Apakah Opec Merupakan Kartel?: Pendekatan Kausalitas Granger dalam Kerangka Vector Autoregressive

One would believe that The Organization of Petroleum Exporting Countries (OPEC) is certainly a cartel which curbs production in order to raise the price of its product as well as to share the market among its members. Did energy shock of the 1970\u27s engineered by an effective cartel of OPEC members acting to share the market by controlling output and influencing market prices? One would also expect OPEC\u27s production to significantly affect the market price of oil as the organization is often accused of curbing production in order to raise prices. This paper tries to determine whether OPEC has the power of affecting the market price of oil and or vice versa. This study uses the Toda and Yamamoto (1995) procedure for testing for Granger non-causality in Vector Autoregressive (VAR) models that involves variables that are integrated of an arbitrary order and that are possibly cointegrated. The results indicate that there is no statistically significant causal relationship between real crude oil price and OPEC production in either direction for full sample period 1974 – 2005. Instead, we find that real crude oil price Granger cause OPEC production in 2 different sub samples period, but not in other direction. As overall we reject cartel hypothesis for OPEC as a whole

Single-Antibody, Targeted Nanoparticle Delivery of Camptothecin

We have developed a new method for assembling targeted nanoparticles that utilizes the complexation between targeting agents that contain boronic acids and polymer–drug conjugates that possess diols. Here, we report the first <i>in vivo</i>, antitumor results of a nanoparticle formed via this new assembly methodology. A nanoparticle consisting of a mucic acid polymer conjugate of camptothecin (CPT), MAP–CPT, and containing on average one Herceptin antibody is investigated in nude mice bearing HER2 overexpressing BT-474 human breast cancer tumors. Nontargeted MAP–CPT and antibody-containing MAP–CPT nanoparticles of ca. 30–40 nm diameter and slightly negative zeta potential show prolonged <i>in vivo</i> circulation and similar biodistributions after intravenous tail vein injections in mice. The maximum tolerated dose (MTD) of the nontargeted and Herceptin-containing MAP–CPT nanoparticles is found to be 10 and 8 mg of CPT/kg, respectively, in mice. Mice bearing BT-474 human breast tumors treated with nontargeted MAP–CPT nanoparticles at 8 mg of CPT/kg show significant tumor growth inhibition (mean tumor volume of 63 mm³) when compared to irinotecan at 80 mg/kg (mean tumor volume of 575 mm³) and CPT at 8 mg/kg (mean tumor volume of 808 mm³) at the end of the study. Herceptin antibody treatment at 5.9 mg/kg results in complete tumor regressions in 5 out of 8 mice, with a mean tumor volume of 60 mm³ at the end of the study. Mice treated with MAP–CPT nanoparticles at 1 mg of CPT/kg do not show tumor inhibition. However, all mice receiving administrations of MAP–CPT nanoparticles (1 mg of CPT/kg) that contain on average a single Herceptin molecule per nanoparticle (5.9 mg of Herceptin equivalent/kg) show complete tumor regression by the end of the study. These results demonstrate that the antitumor efficacy of nanoparticles carrying anticancer drugs can be enhanced by incorporating on average a single antibody

Targeted Nanoparticles Assembled via Complexation of Boronic-Acid-Containing Targeting Moieties to Diol-Containing Polymers

The delivery of therapeutics via nanoscaled vehicles for solid cancer treatment can be enhanced by the incorporation of a targeting capability. Here, we describe a new method for assembling a targeted nanoparticle that utilizes the reversible covalent complexation between boronic acids and diols to achieve a targeted nanoparticle for the delivery of the anticancer drug camptothecin (CPT). CPT is conjugated to a biocompatible, hydrophilic copolymer of mucic acid and PEG (MAP). When this polymer–drug conjugate is placed in water, it self-assembles into MAP–CPT nanoparticles of ca. 30 nm (diameter) and slightly negative zeta potential. The antibody Herceptin is attached to a boronic acid via a polyethylene glycol (PEG) spacer, and this boronic acid-containing targeting moiety is complexed with the diol-containing MAP to form a targeted MAP–CPT nanoparticle. The addition of Herceptin targeting agent to the MAP–CPT nanoparticles yields targeted MAP–CPT nanoparticles with increased nanoparticle size to ca. 40 nm (diameter). The main mechanisms of CPT release from MAP–CPT nanoparticles are found by <i>in vitro</i> analysis to be hydrolysis and nanoparticle disruption by fat. Cellular uptake of nanoparticles is enhanced by 70% compared to nontargeted version by the incorporation of a single Herceptin antibody targeting agent per nanoparticle. This single Herceptin antibody targeted MAP–CPT nanoparticle system carries ca. 60 CPT molecules per nanoparticle and shows prolonged plasma circulation with an elimination half-life of 21.2 h and AUC value of 2766 μg.h/mL at a 10 mg CPT/kg tail vein injection in mice

Combinatorial treatment shows the greatest efficacy in inhibiting cell growth and limiting colony formation.

<p>A. The expression levels of LSD1 in bladder cancers, T-cell acute lymphoblastic leukemia, colon adenoma and their normal counterparts were obtained from ONCOMINE. Numbers in the parentheses indicate number of samples used to generate box plots. B-D. Population doubling times for control (black), clorgyline treated (yellow), 5-Aza-CdR treated (red) and combinatorial treatment treated (green) in T24, HL60 and HCT116 cells. The corresponding numbers of hours are listed in the table below each graph. E. Quantification of number of colonies produced by colony formation assays in T24 and HCT116 cells after indicated treatments.</p

Combinatorial treatment elicits a synergistic effect in up-regulating genes in HL60 cells.

<p>A. Gene expression log2 difference is plotted on the x-axis, and the –log10 (p-value) is plotted on the y-axis. Probes that are identified as significantly different between two groups are colored in red. B. Venn intersects of the number of genes that are up-regulated upon the indicated treatment. C. Expression status obtained from ONCOMINE of 20 genes, whose expression was synergistically reactivated in HL60 cells, in peripheral blood mononuclear and chronic lymphocytic leukemia.</p

Additional file 19 of Dynamic transcriptome profiling exploring cold tolerance in forensically important blow fly, Aldrichina grahami (Diptera: Calliphoridae)

Additional file 19: Table S6. Primers used for qPCR validation

Additional file 14 of Dynamic transcriptome profiling exploring cold tolerance in forensically important blow fly, Aldrichina grahami (Diptera: Calliphoridae)

Additional file 14: Figure S10. Functional annotation of assembled sequences of DEGs of third-instar larvae at 20 °C (H3) vs third-instar larvae at 4 °C (L3) based on gene ontology (GO) categorization. Unigenes were annotated in three categories: biological process, cellular components, and molecular functions

Additional file 6 of Dynamic transcriptome profiling exploring cold tolerance in forensically important blow fly, Aldrichina grahami (Diptera: Calliphoridae)

Additional file 6: Figure S4. The series-clusters for DEGs in the second-instar larvae stage. Each cluster of DEGs showed similar expression change in second-instar larvae at 20 °C (H2), second-instar larvae at 12 °C (M2), and second-instar larvae at 4 °C (L2)

DataSheet_1_Insulin-binding protein-5 down-regulates the balance of Th17/Treg.docx

The inflammatory response plays critical important role in tissue hemostasis. Our previous study showed insulin-binding protein-5 (IGFBP5) could enhance the regeneration of tissue defect under inflammation condition, but the function of IGFBP5 in controlling inflammation and regulating immune responses remains unclear. In present study, we studied the regulatory effect of IGFBP5 on T cell immune response in vitro, and the maintenance of Th17/Treg balance in vivo by using dextran sulfate sodium salt (DSS)-induced colitis in mice. The results showed that IGFBP5 inhibited the differentiation of CD4+ T cells into Th17 subset while promoted its differentiation into Treg subsets. Further results of animal experiments demonstrated that recombinant IGFBP5 reversed the imbalance of Th17/Treg and alleviated the severity of DSS-induced colitis. The percentage of Th17 cells decreased and the percentage of Treg cells increased in the inflamed colon tissue and mesenteric lymph nodes of mice with colitis after IGFBP5 treatment. Besides, pro-inflammatory cytokines such as TNF-α, IL-1β and IFN-γ in serum were suppressed after the treatment of IGFBP5. Moreover, the function of IGFBP5 in regulating Th17/Treg balance could be inhibited by the inhibitors of ERK or JNK pathway. In conclusion, all these data showed that IGFBP5 could regulate Th17/Treg balance via ERK or JNK pathways. The findings of our study provide a theoretical basis for the application of IGFBP5 in inflammatory diseases.</p

Time series analysis of Weibo discussion heat.

Time series analysis of Weibo discussion heat.</p