1,290 research outputs found

    CELL SORTING IN THE PRESENCE OF CYTOCHALASIN B

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    The ability of cytochalasin B to inhibit ruffled membrane activity and cellular locomotion of vertebrate cells in monolayer culture prompted its use to study the necessity for this kind of active cellular locomotion in cell sorting in heterotypic cell aggregates. Cell sorting was inhibited in chick embryo heart-pigmented retina aggregates but a remarkable degree of sorting did occur in neural retina-pigmented retina aggregates. In these experiments, the levels of cytochalasin B employed (5 or 10 µg/ml) are sufficient to inhibit completely locomotion of these cell types in monolayer culture. It is proposed that the degree of cell movement achieved during sorting in neural retina-pigmented retina aggregates in the presence of cytochalasin B is the result of changes in cell contact resulting from adhesive interaction of cells. The effect of cytochalasin B on the initial aggregation of dissociated cells was also tested. With the cell types used in this study (chick embryo neural retina and limb bud), aggregation was not affected for a period of several hours

    Capture of lipopolysaccharide (endotoxin) by the blood clot: A comparative study

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    In vertebrates and arthropods, blood clotting involves the establishment of a plug of aggregated thrombocytes (the cellular clot) and an extracellular fibrillar clot formed by the polymerization of the structural protein of the clot, which is fibrin in mammals, plasma lipoprotein in crustaceans, and coagulin in the horseshoe crab, Limulus polyphemus. Both elements of the clot function to staunch bleeding. Additionally, the extracellular clot functions as an agent of the innate immune system by providing a passive anti-microbial barrier and microbial entrapment device, which functions directly at the site of wounds to the integument. Here we show that, in addition to these passive functions in immunity, the plasma lipoprotein clot of lobster, the coagulin clot of Limulus, and both the platelet thrombus and the fibrin clot of mammals (human, mouse) operate to capture lipopolysaccharide (LPS, endotoxin). The lipid A core of LPS is the principal agent of gram-negative septicemia, which is responsible for more than 100,000 human deaths annually in the United States and is similarly toxic to arthropods. Quantification using theLimulus Amebocyte Lysate (LAL) test shows that clots capture significant quantities of LPS and fluorescent-labeled LPS can be seen by microscopy to decorate the clot fibrils. Thrombi generated in the living mouse accumulate LPS in vivo. It is suggested that capture of LPS released from gram-negative bacteria entrapped by the blood clot operates to protect against the disease that might be caused by its systemic dispersal

    Interaction of pathogenic vibrio bacteria with the blood clot of the Pacific white shrimp, Litopenaeus vannamei

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    Author Posting. © Marine Biological Laboratory, 2014. This article is posted here by permission of Marine Biological Laboratory for personal use, not for redistribution. The definitive version was published in Biological Bulletin 226 (2014): 102-110.In addition to its roles in hemostasis and wound repair, the blood clot plays an underappreciated role in innate immunity, where the established clot serves as a barrier to microbial penetration into the internal milieu and where the early clot entraps and immobilizes microbes that have entered wounds to the integuments. In this report we document the behavior of the pathogenic gram-negative bacterium Vibrio harveyi that has been entrapped in the fabric of the extracellular blood clot of one of its target organisms, the Pacific white shrimp, Litopenaeus vannamei. The freshly entrapped bacteria are held tightly by the clot, losing even Brownian motility, but by 1 h post-entrapment, a fraction of the bacteria have established small domains of fibrinolysis that enlarge progressively, enabling bacteria to escape from the clot's embrace. Escape is dependent on the actions of both serine- and metallo-proteases released from the bacterial cells.This research was financially supported by a student fellowship for Vorrapon Chaikeeratisak from the Royal Golden Jubilee Ph.D. program under the Thailand Research Fund (TRF) and by grant 0344360 from the National Science Foundation (PBA)

    CBT for difficult-to-treat depression: self-regulation model

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    Background:Cognitive behavioural therapy (CBT) is an effective treatment for depression but a significant minority of clients do not complete therapy, do not respond to it, or subsequently relapse. Non-responders, and those at risk of relapse, are more likely to have adverse childhood experiences, early-onset depression, co-morbidities, interpersonal problems and heightened risk. This is a heterogeneous group of clients who are currently difficult to treat.Aim:The aim was to develop a CBT model of depression that will be effective for difficult-to-treat clients who have not responded to standard CBT.Method:The method was to unify theory, evidence and clinical strategies within the field of CBT to develop an integrated CBT model. Single case methods were used to develop the treatment components.Results:A self-regulation model of depression has been developed. It proposes that depression is maintained by repeated interactions of self-identity disruption, impaired motivation, disengagement, rumination, intrusive memories and passive life goals. Depression is more difficult to treat when these processes become interlocked. Treatment based on the model builds self-regulation skills and restructures self-identity, rather than target negative beliefs. A bespoke therapy plan is formed out of ten treatment components, based on an individual case formulation.Conclusions:A self-regulation model of depression is proposed that integrates theory, evidence and practice within the field of CBT. It has been developed with difficult-to-treat cases as its primary purpose. A case example is described in a concurrent article (Barton et al., 2022) and further empirical tests are on-going

    Recurrent depression and relational trauma: a single case of memory processing

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    Cognitive behavioural therapy (CBT) is an effective treatment for depression, but a significant minority of clients are difficult to treat, including those with histories of relational trauma. The model of Beck et al. (1979) proposes that adverse childhood experiences lead to negative core beliefs, and these create a susceptibility to depression. However, Beck’s model does not identify trauma as a subset of adverse experiences. An alternative view is that traumatised clients internalise conflicting representations of self and it is conflict, interacting with trauma memories, that creates a vulnerability for depression. In this formulation, methods from the treatment of post-traumatic stress disorder (PTSD) could be incorporated into the treatment of depression, to emotionally process trauma memories and resolve self-identity conflicts. The aims of this study were to: (1) report the treatment of a 67-year-old man with recurrent depression and a history of prolonged relational trauma, and (2) to explore how memory processing from the treatment of PTSD can be incorporated into the treatment of recurrent depression. A single case observational design was used in the long-term treatment of a depressed traumatised client. The client received 47 individual sessions over 19 months in routine clinical practice in a tertiary CBT service. He completed repeated measures of mood, memory intrusions and sleep disruption. The client responded well to treatment with clinically significant improvements across measures of mood, memory and sleep. The effects were sustained over an 18-month follow-up. Memory processing was successfully integrated into a high-intensity treatment for recurrent depression. This is a promising approach for depressed clients with histories of relational trauma

    CELL SORTING IN THE PRESENCE OF CYTOCHALASIN B

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    Design of a 100 kW Concentrated Solar Power on Demand Volumetric Receiver With Integral Thermal Energy Storage Prototype

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    A new concept of Thermal Energy Storage (TES) system based on current available technologies is being developed under the framework of the Masdar Institute (MI) and Massachusetts Institute of Technology (MIT) collaborative Flagship Program. The key feature of this concept lies on concentrating sun light directly on the molten salt storage tank, avoiding the necessity of pumping the salts to the top of a tower thereby avoiding thermal losses and pumping and electric tracing needs inherent in most conventional CSP plants. This Concentrated Solar Power on Demand (CSPonD) volumetric receiver/TES unit prototype will be tested in the existing MI heliostat field and beam down tower in Abu Dhabi (UAE) which will collect and redirect solar energy to an upwards-facing final optical element (FOE). These energy will be concentrated on the aperture of the prototype designed to store 400 kWh of energy allowing 16 hours of continuous production after sunset using Solar Salt (60%NaNO3 + 40%KNO3) as storage material. The tank is divided in two volumes: one cold in the bottom region, where Solar Salt is at 250 °C and another hot on the upper region, at 550 °C. A moving divider plate with active control separates both volumes. The plate includes mixing enhancement features to help with convection on the hot volume of salts. It’s expected that results will demonstrate the technical feasibility and economic viability of this concept allowing its scale up at commercial size

    Potential gains in life expectancy from reducing amenable mortality among people diagnosed with serious mental illness in the United Kingdom.

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    BACKGROUND: To estimate the potential gain in life expectancy from addressing modifiable risk factors for all-cause mortality (excluding suicide and deaths from accidents or violence) across specific serious mental illness (SMI) subgroups, namely schizophrenia, schizoaffective disorders, and bipolar disorders in a Western population. METHODS: We have used relative risks from recent meta-analyses to estimate the population attribution fraction (PAF) due to specific modifiable risk factors known to be associated with all-cause mortality within SMI. The potential gain in life expectancy at birth, age 50 and age 65 years were assessed by estimating the combined effect of modifiable risk factors from different contextual levels (behavioural, healthcare, social) and accounting for the effectiveness of existing interventions tackling these factors. Projections for annual gain in life expectancy at birth during a two-decade was estimated using the Annual Percentage Change (APC) formula. The predicted estimates were based on mortality rates for year 2014-2015. RESULTS: Based on the effectiveness of existing interventions targeting these modifiable risk factors, we estimated potential gain in life expectancy at birth of four (bipolar disorders), six (schizoaffective disorders), or seven years (schizophrenia). The gain in life expectancy at age 50 years was three (bipolar disorders) or five (schizophrenia and schizoaffective disorders) years. The projected gain in life expectancy at age 65 years was three (bipolar disorders) or four (schizophrenia and schizoaffective disorders) years. CONCLUSIONS: The implementation of existing interventions targeting modifiable risk factors could narrow the current mortality gap between the general and the SMI populations by 24% (men) to 28% (women). These projections represent ideal circumstances and without the limitation of overestimation which often comes with PAFs
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