Mass Transfer and Volume Changes in French Fries During Air Frying

An erratum to this article can be found at http://dx.doi.org/10.1007/s11947-012-0904-8 (The graph located in the left upper corner of Fig. 2 is incorrect)The production of healthier fried foods requires the adaptation of industrial processes. In this context, air frying is an alternative to deep oil frying to obtain French fries with lower fat content. Kinetic analysis of compositional changes and main fluxes involved in air frying were carried out, and the results were compared to those obtained for deep oil frying. The influence of the type of sample (unpretreated, frozen, or blanched potatoes) was also analyzed. The results showed that oil uptake is much lower in air frying although a much longer processing time is required. Also, water loss and thus the loss of volume were much higher in air frying compared to the conventional process.The authors would like to thank the Universitat Politecnica de Valencia (PAID-06-09-2876) for the financial support given to this investigation.Andrés Grau, AM.; Argüelles Foix, AL.; Castelló Gómez, ML.; Heredia Gutiérrez, AB. (2013). Mass Transfer and Volume Changes in French Fries During Air Frying. Food and Bioprocess Technology. 6(8):1917-1924. https://doi.org/10.1007/s11947-012-0861-2S1917192468Aguilar, C. N., Anzaldúa-Morales, R., Talamás, R., & Gastélum, G. (1997). Low-temperature blanch improves textural quality of French-fries. Journal of Food Science, 62, 568–571.AOAC. (1980). Official methods of analysis (12th ed.). Washington, D.C., USA: Association of Official Analytical Chemists.Califano, A. N., & Calvelo, A. (1987). Adjustment of surface concentration of reducing sugars before frying of potato strips. Journal of Food Processing and Preservation, 12, 1–9.Clark, J. P. (2003). Happy birthday, potato chip! And other snack developments. Food Technology, 57(5), 89–92.Debnath, S., Bhat, K. K., & Rastogi, N. K. (2003). Effect of pre-drying on kinetics of moisture loss and oil uptake during deep fat frying of chickpea flour-based snack food. LWT—Food Science and Technology, 36, 91–98.Du Pont, M. S., Kirby, A. B., & Smith, A. C. (1992). Instrumental and sensory tests of cooked frozen French fries. International Journal of Food Science and Technology, 27, 285–295.Dueik, V., Robert, P., & Bouchon, P. (2010). Vacuum frying reduces oil uptake and improves the quality parameters of carrot crisps. Food Chemistry, 119(3), 1143–1149.Hubbard, L. J., & Farkas, B. E. (2000). Influence of oil temperature on convective heat transfer during immersion frying. Journal of Food Processing and Preservation, 24(2), 143–162.Krokida, M. K., Oreopoulou, V., & Maroulis, Z. B. (2000). Water loss and oil uptake as a function of frying time. Journal of Food Engineering, 44, 39–46.Mestdagh, F., De Wilde, T., Fraselle, S., Govaert, Y., Ooghe, W., Degroodt, J. M., Verhé, R., Van Peteghem, C., & De Meulenaer, B. (2008). Optimization of the blanching process to reduce acrylamide in fried potatoes. LWT- Food Science and Technology, 41(9), 1648–1654.Mohsenin, N. M. (1986). Physical properties of plant and animal materials. Nueva York: Gordon and Breach.Moyano, P. C., & Pedreschi, F. (2006). Kinetics of oil uptake during frying of potato slices: effect of pre-treatments. LWT- Food Science and Technology, 39, 285–291.Ngadi, M. O., Wang, Y., Adedeji, A. A., & Raghavan, G. S. V. (2009). Effect of microwave pretreatment on mass transfer during deep-fat frying of chicken nugget. LWT- Food Science and Technology, 42(1), 438–440.Pedreschi, F., & Moyano, P. (2005). Oil uptake and texture development in fried potato slices. Journal of Food Engineering, 70(4), 557–563.Saguy, S., & Dana, D. (2003). Integrated approach to deep fat frying: engineering, nutrition, health and consumer aspects. Journal of Food Engineering, 56, 143–152.Troncoso, E., & Pedreschi, F. (2009). Modeling water loss and oil uptake during vacuum frying of pre-treated potato slices. LWT- Food Science and Technology, 42(6), 1164–1173

Phase III randomised trial of doxorubicin-based chemotherapy compared with platinum-based chemotherapy in small-cell lung cancer

This randomised trial compared platinum-based to anthracycline-based chemotherapy in patients with small-cell lung cancer (limited or extensive stage) and ⩽2 adverse prognostic factors. Patients were randomised to receive six cycles of either ACE (doxorubicin 50 mg/m2 i.v., cyclophosphamide 1 g/m2 i.v. and etoposide 120 mg/m2 i.v. on day 1, then etoposide 240 mg/m2 orally for 2 days) or PE (cisplatin 80 mg/m2 and etoposide 120 mg/m2 i.v. on day 1, then etoposide 240 mg/m2 orally for 2 days) given for every 3 weeks. For patients where cisplatin was not suitable, carboplatin (AUC6) was substituted. A total of 280 patients were included (139 ACE, 141 PE). The response rates were 72% for ACE and 77% for PE. One-year survival rates were 34 and 38% (P=0.497), respectively and 2-year survival was the same (12%) for both arms. For LD patients, the median survival was 10.9 months for ACE and 12.6 months for PE (P=0.51); for ED patients median survival was 8.3 months and 7.5 months, respectively. More grades 3 and 4 neutropenia (90 vs 57%, P<0.005) and grades 3 and 4 infections (73 vs 29%, P<0.005) occurred with ACE, resulting in more days of hospitalisation and greater i.v. antibiotic use. ACE was associated with a higher risk of neutropenic sepsis than PE and with a trend towards worse outcome in patients with LD, and should not be studied further in this group of patients

11q13 amplification status and human papillomavirus in relation to p16 expression defines two distinct etiologies of head and neck tumours

Two distinct etiologies of head and neck squamous cell carcinoma (HNSCC) have been proposed, DNA damage owing to tobacco and alcohol exposure and human papillomavirus (HPV) oncogene-mediated transformation. Common genetic alterations in HNSCC include TP53 mutations, 11q13 amplification (amp) and CDKN2A/p16 mutations or promoter methlyation. However, in HPV+ HNSCC it is frequent to observe wild-type TP53 and expression of p16. The relationship of this unusual pattern with 11q13 amp has not been tested. In a retrospective study on 125 HNSCC patients, only 17% (five out of 30) of HPV+ vs 44% (39 out of 89) of HPV − tumours expressed 11q13 amp (adjusted odds ratio (OR)=0.2, 95% confidence interval (CI)=0.1–0.6). A subpopulation of tumours (n=69) were classified according to the three molecular markers, TP53, p16 and 11q13 amp. In addition to wild-type TP53, and p16 expression, HPV+ tumours were more likely not to be amplified at 11q13 (OR=6.5, 95% CI=1.8–23.9). As HPV+ HNSCC lack the genetic alterations which are common in other tumours, we hypothesise that HPV infection may represent an early event in the HNSCC carcinogenic process, thus suggesting a distinct molecular pathway

Contractility Dominates Adhesive Ligand Density in Regulating Cellular De-adhesion and Retraction Kinetics

Cells that are enzymatically detached from a solid substrate rapidly round up as the tensile prestress in the cytoskeleton is suddenly unopposed by cell–ECM adhesions. We recently showed that this retraction follows sigmoidal kinetics with time constants that correlate closely with cortical stiffness values. This raises the promising prospect that these de-adhesion measurements may be used for high-throughput screening of cell mechanical properties; however, an important limitation to doing so is the possibility that the retraction kinetics may also be influenced and potentially rate-limited by the time needed to sever matrix adhesions. In this study, we address this open question by separating contributions of contractility and adhesion to cellular de-adhesion and retraction kinetics. We first develop serum-free conditions under which U373 MG glioma cells can be cultured on substrates of fixed fibronectin density without direct matrix contributions from the medium. We show that while spreading area increases with ECM protein density, cortical stiffness and the time constants of retraction do not. Conversely, addition of lysophosphatidic acid (LPA) to stimulate cell contractility strongly speeds retraction, independent of the initial matrix protein density and LPA’s contributions to spreading area. All of these trends hold in serum-rich medium commonly used in tissue culture, with the time constants of retraction much more closely tracking cortical stiffness than adhesive ligand density or cell spreading. These results support the use of cellular de-adhesion measurements to track cellular mechanical properties

Differential Analysis of Ovarian and Endometrial Cancers Identifies a Methylator Phenotype

Despite improved outcomes in the past 30 years, less than half of all women diagnosed with epithelial ovarian cancer live five years beyond their diagnosis. Although typically treated as a single disease, epithelial ovarian cancer includes several distinct histological subtypes, such as papillary serous and endometrioid carcinomas. To address whether the morphological differences seen in these carcinomas represent distinct characteristics at the molecular level we analyzed DNA methylation patterns in 11 papillary serous tumors, 9 endometrioid ovarian tumors, 4 normal fallopian tube samples and 6 normal endometrial tissues, plus 8 normal fallopian tube and 4 serous samples from TCGA. For comparison within the endometrioid subtype we added 6 primary uterine endometrioid tumors and 5 endometrioid metastases from uterus to ovary. Data was obtained from 27,578 CpG dinucleotides occurring in or near promoter regions of 14,495 genes. We identified 36 locations with significant increases or decreases in methylation in comparisons of serous tumors and normal fallopian tube samples. Moreover, unsupervised clustering techniques applied to all samples showed three major profiles comprising mostly normal samples, serous tumors, and endometrioid tumors including ovarian, uterine and metastatic origins. The clustering analysis identified 60 differentially methylated sites between the serous group and the normal group. An unrelated set of 25 serous tumors validated the reproducibility of the methylation patterns. In contrast, >1,000 genes were differentially methylated between endometrioid tumors and normal samples. This finding is consistent with a generalized regulatory disruption caused by a methylator phenotype. Through DNA methylation analyses we have identified genes with known roles in ovarian carcinoma etiology, whereas pathway analyses provided biological insight to the role of novel genes. Our finding of differences between serous and endometrioid ovarian tumors indicates that intervention strategies could be developed to specifically address subtypes of epithelial ovarian cancer

Microfabricated Physical Spatial Gradients for Investigating Cell Migration and Invasion Dynamics

We devise a novel assay that introduces micro-architectures into highly confining microchannels to probe the decision making processes of migrating cells. The conditions are meant to mimic the tight spaces in the physiological environment that cancer cells encounter during metastasis within the matrix dense stroma and during intravasation and extravasation through the vascular wall. In this study we use the assay to investigate the relative probabilities of a cell 1) permeating and 2) repolarizing (turning around) when it migrates into a spatially confining region. We observe the existence of both states even within a single cell line, indicating phenotypic heterogeneity in cell migration invasiveness and persistence. We also show that varying the spatial gradient of the taper can induce behavioral changes in cells, and different cell types respond differently to spatial changes. Particularly, for bovine aortic endothelial cells (BAECs), higher spatial gradients induce more cells to permeate (60%) than lower gradients (12%). Furthermore, highly metastatic breast cancer cells (MDA-MB-231) demonstrate a more invasive and permeative nature (87%) than non-metastatic breast epithelial cells (MCF-10A) (25%). We examine the migration dynamics of cells in the tapered region and derive characteristic constants that quantify this transition process. Our data indicate that cell response to physical spatial gradients is both cell-type specific and heterogeneous within a cell population, analogous to the behaviors reported to occur during tumor progression. Incorporation of micro-architectures in confined channels enables the probing of migration behaviors specific to defined geometries that mimic in vivo microenvironments

Effects of Hormone Agonists on Sf9 Cells, Proliferation and Cell Cycle Arrest

Methoxyfenozide and methoprene are two insecticides that mimic the action of the main hormones involved in the control of insect growth and development, 20-hydroxyecdysone and juvenile hormone. We investigated their effect on the Spodoptera frugiperda Sf9 cell line. Methoxyfenozide was more toxic than methoprene in cell viability tests and more potent in the inhibition of cellular proliferation. Cell growth arrest occurred in the G2/M phase after a methoprene treatment and more modestly in G1 after methoxyfenozide treatment. Microarray experiments and real-time quantitative PCR to follow the expression of nuclear receptors ultraspiracle and ecdysone receptor were performed to understand the molecular action of these hormone agonists. Twenty-six genes were differentially expressed after methoxyfenozide treatment and 55 genes after methoprene treatment with no gene in common between the two treatments. Our results suggest two different signalling pathways in Sf9 cells

Bcl11b sets pro-T cell fate by site-specific cofactor recruitment and by repressing Id2 and Zbtb16

Multipotent progenitor cells confirm their T cell–lineage identity in the CD4^–CD8^– double-negative (DN) pro-T cell DN2 stages, when expression of the essential transcription factor Bcl11b begins. In vivo and in vitro stage-specific deletions globally identified Bcl11b-controlled target genes in pro-T cells. Proteomics analysis revealed that Bcl11b associated with multiple cofactors and that its direct action was needed to recruit those cofactors to selective target sites. Regions near functionally regulated target genes showed enrichment for those sites of Bcl11b-dependent recruitment of cofactors, and deletion of individual cofactors relieved the repression of many genes normally repressed by Bcl11b. Runx1 collaborated with Bcl11b most frequently for both activation and repression. In parallel, Bcl11b indirectly regulated a subset of target genes by a gene network circuit via the transcription inhibitor Id2 (encoded by Id2) and transcription factor PLZF (encoded by Zbtb16); Id2 and Zbtb16 were directly repressed by Bcl11b, and Id2 and PLZF controlled distinct alternative programs. Thus, our study defines the molecular basis of direct and indirect Bcl11b actions that promote T cell identity and block alternative potentials