Interventionelle Therapieverfahren bei akuter nekrotisierender Pankreatitis

The clinical course of acute pancreatitis is variable. Severe pancreatitis is observed in up to 20% of cases and is associated with high mortality rates of up to 40%. The most serious complication is the infection of the (peri-)pancreatic necroses. The therapeutic goal is debridement of the infected material. Whereas surgical methods still represent the gold standard, minimally invasive interventional approaches are gaining importance. This article reviews the different interventional procedures, particularly percutaneous, CT-guided drainage and necrosectomy. Furthermore, an overview of published studies about interventional therapy in patients with acute necrotizing pancreatitis is given.     

Outpatient triplet management: a contemporary review

The antepartum management of 198 women who were delivered of triplets between 1985 and 1988 is reviewed. Women were managed with the assistance of ambulatory perinatal nursing to provide outpatient surveillance. Modified bed rest, prophylactic tocolysis, and betamethasone were liberally used and patients were hospitalized only when obstetrically indicated. The most common antepartum complication was preterm labor (66.2%) and the success of therapy with tocolytic agents is described. The mean gestational age and birth weight at delivery were 33.6 +/- 3 weeks (mean +/- SD) and 1871 +/- 555 gm, respectively. Comparison of the gestational age distribution at delivery with previous reviews demonstrates fewer deliveries less than 29 weeks' gestation and significantly more deliveries between 32 and 37 weeks' gestation. Cesarean delivery occurred in 94% of the triplets, which eliminated birth order as a factor that affects survival. The corrected perinatal survival rate was 95% in this contemporary review of outpatient triplet management and represents a major improvement in the expected outcome for triplets.     

Discrimination between low dietary zinc and endotoxin exposure: a model study on weaning rats

To establish a parameter for zinc status that is independent of the occurrence of infection, we studied the effects of low dietary zinc and endotoxin in weaning rats 21 d after 65Zn intubation. We monitored aspects of zinc status (tissue zinc content, 65Zn distribution, and specific 65Zn activity in tissue) and 65Zn metabolism (absorption, excretion, and biologic half-life), as well as weight gain, feed conversion, and dietary zinc use. The low zinc diet induced classical deficiency with losses of bone zinc, resulting in lower content (7.4 versus 19.6 mumol) and higher spec act (17 versus 8 kBq/mumol). Other tissue-specific and plasma-specific activities were also higher (overall, 20 versus 8 kBq/mumol; plasma, 8 versus 4 kBq/mumol). Endotoxin caused lower total-plasma zinc (0.04 versus 0.05 mumol) but did not affect spec act (4 kBq/mumol); combined endotoxin and low-zinc diet caused low total-plasma zinc (0.01 mumol) and high spec act, as did the low-zinc diet alone (12 kBq/mumol). We conclude that plasma-spec act (or stable isotope enrichment) can serve as an index for nutritional zinc status during recurrent infection.     

Sports injury experiences from the Western Australian Sports Injury Cohort Study

OBJECTIVE: The Western Australian Sports Injury Study is the first prospective cohort study of sports injuries sustained during community-level sports participation in Australia. METHODS: The players were nonprofessional/non-elite participants of hockey, Australian football, basketball and netball from metropolitan Perth. Players completed a baseline questionnaire relating to their sports injury history, training practices, protective equipment use, demographic profile, general health and lifestyle factors. Sports participation and injury experiences were monitored by monthly telephone surveys over two consecutive five-month winter sporting seasons during 1997 and 1998. RESULTS: Of the 1,512 players recruited into the initial cohort, 966 (i.e. 64%) responded to at least 700% of the callback surveys over the two-year follow-up. Across all sports, the injury incidence rate was 16.1 injuries/ 1,000 exposure hours (both games and training). Injury rates were highest in Australian football and lowest in netball. Lower limb injuries were twice as common as those to the upper limb (67% vs. 31%). Three-quarters of injured players sought treatment from a health care practitioner. CONCLUSIONS AND IMPLICATIONS: This is the first longitudinal study of injuries to community-based sports participants in Australia. Compared with elite sports participants, the risk of injury is relatively low. The results provide valuable direction for the design and conduct of further aetiological studies.     

Increased arginase activity underlies allergen-induced deficiency of cNOS-derived nitric oxide and airway hyperresponsiveness

1. A deficiency of constitutive nitric oxide synthase (cNOS)-derived nitric oxide (NO), due to reduced availability of L-arginine, importantly contributes to allergen-induced airway hyperresponsiveness (AHR) after the early asthmatic reaction (EAR). Since cNOS and arginase use L-arginine as a common substrate, we hypothesized that increased arginase activity is involved in the allergen-induced NO deficiency and AHR. 2. Using a guinea-pig model of allergic asthma, we addressed this hypothesis by examining the effects of the specific arginase inhibitor N(omega)-hydroxy-nor-L-arginine (nor-NOHA) on the responsiveness to methacholine of isolated perfused tracheae from unchallenged control animals and from animals 6 h after ovalbumin challenge. Arginase activity in these preparations was investigated by measuring the conversion of L-[14C]arginine to [14C]urea. 3. Airways from allergen-challenged animals showed a 2 fold (P<0.001) increase in responsiveness to intraluminal (IL) administration of methacholine compared to controls. A similar hyperresponsiveness (1.8 fold, P<0.01) was observed in control airways incubated with the NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, 0.1 mM, IL), while L-NAME had no further effect on the airways from challenged animals. 4. Remarkably, 5 microM nor-NOHA (IL) normalized the hyperresponsiveness of challenged airways to basal control (P<0.001), and this effect was fully reversed again by 0.1 mM L-NAME (P<0.05). Moreover, arginase activity in homogenates of the hyperresponsive airways was 3.5 fold (P<0.001) enhanced compared to controls. 5. The results indicate that enhanced arginase activity contributes to allergen-induced deficiency of cNOS-derived NO and AHR after the EAR, presumably by competition with cNOS for the common substrate, L-arginine. This is the first demonstration that arginase is involved in the pathophysiology of asthma.     

Cyclin D3 activates Caspase 2, connecting cell proliferation with cell death

Precancerous cells that enter S phase without appropriate growth and viability factors undergo programmed cell death, suggesting that apoptosis may help guarantee organismic integrity [Evan, G. & Littlewood, T. (1998) Science 281, 1317-1322]. However, the connection between proliferation and cell death has remained unclear. Here, we show that the positive cell cycle regulator cyclin D3 [Matsushime H., Roussel M. F., Ashmun, R. A. & Sherr, C. J. (1991) Cell 65, 701-713] interacts with the death enzyme Caspase 2 [Wang, L., Miura, M., Bergeron, L., Zhu, H. & Yuan, J. (1994) Cell 78, 739-750]. Directed expression of cyclin D3 and Caspase 2 in human cells potentiated apoptosis compared with expression of Caspase 2 alone. Cyclin D3 expression increased the amount of cleaved (active) Caspase 2. We describe a PCR mutagenesis/ligation/two-hybrid/green fluorescent protein approach that facilitates the isolation of missense mutant proteins defective in interaction with particular partners absent other phenotypes or knowledge of the system. We used this approach to isolate Caspase 2 mutants that did not bind cyclin D3 (noninteractors). Noninteractors were sensitive to apoptosis-dependent proteolysis, but did not potentiate apoptosis. Noninteractors did not block apoptosis caused by wild-type Caspase 2. Our results are consistent with the idea that an interaction with cyclin D3 may stabilize Caspase 2, and suggest that a physical interaction between cyclin D3 and Caspase 2 connects the genetic networks that govern cell-cycle progression with those that govern cell death.     

The diffusion of information technology among health maintenance organizations

This article examines the information technology functions, staffing and cost, services provided, and advanced technologies among health maintenance organizations (HMOs) using a national sample of HMOs from mid-1995. HMOs have a well-developed capability to use data from administrative functions, such as claims processing. Nationally affiliated HMOs and HMOs in markets with greater HMO penetration support more IT functions. Relatively little work has been completed integrating clinical with administrative systems.