Research alignment in the U.S. national park system: Impact of transformative science policy on the supply and demand for scientific knowledge for protected area management.

The US National Park System encompasses diverse environmental and tourism management regimes, together governed by the 1916 Organic Act and its dual mandate of conservation and provision of public enjoyment. However, with the introduction of transformative science policy in the 2000's, the mission scope has since expanded to promote overarching science-based objectives. Yet despite this paradigm shift instituting "science for parks, parks for science", there is scant research exploring the impact of the National Park Science Policy on the provision of knowledge. We address this gap by developing a spatiotemporal framework for evaluating research alignment, here operationalized via quantifiable measures of supply and demand for scientific knowledge. Specifically, we apply a machine learning algorithm (Latent Dirichlet analysis) to a comprehensive park-specific text corpus (combining official needs statements -i.e. demand- and scientific research metadata -i.e. supply-) to define a joint topic space, which thereby facilitates quantifying the direction and degree of alignment at multiple levels. Results indicate an overall robust degree of research alignment, with misaligned topics tending to be over-researched (as opposed to over-demanded), which may be favorable to many parks, but is inefficient from the park system perspective. Results further indicate that the transformative science policy exacerbated the misalignment in mandated research domains. In light of these results, we argue for improved decision support mechanisms to achieve more timely alignment of research efforts towards distinctive park needs, thereby fostering convergent knowledge co-production and leveraging the full value of National Parks as living laboratories.

[Controlled evaluation of a high-resolution three-dimensional magnetic detector system (3D-MAGMA) as a proof of concept - examination of healthy volunteers before and after application of Metoclopramide (MCP)]. / Kontrollierte Evaluierung des 3-dimensionalen, magnetischen Markermonitorings (3D-MAGMA) in einer Proof-of-Concept-Studie - Untersuchungen vor und nach Gabe von Metoclopramid (MCP) bei gesunden Probanden.

BACKGROUND: Changes in gastric and small bowel motility are a common clinical problem. Currently diagnostic options are limited because each method harbors certain disadvantages. It has been shown that the high-resolution three-dimensional magnetic detector system 3D-MAGMA is capable of reliably measuring gastric and small intestine motor activity. This system allows precise localization of a small magnetic marker and determination of its three-dimensional orientation inside a human body. The aim of the current study was to determine if 3D-MAGMA is reliably able to detect changes in gastric and small bowel motility under controlled conditions. MCP was used as a well known prokinetic agent to shorten the gastric and small bowel passage. PATIENTS AND METHODS: 8 healthy volunteers (fasting) underwent motility testing of the stomach and small bowel by 3D-MAGMA with and without administration of MCP (10 mg orally). Among other data the time the capsule needed to pass through the stomach and the duodenum and the time the capsule needed to pass through the first 50 cm of the jejunum were recorded. RESULTS: The retention time of the capsule in the stomach under physiological conditions was 49.1 minutes (median; min. 18 min; max. 88.8 min). The median time the capsule needed to pass through the duodenum was 13.8 minutes (median; min. 1.7 min; max. 24.8 min). The time the capsule needed to pass through the first 50 cm of the jejunum under physiological conditions was 33.0 minutes (median; min. 20.2 min; max. 67.2 min). The retention time of the capsule in the stomach decreased significantly after administration of MCP to 20.9 minutes (median; min. 1.7 min; max. 62.8 min; p = 0.008). The time the capsule needed to pass through the duodenum was also reduced to 7.1 minutes (median; min. 3.1 min; max. 18.3 min; p = 0.055). The time the capsule needed to pass through the first 50 cm of the jejunum was also reduced to 21.7 minutes (median; min. 10.7 min; max. 31.2 min; p = 0.069). DISCUSSION: 3D-MAGMA is able to accurately detect changes in gastric and small bowel motility. Its clinical use appears conceivable especially in patients with diseases that have impact on gastric and small bowel motility.

[Jejunal ulcerations - a diagnostic challenge in a patient with coeliac disease]. / Jejunale Ulzerationen - eine diagnostische Herausforderung bei einem Patienten mit Zöliakie.

A subset of patients with coeliac disease (CD) suffers persistent or recurrent complaints despite a strict adherence to a gluten-free diet (GFD) that can be caused by refractory coeliac disease (RCD). We present a patient with weight loss and signs of malassimilation secondary to villous atrophy and jejunal ulcerations complicating known CD. We demonstrate a stepwise approach to the diagnosis and subtyping of RCD and to rule out important alternative causes of jejunal ulcerations. RCD can be classified as type I based on the absence or as type II based on the presence of an aberrant intestinal mucosal lymphocyte population. RCD type I shows a more benign course as these patients usually improve on a treatment consisting of nutritional support and immunosuppressive therapies such as budesonide or azathioprine. In contrast, clinical response to standard therapies in RCD type II is less certain and the prognosis is poor. Several groups suggest that RCD type II should be regarded as low-grade intraepithelial lymphoma which frequently transforms into an aggressive enteropathy associated T-cell lymphoma with a high mortality rate. Therefore, a rapid differentiation of RCD type I and RCD type II is a major clinical challenge to early initiate appropriate treatment modalities.

A spatial assessment of baseline nutrient and water quality values in the Ashepoo-Combahee-Edisto (ACE) Basin, South Carolina, USA.

The Ashepoo-Combahee-Edisto (ACE) Basin (South Carolina, USA) National Estuarine Research Reserve System (NERRS) encompasses some of the least developed USA coastline. Yet, periodic sampling showed that certain regions have higher nutrient, fecal coliform, and chlorophyll a levels, often with lower dissolved oxygen, than other South Carolina estuaries. To evaluate the spatial extent of these issues, a summer (2008) baseline study was conducted. Physical water quality, total nitrogen and phosphorus, chlorophyll a, dissolved organic carbon, and suspended solids were measured from surface waters of 67 stations (30 tidal creek, 37 open water). Nutrient and chlorophyll a levels were significantly (p<0.01) and negatively correlated with the extent of open water (% land cover), and chlorophyll a and nitrogen levels were, at times, elevated relative to concentrations typical of other estuaries in the state, reinforcing previous findings. This survey also identified several creeks not previously monitored that exhibited elevated nutrients.

[Impact of implementation strategies on adherence rates to colorectal cancer (CRC) guidelines after polypectomy in a university hospital]. / Einfluss von Weiterbildungsmaßnahmen auf die leitliniengerechten Nachsorgeempfehlungen nach Polypektomie aus dem Dickdarm in einem Universitätsklinikum.

BACKGROUND: Colorectal cancer (CRC) is the second most common malignancy in Germany. Screening colonoscopies with polypectomy have been demonstrated to reduce the incidence of CRC. Detailed recommendations on scheduling screening and follow-up colonoscopies have therefore been included into national guidelines. Knowledge about CRC guidelines and adherence to guideline recommendations varies greatly among physicians. METHODS: We combined different implementation strategies (training courses, case discussion, handouts, wall charts) to improve adherence of recommendations for scheduling follow-up colonoscopy. To assess adherence, written recommendations given at discharge after inpatient treatment for polypectomy were analysed before (n = 111) and after (n = 83) the implementation of the above-mentioned implementation measures. Additional factors possibly influencing the recommendations of physicians were collected (histology, polyp size). RESULTS: The adherence to the CRC guideline before implementation of the above-mentioned measures was moderate. After intervention, there was a non-significant increase from 47 % to 53 %. Senior physician review and editing of the discharge summaries improved guideline adherence of recommendations to 69 %. Neither the education level of residents nor their affiliation to a certain department had an impact on the quality of the recommendations. Histology and in particular information on the resection status of the polyps in the pathology report (complete versus incomplete resection) had an influence of the recommended schedule. Furthermore, size of the polyps, but not the number, had a statistically significant influence on the quality of the recommendations. CONCLUSIONS: The inadequate improvement of guideline adherence can possibly be explained by the insufficient interactive and repetitive character of interventions. As the histology reports seem to have an influence on the recommendations in regards to the interval to the next colonoscopy, interdisciplinary teaching is necessary to improve guideline concurrent care.

[Enteroscopy and imaging in sclerosing mesenteritis]. / Enteroskopie und Bildgebung bei sklerosierender Mesenteritis.

Sclerosing mesenteritis is a rare, benign, and chronic fibrosing inflammatory disease of the mesenteric fatty tissue. Its aetiology is unknown. In the present report we describe a 56-year-old women who presented with postprandial abdominal pain, and weight loss. Ultrasound, computed tomography, and magnetic resonance imaging revealed a mesenteric mass of 15 cm. The findings were typical for this disease. Additionally the patient underwent a single ballon enteroscopy in which the mucosa showed a considerable hyperergic reaction. The histological examination of the ileum was appropriate to support the suspicion. The patient's symptoms responded to a therapy with tamoxifen.

Surveillance strategies in inflammatory bowel disease.

Patients with longstanding ulcerative colitis (UC) are at increased risk of developing colorectal cancer (CRC). Although data for CRC risk in Crohn's disease (CD) are limited, it has been suggested that the risk is comparable to UC. Current strategies for the prevention and early detection of cancer in this high risk population are based on the concept of an inflammation-neoplasia-carcinoma sequence. To reduce CRC mortality in inflammatory bowel disease (IBD), colonoscopic surveillance with random and targeted biopsies are recommended to detect early neoplasia. The introduction of novel endoscopic techniques such as conventional or virtual chromoendoscopy to facilitate targeted biopsies or confocal laser endomicroscopy to further characterise suspicious lesions has become increasingly associated with enhanced neoplasia detection. However, there is only indirect evidence that such surveillance strategies are likely to be effective in reducing the risk of death from IBD-associated CRC. Furthermore, new data suggests that surveillance strategies largely based upon disease duration are leading to delayed or missed diagnosis of early CRC in a substantial number of patients. Therefore, current surveillance guidelines seem to lack efficacy and need to be reassessed.

Airway inflammation in children with tracheostomy.

We hypothesised that long-term tracheostomy in infants and children may perpetuate chronic airway inflammation and airway remodeling due to easier access to the lungs for microorganisms. Pulmonary surfactant represents an important part of the initial host defense, and in particular, the surfactant proteins (SP) A and D may directly interact with invading microorganisms and also modulate the activity of local immune cells. The goals of this study were to determine the presence and intensity of a peripheral airway inflammation and of potential deficiency states of surfactant proteins in nonsymptomatic children with tracheostomy. Bronchoalveolar lavage (BAL) cell pattern, bacteria and viruses recovered, and concentrations of SP-A, SP-B, SP-C, and SP-D were assessed in 46 children (4.3 years (1.6-6)) median (range) carrying a tracheostomy for 2.4 years (1.3-4.9), and were compared to 16 children with no lung disease. Children with tracheostomy had an increased total number of cells, increased neutrophils, and more frequently bacteria, but no viruses were recovered. SP-D concentration was reduced by 50% on average (P = 0.0002). SP-A, SP-B, and SP-C were not different between the two groups. SP-D was inversely correlated to neutrophils, and high numbers of bacteria were associated with lower SP-D concentrations. We suggest that bacteria and low SP-D support neutrophilic inflammation in the lower respiratory tract of nonsymptomatic with children with tracheostomy.

Pathways from obesity to diabetes.

The relationship between obesity and type 2 diabetes has been known for decades and the recent important increase in such diseases represents a major medical problem worldwide. Several prospective studies present both impaired insulin release and insulin resistance as the major factors for the development of type 2 diabetes. The factor that dominates in obesity is the permanent elevation of plasma FFA and the predominant utilization of lipids by the muscle inducing a diminution of glucose uptake and, therefore, insulin resistance. The rise in insulin secretion appears to be a compensatory mechanism that responds to the increased levels of circulating glucose. The fall in insulin secretion occurs as a late phenomenon. The present review aims at analysing the mechanisms that lead human obesity to type 2 diabetes and using the pathophysiological information for the prevention of diabetes. The partial reversibility of the evolution of obesity towards diabetes is well demonstrated today by lifestyle changes and multidisciplinary weight loss programs.

Endogenous glucose production, gluconeogenesis and liver glycogen concentration in obese non-diabetic patients.

Resting, post-absorptive endogenous glucose production (EGP), fractional gluconeogenesis and liver glycogen concentration were assessed in 6 lean and 5 obese non-diabetic subjects undergoing elective abdominal surgery. During the 2 days preceding these measurements, 0.3 g/day U-13C glucose had been added to their usual diet to label their endogenous glycogen stores. On the morning of day 3, EGP was measured with 6,6-2H glucose. Their endogenous 13C glycogen enrichment was calculated from 13CO2 and respiratory gas exchanges. Fractional gluconeogenesis was assessed as 1-(13C glucose/13C glycogen)100. EGP was similar in lean subjects (113 +/- 5 mg/min) and in obese subjects (111 +/- 6). Fractional gluconeogenesis was higher in obese (59 +/- 10%) than in lean subjects (29 +/- 8%). However, overall EGP remained constant due to a decrease in glycogenolysis. Since an increased gluconeogenesis and a decreased glycogenolysis may both contribute to increase liver glycogen concentration in obesity, hepatic glycogen concentrations were assessed in hepatic needle biopsies obtained during surgery. Hepatic glycogen concentrations were increased in obese patients (515 +/- 38 mg/g protein) compared to lean subjects (308 +/- 58, p < 0.05). It is concluded that in obese patients: a) fractional gluconeogenesis is increased; b) overall EGP is unchanged due to a proportional inhibition of glycogenolysis; c) liver glycogen concentration is increased.

Effect of lipid oxidation on the regulation of glucose utilization in obese patients.

The effect of changes in lipid oxidation on glucose utilization (storage and oxidation) was studied in seven nondiabetic obese patients. They participated in three protocols in which: (1) Intralipid (to raise plasma FFA concentrations), (2) beta-pyridylcarbinol [a precursor of nicotinic acid, to lower plasma free fatty acids (FFA) concentrations], or (3) isotonic saline were infused over 2 h. Thereafter, these infusions were discontinued, and a 2-h euglycemic, hyperinsulinemic clamp was performed to measure glucose uptake. All studies were carried out in combination with indirect calorimetry to measure oxidative and nonoxidative glucose disposal (glucose storage). The high plasma FFA concentrations (1024 +/- 57 mumol/l) and lipid oxidation rates (1.1 +/- 0.1 mg/kg.min) found at the end of the Intralipid infusion and the low plasma FFA concentrations (264 +/- 26 mumol/l) and lipid oxidation rates (0.7 +/- 0.1 mg/kg.min) found at the end of the beta-pyridylcarbinol infusions resulted in significantly different rates of total and nonoxidative glucose disposal during the insulin clamp. The values were 2.6 +/- 0.6 mg/kg.min after Intralipid and 4.1 +/- 1.0 mg/kg.min after beta-pyridylcarbinol for total glucose disposal, and 0.4 +/- 0.4 and 1.6 +/- 0.8, respectively for nonoxidative glucose disposal. In conclusion, these observations show that changes in lipid oxidation rates preceding a glucose load influence glucose disposal and glycogen storage in obese subjects.

Regulation of nutrient metabolism and energy expenditure.

The requisites for energy expenditure are covered mainly by two major substrates, glucose and free fatty acids (FFA). Their regulation and metabolism differ. After carbohydrate ingestion, glucose is rapidly oxidized or stored in muscles and liver. There is a constant alternance between glucose storage as glycogen after meals and glycogen mobilization in the postabsorptive state when plasma glucose has returned to the basal state. Impairment of this alternance, in particular when glycogen stores are not being used, may lead to glucose intolerance and insulin resistance. Ingestion of lipids is not followed by an immediate increase in lipid oxidation, but FFA are stored as triglycerides in different tissues. Lipolysis occurs in the fasting state from tissue triglycerides and favors lipid oxidation. Lipid oxidation is typically increased in obesity. The preferential use of FFA from triglyceride stores for energy expenditure in obesity is responsible for the decrease in glucose mobilization from glycogen stores. This leads to a negative feedback of muscle and liver glycogen on glycogen synthase activity and consequently on glucose storage. It results in glucose intolerance after carbohydrate ingestion. Diabetes develops in obesity, usually after a long period of glucose intolerance, when glycemia does not return to the basal state. In obesity, glucose intolerance and insulin resistance can be prevented, or if already existing, can be decreased by stimulating glycogen mobilization by exercise, thermogenesis-stimulating drugs, and weight loss, which reduces fat stores and decreases lipid oxidation.

[From obesity to diabetes]. / De l'obesité au diabéte.

The frequent development of Type 2 diabetes in the obese suggests a relationship between obesity and diabetes. This study presents evidence for a continuum form obesity to diabetes via glucose intolerance and hyperinsulinemic diabetes. The defect which seems to be at the origin of this development resides in the increase in lipid oxidation already present in the early stages of obesity. It reflects the increased utilisation of fatty acids for energy purpose in the obese, at the expenses of glucose. In non-diabetic obese subjects, insulin resistance can be demonstrated by the inhibition of glucose storage during a euglycemic, hyperinsulinemic, clamp. This defect in glucose storage is not observed during a oral glucose tolerance test (OGTT), as it is compensated by hyperinsulinemia and hyperglycemia during glucose tolerance. Glucose tolerance appears with the inhibition of glucose oxidation by the augmented lipid oxidation. This decreased glucose utilization causes a slowdown of the utilization of glycogen stores which leads, as a consequence, to the inhibition of glycogen synthase by its product, glycogen. Diabetes appears when the increase in glycemia and insulinemia does not compensate any more for the inhibition of glucose storage. The rise in basal glycemia simultaneously with the fall in glucose storage corresponds to the transition to diabetes. The decreased glucose mobilization together with the inhibition of glycogen phosphorylase are such in the diabetic patient that glycogen stores tend to remain full and glycogen synthase is inhibited by negative feedback. The retrograde inhibition of glycogen stores on glycogen synthase activity brings up incapacity to store glucose and leads to a rise in glycemia. Finally, the evolution of obesity to diabetes leads to a decrease in insulin secretion with increase in hepatic glucose production through gluconeogenesis and decreased capacity to store glucose. Therapeutic implications are discussed in this review.

Effect of a novel beta-adrenoceptor agonist (Ro 40-2148) on resting energy expenditure in obese women.

The aim of this single-blind, placebo-controlled study was to investigate the effects of the new beta-adrenergic compound Ro 40-2148 on resting energy expenditure (REE) at rest and after an oral glucose load in non-diabetic obese women before and after two weeks of treatment. After one week of placebo administration and after an overnight fast and one hour rest, REE and glucose and lipid oxidation rates were measured by indirect calorimetry (hood system) before and for 6 h after a single dose of placebo solution. A 75 g oral glucose tolerance test (OGTT) was performed during this period starting 90 min after the placebo administration. During the following two weeks, using a randomization design, six patients received Ro 40-2148 at a dose of 400 mg diluted in 100 ml water twice a day (i.e. 800 mg per day), while six others continued with the placebo administration. The same tests and measurements were repeated after two weeks, except for the treatment group which received the drug instead of the placebo. The 14-day period of drug administration did not increase REE measured in post-absorptive conditions. Similarly, there was no acute effect on REE of a 400 mg dose of Ro 40-2148. In contrast, glucose-induced thermogenesis was significantly increased after two weeks in the treatment group (means +/- s.e.m.: 3.7 +/- 1.3%, P = 0.047), while no change was observed in the placebo group (-0.8 +/- 0.7%, not significant). Since there was no significant change in the respiratory quotient, the increase in energy expenditure observed in the treatment group was due to stimulation of both lipid and glucose oxidation. The drug induced no variations in heart rate, blood pressure, axillary temperature or in plasma glucose, insulin and free fatty acid levels. In conclusion, this study shows that Ro 40-2148 activates glucose-induced thermogenesis in obese non-diabetic patients.