Merits of Ratifying and Implementing the Cartagena Protocol on Biosafety

In a meeting in Cartagena, Colombia in February 1999, parties to the CBD, known as the Conference of the Parties ( COP ), could not agree on the proposed biosafety protocol drafted in prior meetings.3 However, in January 2000, in a meeting in Montreal, the parties to the CBD finally adopted the draft protocol, naming it the Cartagena Protocol on Biosafety ( Cartagena Protocol or Protocol ). 4 When the Cartagena Protocol opened for signature at the CBD\u27s COP meeting in Nairobi in May 2000, sixty-four governments and the European Union signed the Protocol . Presently, eighty-one parties have signed the Protocol, while only two have ratified it.6 However, the Protocol will only enter into legal force after fifty parties have ratified it. 7 This comment argues that each party to the COP should ratify and implement the Protocol as soon as possible. This comment also critiques the provisions of the Protocol and alternatives to the Protocol, namely the voluntary regulation of GMOs. Part II begins with a discussion of the background of GMOs. Next, Part III discusses the World Trade Organization\u27s Agreement on the Application of Sanitary and Phytosanitary Measures ( SPS Agreement ) and its agricultural safety provisions. Part IV continues with a description of the CBD, the history of the development of the Cartagena Protocol, and a discussion of important Protocol language. Part V analyzes the merits of the Protocol and why it should be ratified and implemented. Finally, this comment concludes with a discussion of alternatives to the Protocol, with an emphasis on voluntary regulations

Working with God Images in Spiritual Care Education

Looking at various images of God and how to approach using images of God in teaching and providing spiritual care

Merits of Ratifying and Implementing the Cartagena Protocol on Biosafety

In a meeting in Cartagena, Colombia in February 1999, parties to the CBD, known as the Conference of the Parties ( COP ), could not agree on the proposed biosafety protocol drafted in prior meetings.3 However, in January 2000, in a meeting in Montreal, the parties to the CBD finally adopted the draft protocol, naming it the Cartagena Protocol on Biosafety ( Cartagena Protocol or Protocol ). 4 When the Cartagena Protocol opened for signature at the CBD\u27s COP meeting in Nairobi in May 2000, sixty-four governments and the European Union signed the Protocol . Presently, eighty-one parties have signed the Protocol, while only two have ratified it.6 However, the Protocol will only enter into legal force after fifty parties have ratified it. 7 This comment argues that each party to the COP should ratify and implement the Protocol as soon as possible. This comment also critiques the provisions of the Protocol and alternatives to the Protocol, namely the voluntary regulation of GMOs. Part II begins with a discussion of the background of GMOs. Next, Part III discusses the World Trade Organization\u27s Agreement on the Application of Sanitary and Phytosanitary Measures ( SPS Agreement ) and its agricultural safety provisions. Part IV continues with a description of the CBD, the history of the development of the Cartagena Protocol, and a discussion of important Protocol language. Part V analyzes the merits of the Protocol and why it should be ratified and implemented. Finally, this comment concludes with a discussion of alternatives to the Protocol, with an emphasis on voluntary regulations

Solutions of Penrose's Equation

The computational use of Killing potentials which satisfy Penrose's equation is discussed. Penrose's equation is presented as a conformal Killing-Yano equation and the class of possible solutions is analyzed. It is shown that solutions exist in spacetimes of Petrov type O, D or N. In the particular case of the Kerr background, it is shown that there can be no Killing potential for the axial Killing vector.Comment: To appear in J. Math. Phy

Aluminum inhibits hemoglobin synthesis but enhances iron uptake in friend erythroleukemia cells

Aluminum inhibits hemoglobin synthesis but enhances iron uptake in Friend erythroleukemia cells. Aluminum (Al) overload in dialysis patients and experimental animals is associated with the development of anemia. However, the precise mechanisms of erythrocyte Al uptake and toxicity are poorly understood. Al accumulation, hemoglobin (Hb) synthesis and cell growth were evaluated in dimethysulfoxide (DMSO)-induced Friend erythroleukemia cells (FEC), a model system for erythroid differentiation. FEC were grown in media containing either Al citrate, transferrin-aluminum (Tf-Al), Tf or no additions. Al accumulation occurring only in cells grown in Tf-Al containing media was detected at 24 hours and increased linearly up to 96 hours after induction. By 96 hours, 200 ± 36 µg Al/liter lysed cells were detected in Tf-Al grown cells versus 5 ± 1 µg Al/liter lysed cells in cells grown in Al citrate (P < 0.001). Tf-Al inhibited Hb synthesis at 72 hours after induction. At 96 hours 50 ± 15% cells were benzidine positive when grown in Tf-Al compared to 76 ± 15% in Al citrate (P < 0.001). FEC grown in increasing concentrations of Tf-Al (100 to 500 µg/ml) showed inhibition of Hb synthesis at lower concentrations of Tf-Al at 100 µg/ml than for cell growth at 300 µg/ml. Higher concentrations of Tf-Al (>300 µg/ml) did not further inhibit Hb synthesis or cell growth. Iron (Fe) and Tf uptake were increased in Al loaded FEC compared to control cells. The increased Tf uptake was probably the result of increased Tf receptor expression on FEC since Tf cell cycling time was unchanged. These data indicate that Al utilizes the Tf uptake pathway for entry into erythrocyte precursors. Al is toxic at sites distal to Fe uptake, possibly at the heme and/or globin synthetic pathways, resulting in decreased Hb synthesis and cell growth

Se-Jin Lee, myostatin discoverer, elected to the National Academy of Science

Se-Jin Lee was elected member to the National Academy of Sciences on 28 April 2012. Dr Lee is responsible for the discovery of myostatin, a critical regulator of skeletal muscle mass and function. He also determined the primary binding receptor for myostatin, and has characterized additional transforming growth factor–β family members acting in this pathway

Validation of machine learning models to detect amyloid pathologies across institutions.

Semi-quantitative scoring schemes like the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) are the most commonly used method in Alzheimer's disease (AD) neuropathology practice. Computational approaches based on machine learning have recently generated quantitative scores for whole slide images (WSIs) that are highly correlated with human derived semi-quantitative scores, such as those of CERAD, for Alzheimer's disease pathology. However, the robustness of such models have yet to be tested in different cohorts. To validate previously published machine learning algorithms using convolutional neural networks (CNNs) and determine if pathological heterogeneity may alter algorithm derived measures, 40 cases from the Goizueta Emory Alzheimer's Disease Center brain bank displaying an array of pathological diagnoses (including AD with and without Lewy body disease (LBD), and / or TDP-43-positive inclusions) and levels of Aβ pathologies were evaluated. Furthermore, to provide deeper phenotyping, amyloid burden in gray matter vs whole tissue were compared, and quantitative CNN scores for both correlated significantly to CERAD-like scores. Quantitative scores also show clear stratification based on AD pathologies with or without additional diagnoses (including LBD and TDP-43 inclusions) vs cases with no significant neurodegeneration (control cases) as well as NIA Reagan scoring criteria. Specifically, the concomitant diagnosis group of AD + TDP-43 showed significantly greater CNN-score for cored plaques than the AD group. Finally, we report that whole tissue computational scores correlate better with CERAD-like categories than focusing on computational scores from a field of view with densest pathology, which is the standard of practice in neuropathological assessment per CERAD guidelines. Together these findings validate and expand CNN models to be robust to cohort variations and provide additional proof-of-concept for future studies to incorporate machine learning algorithms into neuropathological practice

Anticancer activity of the iron facilitator LS081

<p>Abstract</p> <p>Background</p> <p>Cancer cells have increased levels of transferrin receptor and lower levels of ferritin, an iron deficient phenotype that has led to the use of iron chelators to further deplete cells of iron and limit cancer cell growth. As cancer cells also have increased reactive oxygen species (ROS) we hypothesized that a contrarian approach of enhancing iron entry would allow for further increased generation of ROS causing oxidative damage and cell death.</p> <p>Methods</p> <p>A small molecule library consisting of ~11,000 compounds was screened to identify compounds that stimulated iron-induced quenching of intracellular calcein fluorescence. We verified the iron facilitating properties of the lead compound, LS081, through ⁵⁵Fe uptake and the expression of the iron storage protein, ferritin. LS081-induced iron facilitation was correlated with rates of cancer cell growth inhibition, ROS production, clonogenicity, and hypoxia induced factor (HIF) levels.</p> <p>Results</p> <p>Compound LS081 increased ⁵⁵Fe uptake in various cancer cell lines and Caco2 cells, a model system for studying intestinal iron uptake. LS081 also increased the uptake of Fe from transferrin (Tf). LS081 decreased proliferation of the PC-3 prostate cancer cell line in the presence of iron with a lesser effect on normal prostate 267B1 cells. In addition, LS081 markedly decreased HIF-1α and -2α levels in DU-145 prostate cancer cell line and the MDA-MB-231 breast cancer cell lines, stimulated ROS production, and decreased clonogenicity.</p> <p>Conclusions</p> <p>We have developed a high through-put screening technique and identified small molecules that stimulate iron uptake both from ferriTf and non-Tf bound iron. These iron facilitator compounds displayed properties suggesting that they may serve as anti-cancer agents.</p