IL-6 and G-CSF levels in amniotic fluid during the second trimester in normal and abnormal pregnancies

Activity levels of cytokines were measured by stimulation of the cell lines NFS-60, 7TD1, and TF-1. In 39 samples of amniotic fluid, levels of Granulocyte-Stimulating Factor (G-CSF) were 1434±2063 (mean±SD) and of Interleukin (IL-6) 546±1071 pg/ml; Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) was not detectable. IL-6 was correlated to G-CSF (r=0.3; p=0.003). G-CSF (p=0.0002) and IL-6 (p=0.006) were influenced by Alpha-Fetoprotein (AFP) and G-CSF by rhesus-incompatibility (p=0.0004). These findings suggest that cytokines such as IL-6 and G-CSF play some role in physiological and pathological pregnancy.Abbreviations G-CSF granulocyte-colony stimulating factor - GM-CSF granulocyte-macrophage colony stimulating factor - M-CSF macrophage-colony stimulating factor - CSF colonystimulating factor - IL-6 interleukin-6 - IL-11 interleukin-11 - AFP alpha-fetoprotein - NFS-60 cell line - 7TD1 cell line - TF-l cell line - rh recombinant human - MTT 3-(4,5-dimethylthiazol2-yl)-2,5-diphenyl tetrazolium bromide - FCS fetal calf serum - RPMI 1640 nutrient solution - ATCC American Tissue Culture Collection Correspondence to: E. Weimann     

Sonographic diagnosis of an aneurysm of the superior mesenteric artery

This is a report on a patient with a mycotic aneurysm of the superior mesenteric artery proved by histology. Because of a marked intolerance of contrast media we abstained from angiography. It is shown that real-time sonography gives a definite diagnosis, if the multiple vascular structures of the upper abdomen are precisely identified.     

Congenital NOS2 deficiency protects mice from LPS-induced hyporesponsiveness to inhaled nitric oxide

BACKGROUND: In animal models, endotoxin (lipopolysaccharide) challenge impairs the pulmonary vasodilator response to inhaled nitric oxide (NO). This impairment is prevented by treatment with inhibitors of NO synthase 2 (NOS2), including glucocorticoids and L-arginine analogs. However, because these inhibitors are not specific for NOS2, the role of this enzyme in the impairment of NO responsiveness by lipopolysaccharide remains incompletely defined. METHODS: To investigate the role of NOS2 in the development of lipopolysaccharide-induced impairment of NO responsiveness, the authors measured the vasodilator response to inhalation of 0.4, 4, and 40 ppm NO in isolated, perfused, and ventilated lungs obtained from lipopolysaccharide-pretreated (50 mg/kg intraperitoneally 16 h before lung perfusion) and untreated wild-type and NOS2-deficient mice. The authors also evaluated the effects of breathing NO for 16 h on pulmonary vascular responsiveness during subsequent ventilation with NO. RESULTS: In wild-type mice, lipopolysaccharide challenge impaired the pulmonary vasodilator response to 0.4 and 4 ppm NO (reduced 79% and 45%, respectively, P < 0.001), but not to 40 ppm. In contrast, lipopolysaccharide administration did not impair the vasodilator response to inhaled NO in NOS2-deficient mice. Breathing 20 ppm NO for 16 h decreased the vasodilator response to subsequent ventilation with NO in lipopolysaccharide-pretreated NOS2-deficient mice, but not in lipopolysaccharide-pretreated wild-type, untreated NOS2-deficient or untreated wild-type mice. CONCLUSIONS: In response to endotoxin challenge, NO, either endogenously produced by NOS2 in wild-type mice or added to the air inhaled by NOS2-deficient mice, is necessary to impair vascular responsiveness to inhaled NO. Prolonged NO breathing, without endotoxin, does not impair vasodilation in response to subsequent NO inhalation. These results suggest that NO, plus other lipopolysaccharide-induced products, are necessary to impair responsiveness to inhaled NO in a murine sepsis model.     

Inhalation of the Phosphodiesterase-3 Inhibitor Milrinone Attenuates Pulmonary Hypertension in a Rat Model of Congestive Heart Failure

Background: Most patients with congestive heart failure (CHF) develop pulmonary venous hypertension, but right ventricular afterload is frequently further elevated by increased pulmonary vascular resistance. To investigate whether inhalation of a vasodilatory phosphodiesterase-3 inhibitor may reverse this potentially detrimental process, the authors studied the effects of inhaled or intravenous milrinone on pulmonary and systemic hemodynamics in a rat model of CHF.

Methods: In male Sprague-Dawley rats, CHF was induced by supracoronary aortic banding, whereas sham-operated rats served as controls. Milrinone was administered as an intravenous infusion (0.2-1 [mu]g [middle dot] kg body weight-1 [middle dot] min-1) or by inhalation (0.2-5 mg/ml), and effects on pulmonary and systemic hemodynamics and lung water content were measured.

Results: In CHF rats, intravenous infusion of milrinone reduced both pulmonary and systemic arterial blood pressure. In contrast, inhalation of milrinone predominantly dilated pulmonary blood vessels, resulting in a reduced pulmonary-to-systemic vascular resistance ratio. Repeated milrinone inhalations in 20-min intervals caused a stable reduction of pulmonary artery pressure. No hemodynamic effects were detected when 0.9% NaCl was administered instead of milrinone or when milrinone was inhaled in sham-operated rats. No indications of potentially adverse effects of milrinone inhalation in CHF, such as left ventricular volume overload, were detected. Moreover, lung edema was significantly reduced by repeated milrinone inhalation.     

Granulocyte Colony-stimulating Factor Supports Liver Regeneration in a Small-for-size Liver Remnant Mouse Model

Experimental partial hepatectomy of more than 80% of the liver weight bears an increased mortality in rodents, due to impaired hepatic regeneration in small-for-size liver remnants. Granulocyte colony-stimulating factor (G-CSF) promotes progenitor cell expansion and mobilization and also has immunomodulatory properties. The aim of this study was to determine the effect of systemically administered G-CSF on liver regeneration and animal survival in a small-for-size liver remnant mouse model. Mice were preconditioned daily for 5 days with subcutaneous injections of 5 μg G-CSF or aqua ad injectabile. Subsequently, 83% partial hepatectomy was performed by resecting the median, the left, the caudate, and the right inferior hepatic lobes in all animals. Daily sham or G-CSF injection was continued. Survival was significantly better in G-CSF-treated animals (P < 0.0001). At 36 and 48 h after microsurgical hepatic resection, markers of hepatic proliferation (Ki67, BrdU) were elevated in G-CSF-treated mice compared to sham injected control animals (P < 0.0001) and dry liver weight was increased (P < 0.05). G-CSF conditioning might prove to be useful in patients with small-for-size liver remnants after extended hepatic resections due to primary or secondary liver tumors or in the setting of split liver transplantation. Presented at the Forty-seventh Annual Meeting of The Society for Surgery of the Alimentary Tract, Los Angeles, CA, May 14–19, 2006 (poster presentation).     

Initial fixation strength of a new hybrid technique for femoral ACL graft fixation: the bone wedge technique

Background Aperture fixation with interference screws matching the diameter of the tunnel is associated with the risk of graft laceration and graft rotation. Hypothesis A hybrid fixation technique (extracortical and aperture fixation) with undersized interference screw placed behind a bone wedge provides a higher fixation strength as aperture fixation with a screw alone matching the size of the tunnel. Study design Experimental laboratory study. Methods We evaluated the initial fixation strength (single cycle and cyclic loading tests) of hybrid and interference screw aperture fixation using different sized interference screws in porcine knees. Results Analysis of yield load, maximum load and stiffness in the single cycle loading test showed no statistically significant differences for hybrid fixation with a 1 mm undersized screw and aperture fixation with a screw matching the size of the tunnel. The use of an undersized screw alone resulted in low fixation strength. Conclusion The initial fixation strength of the hybrid technique with undersized screws is comparable to that of interference screw fixation matching the size. Clinical relevance The new “bone wedge fixation” is an alternative for ACL graft fixation without the risk of graft laceration and graft rotation.     

Emptying of the gastric substitute after total gastrectomy. Jejunal interposition versus Roux-y esophagojejunostomy.

Emptying of the gastric substitute and small bowel transit time of a 99mTc-labeled solid test meal were measured in 20 tumor-free patients 13 to 63 (median, 35) months after total gastrectomy with Roux-y (n = 11) and jejunal interposition (n = 9) reconstruction. The emptying half-times ranged from 2 minutes to greater than 20 minutes. Rapid emptying was associated with dumping symptoms (p less than 0.03) and shorter orocoecal transit-time (p less than 0.05). Serum glucose concentrations rose more quickly in jejunal interposition, but the areas under the curve were identical in both groups. The median insulin-to-glucose ratio (areas under the curve) during the 20 minutes after the meal was 11.4 in jejunal interposition and 7.1 in Roux-y esophagojejunostomy (NS). Interposition cases had regained a significantly higher percentage (89%) of their premorbid weight than patients with Roux-y (78%; p less than 0.05). The weight/height2 ratio was above the 50th centile in 45% of interpositions, but below the 50th centile in all patients after the Roux-y mode of reconstruction (p less than 0.05). It is concluded that the emptying velocity of the gastric substitute has no impact on postoperative weight gain. The authors contend that the concept of a gastric substitute pouch is not supported by the findings of this study.     

Hyaluronan-independent adhesion of CD44H+ and CD44v10+ lymphocytes to dermal microvascular endothelial cells and keratinocytes.

We have recently shown the CD44 variant isoform 10 (CD44v10) to be expressed on reactive as well as malignant cutaneous lymphocytes; however, the functional consequences of CD44v10 expression on lymphocytes are not elucidated. By using appropriately transfected lymphatic cells we analyzed the role of CD44v10 on lymphocytes in cell-matrix adhesion and homotypic and heterotypic cell-cell adhesion assays. Despite a low binding affinity to hyaluronan, CD44v10-expressing lymphocytes exhibited heterotypic cell-cell adhesion to inflamed dermal microvascular endothelium and keratinocytes, as indicated by Stamper-Woodruff assays on tissue sections of delayed type hypersensitivity reactions and adhesion assays with cultured keratinocytes and cytokine-stimulated human dermal microvascular endothelial cells. Antibody-blocking assays excluded interaction of CD44v10 with the principal CD44 ligand hyaluronan as well as involvement of selectins or integrins in these heterotypic cell-cell adhesion assays. In contrast, cellular aggregation assays with fluorescence-labeled CD44v10- and CD44H-expressing lymphocytes revealed homotypic CD44v10/CD44v10 binding as well as binding of CD44v10 with CD44H. Heterotypic cell-cell adhesion assays with ultraviolet-A-irradiated CD44v-negative cytokine-stimulated endothelial cells demonstrated binding kinetics of CD44v10-expressing lymphocytes paralleling those of endothelial CD44H expression. These results imply that a hyaluronan-independent CD44v10/CD44H-mediated pathway is involved in lymphocyte infiltration into the dermis and epidermis of inflamed skin and suggest modulation of CD44H expression on inflamed dermal microvascular endothelium as a mechanism of ultraviolet-A-induced therapeutic effects on the skin.