A rare hybrid solar eclipse has taken place, switching between a total eclipse (where the moon completely covers the sun) and an annular one (where a halo of sunlight is visible around the moon) (The hybrid solar eclipse – in pictures
For those who suffer from diabetes, the pain that comes with pricking one's finger often discourages consistent blood glucose monitoring.
Tear glucose has been suggested previously as a potential approach for the noninvasive estimation of blood glucose. While the topic remains unresolved, an overview of previous studies suggests the importance of a tear sampling approach and warrants new technology development. A concept device is presented that meets the needs of a tear glucose biosensor.
Three approaches to chronoamperometric glucose sensing were evaluated, including glucose oxidase mediated by potassium ferricyanide or oxygen with a hydrogen peroxide catalyst, Prussian blue, and potassium ferricyanide-mediated glucose dehydrogenase. For tear sampling, calcium alginate, poly(2-hydroxyethyl methacrylate), and polyurethane foam were screened as an absorbent tear sampling material. A quantitative model based on the proposed function of concept device was created.For glucose sensing, it was found that potassium ferricyanide with glucose dehydrogenase was ideal, featuring oxygen insensitivity, long-term stability, and a lower limit of detection of 2 μM glucose.Polyurethane foam possessed all of the required characteristics for tear sampling, including reproducible sampling from a hydrogel-simulated, eye surface (4.2 ± 0.5 μl; n = 8). It is estimated that 100 μM of glucose tear fluid would yield 135 nA (14.9% relative standard deviation).
While the device has numerous challenges ahead, such as obtaining reproducible results, proof-of-concept has been demonstrated and the project has received backing from Mayo Clinic and BioAccel, an Arizona biomedical commercialization non-profit.
Authors: Murray R. Grant, Kemal Kazan & John M. Manners
With expansion of our understanding of pathogen effector strategies and the multiplicity of their host targets, it is becoming evident that novel approaches to engineering broad-spectrum resistance need to be deployed. The increasing availability of high temporal gene expression data of a range of plant–microbe interactions enables the judicious choices of promoters to fine-tune timing and magnitude of expression under specified stress conditions. We can therefore contemplate engineering a range of transgenic lines designed to interfere with pathogen virulence strategies that target plant hormone signalling or deploy specific disease resistance genes. An advantage of such an approach is that hormonal signalling is generic so if this strategy is effective, it can be easily implemented in a range of crop species. Additionally, multiple re-wired lines can be crossed to develop more effective responses to pathogens.
The previous two collections in the excellent The Best Australian Science Writing 2013 series have contained forewords written by Nobel laureates, so in pursuit of balance - I assume - this year's foreword is written by someone who is quite...
Researchers from Rice University's Center for Theoretical Biological Physics have deciphered the operating principles of a genetic circuit that allows cancer to metastasize.
“Cancer cells behave in complex ways, and this work shows how such complexity can arise from the operation of a relatively simple decision-making circuit,” said study co-author Eshel Ben-Jacob, a senior investigator at Rice’sCenter for Theoretical Biological Physics (CTBP) and adjunct professor of biochemistry and cell biology at Rice. “By stripping away the complexity and starting with first principles, we get a glimpse of the ‘logic of cancer’ — the driver of the disease’s decision to spread.”
In the PNAS study, Ben-Jacob and CTBP colleagues José Onuchic, Herbert Levine, Mingyang Lu and Mohit Kumar Jolly describe a new theoretical framework that allowed them to model the behavior of microRNAs in decision-making circuits. To test the framework, they modeled the behavior of a decision-making genetic circuit that cells use to regulate the forward and backward transitions between two different cell states, the epithelial and mesenchymal. Known respectively as the E-M transition (EMT) and the M-E transition (MET), these changes in cell state are vital for embryonic development, tissue engineering and wound healing. During the EMT, some cells also form a third state, a hybrid that is endowed with a special mix of both epithelial and mesenchymal abilities, including group migration.
The EMT transition is also a hallmark of cancer metastasis. Cancer cells co-opt the process to allow tumor cells to break away, migrate to other parts of the body and establish a new tumor. To find ways to shut down metastasis, cancer researchers have conducted dozens of studies about the genetic circuitry that activates the EMT.
One clear finding from previous studies is that a two-component genetic switch is the key to both the EMT and MET. The switch contains two specialized pairs of proteins. One pair is SNAIL and microRNA34 (SNAIL/miR34), and the other is ZEB and microRNA200 (ZEB/miR200). Each pair is “mutually inhibitory,” meaning that the presence of one of the partners inhibits the production of the other.
In the mesenchymal cell state — the state that corresponds to cancer metastasis — both SNAIL and ZEB must be present in high levels. In the epithelial state, the microRNA partners dominate, and neither ZEB nor SNAIL is available in high levels.
“Usually, if you have two genes that are mutually limiting, you have only two possibilities,” Ben-Jacob said. “In the first case, gene A is highly expressed and inhibits gene B. In the other, gene B is highly expressed and it inhibits A. This is true in the case of ZEB and miR200. One of these is ‘on’ and the other is ‘off,’ so it’s clear that this is the decision element in the switch.”
SNAIL and miR34 interact more weakly. As a result, both can be present at the same time, with the amount of each varying based upon inputs from a number of other proteins, including several other cancer genes.
“One of the most important things the model showed us was how SNAIL and miR34 act as an integrator,” Ben-Jacob said. “This part of the circuit is acted on by multiple cues, and it integrates those signals and feeds information into the decision element. It does this based upon the level of SNAIL, which activates ZEB and inhibits miR200.”
My last post looked at an article published by The Economist on why research can be unreliable. The link in the title above is to part two: Trouble at the Lab.
One of the most fascinating topics here is a sting mounted by John Bohannon, in collaboration with editors at Science.
Bohannon concocted a manuscript that was entirely false - flawed data, no ethics approval, manufactured authors and institutions. He submitted the manuscript to a number of open access journals. The result: 98 rejected the paper, 157 accepted it.
And as to the idea that you can't clone something by simply moving it, consider the following (horrifying) thought experiment: You have a replication machine that can only work by taking a human heart and building up around ...
Andreina De Leon Carmenatis's insight:
cuestión muy discutida en los últimos años, ¿creen ustedes que debemos hacer este tipo de prácticas ? Personalmente creo que la clonación es un sector muy arriesgado en el que jugar, sobre todo si estamos hablando de embriones, en estas prácticas entra en juego no solo la ética de cada científico, sino támbien la consideración de la diversidad génetica, el uso no controlado de clonación, el efecto en el futuro individuo....
Piensen en todo ello y hagan un balance de riesgo y beneficio
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