangsung dari Mei hingga Juni 2012. Hasil penelitian menunjukkan bahwa, respon tanaman mentimun terhadap kombinasi jumlah tanaman per polibag dan pemangkasan pucuk berbeda-beda. Secara kuantitas, kombinasi 1 tanaman per polibag dan pemangkasan dengan menyisakan 12 ruas menghasilkan bobot buah yang lebih tinggi daripada perlakuan lain. Sedangkan secara kualitas, kombinasi 1 tanaman per polibag dan tanpa pemangkasan menghasilkan buah dengan kualitas grade A terbanyak diantara perlakuan lainnya

Pengaruh Dukungan Organisasional, Pemberdayaan Karyawan, dan Kapabilitas Ti terhadap Keinovasian USAha Kecil Menengah (UKM) Studi Empiris : UKM di Sleman, D.i. YOGYAKARTA

Penelitian ini bersifat ex-post facto dan kausal komparatif yang bertujuan untuk mengetahui: 1) pengaruh Kapabilitas TI terhadap Keinovasian, (2) pengaruh Dukungan Organisasional terhadap Keinovasian, dan (3) pengaruh Pemberdayaan Karyawan terhadap Keinovasian. Populasi penelitian ini adalah Perusahaan berskala kecil menengah atau UKM di Kabupaten Sleman DIY. Sampel yang digunakan pada penelitian ini adalah UKM yang berjumlah 70 responden di kabupaten Sleman DIY. Teknik pengumpulan data dilakukan dengan menggunakan kuesioner atau angket. Data yang terkumpul dianalisis dengan menggunakan uji asumsi klasik, dan regresi sederhana. Hasil penelitian ini menunjukkan bahwa: (1) Terdapat pengaruh positif dan signifikan Kapabilitas TI terhadap Keinovasian yang ditunjukkan dengan nilai R2(x1y)= 0,511,thitung= 8,425> ttabel =2,000 dan dengan signifikansi (0,000 ttabel =2,000 dan dengan signifikansi (0,000 ttabel =2,000 dan dengan signifikansi (0,000 < 0,050). Dengan demikian dapat disimpulkan bahwa pemanfaatan teknologi, dukungan terhadap kontribusi karyawan, dan pemberdayaan karyawan dapat semakin meningkatkan keinovasian dalam UKM yang pada akhirnya akan berdampak baik pada kinerja dan keefisienan aktivitas bisnis Perusahaan

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

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

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

Magnetic resonance detects metabolic changes associated with chemotherapy-induced apoptosis

Apoptosis was induced by treating L1210 leukaemia cells with mechlorethamine, and SW620 colorectal cells with doxorubicin. The onset and progression of apoptosis were monitored by assessing caspase activation, mitochondrial transmembrane potential, phosphatidylserine externalization, DNA fragmentation and cell morphology. In parallel, 31P magnetic resonance (MR) spectra of cell extracts were recorded. In L1210 cells, caspase activation was detected at 4 h. By 3 h, the MR spectra showed a steady decrease in NTP and NAD, and a significant build-up of fructose 1,6-bisphosphate (F-1,6-P) dihydroxyacetonephosphate and glycerol-3-phosphate, indicating modulation of glycolysis. Treatment with iodoacetate also induced a build-up of F-1,6-P, while preincubation with two poly(ADP-ribose) polymerase inhibitors, 3-aminobenzamide and nicotinamide, prevented the drop in NAD and the build-up of glycolytic intermediates. This suggested that our results were due to inhibition of glyceraldehyde-3-phosphate dehydrogenase, possibly as a consequence of NAD depletion following poly(ADP-ribose) polymerase activation. Doxorubicin treatment of the adherent SW620 cells caused cells committed to apoptosis to detach. F-1,6-P was observed in detached cells, but not in treated cells that remained attached. This indicated that our observations were not cell line- or treatment-specific, but were correlated with the appearance of apoptotic cells following drug treatment. The 31P MR spectrum of tumours responding to chemotherapy could be modulated by similar effects

LRRK2 deficiency induced mitochondrial Ca2+ efflux inhibition can be rescued by Na+/Ca2+/Li+ exchanger upregulation

Variants of leucine-rich repeat kinase 2 (lrrk2) are associated with an increased risk in developing Parkinson’s disease (PD). Mitochondrial dysfunction and specifically mitochondrial Ca2+ handling has been linked to the pathogenesis of PD. Here we describe for the second time a mitochondrial Ca2+ efflux deficiency in a model displaying alterations in a PD-associated risk protein. LRRK2 deletion, inhibition and mutations led to an impaired mitochondrial Ca2+ extrusion via Na+/Ca2+/Li+ exchanger (NCLX) which in turn lowered mitochondrial permeability transition pore (PTP) opening threshold and increased cell death. The mitochondrial membrane potential was found not to be the underlying cause for the Ca2+ extrusion deficiency. NCLX activity was rescued by a direct (phosphomimetic NCLX mutant) and indirect (protein kinase A) activation which in turn elevated the PTP opening threshold. Therefore, at least two PD-associated risk protein pathways appear to converge on NCLX controlling mitochondrial Ca2+ extrusion and therefore mitochondrial health. Since mitochondrial Ca2+ overload has been described in many neurological disorders this study warrants further studies into NCLX as a potential therapeutic target

HBsAg Inhibits the Translocation of JTB into Mitochondria in HepG2 Cells and Potentially Plays a Role in HCC Progression

Background and Aims: The expression of the jumping translocation breakpoint (JTB) gene is upregulated in malignant liver tissues; however, JTB is associated with unbalanced translocations in many other types of cancer that suppress JTB expression. No comprehensive analysis on its function in human hepatocellular carcinoma (HCC) has been performed to date. We aimed to define the biological consequences for interaction between JTB and HBsAg in HCC cell lines. Methods: We employed the stable transfection to establish small HBsAg expressing HepG2 cell line, and stably silenced the JTB expression using short hairpin RNA in HepG2 cell line. The effects of JTB and small HBsAg in vitro were determined by assessing cell apoptosis and motility. Results: Silencing of JTB expression promoted cancer cell motility and reduced cell apoptosis, which was significantly enhanced by HBs expression. Expression of HBsAg inhibited the translocation of JTB to the mitochondria. Furthermore, silencing of the JTB resulted in an increase in the phosphorylation of p65 in HepG2 cells and HepG2-HBs cells, whereas HBsAg expression decreased the phosphorylation of p65. The silencing of JTB in HepG2-HBs cells conferred increased advantages in cell motility and anti-apoptosis. Conclusion: HBsAg inhibited the translocation of JTB to the mitochondria and decreased the phosphorylation of p65 through the interaction with JTB, After JTB knockdown, HBsAg exhibited a stronger potential to promote tumor progression. Our data suggested that JTB act as a tumor suppressor gene in regards to HBV infection and its activation might be applied as a therapeutic strategy for in control of HBV related HCC development.National Natural Science Foundation of China [30971362, 81072013]; Fundamental Research Funds for the Central Universities in China [2010111082]; Key Projects for Technology Plan of Fujian Province in China [2009D020]; Foundation of Health Bureau of Fujian in China [2007CXB8, 3502z20077046]; Foundation of Health Bureau of Xiamen in China [2007CXB8, 3502z20077046