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.

[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.

Effect of beta and alpha adrenergic blockade on glucose-induced thermogenesis in man.

After intravenous glucose/insulin infusion there is an increase in oxygen consumption and energy expenditure that has been referred to as thermogenesis. To examine the contribution of the beta and alpha adrenergic nervous system to this thermogenic response, 12 healthy volunteers participated in three studies: (a) euglycemic insulin (plasma insulin approximately 100 microunits/ml) clamp study (n = 12); (b) insulin clamp study after beta adrenergic blockade with intravenous propranolol for 1 h (n = 12); (c) insulin clamp study after alpha adrenergic blockade with phentolamine for 1 h (n = 5). During the control insulin clamp study total glucose uptake, glucose oxidation and nonoxidative glucose uptake averaged 7.85 +/- 0.47, 2.62 +/- 0.22, and 5.23 +/- 0.51 mg/kg X min. After propranolol infusion, insulin-mediated glucose uptake was significantly reduced, 6.89 +/- 0.41 (P less than 0.02). This decrease was primarily the result of a decrease in glucose oxidation (1.97 +/- 0.19 mg/kg X min, P less than 0.01) without any change in nonoxidative glucose metabolism. Phentolamine administration had no effect on total glucose uptake, glucose oxidation, or nonoxidative glucose disposal. The increments in energy expenditure (0.10 +/- 0.01 vs. 0.03 +/- 0.01 kcal/min) and glucose/insulin-induced thermogenesis (4.9 +/- 0.5 vs. 1.5 +/- 0.5%) were reduced by 70% during the propranolol/insulin clamp study. The increments in energy expenditure (0.12 +/- 0.03 kcal/min) and thermogenesis (5.0 +/- 1.5%) were not affected by phentolamine. These results indicate that activation of the beta adrenergic receptor plays an important role in the insulin/glucose-mediated increase in energy expenditure and thermogenesis. In contrast, the alpha adrenergic receptor does not appear to participate in this response.

Radioimmunoassay of human plasma trypsin.

A radioimmunoassay has been developed for the determination of human trypsin (3.4.21.4) in plasma. It allows the measurement of trypsin concentration in spite of the presence of plasma or pancreatic inhibitors. The human trypsin used as a standard and for labelling was isolated from pancreatic tissue and purified by affinity chromatography. The antiserum was obtained from guinea-pigs immunized with partially purified human trypsin. In the radioimmunoassay, the values of trypsin in serial dilutions of plasma were parallel to those of the standard curves. The assay was shown to be reproducible, sensitive and specific. However, the two antisera used did not distinguish between the enzyme and its proenzyme. In normal subjects, plasma values were found to be around 400 ng/ml. They were 10-40 times higher in patients with acute pancreatitis. The method appears to be much more specific for the diagnosis of acute pancreatitis than the current determinations of amylase and lipase activity.

Insulin sensitivity and exogenous insulin clearance in Graves' disease. Measurement by the glucose clamp technique and continuous indirect calorimetry.

Insulin sensitivity was measured in a group of seven thyrotoxic patients and in a group of seven normal subjects by means of the glucose clamp technique. Infusion of insulin at a rate of 0.80 +/- 0.05 mU/kg X min in the hyperthyroid patients and of 0.55 +/- 0.04 mU/kg X min in the control group was performed to obtain a steady-state plasma insulin concentration of approximately 50 microU/ml. Substrate oxidation rates were measured in the postabsorptive state and during the 2 h of the clamp by means of continuous indirect calorimetry. In the postabsorptive state, hyperthyroid patients presented a preferential oxidation of lipids. During the period 60-120 min of the clamp, mean plasma glucose (92 +/- 2 versus 93 +/- 2 mg/dl), insulin (50 +/- 5 versus 58 +/- 3 microU/ml), and total glucose metabolism (5.8 +/- 0.7 versus 6.1 +/- 0.3 mg/kg X min) were similar in the hyperthyroid patients and the control subjects. The rate of glucose oxidation was higher in hyperthyroid patients than in control subjects (4.3 +/- 0.5 versus 2.2 +/- 0.2 mg/kg X min, P less than 0.001), while that of lipid oxidation was similar in both groups (0.6 +/- 0.2 versus control 0.7 +/- 0.1 mg/kg X min). The calculated metabolic clearance rate of insulin was markedly higher in the hyperthyroid patients (1144 +/- 132 ml/min) than in the normal subjects (812 +/- 56 ml/min, P less than 0.025). It is concluded that insulin sensitivity is not altered in the thyrotoxic state. The major route of insulin-stimulated glucose disposal in the hyperthyroid patients appears to be glucose oxidation.

Modifications of glucose storage and oxidation in nonobese diabetics, measured by continuous indirect calorimetry.

A new application of continuous indirect calorimetry is described for measuring the disposal of a glucose load. In a group of 10 normal subjects, 3 h after a 100 g oral glucose load, 20 g glucose was oxidized at basal rate, 19 g in response to the load and 63 g stored, while a decrease of 2 g was observed in the glucose space (GS). In a group of four type I, insulin-dependent diabetics, both glucose oxidation (9 g at the basal rate and 4 g in response to the load) and glucose storage (9 g) were markedly decreased, with the remainder either being lost in the urine (36 g) or remaining in the glucose space (42 g). In a group of eight nonobese type II, non-insulin-dependent diabetics, glucose oxidation both in the basal rate and in response to the load was slightly decreased (13 and 14 g, respectively) and glucose storage decreased to 40 g. These results suggest that, in type I diabetics, complete insulin deficiency seriously impairs two major mechanisms regulating glucose homeostasis, i.e., glucose storage and oxidation, while, in type II diabetics, the remaining insulin secretion attentuates these disturbances.

Role of lipid oxidation in pathogenesis of insulin resistance of obesity and type II diabetes.

Increased lipid oxidation is generally observed in subjects with obesity and diabetes and has been suggested to be responsible for the insulin resistance associated with these conditions. We measured, by continuous indirect calorimetry, lipid and glucose oxidation and nonoxidative glucose disposal in 82 obese subjects during a 100-g oral glucose tolerance test (OGTT) and in 26 during a euglycemic insulin (40 mU.min-1.m-2) clamp. The obese subjects were subdivided into those with normal glucose tolerance (group A), those with impaired glucose tolerance (group B), and those with overt diabetes (group C). Forty-five healthy nonobese subjects were subdivided into a young and an older control group, which were age-matched to the nondiabetic obese (groups A and B) and diabetic obese (group C) subjects, respectively. In the postabsorptive state, as well as in response to insulin stimulation (both OGTT and insulin clamp), lipid oxidation was significantly increased in all three obese groups in comparison with either young or older controls. Basal glucose oxidation was significantly decreased in obese nondiabetic and obese glucose--intolerant subjects (groups A and B) compared with age-matched controls. During the OGTT and during the insulin clamp, insulin-stimulated glucose oxidation was decreased in all three obese groups. In contrast, nonoxidative glucose disposal was markedly inhibited in nondiabetic and diabetic obese patients during the euglycemic insulin clamp but not during the OGTT. After glucose ingestion, nonoxidative glucose uptake was normal in nondiabetic obese and glucose-intolerant obese subjects and decreased in diabetic obese subjects. Statistical analysis revealed that lipid and glucose oxidation were strongly and inversely related in the basal state, during euglycemic insulin clamp, and during OGTT. The negative correlation between lipid oxidation and nonoxidative glucose uptake, although significant, was much weaker. Fasting and post-OGTT hyperglycemia were the strongest (negative) correlates of nonoxidative glucose disposal in both single and multiple regression models. We conclude that 1) reduced glucose oxidation and reduced nonoxidative glucose disposal partake of the insulin resistance of nondiabetic obese and diabetic obese individuals; 2) hyperglycemia provides a compensatory mechanism for the defect in nonoxidative glucose disposal in nondiabetic obese subjects; however, this compensation is characteristically lost when overt diabetes ensues; and 3) increased lipid oxidation may contribute, in part, to the defects in glucose oxidation and nonoxidative glucose uptake in obesity.

Energy and substrate metabolism in obesity and postobese state.

The total energy expenditure (EE) of human beings is represented by basal metabolic rate (which corresponds to 60-70% of EE), dietary-induced thermogenesis (10% of EE), and the energy expended in physical activity (20-30% of EE). Obese individuals have an increased total EE compared with lean subjects; this increase is essentially due to an increased lean body mass concomitant with obesity, and is completely reverted after weight loss. Glucose-induced thermogenesis (GIT), measured during an oral glucose tolerance test (OGTT) or hyperinsulinemic-euglycemic clamps, has been found to be decreased in obese individuals, although some discrepancy exists between studies. The observed decreases in GIT show a gradation, increasing progressively from obese patients with normal glucose tolerance to obese patients with impaired glucose tolerance (IGT) to obese patients with non-insulin-dependent diabetes mellitus (NIDDM) and an increased insulin response after OGTT to obese patients with NIDDM and a hypoinsulinemic response after OGTT. The defect in GIT appears to be related to impairment in nonoxidative glucose storage and with the degree of insulin resistance. Obese patients after weight loss show a further decrease in GIT after OGTT or during a euglycemic clamp, which remains unclear. Obese patients have an increased basal lipid oxidation and a decreased suppression of lipid oxidation after OGTT or during a euglycemic clamp. Glucose oxidation and storage are both markedly decreased during a euglycemic clamp. In contrast, the defect in glucose storage is less apparent after OGTT, due to the compensatory effect of hyperglycemia and hyperinsulinemia.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Prolonged corticotropic action of synthetic human ACTH in man.

The corticotropic activities of synthetic human ACTH (revised structure), synthetic porcine ACTH (unrevised structure) and synthetic 1-24ACTH were compared in 8 normal men by measuring the magnitude and duration of the elevation of plasma 11-hydroxy-corticosteroids following the injection of 1 mg of the peptides. The duration of response was significantly longer after human ACTH than following porcine or 1-24ACTH, although the initial responses were identical. This difference was noted after both intramuscular and intravenous administration. The data suggest that the carboxyterminal of the ACTH peptide is of some importance for biological activity and that biological species specificity may exist.

Study on the relationship between plasma prolactin levels and androgen metabolism in man.

The purpose of the study was to investigate the effect of hyperprolactinemia on the metabolism of androgens in man. A group of 6 normal men was treated for 4 consecutive days, on separate periods, with Sulpiride which is known to raise plasma prolactin (PRL) concentration. The effect of the treatment on plasma steroids was verified in basal conditions and under stimulation by HCG. In the controls, a parallel rise in testosterone (T) and dihydrotestosterone (DHT) was observed in response to HCG stimulation. In experimental hyperprolactinemia, the rise in T in response to HCG, similar to that of the controls, was accompanied by a markedly diminished rise in DHT. Similar results were observed in a patient with hyperprolactinemia following apparent accidental section of the pituitary stalk. These data demonstrate the interference of increased levels of PRL in the metabolism of testosterone into the active DHT form by 5alpha-reductase. They suggest that this mechanism could possibly impair the gonadal function in man.

Study of glucose and lipid metabolism by continuous indirect calorimetry in Graves' disease: effect of an oral glucose load.

Glucose and lipid metabolism were studied in 12 patients with hyperthyroid Graves' disease for 3 h during an oral glucose tolerance test (100 g) by continuous indirect calorimetry. In the postabsorptive state, glucose oxidation was not different from that in normal subjects, but lipid oxidation was significantly increased. Impaired glucose tolerance was found, but total glucose oxidation increased after the glucose load to 47.1 +/- 2.0 (+/- SEM) vs. 33.4 +/- 1.4 g/3 h in the control group (P less than 0.001). Total glucose oxidation corresponded, in hyperthyroid patients, to the highest rate obtained with progressively increasing insulin and glucose administration in normal man. Glucose storage was clearly lower in hyperthyroid patients. After treatment in 7 patients, glucose tolerance improved significantly, and the metabolic patterns almost normalized. In the 12 hyperthyroid patients and the 7 patients after treatment (n = 19), a correlation was found between total serum T3 concentration and both basal lipid oxidation and suprabasal glucose oxidation. It is concluded that the decrease in glucose tolerance in hyperthyroidism cannot be explained by an alteration in glucose oxidation, but, rather, by a defect in nonoxidative glucose uptake in the periphery.

Free cortisol index: a rapid and simple estimation of free cortisol in human plasma.

A rapid and simple method for the estimation of free (nonprotein-bound) cortisol in human plasma is described. Total plasma cortisol (F) was determined by a competitive protein binding assay. An estimate of the saturation of Corticosteroid Binding Globulin was obtained by the use of "charcoal cortisol uptake" (CFU). "Charcoal cortisol uptake ratio" (CFUR) was defined as the ratio of the CFU of the unknown plasma to that of a reference serum pool. Free cortisol index (FFI) was calculated as (total plasma F) times (CFUR). Percent free cortisol and free cortisol concentration (FF) was determined by equilibrium dialysis at 37 C. 169 plasma samples with an F range of 0.8-61.2 mug/100 ml from 18 normal, 10 ACTH-stimulated, 17 estrogen-treated and 12 pregnant subjects were analyzed. A highly significant correlation between FFI and FF was found (r = 0.952). Inter-assay coefficients of variation were 7% for total plasma F and 3.5% for CFU. The method allows the rapid processing of large numbers of samples and can be performed on 0.2 ml of plasma.