Search

Purpose: The purpose of this study was to use Watkins and Marsick model of a learning organization (1993, 1996), the dimensions of the learning organization questionnaire as a framework for interdisciplinary network collaboration and knowledge sharing. Design/methodology/approach: The research team used a mixed-methods approach for data collection. Survey data was collected from 181 networks. In addition, data was collected from two focus groups with six participants each. Findings: Results, in general, showed that the learning organization culture could be used as a framework for interdisciplinary network collaboration. In particular, results showed that shared vision, imbedded systems and knowledge sharing were key driving forces required for successful collaboration. Research limitations/implications: Theoretical and practical implications were discussed, and conditions for learning organization culture for networks were established. Originality/value: People in a network era need more than training; they need ongoing, interdisciplinary, collaborative support to solve complex problems. Organizations can only work effectively if barriers to organizational learning were removed. This originality of this paper lies in applying learning organization framework at the network level.

This study aimed to isolate the conditions under which aversive stimulation is experienced as more or less discomforting/unpleasant. Discomfort was induced by playing loud noises through headphones while participants performed computer tasks. We employed 4 main conditions. Condition 1: the acceptance-based protocol (ACT), intended to integrate discomfort in a valued direction, was implemented before the Inclusion Task (task performance could continue despite the presence of the noise). Subsequently, the experiential avoidance-based protocol (EA), intended to promote a relation of opposition between discomfort and valued actions, was implemented before the Opposition Task (task performance was suspended until the participants eliminated the sounds). Condition 2: this order was reversed. Conditions 3 and 4: the tasks were presented without any protocol. The ACT protocol produced the lowest level of discomfort, particularly when it was implemented before participants had experimental experience in trying to control discomfort. Two postcontrol conditions confirmed this result. Implications for prevention and treatment of psychological suffering are discussed. (Contains 1 table and 5 figures.)

This study compares the effect of an acceptance-based protocol (ACT) and a cognitive control-based (CONT) protocol on three measures of pain coping: tolerance, self-report, and believability. Specific methodological controls were employed to further isolate the role of the value of participating in a pain task, compared to previous investigations on the alteration of the function of aversive stimulation. Twenty participants were randomly assigned to one of the conditions (ACT vs. CONT), and a pre-post design was used. In the ACT condition, the protocol established a relation of coordination between the pain-related thoughts and the actions in the valued direction. In the CONT condition, the protocol established a relation of opposition between the same aspects. Results show an increase in pain tolerance and a reduction of self-reported pain at posttest for both conditions. However, ACT participants showed significantly lower believability of pain than did CONT participants. Conceptual and clinical implications are discussed. (Contains 2 tables and 1 figure.)

The environmental and health implications caused by volatile organic compounds (VOCs) from gasoline emissions require the development of adsorbents to overcome the slow and ineffective gas-phase adsorption of microporous activated carbons in automotive containers. This research presents the physicochemical properties of a novel adsorbent prepared from lignocellulosic waste biochar and carbon nanostructures synthetized by applying carbon pulses at low temperature of chemical vapor deposition. Moreover, the kinetic adsorption of aliphatic and aromatic VOCs as model gasoline emissions was explored. Electron microscopy analysis displayed the growth of carbon nanotubes, carbon nanofibers, and onion-like carbon, doubling the biochar surface area from 120 to 240 m2 g−1, without developing micropores. Raman analysis suggested that the growth of carbon nanostructures on the biochar promoted a higher graphitization degree of the adsorbent, inducing a more hydrophobic and basic surface (pH PZC = 10.3). Results unveiled a 1.30–1.81-fold increase in adsorption capacity for aliphatic and aromatic VOCs after improving the biochar with carbon nanostructures. This novel composite had up to 2.60 and 0.98 times more benzene and toluene uptake, respectively, than a commercial activated carbon, as well as a similar removal capacity for pentene and hexane molecules. Additional finding of this study provided evidence that the VOCs adsorption is not only related to the textural properties of the novel composite, but also to its surface chemistry. Overall, the present novel composite offers a promising approach for gasoline emissions recovery as a potential alternative to commercial activated carbon. [Display omitted] • Adsorbents were developed from waste biomass to capture automotive emissions. • Pulses CVD increased biochar surface but no microporosity. • Removal rates of up to 0.98 times faster than AC were achieved. • Remarkable adsorption capacity of the smaller VOCs was accomplished. • Improved biochar had a high selectivity for nonpolar aromatic VOCs. [ABSTRACT FROM AUTHOR]

Background: Increased resting heart rate (RHR) is a predictor of mortality. RHR is influenced by cardiorespiratory fitness (CRF). Little is known about the combined associations of RHR and CRF on cancer mortality. Methods: 50,108 men and women (mean age 43.8 years) were examined between 1974 and 2002 at the Cooper Clinic in Dallas, Texas. RHR was measured by electrocardiogram and categorized as <60, 60-69, 70-79, or =80 beats/minute. CRF was quantified by maximal treadmill test and dichotomized as unfit and fit corresponding to the lower 20% and the upper 80%, respectively, of the age- and sex-specific distribution of treadmill exercise duration. The National Death Index was used to ascertain vital status. Cox regression was used to compute HRs and 95% confidence intervals (CI) for cancer mortality across RHR categories. Results: During a mean follow-up of 15.0 ± 8.6 years, 1,090 cancer deaths occurred. Compared with RHR <60 beats/minute, individuals with RHR =80 beats/minute had a 35% increased risk of overall cancer mortality (HR, 1.35; 95% CI, 1.06-1.71) after adjusting for confounders, including CRF. Compared with "fit and RHR <80 beats/minute", HRs (95% CI) for cancer mortality were 1.41 (1.20-1.66), 1.51 (1.11-2.04), and 1.78 (1.30-2.43) in "unfit and RHR <80," "fit and RHR =80," and "unfit and RHR =80 beats/minute," respectively. Conclusions: RHR =80 beats/minute is associated with an increased risk of overall cancer mortality. High CRF may help lower the risk of cancer mortality among those with high RHR. [ABSTRACT FROM AUTHOR]

This paper explains the evaluation method applied to a specific capstone course, called "Ubiquitous computing", taught in different Computer Science Degrees of the University of Alcala (Spain). Along the previous editions of the course several issues have been discovered, which are intended to be solved with the proposed method that was used as evaluation system of the subject in year 2016-2017. The issues are related to the number of students of each degree that compose the group each year, the contents' deviation, the low marks obtained in previous years, the methodological mismatch in relation with other subjects and the bad alignment of the evaluation method used before. With the idea of obtaining better marks, a closer experience to the real situation in software companies and higher satisfaction level of the students, the learning experience proposed implies teamwork, a project-based learning perspective and a balanced use of the technologies. Taking the results obtained through its implantation along the last academic year, it can be concluded that the evaluation method shown in this document enhances the learning process and the contents are closer to the course initial conception, and students got more involved and obtained better results. [ABSTRACT FROM AUTHOR]

DNA double-strand breaks (DSBs) are among the most deleterious lesions that can challenge genomic integrity. Concomitant to the repair of the breaks, a rapid signaling cascade must be coordinated at the lesion site that leads to the activation of cell cycle checkpoints and/or apoptosis. In this context, ataxia telangiectasia mutated (ATM) and ATM and Rad-3-related (ATR) protein kinases are the earliest signaling molecules that are known to initiate the transduction cascade at damage sites. The current model places ATM and ATR in separate molecular routes that orchestrate distinct pathways of the checkpoint responses. Whereas ATM signals DSBs arising from ionizing radiation (IR) through a Chk2-dependent pathway, ATR is activated in a variety of replication-linked DSBs and leads to activation of the checkpoints in a Chk1 kinase-dependent manner. However, activation of the G2/M checkpoint in response to IR escapes this accepted paradigm because it is dependent on both ATM and ATR but independent of Chk2. Our data provides an explanation for this observation and places ATM activity upstream of ATR recruitment to IR-damaged chromatin. These data provide experimental evidence of an active cross talk between ATM and ATR signaling pathways in response to DNA damage. [ABSTRACT FROM AUTHOR]

Chitosan-based film with and without antagonistic yeast was prepared and its effect against Penicillium italicum was evaluated. The biocompatibility of yeast cells in the developed films was assessed in terms of population dynamics. Furthermore, the impact on physicochemical properties of the prepared films with and without yeast cells incorporated were evaluated in terms of thickness, mechanical properties, color and opacity. Chitosan films with the antagonistic yeast entrapped exhibited strong antifungal activity by inhibiting the mycelial development (55%), germination (45%) and reducing the sporulation process (87%). Chitosan matrix at 0.5% and 1.0% was maintained over 9 days of cell viability. However, at 1.5% of chitosan the population dynamics was strongly affected. The addition of yeast cells only impacted color values such as a*, b*, chroma and hue angle when 1.0% of chitosan concentration was used. Conversely, luminosity was not affected in the presence of yeast cells as well as the opacity. Besides, the addition of antagonistic yeast improved the mechanical resistance of the films. The addition of D. hansenii in chitosan films improve their efficacy for controlling P. italicum, and besides showed desirable characteristics for future use as packaging for citrus products.

The hematopoietic system undergoes many changes during aging, but the causes and molecular mechanisms behind these changes are not well understood. Wang et al. have recently implicated a circadian rhythm gene, Per2, as playing a role in the DNA damage response and in the expression of lymphoid genes in aged hematopoietic stem cells., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

The generation of induced pluripotent stem cells (iPSC) from adult somatic cells is one of the most remarkable discoveries in recent decades. However, several works have reported evidence of genomic instability in iPSC, raising concerns on their biomedical use. The reasons behind the genomic instability observed in iPSC remain mostly unknown. Here we show that, similar to the phenomenon of oncogene-induced replication stress, the expression of reprogramming factors induces replication stress. Increasing the levels of the checkpoint kinase 1 (CHK1) reduces reprogramming-induced replication stress and increases the efficiency of iPSC generation. Similarly, nucleoside supplementation during reprogramming reduces the load of DNA damage and genomic rearrangements on iPSC. Our data reveal that lowering replication stress during reprogramming, genetically or chemically, provides a simple strategy to reduce genomic instability on mouse and human iPSC.

Growth hormone receptor (Ghr) signaling is important in a wide variety of cellular processes including aging; however, the role of Ghr signaling in hematopoietic stem cell (HSC) biology remains unexplored. Within the hematopoietic system, Ghr is expressed in a highly HSC-specific manner and is significantly upregulated during aging. Exposure of young and old HSCs to recombinant growth hormone ex vivo led to diminished short-term reconstitution and restored B-cell output from old HSCs. Hematopoietic-specific genetic deletion of Ghr neither impacted steady-state hematopoiesis nor serial transplantation potential. Repeat challenge with 5-fluorouracil showed that Ghr was dispensable for HSC activation and homeostatic recovery in vivo and, after challenge, Ghr-deficient HSCs functioned normally through serial transplantation. Although exogenous Gh induces age-dependent HSC effects, these results indicate that Ghr signaling appears largely dispensable for HSC function and aging., (© 2014 by The American Society of Hematology.)

Self-renewal is the hallmark feature both of normal stem cells and cancer stem cells. Since the regenerative capacity of normal haematopoietic stem cells is limited by the accumulation of reactive oxygen species and DNA double-strand breaks, we speculated that DNA damage might also constrain leukaemic self-renewal and malignant haematopoiesis. Here we show that the histone methyl-transferase MLL4, a suppressor of B-cell lymphoma, is required for stem-cell activity and an aggressive form of acute myeloid leukaemia harbouring the MLL-AF9 oncogene. Deletion of MLL4 enhances myelopoiesis and myeloid differentiation of leukaemic blasts, which protects mice from death related to acute myeloid leukaemia. MLL4 exerts its function by regulating transcriptional programs associated with the antioxidant response. Addition of reactive oxygen species scavengers or ectopic expression of FOXO3 protects MLL4(-/-) MLL-AF9 cells from DNA damage and inhibits myeloid maturation. Similar to MLL4 deficiency, loss of ATM or BRCA1 sensitizes transformed cells to differentiation, suggesting that myeloid differentiation is promoted by loss of genome integrity. Indeed, we show that restriction-enzyme-induced double-strand breaks are sufficient to induce differentiation of MLL-AF9 blasts, which requires cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) activity. In summary, we have uncovered an unexpected tumour-promoting role of genome guardians in enforcing the oncogene-induced differentiation blockade in acute myeloid leukaemia.

Replicative stress (RS) is a type of endogenous DNA damage that cells suffer every time they duplicate their genomes, and which is further boosted by oncogenes. In mammals, the RS response (RSR) is coordinated by ATR and Chk1 kinases. We sought to develop a mammalian organism that is selectively protected from RS. To this end, mice carrying an extra copy of the Chk1 gene were generated. In vitro, Chk1 transgenic cells are protected from RS-inducing agents. Moreover, an extra Chk1 allele prolongs the survival of ATR-Seckel mice, which suffer from high levels of RS, but not that of ATM-deficient mice, which accumulate DNA breaks. Surprisingly, increased Chk1 levels favor transformation, which we show is associated with a reduction in the levels of RS induced by oncogenes. Our study provides the first example where supra-physiological levels of a tumor suppressor can promote malignant transformation, which is a result of the protection from the RS found in cancer cells.

One of the current models of cancer proposes that oncogenes activate a DNA damage response (DDR), which would limit the growth of the tumor in its earliest stages. In this context, and in contrast to studies focused on the acute responses to a one-time genotoxic insult, understanding how cells respond to a persistent source of DNA damage might become critical for future studies in the field. We here report the discovery of a novel damage-responsive pathway, which involves p27(Kip1) and retinoblastoma tumor suppressors and is only implemented after a persistent exposure to clastogens. In agreement with its late activation, we show that this pathway is critical for the maintenance, but not the initiation, of the cell cycle arrest triggered by DNA damage. Interestingly, this late response is independent of the canonical ataxia telangiectasia mutated-dependent and ataxia telangiectasia mutated and Rad3-related-dependent DDR but downstream of p38 mitogen-activated protein kinase. Our results might help to reconcile the oncogene-induced DNA damage model with the clinical evidence that points to non-DDR members as the most important tumor suppressors in human cancer.

The ATR kinase is a key transducer of "replicative stress," the type of genomic damage that has been postulated to be induced by oncogenes. Here we describe a cellular system in which we can unleash ATR activity at will, in the absence of any actual damage or additional signaling pathways triggered by DNA breaks. We demonstrate that activating ATR is sufficient to promote cell cycle arrest and, if persistent, triggers p53-dependent but Ink4a/ARF-independent senescence. Moreover, we show that an ectopic activation of ATR leads to a G1/S arrest in ATM-/- cells, providing the first evidence of functional complementation of ATM deficiency by ATR. Our system provides a novel platform for the study of the specific functions of ATR signaling and adds evidence for the tumor-suppressive potential of the DNA damage response.