Influence of selected packaging materials on some quality aspects of pressure-assisted thermally processed carrots during storage

Role of packaging barrier properties and storage conditions on pressure-assisted thermally processed (PATP) carrot quality were investigated. Samples were packaged in pouches fabricated using three packaging materials (Nylon/EVOH/EVA, Nylon/EVA and MetPET/PE) and processed at 600 MPa and 110 °C for 10 minutes. Processed pouches were stored at 25 and 37 °C, and withdrawn over 12 weeks. Samples were analyzed for color, β-carotene and total plate count. Oxygen and water vapor transmission rates (OTR, WVTR), melting point and enthalpy of fusion of the packages were evaluated. PATP treatment resulted in product shelf-stability during storage. Packaging type and storage conditions significantly influenced the product color and β-carotene content. Nylon/EVOH/EVA package best preserved carrot quality. PATP increased OTR of the MetPET/PE and degraded carrot color and β-carotene during storage. Raw carrots had 11.13 mg/100g β-carotene content. PATP treatment followed by 12 weeks storage at 37 °C reduced the β-carotene content of carrots packaged in Nylon/EVOH/EVA, Nylon/EVA and MetPET/PE to 7.19, 0.04 and 0.06 mg/100g, respectively. Similarly, the red color of carrot samples (25.51 for raw carrots) decreased to 19.85, 3.44 and 7.20 for Nylon/EVOH/EVA, Nylon/EVA and MetPET/PE, respectively. The study demonstrated the importance of high barrier packaging materials in preserving PATP-treated carrot quality.     

Multilevel diffractive elements in SiO2 by electron beam lithography and proportional etching with analogue negative resist

Abstract

A negative low-contrast electron beam resist X AR-N 7700/18 is introduced, which provides a nearly linear dose-to-depth curve at electron acceleration voltages below 20 kV, and is therefore an excellent material for fabrication of multilevel diffractive optics. Direct electron beam recording at 12.5kV is used to pattern analogue surface profiles in this resist, and proportional reactive ion etching (RIE) is employed to transfer the profile into the SiO₂ substrate. It is shown that errors in resist-profile scale can be corrected by proper adjustment of the radio-frequency power or chamber pressure in RIE. The reproducibility of the profile scale is better than 2%. Transmission-type blazed gratings, array illuminators, and pattern projection elements are demonstrated.     

The MKK6/p38 stress kinase cascade is critical for tumor necrosis factor-alpha-induced expression of monocyte-chemoattractant protein-1 in endothelial cells

Monocyte chemoattractant protein-1 (MCP-1), a member of the C-C subfamily of chemokines, is important for the local recruitment of leukocytes to sites of inflammatory challenge. Here, we investigated endothelial signaling pathways involving members of the mitogen-activated protein (MAP) kinase superfamily and studied their role for MCP-1 expression in endothelium. We show that tumor necrosis factor-alpha (TNF-alpha), a potent inflammatory activator of endothelium, leads to activation of MAP kinases ERK, p38, and JNK in human umbilical vein endothelial cells (HUVEC). Contribution of MAP kinase pathways to TNF-alpha-induced synthesis of endothelial MCP-1 was then studied by pharmacologic inhibition and transient expression of dominant negative or constitutively active kinase mutants using flow cytometry, Northern blot, and luciferase reporter gene assays. Inhibition of Raf/MEK/ERK or SEK/JNK pathways had no significant effect on MCP-1 levels, whereas blocking the MKK6/p38 pathway by p38 inhibitors SB203580 or SB202190 or by a dominant negative mutant of MKK6, the upstream activator of p38, strongly inhibited TNF-alpha-induced expression of MCP-1. Consistent with that finding, expression of wild-type or constitutively active MKK6 significantly enhanced the effect of limiting TNF-alpha concentrations on MCP-1 synthesis. These data suggest a crucial role for the MKK6/p38 stress kinase cascade in TNF-alpha-mediated endothelial MCP-1 expression.     

Homozygous deletion of the p16/MTS1 gene in pediatric acute lymphoblastic leukemia is associated with unfavorable clinical outcome

The p16 gene (MTS1, CDKN2, p16INK4A, CDKI) encoding an inhibitor of cyclin-dependent kinase 4 (cdk4) has been found to be deleted in various types of tumors, including leukemia, and is thought to code for a tumor suppressor gene. Our preliminary findings on eight pediatric patients with acute lymphoblastic leukemia (ALL) suggested that the survival of patients carrying a homozygous p16 gene deletion was significantly inferior to that of those without a deletion. The present study on 48 patients tested the hypothesis that the clinical outcome for pediatric ALL patients is correlated with the presence or absence of the p16 gene. Overall, nine of 48 children (18.3%) carried a homozygous p16 deletion. Such deletions were significantly more common (P = .003) among T-ALL patients (five of eight, 62.5%) than among precursor-B-ALL patients (four of 40, 10.0%). Of nine patients exhibiting p16 deletions, eight (88.9%) were classified as high-risk patients by the recognized prognostic factors of age, white blood cell count, and T-cell phenotype. The 4-year event-free survival in the study population as a whole was 72.7%. Without adjustment for other risk factors (univariate model), the presence of a homozygous p16 deletion was associated with a markedly increased probability of both relapse (P = .0003) and death (P = .002). These findings raise the question of whether the p16 deletion itself confers an increased risk of relapse after adjusting for the known risk factors. In this analysis, the estimated risk multiplier factor for relapse in patients carrying the p16 deletion was 14.0 (P = .0004) and for the risk of death 15.6 (P = .0008). We therefore conclude that the presence of a homozygous p16 deletion may well be an important risk factor for both relapse and death in childhood ALL, and that its prognostic effect is not a consequence of confounding by other factors already known to influence outcome in this disease.     

Veno-venous extracorporeal lung assist with concurrent distal aortic perfusion: repair of ruptured aorta in a patient with dense ARDS

Extracorporeal lung assist (ECLA) allowed surgical repair of a ruptured descending thoracic aorta to be performed in a patient with profound respiratory failure. Dense acute respiratory distress syndrome (ARDS) developed during his 15-day hospitalization at a regional trauma center. After transfer to a Level I facility, an additional injury was diagnosed: traumatic rupture of the aorta, contained within a pseudoaneurysm. ECLA by the veno-venous route was required immediately preoperatively and distal aortic perfusion was performed during the aortic repair. Despite deflation of the left lung, the patient was oxygenated and ventilated adequately during surgery. Cross-clamp time was 48 minutes. The patient was weaned from ECLA by the fifth postoperative day. To our knowledge, this is the first report of concurrent veno-venous pulmonary support with distal aortic perfusion.     

Why and How Urban Residents Resisted a Proposed Gas-Fired Power Station

New urban infrastructure including lower-carbon energy facilities are increasingly met with community resistance during the public participation phase of planning. Resistance can confound the implementation of government climate change and energy policies. A qualitative case study using social capital and place-attachment analytical lenses is conducted to build knowledge about the social factors involved in a Canberra community's resistance to a gas-fired power station. Analysis reveals that while social capital explains how resistance occurred, a threatened disruption to place attachment explains why. We conclude that public participation processes informed by community social capital and place attachment characteristics would help developers and planners pre-empt resistance.     

Fetal cells in maternal blood: recovery by charge flow separation

PURPOSE: To screen patients with abdominal aortic aneurysm for popliteal aneurysm and investigate cardiovascular and genetic risk factors associated with aneurysmal disease at more than one site (generalised aneurysmal disease). SUBJECTS, DESIGN AND SETTING: All patients referred to the Regional Vascular Surgical Service at Charing Cross Hospital with unruptured abdominal aortic aneurysm between 1989 and 1993 were screened for popliteal aneurysms, using ultrasonography. MAIN OUTCOME MEASURES: Palpation of a popliteal aneurysm or ultrasonographic detection of popliteal dilatation, where the ratio maximum popliteal fossa diameter/suprageniculate popliteal diameter was > or = 1.5, in relation to cardiovascular and genetic risk factors. RESULTS: Clinical examination detected popliteal aneurysms in only 11/232 patients (5%), but ultrasonography demonstrated the presence of popliteal aneurysm in a further 13 patients, 24/232 in total (10%). Multivariate regression identified four independent factors associated with popliteal dilatation disease: age (p = 0.046), height (p = 0.006), systolic hypertension (p = 0.037) and triglyceride concentration (p = 0.009). Generalised aneurysmal disease and systolic blood pressure were associated with polymorphic variation in the fibrillin-1 gene, but not with variations in the apolipoprotein B and type III collagen genes. CONCLUSIONS: Few patients with abdominal aortic aneurysm (10%) also have popliteal aneurysms: the risk of popliteal dilatation increases with age, height, systolic blood pressure, triglyceride concentration and fibrillin genotype. The strong interaction between fibrillin genotype and blood pressure may contribute to the familial tendency to aortic aneurysm.     

No evidence for inhibition of human glutathione reductase by valproic acid

The human red blood cell enzyme glutathione reductase (GR) was reported to be inhibited by the anticonvulsant drug valproic acid (VPA) [Cotariu et al., Biochem Pharmacol 43: 425-429, 1992]. When attempting to reproduce and extend these experiments, we could not detect any significant effect of VPA on glutathione reductase in haemolysates from 20 healthy children and 10 children under VPA therapy, no matter which concentration of the drug (0.9 or 1.8 mM in a haemolysate diluted by a factor of 50 or 1.8 mM directly in the assay), which incubation time (0-60 min) and which assay system were chosen. An influence of VPA on FAD-free apoglutathione reductase was also excluded. GR-activities of 10 children under VPA therapy (1.08 +/- 0.14 U/mL blood or 7.57 +/- 0.94 U/g Hb) were almost identical with the activities of age- and sex-matched controls (1.04 +/- 0.17 U/mL or 7.79 +/- 1.32 U/g Hb). No correlation between erythrocyte GR activity and serum levels of VPA was observed. Finally, incubation of crystalline human GR with VPA did not lead to enzyme inhibition; rather, in most experiments the enzyme was stabilized by incubation with VPA. Possible explanations for the discrepancies between the results of Cotariu et al. and our data are discussed.     

Gastrointestinal hormones as potential adjuvant treatment of exocrine pancreatic adenocarcinoma

Arterial hemodynamics and wall mechanics are important considerations for the vascular clinician for a number of reasons. Hemodynamics and wall mechanics both have been shown to be affecters of disease formation. It is important for the practicing vascular surgeon to know how disease affects both blood flow and wall mechanics and to understand the consequence of hemodynamics on arterial reconstructions. In this article, we summarize the basic concepts of arterial hemodynamics and wall mechanics as they relate to the development of arterial pathology. A few practical mathematical relationships and examples are provided for both illustration and utilization. We also discuss the use of computer models for the estimation of wall stresses in individual abdominal aortic aneurysms.