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"Martin, S J"
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INFOGEST static in vitro simulation of gastrointestinal food digestion
Developing a mechanistic understanding of the impact of food structure and composition on human health hasincreasingly involved simulating digestion in the upper gastrointestinal tract. These simulations have used a wide range of different conditions that often have very little physiological relevance, and this impedes the meaningful comparison of results. The standardized protocol presented here is based on an international consensus developed by the COST INFOGEST network. The method is designed to be used with standard laboratory equipment and requires limited experience to encourage a wide range of researchers to adopt it. It is a static digestion method that uses constant ratios of meal to digestive fluids and a constant pH for each step of digestion. This makes the method simple to use but not suitable for simulating digestion kinetics. Using this method, food samples are subjected to sequential oral, gastric and intestinal digestion while parameters such as electrolytes, enzymes, bile, dilution, pH and time of digestion are based onavailable physiological data. This amended and improved digestion method (INFOGEST 2.0) avoids challenges associated with the original method, such as the inclusion of the oral phase and the use of gastric lipase. The method can be used to assess the endpoints resulting from digestion of foods by analyzing the digestion products (e.g., peptides/amino acids, fatty acids, simple sugars) and evaluating the release of micronutrients from the food matrix. The whole protocol can be completed in ~7 d, including ~5 d required for the determination of enzyme activities.
Journal Article
Harsh environments promote alloparental care across human societies
Alloparental care is central to human life history, which integrates exceptionally short interbirth intervals and large birth size with an extended period of juvenile dependency and increased longevity. Formal models, previous comparative research, and palaeoanthropological evidence suggest that humans evolved higher levels of cooperative childcare in response to increasingly harsh environments. Although this hypothesis remains difficult to test directly, the relative importance of alloparental care varies across human societies, providing an opportunity to assess how local social and ecological factors influence the expression of this behaviour. We therefore, investigated associations between alloparental infant care and socioecology across 141 non-industrialized societies. We predicted increased alloparental care in harsher environments, due to the fitness benefits of cooperation in response to shared ecological challenges. We also predicted that starvation would decrease alloparental care, due to prohibitive energetic costs. Using Bayesian phylogenetic multilevel models, we tested these predictions while accounting for potential confounds aswell as for population history. Consistent with our hypotheses, we found increased alloparental infant care in regions characterized by both reduced climate predictability and relatively lower average temperatures and precipitation.We also observed reduced alloparental care under conditions of high starvation. These results provide evidence of plasticity in human alloparenting in response to ecological contexts, comparable to previously observed patterns across avian and mammalian cooperative breeders. This suggests convergent social evolutionary processes may underlie both inter- and intraspecific variation in alloparental care.
Journal Article
Deformed wing virus variant shift from 2010 to 2016 in managed and feral UK honey bee colonies
Deformed wing virus (DWV) has been linked to the global decline of honey bees. DWV exists as three master variants (DWV-A, DWV-B, and DWV-C), each with differing outcomes for the honey bee host. Research in the USA showed a shift from DWV-A to DWV-B between 2010 to 2016 in honey bee colonies. Likewise, in the UK, a small study in 2007 found only DWV-A, whereas in 2016, DWV-B was the most prevalent variant. This suggests a shift from DWV-A to DWV-B might have occurred in the UK between 2007 and 2016. To investigate this further, data from samples collected in 2009/10 (n = 46) were compared to existing data from 2016 (n = 42). These samples also allowed a comparison of DWV variants between Varroa-untreated (feral) and Varroa-treated (managed) colonies. The results revealed that, in the UK, DWV-A was far more prevalent in 2009/10 (87%) than in 2016 (43%). In contrast, DWV-B was less prevalent in 2009/10 (76%) than in 2016 (93%). Regardless if colonies had been treated for Varroa (managed) or not (feral), the same trend from DWV-A to DWV-B occurred. Overall, the results reveal a decrease in DWV-A and an increase in DWV-B in UK colonies.
Journal Article
Necroptosis suppresses inflammation via termination of TNF- or LPS-induced cytokine and chemokine production
TNF promotes a regulated form of necrosis, called necroptosis, upon inhibition of caspase activity in cells expressing RIPK3. Because necrosis is generally more pro-inflammatory than apoptosis, it is widely presumed that TNF-induced necroptosis may be detrimental
in vivo
due to excessive inflammation. However, because TNF is intrinsically highly pro-inflammatory, due to its ability to trigger the production of multiple cytokines and chemokines, rapid cell death via necroptosis may blunt rather than enhance TNF-induced inflammation. Here we show that TNF-induced necroptosis potently suppressed the production of multiple TNF-induced pro-inflammatory factors due to RIPK3-dependent cell death. Similarly, necroptosis also suppressed LPS-induced pro-inflammatory cytokine production. Consistent with these observations, supernatants from TNF-stimulated cells were more pro-inflammatory than those from TNF-induced necroptotic cells
in vivo
. Thus necroptosis attenuates TNF- and LPS-driven inflammation, which may benefit intracellular pathogens that evoke this mode of cell death by suppressing host immune responses.
Journal Article
شراكات المدرسة والأسرة والمجتمع : دليلك للعمل =
كتاب ثري وعملي يشجعك على البدء في بناء شراكة فاعلة بين المدرسة والأسرة والمجتمع ويقدم لك مختلف الأدوات التي تحتاجها لتبدأ ستجد نموذجا مميزا لمساعدة كل مدرسة على بناء خطة العام للشراكة مع الأسر والمجتمع بالتفصيل ستحصل على خطوات تكوين فرق الشراكة في داخل المدرسة ستحصل على نماذج جاهزة للعمل أيضا قوائم بأنشطة هادفة يمكن تنفيذها وأثبتت جدواها عبر دراسات.
BOOK
The unfolded protein response influences therapy outcome and disease progression in chronic lymphocytic leukaemia
Since genomics, epigenomics and transcriptomics have provided only a partial explanation of chronic lymphocytic leukaemia (CLL) heterogeneity, and since concordance between mRNA and protein expression is incomplete, we related the CLL proteome to clinical outcome. CLL samples from patients who received fludarabine-containing chemoimmunotherapy were analysed by mass spectrometry (SWATH-MS). One dataset compared pre-treatment samples associated with an optimal versus suboptimal response, while another compared paired samples collected before treatment and at disease progression. eIF2 signalling (pivotal to the unfolded protein response (UPR)), was identified as the most enriched pathway in both datasets (respective z-scores: − 6.245 and 3.317;
p
< 0.0001), as well as in a fludarabine-resistant CLL cell line established from HG3 cells (z-score: − 2.121;
p
< 0.0001). Western blotting revealed that fludarabine-resistant HG3 cells expressed higher levels of PERK, which phosphorylates the regulatory eIF2α subunit, and lower levels of BiP, an HSP70 molecular chaperone that inactivates PERK but preferentially binds to misfolded proteins during ER stress. The PERK inhibitor, GSK2606414, sensitised resistant, but not sensitive, HG-3 cells to fludarabine without affecting background cell viability or cytotoxicity induced by the BCL-2 inhibitor venetoclax. These findings identify the UPR as a novel determinant of therapy outcome and disease progression in CLL.
Journal Article