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In addition to vascular disease, diabetes is associated with substantial premature death from several cancers, infectious diseases, external causes, intentional self-harm, and degenerative disorders, independent of several major risk factors. (Funded by the British Heart Foundation and others.).
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The existence of a work potential, governing material response when elastic behavior occurs, is shown to provide a concise framework for the structure of inelastic constitutive laws. The discussion includes the identification of differential invariants in conjugate stress and strain variables, an examination and reformulation of postulates leading to "normality rules", and a study of the transmission of constitutive properties from subelements to overall behavior of heterogeneous systems. Also, internal variable representations of inelasticity are examined within this framework.
This Letter describes a quasistationary breakup of an immiscible, inviscid fluid at low capillary numbers. The breakup proceeds in a coflowing, viscous liquid, in a confined geometry of a long and narrow orifice. In contrast to the capillary instability in an unbounded fluid, the collapse proceeds through a series of equilibria, each yielding the minimum interfacial energy of the fluid-fluid interface. The process is slow in comparison to typical relaxation speeds of the interface, and it is reversible. Its quasistatic character of collapse forms the basis for controlled, high-throughput generation of monodisperse fluid dispersions.
The prevalence of type 2 diabetes is increasing dramatically worldwide. Excess adiposity is an important contributor to the development of type 2 diabetes and cardiovascular diseases (1). Insulin resistance, inflammation, hypertension, and dyslipidemia, components of the metabolic syndrome, have been implicated in the effects of adiposity on type 2 diabetes and cardiovascular diseases, but the mechanisms responsible for these detrimental effects of adiposity have not been fully elucidated. Two paradigms are currently areas of intense study: one focused on ectopic fat and the other on the endocrine function of adipose tissue (2). Ectopic fat is present in nonadipose tissues such as the liver, muscle, and probably pancreatic β-cells. Both lipodystrophy (failure to develop adipose tissue) and obesity with full adipose cells are characterized by a lack of fat-storage capacity, resulting in overflow to other tissues of triglycerides and free fatty acids in the form of ectopic fat. Normal physiological processes can be disrupted by this ectopic fat, leading to insulin resistance and impaired insulin secretion. The endocrine function of adipose tissue is an important regulatory process throughout the body that is carried out by signaling proteins secreted by adipose tissue. These signaling proteins are called adipocytokines or adipokines, and they include leptin, adiponectin, resistin, tumor necrosis factor-α, and interleukin-6. Members of the lipocalin family of proteins have large sequence differences but share a common tertiary structure formed by segments termed lipocalin folds (3). Lipocalin folds consist of 8 antiparallel β-sheets that surround a hydrophobic pocket and allow lipocalins to function as transport or carrier proteins. Several human lipocalins have been identified, including retinol-binding protein 4 (RBP4), which has recently been added to the list of adipokines that may link obesity and insulin resistance (4)(5). In this issue of Clinical Chemistry , Dr. Wang and …
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTReaction of threo-dicarbonyl-.pi.-cyclopentadienyl(3,3-dimethylbutyl-1,2-d2)iron with triphenylphosphineGeorge M. Whitesides and David J. BoschettoCite this: J. Am. Chem. Soc. 1969, 91, 15, 4313–4314Publication Date (Print):July 1, 1969Publication History Published online1 May 2002Published inissue 1 July 1969https://doi.org/10.1021/ja01043a064Request reuse permissionsArticle Views254Altmetric-Citations38LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit PDF (259 KB) Get e-Alertsclose Get e-Alerts
Abstract The long-term inflammatory impact of diet could potentially elevate the risk of periodontal disease through modification of systemic inflammation. The aim of the present study was to prospectively investigate the associations between a food-based, reduced rank regression (RRR)-derived, empirical dietary inflammatory pattern (EDIP) and incidence of periodontitis. The study population was composed of 34 940 men from the Health Professionals Follow-Up Study, who were free of periodontal disease and major illnesses at baseline (1986). Participants provided medical and dental history through mailed questionnaires every 2 years and dietary data through validated semi-quantitative FFQ every 4 years. We used Cox proportional hazard models to examine the associations between EDIP scores and validated self-reported incidence of periodontal disease over a 24-year follow-up period. No overall association between EDIP and the risk of periodontitis was observed; the hazard ratio comparing the highest EDIP quintile (most proinflammatory diet) with the lowest quintile was 0·99 (95 % CI 0·89, 1·10, P -value for trend = 0·97). A secondary analysis showed that among obese non-smokers (i.e. never and former smokers at baseline), the hazard ratio for periodontitis comparing the highest EDIP quintile with the lowest was 1·39 (95 % CI 0·98, 1·96, P -value for trend = 0·03). In conclusion, no overall association was detected between EDIP and incidence of self-reported periodontitis in the study population. From the subgroups evaluated, EDIP was significantly associated with increased risk of periodontitis only among non-smokers who were obese. Hence, this association must be interpreted with caution.