Creating new littoral zones in a shallow lake to forward-restore an aquatic food web.

Current rates of habitat loss require science-based predictions on how to restore or newly create lost habitat types. In aquatic ecosystems, littoral zones are key habitats for food web functioning, but they are often replaced by unnatural steep shorelines for water safety. To reverse this trend, knowledge is needed on how to successfully (re)create littoral zones. We quantified the response of an aquatic food web to the large-scale creation of new heterogeneous littoral habitats in shallow lake Markermeer, the Netherlands. Lake Markermeer was formed by dike construction in a former estuary, which created a heavily modified homogeneous 70,000 ha turbid lake lacking littoral habitat. Fish and bird populations declined over the last decades, but classical restoration via return to former marine conditions would compromise water safety and the large spatial scale prohibited biodiversity offsets. Therefore, an innovative "forward-looking restoration" approach was adopted: a 1000 ha archipelago called "Marker Wadden" was constructed without using a historic reference situation to return to. This aimed bottom-up stimulation of the aquatic food web by adding missing gradual land-water transitions and sheltered waters to the lake. After four years, new sheltered shorelines had become vegetated if they were constructed from nutrient-rich sediments. Exposed and sandy shorelines remained free of vegetation. Zooplankton community diversity increased in sheltered waters due to bottom-up processes, which increased food availability for higher trophic levels, including young fish. The creation of sheltered waters increased macroinvertebrate densities threefold, with sediment type determining the community composition. The archipelago became new nursery habitat for 13 of the 24 fish species known to occur in the lake, with up to 10-fold higher abundances under sheltered conditions. We conclude that modifying abiotic conditions can stimulate multiple trophic levels in aquatic food webs simultaneously, even in heavily modified ecosystems. This provides proof-of-principle for the forward-looking restoration approach.

Interferon-gamma inhibits growth of human neuroendocrine carcinoma cells via induction of apoptosis.

Although biotherapy of gastroenteropancreatic neuroendocrine tumors (NET) provides excellent control for the hypersecretion syndrome, tumor regression is rarely observed, implying the need for novel antiproliferative strategies. Here, we demonstrate that human pancreatic QGP-1 NET cells express functionally intact interferon-gamma (IFN-gamma) receptors and downstream effectors, including the putative tumor suppressor interferon regulatory factor-1 (IRF-1). IFN-gamma treatment profoundly inhibited anchorage-dependent and anchorage-independent growth of QGP-1 cells. Concomitant with the onset of growth inhibition, apoptotic cells were detected in cell cycle analyses of IFN-gamma treated cultures. Apoptosis was confirmed by evaluation of DNA fragmentation and PARP cleavage. Immunoblots of IFN-gamma treated QGP-1 cells revealed a substantial upregulation of caspase-1, followed by the appearance of active proteolytic fragments of caspase-3, suggesting that autocatalytic activation of caspase-1 might initiate the caspase cascade. Apoptosis induction by IFN-gamma was also observed in two of four primary cultures established from tumors of patients with for- and midgut NETs, respectively. Taken together our results characterize IFN-gamma as a potent proapoptotic stimulus in a subset of gastrointestinal NETs and suggest an IRF-1 mediated induction of caspase-1 as a relevant underlying mechanism. Based on these results, the potential of IFN-gamma in experimental biotherapeutic treatment of NETs can be further explored.

Use of DNA fingerprinting in international source case finding during a large outbreak of tuberculosis in The Netherlands.

SETTING: Tuberculosis outbreak in a low prevalence country. OBJECTIVE: Description of an international source tracing process in which restriction fragment length polymorphism (RFLP) analysis played an essential role. DESIGN: In 1993 a large scale source tracing process was initiated in Harlingen, a harbour town in the north of The Netherlands, after a child with tuberculous meningitis was reported for which no source could be identified. Traditional contact tracing followed the detection of sources of infection. RFLP was used to map the tuberculosis transmission and identify the source case. RESULTS: The investigation extended from the north to several places in the west of The Netherlands. In total 6519 persons were screened; there were 276 infections, among which 49 cases of active tuberculosis were identified. RFLP analysis of Mycobacterium tuberculosis isolates from all 28 culture positive patients showed the 'Harlingen' type DNA fingerprint. After 5 months source tracing led to the identification of the source case in the United Kingdom. Up to June 1996 altogether 37 patients (The Netherlands 28; the UK 7; Surinam 1; Morocco 1) were found to have isolates with the Harlingen type DNA pattern. Despite a thorough evaluation, in 5 of the 37 patients no relation to the source case or the outbreak in Harlingen could be established. CONCLUSION: RFLP typing proved a very useful instrument in guiding the process of international source tracing and contact investigation.

[Duplex ultrasound imaging of vascularization in venous thrombosis]. / Duplexsonographische Darstellung der Vaskularisation venöser Thrombosen.

Vascularization of venous thrombosis. The degree of organisation of an intravenous thrombus is important for therapeutic interventions and the postthrombotic damage. Changes in echogenicity have already been described in B-mode sonography. We investigated 7 thrombosis in the jugular vein looking for intra-thrombotic vessels that occur during the organisation. In 3 thrombosis arterial vessels were found from the 12th to the 17th day. Such arterial vessels appeared only in a short range of time and only in circumscript areas of the thrombus. The intra-vitam documentation of arterial vessels in an organizating intravenous thrombus may give information about the mechanism of thrombogenesis and about the degree of organisation.

[Border-crossing source tracing in tuberculosis via DNA fingerprint technique]. / Grensoverschrijdende bronopsporing bij tuberculose door DNA-'fingerprint'-techniek.

OBJECTIVE: Description of the value of modern DNA analysis ('restriction fragment length polymorphism'; RFLP) as a method for mapping tuberculosis transmission. DESIGN: Descriptive. SETTING: Social Health Service Noord-Friesland, the Netherlands. METHOD: A large-scale tuberculosis investigation was conducted in Harlingen in 1993 when a 2,5 year old patient with tuberculous meningitis was reported. Source tracing and contact tracing extended from Harlingen to the west of the Netherlands and even abroad. Modern DNA analysis (RFLP) was used to map the tuberculosis transmission. RESULTS: A total of 6519 persons were screened and 276 infected people were identified, of whom 49 were suffering from active tuberculosis. RFLP analysis showed in 27 of them a 'Harlingen' type Mycobacterium tuberculosis DNA pattern identical to that of the index patient. The source patient was finally traced in England. By the end of 1994 3 more patients were found with the same DNA pattern; their relation with the source patient and the outbreak of tbc remained unrevealed. CONCLUSION: The Harlingen outbreak was extensive and characterized by time-consuming source tracing. Modern DNA analysis proved to be a very useful instrument in identifying the source case.

Plasma cytokines following thermal injury and their relationship with patient mortality, burn size, and time postburn.

We measured plasma levels of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), and interleukin-6 (IL-6) following thermal injury. Cytokine levels in the plasma of 27 burned patients were serially screened by ELISA and compared with cytokine levels in 16 healthy laboratory employees. The relationships between cytokine concentrations and patient mortality, burn size, and time postburn were examined. Plasma samples with detectable amounts of IL-1 beta and IL-6 were significantly more frequent in burned patients than in controls, whereas TNF alpha was undetectable in most plasma samples. All nonsurviving burned patients had detectable IL-6 levels; these were significantly higher than those of surviving patients. The IL-1 beta and IL-6 concentrations were highest during the first week after injury and declined over time. The IL-1 beta concentrations were positively correlated with burn size. These findings suggest that IL-1 beta and IL-6 may influence metabolic and immunologic responses in the first few weeks following thermal injury. Tumor necrosis factor alpha was transiently elevated in a small subpopulation of burned patients with no obvious relationship to burn size or time postburn.

Plasma cytokines after thermal injury and their relationship to infection.

OBJECTIVE: The relationship of plasma cytokine levels to infection, core temperature, and to one another in patients with thermal injury was examined. SUMMARY BACKGROUND DATA: The response to infection has been associated with cytokines such as interleukin 1 beta (IL1 beta), interleukin 6 (IL6), and tumor necrosis factor alpha (TNF alpha), and these cytokines have been studied in various inflammatory diseases. The authors previously reported that patients with thermal injury have elevated IL1 beta and IL6 plasma levels and that these cytokines may play different roles in the response to thermal injury. METHODS: IL1 beta, IL6, and TNF alpha were measured by enzyme-linked immunosorbent assay (ELISA) in serial samples of plasma from 27 patients. RESULTS: IL6 and TNF alpha levels were increased in severely infected patients as compared to patients who remained free of infection, and the IL6 level was higher in infected patients who died than those who survived. There was no apparent relationship between IL1 beta levels and infection. IL6 and IL1 beta were positively correlated with core temperature. The correlations between IL6 and IL1 beta, between IL6 and TNF alpha, and between TNF alpha and IL1 beta were significant. CONCLUSIONS: These results suggest that IL6 and TNF alpha play a role in the response of burned patients to infection.

The effects of thermal injury on serum interleukin 1 activity in rats.

Interleukin 1 (IL-1) is present in the blood of burned patients but its pathophysiologic role is not fully understood. Rat models would be useful research tools, if this cytokine could be identified in a complex fluid like blood. We describe a methodology, which revealed IL-1 activity from the serum of burned rats. Serum was collected from 37 rats with 30% total body surface burns and 9 unburned controls. To vary the burn response, the wounds of 17 rats were seeded with nonvirulent Pseudomonas aeruginosa at the time of injury. IL-1 activity was assessed by its capacity to induce IL-2 secretion in murine lymphoma cells (LBRM-33-1A5). Only after the serum had been fractionated, concentrated, and dialyzed, was IL-1 activity uncovered. Sera from burned rats contained five times more IL-1 activity than those from control animals (p < 0.05). There was no difference in serum IL-1 activity between burned and burn-seeded animals. The IL-1 activity was heat labile, and not produced by P. aeruginosa endotoxin, TNF-alpha, or endogenous IL-2 in rat serum. These results confirm that serum IL-1 levels are increased following thermal injury, and that there is no apparent relationship between IL-1 levels and infection. The serum preparation scheme presented in this study offers a reasonable approach to the measurement of serum IL-1 levels in rat models of disease and injury.