Marine phytoplankton community composition data from the Belgian part of the North Sea, 1968-2010

The Belgian Phytoplankton Database (BPD) is a comprehensive data collection comprising quantitative phytoplankton cell counts from multiple research projects conducted since 1968. The collection is focused on the Belgian part of the North Sea, but also includes data from the French and the Dutch part of the North Sea. The database includes almost 300 unique sampling locations and more than 3,000 sampling events resulting in more than 86,000 phytoplankton cell count records. The dataset covers two periods: 1968 to 1978 and 1994 to 2010. The BPD can be accessed online and provides high quality phytoplankton count data. The species taxonomy is updated, and the count values are quality checked and standardized. Important metadata like sampling date, sampling location, sampling depth and methodology is provided and standardized. Additionally, associated abiotic data and biovolume values are available. The dataset allows to conduct analyses of long-term temporal and spatial trends in phytoplankton community structure in the southern part of the North Sea, including changes in phytoplankton phenology and seasonality

Effect of mastication on lipid bioaccessibility of almonds in a randomized human study and its implications for digestion kinetics, metabolizable energy, and postprandial lipemia

Background: The particle size and structure of masticated almonds impact significantly on nutrient release (bioaccessibility) and digestion kinetics. Objectives: To quantify the effects of mastication on the bioaccessibility of intracellular lipid of almond tissue and examine microstructural characteristics of masticated almonds. Design: In a randomized, subject-blind, crossover trial, 17 healthy subjects chewed natural (NA) or roasted almonds (RA) on 4 separate mastication sessions. Particle size distributions (PSDs) of the expectorated boluses were measured using mechanical sieving and laser diffraction (primary outcome). The microstructure of masticated almonds, including the structural integrity of the cell walls (i.e. dietary fiber), was examined using microscopy. Lipid bioaccessibility was predicted using a theoretical model, based on almond particle size and cell dimensions, and then compared to empirically-derived release data. Results: Inter-subject variations (n=15, 2 subjects withdrew) in PSDs of both NA and RA samples were small (e.g. laser diffraction, CV = 12% and 9%, respectively). Significant differences in PSDs were found between these two almond forms (P 500 µm) in masticated almonds. Microstructural examination of the almonds indicated that most intracellular lipid remained undisturbed in intact cells post-mastication. No adverse events were recorded. Conclusions: Following mastication, most of the almond cells remained intact with lipid encapsulated by cell walls. Thus, most of the lipid (>88%) in masticated almonds is not immediately bioaccessible and remains unavailable for digestion and absorption. The lipid encapsulation mechanism provides a convincing explanation for why almonds have a low metabolizable energy content and an attenuated impact on postprandial lipemia. Trial registration number; ISRCTN58438021

Diagnosis and treatment of musculoskeletal chest pain: design of a multi-purpose trial

<p>Abstract</p> <p>Background</p> <p>Acute chest pain is a major health problem all over the western world. Active approaches are directed towards diagnosis and treatment of potentially life threatening conditions, especially acute coronary syndrome/ischemic heart disease. However, according to the literature, chest pain may also be due to a variety of extra-cardiac disorders including dysfunction of muscles and joints of the chest wall or the cervical and thoracic part of the spine. The diagnostic approaches and treatment options for this group of patients are scarce and formal clinical studies addressing the effect of various treatments are lacking.</p> <p>Methods/Design</p> <p>We present an ongoing trial on the potential usefulness of chiropractic diagnosis and treatment in patients dismissed from an acute chest pain clinic without a diagnosis of acute coronary syndrome. The aims are to determine the proportion of patients in whom chest pain may be of musculoskeletal rather than cardiac origin and to investigate the decision process of a chiropractor in diagnosing these patients; further, to examine whether chiropractic treatment can reduce pain and improve physical function when compared to advice directed towards promoting self-management, and, finally, to estimate the cost-effectiveness of these procedures. This study will include 300 patients discharged from a university hospital acute chest pain clinic without a diagnosis of acute coronary syndrome or any other obvious cardiac or non-cardiac disease. After completion of the clinic's standard cardiovascular diagnostic procedures, trial patients will be examined according to a standardized protocol including a) a self-report questionnaire; b) a semi-structured interview; c) a general health examination; and d) a specific manual examination of the muscles and joints of the neck, thoracic spine, and thorax in order to determine whether the pain is likely to be of musculoskeletal origin. To describe the patients status with regards to ischemic heart disease, and to compare and indirectly validate the musculoskeletal diagnosis, myocardial perfusion scintigraphy is performed in all patients 2–4 weeks following discharge. Descriptive statistics including parametric and non-parametric methods will be applied in order to compare patients with and without musculoskeletal chest pain in relation to their scintigraphic findings. The decision making process of the chiropractor will be elucidated and reconstructed using the CART method. Out of the 300 patients 120 intended patients with suspected musculoskeletal chest pain will be randomized into one of two groups: a) a course of chiropractic treatment (therapy group) of up to ten treatment sessions focusing on high velocity, low amplitude manipulation of the cervical and thoracic spine, mobilisation, and soft tissue techniques. b) Advice promoting self-management and individual instructions focusing on posture and muscle stretch (advice group). Outcome measures are pain, physical function, overall health, self-perceived treatment effect, and cost-effectiveness.</p> <p>Discussion</p> <p>This study may potentially demonstrate that a chiropractor is able to identify a subset of patients suffering from chest pain predominantly of musculoskeletal origin among patients discharged from an acute chest pain clinic with no apparent cardiac condition. Furthermore knowledge about the benefits of manual treatment of patients with musculoskeletal chest pain will inform clinical decision and policy development in relation to clinical practice.</p> <p>Trial registration</p> <p>NCT00462241 and NCT00373828</p

Cyclin-dependent kinases 7 and 9 specifically regulate neutrophil transcription and their inhibition drives apoptosis to promote resolution of inflammation

Terminally differentiated neutrophils are short-lived but the key effector cells of the innate immune response, and have a prominent role in the pathogenesis and propagation of many inflammatory diseases. Delayed apoptosis, which is responsible for their extended longevity, is critically dependent on a balance of intracellular survival versus pro-apoptotic proteins. Here, we elucidate the mechanism by which the cyclin-dependent kinase (CDK) inhibitor drugs such as R-roscovitine and DRB (5,6-dichloro-1-beta--ribofuranosylbenzimidazole) mediate neutrophil apoptosis. We demonstrate (by a combination of microarray, confocal microscopy, apoptosis assays and western blotting) that the phosphorylation of RNA polymerase II by CDKs 7 and 9 is inhibited by R-roscovitine and that specific effects on neutrophil transcriptional capacity are responsible for neutrophil apoptosis. Finally, we show that specific CDK7 and 9 inhibition with DRB drives resolution of neutrophil-dominant inflammation. Thus, we highlight a novel mechanism that controls both primary human neutrophil transcription and apoptosis that could be targeted by selective CDK inhibitor drugs to resolve established inflammation