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Biomedical subjects

Franz J Wiedermann

Publications and source records attributed to Franz J Wiedermann.

8 recordsLinked to original sources
PubMed2006

Review on the importance of an emergency kit for physicians in out-of-hospital emergencies.

The importance of an emergency kit for private use by emergency physicians was evaluated. Self-reporting questionnaires were used to assess the satisfaction of emergency physicians who were given a specially adjusted emergency kit for 3 years. Of 73 emergency physicians, 52.1% used the kit at least once during a 3-year interval. Physicians who already used the emergency kit responded more frequently to the importance of having private emergency equipment than those who did not. The kit's low weight and assortment of equipment including ventilation equipment were given higher ratings by users. The majority of physicians regarded a maintenance interval of 6-12 months as sufficient for the emergency equipment. In conclusion, the private emergency kit was used by more than half of the study participants at least once during a 3-year study period. Emergency physicians who used the emergency kit gave it higher ratings than did non-users.

Attitude of Health Personnel↗
PubMed2004

Alveolar granulocyte colony-stimulating factor and alpha-chemokines in relation to serum levels, pulmonary neutrophilia, and severity of lung injury in ARDS.

OBJECTIVES: To determine granulocyte colony-stimulating factor (G-CSF), epithelial neutrophil-activating peptide (ENA)-78, and interleukin (IL)-8 in BAL fluid (BALF), epithelial lining fluid (ELF), and serum for establishing the concentration gradient of G-CSF, ENA-78, and IL-8 between the blood and the alveolar space in ARDS and acute lung injury (ALI); and to evaluate the relationship of G-CSF, IL-8, and ENA-78 to pulmonary neutrophilia and severity of lung injury. DESIGN: Prospective study. SETTING: An adult trauma/surgical ICU. PATIENTS: Nineteen patients with ARDS and 10 patients with ALI. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: BAL and blood sampling simultaneously within 12 h and 24 h after onset of ARDS/ALI; G-CSF was detected in BALF in 18 of 19 patients with ARDS, in 7 of 10 patients with ALI, and in all serum samples. G-CSF in BALF and serum was significantly higher in ARDS than in ALI. ENA-78 was detected in BALF in 14 of 19 patients with ARDS, in 8 of 10 patients with ALI, and in serum of all patients. Levels in BALF and serum were not different between ARDS and ALI. IL-8 was detected in all patients; concentrations in BALF in ARDS were significantly higher than in ALI. Concentrations of G-CSF, ENA-78, and IL-8 in ELF were significantly higher than in serum. G-CSF in BALF and serum and IL-8 in BALF correlated positively with pulmonary neutrophilia. G-CSF in serum and IL-8 in BALF correlated negatively with PaO(2)/fraction of inspired oxygen (FIO(2)) ratio. However, ENA-78 did not show a correlation with neutrophil count or with PaO(2)/FIO(2) ratio. CONCLUSIONS: G-CSF may be pathophysiologically important for accumulation and activation of neutrophils in ARDS. Local G-CSF production is the likely driving force for neutrophils rather than elevation of circulating levels. In comparison to ENA-78, IL-8 seems to be the predominant neutrophil chemoattractant in the early phase of ARDS.

Adult↗
PubMed2003

Association of endogenous G-CSF with anti-inflammatory mediators in patients with acute respiratory distress syndrome.

Upregulation of the anti-inflammatory mediators, soluble tumor necrosis factor-alpha receptors I and II (sTNFRI/RII) and interleukin-1 receptor antagonist (IL-1RA), by granulocyte colony-stimulating factor (G-CSF) may contribute to the pathophysiology of lung injury. We determined the relation of endogenous G-CSF to proinflammatory and anti-inflammatory mediators in bronchoalveolar lavage fluid (BALF) and serum of patients with acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). Nineteen patients with ARDS and 10 with ALI were included in this prospective investigation. BAL was performed within 12 h and 24 h after onset of lung injury. Concentrations of G-CSF, TNF-alpha, IL-6, sTNFRI and sTNFRII, IL-1RA and IL-10 in BALF as well as in serum were determined by ELISA. G-CSF was associated with alveolar neutrophilia. Results in patients with ARDS and ALI exhibited significant positive correlations in BALF of G-CSF levels with that of IL-6, sTNFRII, and IL-1RA and of G-CSF levels in serum with that of serum IL-6, IL-1RA, and IL-10. Given the potential of G-CSF to directly induce anti-inflammatory cytokines in vitro, significant associations of endogenous G-CSF levels with these mediators early in the development of severe lung injury suggest an endogenous anti-inflammatory role of G-CSF in vivo.

Adolescent↗
PubMed2002

Migration of human monocytes in response to procalcitonin.

OBJECTIVE: Circulating serum levels of procalcitonin rise significantly during bacterial infection. Because calcitonin is known to be a monocyte chemoattractant, we investigated whether procalcitonin, a prohormone of calcitonin, also affects leukocyte migration. DESIGN: Prospective, controlled in vitro study. SETTING: University research laboratories. INTERVENTIONS: Forearm venous blood polymorphonuclear neutrophils and monocytes were isolated from healthy human donors. Cell migration was assessed in a blindwell chemotaxis chamber. The distance of migration into filter micropores was measured. To biochemically confirm functional data on cell migration, effects of procalcitonin on cellular levels of cyclic adenosine monophosphate were measured by high-performance liquid chromatography. MEASUREMENTS AND MAIN RESULTS: Both procalcitonin and calcitonin elicited dose-dependent migration of monocytes at concentrations from the femtomolar to the micromolar range. Neutrophils did not migrate toward procalcitonin or calcitonin, nor was their oxygen free radical release affected as measured fluorimetrically. Checkerboard analysis of monocyte locomotion revealed procalcitonin-induced migration as true chemotaxis. Pretreatment of monocytes with procalcitonin or calcitonin rapidly deactivated their migratory response to formyl-Met-Leu-Phe, and both also induced homologous deactivation of migration. Procalcitonin elevated levels of cyclic adenosine monophosphate in monocytes. CONCLUSIONS: In vitro procalcitonin is a monocyte chemoattractant that deactivates chemotaxis in the presence of additional inflammatory mediators. Procalcitonin stimulates cyclic adenosine monophosphate production in monocytes, suggesting that its action may be specific and comparable with calcitonin, which exerts similar functions.

Calcitonin↗
PubMed2002

Involvement of cyclic adenosine monophosphate-dependent protein kinase A and pertussis toxin-sensitive G proteins in the migratory response of human CD14+ mononuclear cells to katacalcin.

Katacalcin (KC) belongs to a small family of polypeptides that are encoded by the calc-1 gene and also include calcitonin (CT) and procalcitonin NH2-terminal cleavage peptide (N-ProCT). Biological roles of KC or N-ProCT are unknown. To determine whether these polypeptides affect leukocyte function, forearm venous blood polymorphonuclear neutrophils and CD14+ peripheral blood mononuclear cells (PBMCs) were isolated from healthy human donors. Cell migration was assessed in a blindwell chemotaxis chamber using nitrocellulose micropore filters. Cellular levels of cyclic adenosine monophosphate (cAMP) were measured by HPLC; activation of protein kinase A was studied by Western blot. Fluorochrome-labeled peptide binding to cells was studied by fluorescence-activated cell sorting (FACS) and intracellular calcium transients were studied by confocal microscopy with FLUO-3. KC elicited concentration-dependent migration of CD14+ PBMC at concentrations from the atomolar to the micromolar range and deactivated attractant-induced chemotaxis. CT N-terminal flanking peptide had no such effect. Neutrophils did not migrate toward any of those peptides and their oxygen-free radical release was not affected as measured fluorometrically. Functional responses of CD14+ PBMC to KC correlated to forskolin-sensitive cAMP accumulation in cells and were inhibited by protein kinase A inhibitor (PKI) and Rp diastereomer of adenosine 3',5'-cyclic monophosphorothioate. Treatment of CD14+ PBMC with KC activated protein kinase A(C alpha). Intracellular calcium was decreased with CT, KC, and procalcitonin (PCT). Binding studies showed that KC might share the binding site with CT and PCT. Data indicate that KC regulates human CD14+ PBMC migration via signaling events involving protein kinase A-dependent cAMP pathways.

Adult↗