A Compression Kit of a Stocking and Three Superimposed Leggings Is Easy to Don and Dose Adjustable.

BACKGROUND: Forty percent of patients with chronic venous insufficiency (CVI) do not wear their indicated and prescribed compression stockings. Difficulties in donning and a feeling of constraint are the most common reasons for non-adherence. OBJECTIVE: The aim was to develop a compression stocking system that is easy to don and dose adjustable. METHODS: A modular compression stocking kit composed of an understocking and three superimposable leggings (SLLLs) was developed. Substocking pressures (P) at the thinnest part above the ankle (cB level) were 17 mm (understocking) + 15 + 10 + 10 mmHg (3 superimposed leggings; Hatra method). Twenty healthy subjects and 20 patients over 65 years with CVI donned the SLLL compression kit. P was measured in vivo (Picopress method) at the transition of the Achilles tendon to the calf muscle (level cB1) during rest and ankle movements (DSI; dynamic stiffness index) and compared with a strong compression stocking of 40 mmHg (S40). RESULTS: Twenty (20/20) patients aged over 65 with CVI (C4-6) successfully donned the SLLL compression kit without aid, compared with 12 (12/20) who were able to don the S40 without aid (p = .02). In vivo resting P at level cB1 was 34.3 mmHg (SLLL) compared with 37.3 mmHg (S40) (p = .1). The DSI was 16.1 (SLLL) compared with 17.9 (p = .79; S40; CVI group). CONCLUSION: The physical properties of the SLLL compression stocking kit correspond to the characteristics of a strong stocking at rest and exercise (DSI). The donning success rate is excellent (100%). A further potential advantage is that the SLLL leg compression kit is dose adjustable, according to indication or patient tolerance. Wearing comfort over periods of several days and clinical effectiveness need to be investigated in future trials.

Ethanol, ethyl and sodium pyruvate decrease the inflammatory responses of human lung epithelial cells via Akt and NF-κB in vitro but have a low impact on hepatocellular cells.

Increases in pro-inflammatory cytokine levels and tissue-infiltrating leukocytes have been closely linked to increased systemic and local inflammation, which result in organ injury. Previously, we demonstrated the beneficial and hepatoprotective anti-inflammatory effects of acute ethanol (EtOH) ingestion in an in vivo model of acute inflammation. Due to its undesirable side-effects, however, EtOH does not represent a therapeutic option for treatment of acute inflammation. Therefore, in this study, we compared the effects of acute EtOH exposure with ethyl pyruvate (EtP) as an alternative anti-inflammatory drug in an in vitro model of hepatic and pulmonary inflammation. Human hepatocellular carcinoma cells Huh7 and alveolar epithelial cells A549 were stimulated with either interleukin (IL) IL-1ß (1 ng/ml, 24 h) or tumor necrosis factor (TNF) (10 ng/ml, 4 h), and then treated with EtP (2.5-10 mM), sodium pyruvate (NaP, 10 mM) or EtOH (85-170 mM) for 1 h. IL-6 or IL-8 release from Huh7 or A549 cells, respectively, was measured by an enzyme­linked immunosorbent assay. Neutrophil adhesion to cell monolayers and CD54 expression were also analyzed. Bcl-2 and Bax gene expression was determined by RT-qPCR, and western blot analysis was performed to determine the mechanisms involved. Treating A549 cells with either EtOH or EtP significantly reduced the IL-1ß- or TNF­induced IL-8 release, whereas treating Huh7 cells did not significantly alter IL-6 release. Similarly, neutrophil adhesion to stimulated A549 cells was significantly reduced by EtOH or EtP, whereas for Huh7 cells the tendency for reduced neutrophil adhesion rates by EtOH or EtP was not significant. CD54 expression was noticeably reduced in A549 cells, but this was not the case in Huh7 cells after treatment. The Bax/Bcl-2 ratio was dose­dependently decreased by EtOH and by high-dose EtP in A549 cells, indicating a reduction in apoptosis, whereas this effect was not observed in Huh7 cells. The underlying mechanisms involve reduced phosphorylation of Akt and nuclear factor-κB (NF-κB) p65. We noted that as with EtP, EtOH reduced the inflammatory response in lung epithelial cells under acute inflammatory conditions. However, due to the low impact which EtP and EtOH had on the hepatocellular cells, our data suggest that both substances exerted different effects depending on the cellular entity. The possible underlying mechanisms involved the downregulation of Akt and the transcription factor NF-κB, but further research on this subject is required.

Decreased inflammatory responses of human lung epithelial cells after ethanol exposure are mimicked by ethyl pyruvate.

BACKGROUND AND PURPOSE: Leukocyte migration into alveolar space plays a critical role in pulmonary inflammation resulting in lung injury. Acute ethanol (EtOH) exposure exerts anti-inflammatory effects. The clinical use of EtOH is critical due to its side effects. Here, we compared effects of EtOH and ethyl pyruvate (EtP) on neutrophil adhesion and activation of cultured alveolar epithelial cells (A549). EXPERIMENTAL APPROACH: Time course and dose-dependent release of interleukin- (IL-) 6 and IL-8 from A549 were measured after pretreatment of A549 with EtP (2.5-10 mM), sodium pyruvate (NaP, 10 mM), or EtOH (85-170 mM), and subsequent lipopolysaccharide or IL-1beta stimulation. Neutrophil adhesion to pretreated and stimulated A549 monolayers and CD54 surface expression were determined. KEY RESULTS: Treating A549 with EtOH or EtP reduced substantially the cytokine-induced release of IL-8 and IL-6. EtOH and EtP (but not NaP) reduced the adhesion of neutrophils to monolayers in a dose- and time-dependent fashion. CD54 expression on A549 decreased after EtOH or EtP treatment before IL-1beta stimulation. CONCLUSIONS AND IMPLICATIONS: EtP reduces secretory and adhesive potential of lung epithelial cells under inflammatory conditions. These findings suggest EtP as a potential treatment alternative that mimics the anti-inflammatory effects of EtOH in early inflammatory response in lungs.

Compliance with school F-milk and non-F milk intake in 3 to 4 and 6 to 7-year-old children.

BACKGROUND: Fluoridated (F) milk schemes are employed in six countries to reduce dental caries in children. To maximise their benefits considerable uptake is required. Measuring compliance and understanding contributing factors is important in evaluating the effectiveness of schemes since it can be unclear whether reported sub-optimal fluoride (F) intakes, measured through urinary F excretion, are due to sub-optimal F contents of milks or lack of compliance with consumption. OBJECTIVES: To determine compliance with milk consumption for children receiving non-F or F milk (containing 0.5 or 0.9 mgF per 189 ml carton) and rationalise the use of compliance data for clinical observational or intervention studies involving F milk schemes. RESEARCH DESIGN: Partially randomised, partial cross-over study. PARTICIPANTS: 50 children aged 3-4 and 6-7y consuming non-F (n=50) and F milk (0.5 mgF; n=15 children; 0.9mg F; n=16 children) at school. RESULTS: Mean compliance for both non-F and F milk was > or =90% in each of the groups studied and showed no statistically significant difference for children using both milks. The 95% central range of proportions of milk consumed for groups of individuals was wider for 0.9mgF milk (25% to 100%) than for 0.5 mgF milk (81% to 100%) although the greatest range of variation in compliance for within individual observations was seen for non-F milk consumption and in older children. CONCLUSION: Assessment of compliance with consumption should be included when dental efficacy of F milk consumption is being investigated or evaluated to quantify F exposure from milk. This is important, particularly if a change in the F dose of F milk might be under consideration.

The amino bisphosphonate ibandronate prevents calciphylaxis in the rat at doses that inhibit bone resorption.

The present experiments were carried out to test the hypothesis that there is a common underlying biochemical mechanism that accounts for the different kinds of soft tissue calcification observed in animals that are treated with toxic doses of vitamin D. In previous studies we showed that lethal doses of vitamin D cause extensive calcification of arteries, lungs, kidneys, and cartilage, and that doses of the amino bisphosphonate ibandronate that inhibit bone resorption completely inhibit each of these soft tissue calcifications and prevent death. In the present experiments we have examined the effect of ibandronate on an entirely different type of calcification, the calciphylaxis induced by administration of a challenger to rats previously treated with sub-lethal doses of vitamin D. These studies show that ibandronate doses that inhibit bone resorption completely inhibit artery calcification as well as, in the same rat, the calciphylactic responses to either subcutaneous injection of 300 mg FeCl3 or intrascapular epilation. Since the vitamin D-treated animals had dramatically increased levels of bone resorption, and concurrent treatment with ibandronate normalized resorption, these results support the hypothesis that soft tissue calcifications in the vitamin D-treated rat may be linked to bone resorption. The ability of ibandronate to inhibit all vitamin D-associated calcifications in the rat cannot be explained by an effect of ibandronate on serum calcium, since serum calcium remained 30% above control levels in the vitamin D-treated animals that also received ibandronate.