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2. Multi-Omic analyses characterize the ceramide/sphingomyelin pathway as a therapeutic target in Alzheimer's disease

Author

Baloni, P, Arnold, M, Buitrago, L, Nho, K, Moreno, H, Huynh, K, Brauner, B, Louie, G, Kueider-Paisley, A, Suhre, K, Saykin, AJ, Ekroos, K, Meikle, PJ, Hood, L, Price, ND, Doraiswamy, PM, Funk, CC, Hernandez, AI, Kastenmueller, G, Baillie, R, Han, X, Kaddurah-Daouk, R, Baloni, P, Arnold, M, Buitrago, L, Nho, K, Moreno, H, Huynh, K, Brauner, B, Louie, G, Kueider-Paisley, A, Suhre, K, Saykin, AJ, Ekroos, K, Meikle, PJ, Hood, L, Price, ND, Doraiswamy, PM, Funk, CC, Hernandez, AI, Kastenmueller, G, Baillie, R, Han, X, and Kaddurah-Daouk, R

Abstract

Dysregulation of sphingomyelin and ceramide metabolism have been implicated in Alzheimer's disease. Genome-wide and transcriptome-wide association studies have identified various genes and genetic variants in lipid metabolism that are associated with Alzheimer's disease. However, the molecular mechanisms of sphingomyelin and ceramide disruption remain to be determined. We focus on the sphingolipid pathway and carry out multi-omics analyses to identify central and peripheral metabolic changes in Alzheimer's patients, correlating them to imaging features. Our multi-omics approach is based on (a) 2114 human post-mortem brain transcriptomics to identify differentially expressed genes; (b) in silico metabolic flux analysis on context-specific metabolic networks identified differential reaction fluxes; (c) multimodal neuroimaging analysis on 1576 participants to associate genetic variants in sphingomyelin pathway with Alzheimer's disease pathogenesis; (d) plasma metabolomic and lipidomic analysis to identify associations of lipid species with dysregulation in Alzheimer's; and (e) metabolite genome-wide association studies to define receptors within the pathway as a potential drug target. We validate our hypothesis in amyloidogenic APP/PS1 mice and show prolonged exposure to fingolimod alleviated synaptic plasticity and cognitive impairment in mice. Our integrative multi-omics approach identifies potential targets in the sphingomyelin pathway and suggests modulators of S1P metabolism as possible candidates for Alzheimer's disease treatment.

Published
2022

5. Concordant peripheral lipidome signatures in two large clinical studies of Alzheimer's disease

Author

Huynh, K, Lim, WLF, Giles, C, Jayawardana, KS, Salim, A, Mellett, NA, Smith, AAT, Olshansky, G, Drew, BG, Chatterjee, P, Martins, I, Laws, SM, Bush, AI, Rowe, CC, Villemagne, VL, Ames, D, Masters, CL, Arnold, M, Nho, K, Saykin, AJ, Baillie, R, Han, X, Kaddurah-Daouk, R, Martins, RN, Meikle, PJ, Huynh, K, Lim, WLF, Giles, C, Jayawardana, KS, Salim, A, Mellett, NA, Smith, AAT, Olshansky, G, Drew, BG, Chatterjee, P, Martins, I, Laws, SM, Bush, AI, Rowe, CC, Villemagne, VL, Ames, D, Masters, CL, Arnold, M, Nho, K, Saykin, AJ, Baillie, R, Han, X, Kaddurah-Daouk, R, Martins, RN, and Meikle, PJ

Abstract

Changes to lipid metabolism are tightly associated with the onset and pathology of Alzheimer's disease (AD). Lipids are complex molecules comprising many isomeric and isobaric species, necessitating detailed analysis to enable interpretation of biological significance. Our expanded targeted lipidomics platform (569 species across 32 classes) allows for detailed lipid separation and characterisation. In this study we examined peripheral samples of two cohorts (AIBL, n = 1112 and ADNI, n = 800). We are able to identify concordant peripheral signatures associated with prevalent AD arising from lipid pathways including; ether lipids, sphingolipids (notably GM3 gangliosides) and lipid classes previously associated with cardiometabolic disease (phosphatidylethanolamine and triglycerides). We subsequently identified similar lipid signatures in both cohorts with future disease. Lastly, we developed multivariate lipid models that improved classification and prediction. Our results provide a holistic view between the lipidome and AD using a comprehensive approach, providing targets for further mechanistic investigation.

Published
2020

8. A blood-based signature of cerebrospinal fluid A beta(1-42) status

Author

Goudey, B., Fung, B.J., Schieber, C., Faux, N.G., Weiner, M.W., Aisen, P., Petersen, R., Jack, C.R., Jagust, W., Trojanowki, J.Q., Toga, A.W., Beckett, L., Green, R.C., Saykin, A.J., Morris, J., Shaw, L.M., Kaye, J., Quinn, J., Silbert, L., Lind, B., Carter, R., Dolen, S., Schneider, L.S., Pawluczyk, S., Beccera, M., Teodoro, L., Spann, B.M., Brewer, J., Vanderswag, H., Fleisher, A., Heidebrink, J.L., Lord, J.L., Mason, S.S., Albers, C.S., Knopman, D., Johnson, K., Doody, R.S., Villanueva-Meyer, J., Chowdhury, M., Rountree, S., Dang, M., Stern, Y., Honig, L.S., Bell, K.L., Ances, B., Morris, J.C., Carroll, M., Creech, M.L., Franklin, E., Mintun, M.A., Schneider, S., Oliver, A., Marson, D., Griffth, R., Clark, D., Geldmacher, D., Brockington, J., Roberson, E., Natelson Love, M., Grossman, H., Mitsis, E., Shah, R.C., deToledo-Morrell, L., Duara, R., Varon, D., Greig, M.T., Roberts, P., Albert, M., Onyike, C., D'Agostino, D., Kielb, S., Galvin, J.E., Cerbone, B., Michel, C.A., Pogorelec, D.M., Rusinek, H., Leon, M.J. de, Glodzik, L., De Santi, S., Doraiswamy, P.M., Petrella, J.R., Borges-Neto, S., Wong, T.Z., Coleman, E., Smith, C.D., Jicha, G., Hardy, P., Sinha, P., Oates, E., Conrad, G., Porsteinsson, A.P., Goldstein, B.S., Martin, K., Makino, K.M., Ismail, M.S., Brand, C., Mulnard, R.A., Thai, G., McAdams-Ortiz, C., Womack, K., Mathews, D., Quiceno, M., Levey, A.I., Lah, J.J., Cellar, J.S., Burns, J.M., Swerdlow, R.H., Brooks, W.M., Apostolova, L., Tingus, K., Woo, E., Silverman, D.H.S., Lu, P.H., Bartzokis, G., Graff-Radford, N.R., Parftt, F., Kendall, T., Johnson, H., Farlow, M.R., Hake, A.M., Matthews, B.R., Brosch, J.R., Herring, S., Hunt, C., Dyck, .H. van, Carson, R.E., MacAvoy, M.G., Varma, P., Chertkow, H., Bergman, H., Hosein, C., Black, S., Stefanovic, B., Caldwell, C., Hsiung, Ging-Yuek Robin, Feldman, H., Mudge, B., Assaly, M., Finger, E., Pasternack, S., Rachisky, I., Trost, D., Kertesz, A., Bernick, C., Munic, D., Mesulam, M.-M., Lipowski, K., Weintraub, S., Bonakdarpour, B., Kerwin, D., Wu, C.-K., Johnson, N., Sadowsky, C., Villena, T., Turner, R.S., Reynolds, B., Sperling, R.A., Johnson, K.A., Marshall, G., Yesavage, J., Taylor, J.L., Lane, B., Rosen, A., Tinklenberg, J., Sabbagh, M.N., Belden, C.M., Jacobson, S.A., Sirrel, S.A., Kowall, N., Killiany, R., Budson, A.E., Norbash, A., Johnson, P.L., Obisesan, T.O., Wolday, S., Allard, J., Lerner, A., Ogrocki, P., Tatsuoka, C., Fatica, P., Fletcher, E., Maillard, P., Olichney, J., DeCarli, C., Carmichael, O., Kittur, S., Borrie, M., Lee, T.-Y., Bartha, R., Johnson, S., Asthana, S., Carlsson, C.M., Potkin, S.G., Preda, A., Nguyen, D., Tariot, P., Burke, A., Trncic, N., Reeder, S., Bates, V., Capote, H., Rainka, M., Scharre, D.W., Kataki, M., Adeli, A., Zimmerman, E.A., Celmins, D., Brown, A.D., Pearlson, G.D., Blank, K., Anderson, K., Flashman, L.A., Seltzer, M., Hynes, M.L., Santulli, R.B., Sink, K.M., Gordineer, L., Williamson, J.D., Garg, P., Watkins, F., Ott, B.R., Querfurth, H., Tremont, G., Salloway, S., Malloy, P., Correia, S., Rosen, H.J., Miller, B.L., Perry, D., Mintzer, J., Spicer, K., Bachman, D., Pomara, N., Hernando, R., Sarrael, A., Relkin, N., Chaing, G., Lin, M., Ravdin, L., Smith, A., Raj, B.A., Fargher, K., Saykin, A., Nho, K., Kling, M., Toledo, J., Shaw, L., Trojanowski, J., Farrer, L., Kastsenmueller, G., Arnold, M., Wishart, D., Wurtz, P., Bhattcharyya, S., Duijin, C. van, Mangravite, L., Han, X., Hankemeier, T., Fiehn, O., Barupal, D., Thiele, I., Heinken, A., Meikle, P., Price, N., Funk, C., Jia, W., Kueider-Paisley, A., Tenebaum, J., Black, C., Moseley, A., Thompson, W., Mahmoudiandehkorki, S., Baillie, R., Welsh-Bohmer, K., Plassman, B., and Epidemiology

Subjects
Male, 0301 basic medicine, Apolipoprotein E, Oncology, medicine.medical_specialty, Amyloid, Amyloid beta, lcsh:Medicine, Article, 03 medical and health sciences, Apolipoproteins E, 0302 clinical medicine, Cerebrospinal fluid, Alzheimer Disease, Predictive Value of Tests, Internal medicine, medicine, Humans, Dementia, Cognitive decline, lcsh:Science, Aged, Aged, 80 and over, Amyloid beta-Peptides, Multidisciplinary, biology, Chemokine CCL26, business.industry, lcsh:R, Alzheimer’s Disease Metabolomics Consortium, Alzheimer’s Disease Neuroimaging Initiative, medicine.disease, Peptide Fragments, 3. Good health, 030104 developmental biology, biology.protein, Chromogranin A, Female, lcsh:Q, Alzheimer's disease, business, Biomarkers, 030217 neurology & neurosurgery, Alzheimer's Disease Neuroimaging Initiative
Abstract

It is increasingly recognized that Alzheimer’s disease (AD) exists before dementia is present and that shifts in amyloid beta occur long before clinical symptoms can be detected. Early detection of these molecular changes is a key aspect for the success of interventions aimed at slowing down rates of cognitive decline. Recent evidence indicates that of the two established methods for measuring amyloid, a decrease in cerebrospinal fluid (CSF) amyloid β1−42 (Aβ1−42) may be an earlier indicator of Alzheimer’s disease risk than measures of amyloid obtained from Positron Emission Tomography (PET). However, CSF collection is highly invasive and expensive. In contrast, blood collection is routinely performed, minimally invasive and cheap. In this work, we develop a blood-based signature that can provide a cheap and minimally invasive estimation of an individual’s CSF amyloid status using a machine learning approach. We show that a Random Forest model derived from plasma analytes can accurately predict subjects as having abnormal (low) CSF Aβ1−42 levels indicative of AD risk (0.84 AUC, 0.78 sensitivity, and 0.73 specificity). Refinement of the modeling indicates that only APOEε4 carrier status and four plasma analytes (CGA, Aβ1−42, Eotaxin 3, APOE) are required to achieve a high level of accuracy. Furthermore, we show across an independent validation cohort that individuals with predicted abnormal CSF Aβ1−42 levels transitioned to an AD diagnosis over 120 months significantly faster than those with predicted normal CSF Aβ1−42 levels and that the resulting model also validates reasonably across PET Aβ1−42 status (0.78 AUC). This is the first study to show that a machine learning approach, using plasma protein levels, age and APOEε4 carrier status, is able to predict CSF Aβ1−42 status, the earliest risk indicator for AD, with high accuracy.

Published
2019

12. Summing curious, slowly convergent, harmonic subseries

Author

Schmelzer, T and Baillie, R

Abstract

The harmonic series diverges. But if we delete from the harmonic series all terms whose denominators contain any string of digits such as "9", "42", or "314159", then the sum of the remaining terms converges. These series converge far too slowly to compute their sums directly. We describe an algorithm to compute these and related sums to high precision. For example, the sum of the series whose denominators contain no "314159" is approximately 2302582.33386. We explain why this sum is so close to 106 log 10 by developing asymptotic estimates for sums that omit strings of length n, as n approaches infinity. The first author is supported by a Rhodes Scholarship.

Published
2016

16. Guidelines for Overseas Eye Surgery Expeditions Using Short-Term Volunteers

Author

Harry S Brown, Izak F Wessels, and Baillie R Brown

Subjects
Blindness, business.industry, medicine.medical_treatment, Medicine, Optometry, Developing country, Eye surgery, Eye care, business, medicine.disease, Checklist, Term (time)
Abstract

Many developing countries face the overwhelming problem of addressing preventable and curable blindness. United States-based ophthalmologists can make important contributions in this regard by volunteering to teach and deliver eye care overseas. However, there are a number of potential risks and difficulties. Surgical Eye Expeditions (SEE) International has developed a logistical outline and planning checklist designed to minimize or avoid such problems. Critical components include a firm timetable, advanced planning, advance contact with a local ophthalmologist or organization, and a thorough understanding of the importance of adapting to the needs of other cultures. With a little planning, the average philanthropic ophthalmologist can make major contributions to individuals and communities in developing nations.

Published
1994

17. Functional annotation of genomic data with metabolic inference

Author

Walzem, R. L., Baillie, R. A., Wiest, M., Davis, R., Watkins, S. M., Porter, T. E., Simon, J., Larry Cogburn, Texas A&M University System, Lipomic Technologies INC., Partenaires INRAE, Department of Animal and Avian Sciences, Unité de Recherches Avicoles (URA), Institut National de la Recherche Agronomique (INRA), Department of Animal and Food Sciences, University of Delaware [Newark], and ProdInra, Migration

Subjects
GENETIC SELECTION, ADIPOSE, CHICKEN LIPID, [SDV.SA.SPA]Life Sciences [q-bio]/Agricultural sciences/Animal production studies, [SDV.SA.SPA] Life Sciences [q-bio]/Agricultural sciences/Animal production studies, METABOLOMICS, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2007

18. Adaptive ARFIMA Models with Applications to Inflation

Author

Morana, C, Baillie, R, MORANA, CLAUDIO, Baillie, RT, Morana, C, Baillie, R, MORANA, CLAUDIO, and Baillie, RT

Abstract

Many previous analyses of inflation have used either long memory or nonlinear time series models. This paper suggests a simple adaptive modification of the basic ARFIMA model, which uses a Flexible Fourier Form to allow for a time varying intercept. Simulation evidence suggests the model provides a good representation of various forms of structural breaks and also that the new model can be efficiently estimated by a QMLE approach. We investigate monthly CPI inflation series for the G7 countries and find evidence of stable long memory parameters across regimes and also of significant nonlinear effects. The estimated adaptive ARFIMA models generally have less persistent long memory parameters than previous studies, with the estimated time dependent intercept being an important component. The model is also supplemented with an adaptive FIGARCH component, yielding a double nonlinear long memory model.

Published
2012

19. Candidate gene-based association genetics analysis of herbage quality traits in perennial ryegrass (Lolium perenne L.)

Author

Pembleton, L. W., primary, Wang, J., additional, Cogan, N. O. I., additional, Pryce, J. E., additional, Ye, G., additional, Bandaranayake, C. K., additional, Hand, M. L., additional, Baillie, R. C., additional, Drayton, M. C., additional, Lawless, K., additional, Erb, S., additional, Dobrowolski, M. P., additional, Sawbridge, T. I., additional, Spangenberg, G. C., additional, Smith, K. F., additional, and Forster, J. W., additional

Published
2013
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34. Copper deficiency induces hepatic fatty acid synthase gene transcription in rats by increasing the nuclear content of mature sterol regulatory element binding protein 1.

Author

Tang, Zhongren, Gasperkova, Daniela, Tang, Z, Gasperkova, D, Xu, J, Baillie, R, Lee, J H, and Clarke, S D

Subjects
PHYSIOLOGICAL effects of copper, DNA, TRANSCRIPTION factors, FATTY acids, RNA metabolism, ANIMAL experimentation, COMPARATIVE studies, COPPER, ENZYMES, GENETIC disorders, LIPID metabolism disorders, LIVER, RESEARCH methodology, MEDICAL cooperation, PROTEINS, RATS, RESEARCH, RNA, WESTERN immunoblotting, DNA-binding proteins, EVALUATION research
Abstract

Dietary copper (Cu) deficiency results in an accelerated rate of hepatic fatty acid synthase gene transcription and an enhanced rate of hepatic lipid synthesis. Because the nuclear transcription factor sterol regulatory element binding protein-1 (SREBP-1) is a strong enhancer of fatty acid synthase promoter activity, it was hypothesized that Cu deficiency induces fatty acid synthase gene transcription by increasing the nuclear localization of mature SREBP-1. Male weanling rats were pair-fed a Cu-adequate (6.0 mg/kg) or Cu-deficient (0.6 mg/kg) diet (AIN-93) for 28 d. DNase I hypersensitivity site mapping of the hepatic fatty acid synthase gene revealed the presence of four major hypersensitivity sites located at -8700 to -8600, -7300 to -6900, -600 to -400 and -100 to +50. Although Cu deficiency did not change the hypersensitivity site pattern or intensity, in vitro footprinting of the region between -100 and +50 indicated that Cu deficiency enhanced DNA protein interactions within this region. The sequence between -68 and -58 contains the DNA recognition sequence for SREBP-1 and upstream stimulatory element-1 (USF-1). Western blot analysis revealed that the dietary Cu deficiency increased the hepatic nuclear content of mature SREBP-1 by 150% (P: < 0.05), and it concomitantly decreased the membrane content of precursor SREBP-1 by 45% (P: < 0.05). Changes in the hepatic distribution of SREBP-1 associated with Cu deficiency were not accompanied by changes in SREBP-1 mRNA. The nuclear content of USF-1 was unaffected by dietary Cu status. The hepatic increase in mature SREBP-1 of Cu-deficient rats was accompanied by a 400% increase and an 80% decrease in the abundance of fatty acid synthase and cholesterol 7-alpha hydroxylase mRNA, respectively. hepatic These data indicate that a Cu deficiency stimulates hepatic lipogenic gene expression by increasing the hepatic translocation of mature SREBP-1. [ABSTRACT FROM AUTHOR]

Published
2000
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38. Cytosolic and nuclear distribution of PPARgamma2 in differentiating 3T3-L1 preadipocytes.

Author

Thuillier, P, Baillie, R, Sha, X, and Clarke, S D

Abstract

In light of the pivotal role that PPARgamma2 plays in the expression of fat specific genes (e.g., A-FABP), we have examined the hypothesis that a rise in PPARgamma2 protein is required for the expression of A-FABP, and that the acceleration of fat cell differentiation by the thiazolidinedione agent, pioglitazone (PIOG), reflects an increase in the abundance of PPARgamma2 mRNA and protein. Western analyses surprisingly revealed that undifferentiated 3T3-L1 fibroblasts contained significant levels of PPARgamma2 protein; that the amount of total cellular PPARgamma2 only increased 2-fold during differentiation; and that the levels of PPARgamma2 protein and mRNA were not increased by PIOG even though fat cell differentiation was accelerated by PIOG as revealed by a 20-fold increase in A-FABP expression. Cell fractionation studies revealed that PPARgamma2 was evenly distributed between the cytosolic and nuclear compartments in both undifferentiated and differentiating 3T3-L1 cells. Immunocytochemical studies with a PPARgamma2-specific antibody indicated that PPARgamma2 was diffusely distributed throughout the cytosol of undifferentiated 3T3-L1 cells, but as the differentiation progressed, the PPARgamma2 became focused around the developing lipid droplets. In contrast to PPARgamma2, undifferentiated 3T3-L1 cells contained no measurable quantities of RXRalpha, but once fat cell differentiation was initiated by treatment with IBMX and dexamethasone, the cellular content of RXRalpha increased several fold. The rise in RXRalpha content paralleled the induction of A-FABP, but the expression of RXRalpha was not enhanced by PIOG. Although the amount of PPARgamma2 and RXRalpha was unaffected by PIOG, gel shift assays revealed that PIOG stimulated PPARgamma2/RXRalpha binding to the adipose response element of A-FABP by 5-fold in less than 12 h. Apparently, RXRalpha rather than PPARgamma2 is the pivotal trans-factor essential for the initiation of terminal fat cell differentiation. However, the high cytsolic content of PPARgamma2 and its association with the lipid droplet of differentiating 3T3-L1 cells suggests PPARgamma2 may possess a cytosolic function in the developing fat cell.

Published
1998

41. A novel 3T3-L1 preadipocyte variant that expresses PPARgamma2 and RXRalpha but does not undergo differentiation.

Author

Baillie, R A, Sha, X, Thuillier, P, and Clarke, S D

Abstract

This report describes a novel adipocyte-like cell line termed 3T3-L1/RB1 that was derived from preadipocyte cell line, 3T3-L1. The 3T3-L1/RB1 cells continued to divide after reaching confluence, formed foci, and constitutively expressed a low level of adipose fatty acid binding protein (A-FABP) mRNA. However, 3T3L-1/RB cells did not undergo terminal differentiation as indicated by the failure of insulin and thiazolidendiones to induce the expression of A-FABP, lipoprotein lipase, and fatty acid synthase. We hypothesized that the 3T3-L1/RB1 variant did not respond to differentiation stimuli because it did not express either peroxisomal proliferator activated receptor gamma2 (PPARgamma2) or its heterodimer partner, retinoid X receptor alpha (RXRalpha). Surprisingly, Western blots revealed that 3T3-L1/ RB1 cells contained both PPARgamma2 and RXRalpha proteins at levels equal to or greater than that of the parent cell line. However, gel retardation assays using the adipose response element from A-FABP and nuclear protein extracts from 3T3-L1/RB1 cells treated with insulin or pioglitazone revealed that nuclear protein extracts from 3T3-L1/RB1 cells had very little ability to bind the PPARgamma2 recognition sequence of the A-FABP gene. These data suggest that the 3T3-L1/RB1 variant contains a mutation that may prevent ligand activation of PPARgamma2, and the subsequent conversion of 3T3-L1/RB1 cells to mature fat cells.

Published
1998

42. Regulation of the action of steroid/thyroid hormone receptors by medium-chain fatty acids.

Author

Thurmond, D C, Baillie, R A, and Goodridge, A G

Abstract

Triiodothyronine (T3) causes a 30-fold increase in transcription of the malic enzyme gene in chick embryo hepatocytes; medium-chain fatty acids (MCFAs) inhibit this increase. T3 action is mediated by T3 receptors (TRs) that bind to T3 response elements (T3REs) in this gene's 5'-flanking DNA. In transiently transfected hepatocytes, fragments of 5'-flanking DNA of the malic enzyme gene or artificial T3REs that conferred T3 stimulation also conferred MCFA inhibition to linked reporter genes. Thus, MCFA inhibition may be mediated through cis-acting T3REs and trans-acting TRs, distinguishing MCFA action from that of other fatty acids which act through unique sequence elements. Using binding assays and overexpression of TR, we showed that MCFAs inhibited the transactivating but not the silencing function of TR and did not alter binding of T3 to TR or of TR to T3RE. The C-terminal ligand-binding domain of TR was sufficient to confer stimulation by T3, but not inhibition by MCFA. Inhibition of transactivation by MCFA was specific: ligand-stimulated transcription from T3 or estrogen response elements was inhibited, but that from glucocorticoid or cyclic AMP response elements was not. We propose that MCFAs or metabolites thereof influence the activity of a factor(s) that interacts with the T3 and estrogen receptors to inhibit ligand-stimulated transcription.

Published
1998

45. PTFE (Polytetrafluoroethylene) Resin Selection for High Performance Wire and Cable

Author

DU PONT DE NEMOURS (E I) AND CO WILMINGTON DE POLYMER PRODUCTS DEPT, Baillie,R. L., Bednarczyk,J. J., Mehta,P., DU PONT DE NEMOURS (E I) AND CO WILMINGTON DE POLYMER PRODUCTS DEPT, Baillie,R. L., Bednarczyk,J. J., and Mehta,P.

Abstract

Polytetrafluoroethylene (PTFE) resins have been used for over 30 years in high performance wire and cable applications because of their unique electrical, thermal and chemical properties. Wire insulated with PTFE is used successfully in aircraft, computers, military and industrial electronics, and other demanding applications. In some instances however, PTFE insulation has cracked during service. The following discussion deals with this problem by comparing the stress crack resistance of six different commercial grades of PTFE resin using insulated wire samples in an accelerated stress cracking test. Results are related to important resin properties including standard specific gravity (SSG) and thermal stability (TII). A theory describing the cracking mechanism is discussed and a new test for stress crack susceptibility is developed based on that theory. (Author), This article is from 'Proceedings of the International Wire and Cable Symposium (35th) Held in Reno, Nevada on 18-20 November 1986,' AD-A180 828, p47-54.

Published
1986

48. High levels of apoptosis are associated with improved survival in non-small cell lung cancer

Author

Michaelina Macluskey, Baillie, R., Chandrachud, L. M., Pendleton, N., and Schor, A. M.

Subjects
Lung Neoplasms, Neovascularization, Pathologic, Carcinoma, Non-Small-Cell Lung, Carcinoma, Squamous Cell, In Situ Nick-End Labeling, Humans, Apoptosis, Cell Count, Life Tables, Adenocarcinoma, Prognosis, Survival Analysis
Abstract

Tumour growth is accompanied by angiogenesis and reduced apoptosis in experimental animals. The aim of this study was to examine the prognostic value of apoptosis and the association between apoptosis and vascularity in non-small cell lung cancer (NSCLC). Following in-situ end-labelling of DNA, apoptotic cells were quantified by three different indices: as a percentage, either counting total cells (AI-tc) or point-counting (AI-pc), or as cells per area (AI-area). Blood vessels were stained with vWF antibody and vascularity was quantified by three methods. Median values for AI-tc, AI-pc and AI-area were 0.38, 0.32 and 10.7, respectively. High values were associated with improved survival, reaching statistical significance for AI-area (p0.05). All three apoptotic indices were significantly correlated with each other, but no correlation was found between indices of apoptosis and vascularity. As previously reported, vascularity had no prognostic value. These results indicate that, in NSCLC, vascularity is not informative, but apoptotic index may be a useful prognostic factor.

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