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Temporal changes in concentrations of lipids and apolipoprotein B among adults with diagnosed and undiagnosed diabetes, prediabetes, and normoglycemia: findings from the National Health and Nutrition Examination Survey 1988–1991 to 2005–2008
Earl S Ford, Chaoyang Li, Allan Sniderman
Cardiovascular Diabetology , 2013, DOI: 10.1186/1475-2840-12-26
Abstract: We used data from 3202 participants aged ≥20 years from the National Health and Nutrition Examination Survey (NHANES) III (1988–1991) and 3949 participants aged ≥20 years from NHANES 2005–2008.Among participants of all four groups, unadjusted and adjusted mean concentrations of total cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B, but not triglycerides, decreased significantly. Among participants with prediabetes and normoglycemia, unadjusted and adjusted mean concentrations of high-density lipoprotein cholesterol increased significantly. Adjusted mean log-transformed concentrations of triglycerides decreased in adults with undiagnosed diabetes and prediabetes. During 2005–2008, unadjusted concentrations of apolipoprotein B ≥80 mg/dl were observed in 72.8% of participants with diagnosed diabetes, 87.9% of participants with undiagnosed diabetes, 86.6% of participants with prediabetes, and 77.2% of participants with normoglycemia. The unadjusted use of cholesterol-lowering medications rose rapidly, especially among participants with diabetes (from ~1% to ~49%, P <0.001). The use of fenofibrate, gemfibrozil, and niacin rose significantly only among adults with diagnosed diabetes (from ~2% to ~8%, P?=?0.011).Lipid profiles of adults with diabetes improved during the approximately 16-year study period. Nevertheless, large percentages of adults continue to have elevated concentrations of apolipoprotein B.During the last several decades, diabetes has emerged as a major public health problem in the United States as the incidence and prevalence of obesity has escalated rapidly [1,2]. The lifetime probability of developing this disease is approximately 32.8% for men and 38.5% for women [3], and an estimated 25.6 million adults have diabetes [4]. Furthermore, diabetes has an enormous impact on health care costs in the United States; in 2007, for example, the economic costs attributable to this condition were est
Leptin and adiponectin in relation to body fat percentage, waist to hip ratio and the apoB/apoA1 ratio in Asian Indian and Caucasian men and women
Jessica Smith, Maha Al-Amri, Allan Sniderman, Katherine Cianflone
Nutrition & Metabolism , 2006, DOI: 10.1186/1743-7075-3-18
Abstract: A cross-sectional study comparing leptin, adiponectin, lipoproteins and anthropometric parameters in Asian Indian men and women to Caucasian men and women (4 groups). Anthropometric data (BMI, BF%, WHR), circulating lipids (apoA1, apoB, total cholesterol, and HDL-cholesterol), leptin and adiponectin were measured.Asian Indian men and women had higher leptin and lower adiponectin concentrations then Caucasian men and women, respectively. Leptin (positively) and adiponectin (negatively) correlated with anthropometric parameters and lipoproteins in all four groups. Using stepwise forward multiple regression, a model including TC/HDL-C ratio, WHR, BF%, hip circumference and waist circumference predicted 74.2% of leptin concentration in men. In women, apoB, BF%, waist circumference and age predicted 77.5% of leptin concentration. Adiponectin concentrations in men were predicted (30.2%) by HDL-C, total cholesterol, hip circumference and BF% while in women 41.2% of adiponectin concentration was predicted by the apoB/apoA1 ratio, WHR and age.As is evident from our data, there is a strong relationship between leptin, adiponectin, and abdominal obesity with increased CVD risk, as assessed by the apoB/apoA1 ratio. Dysregulation of these parameters may account for the increased risk of CVD in Asian Indians.Asian Indian men and women have a higher incidence and mortality rate from cardiovascular disease (CVD) than Caucasian men and women, yet the pathology behind this increased susceptibility is not fully understood [1-3]. Within India there has been a drastic increase in the incidence of CVD as a result of improving social and economic conditions [4,5]. Even immigrants within the same environment, when compared to Europeans or Caucasians, have a 1.5 to 4.0 times higher mortality rate from CVD and this risk increases with duration of residence [2,6,7].Factors such as body fat percentage (BF%), body fat distribution, dyslipidemia, and adipose tissue derived hormones (specifically
Gender Consideration in Sustainable Land Management Project Activities on the Highlands of Kilimanjaro Region: Lessons and Future Outlook  [PDF]
Wakuru Magigi, Allan Sathiel
Open Journal of Soil Science (OJSS) , 2014, DOI: 10.4236/ojss.2014.45022
Abstract: The paper contributes on understanding gender considerations into Sustainable Land Management (SLM) project activities on the Highlands of Kilimanjaro Region. Specifically, it documents gender profile and assesses the project activities along with gender considerations, where critical issues, risks and opportunities in relation to gender mainstreaming in SLM project activities are highlighted. It evaluates also the capacity for mainstreaming gender issues into the institutions involved in project implementation. The study employed structured interview and consultative meetings methods with key actors identified. A total of 500 respondents were interviewed in the project catchment areas in the region. Data were analyzed using the Statistical Package for Social Scientists (SPSS). The paper winds up by consolidating key strategic areas for intervention as future outlook and lessons which manifests benchmarks for the Kilimanjaro region to adopt a more programmatic approach to sustainable land management and elsewhere of the same in other cities with the same context in Sub-Saharan Africa.
The Heart of Learning  [PDF]
Allan M. MacKinnon
Creative Education (CE) , 2013, DOI: 10.4236/ce.2013.412A2003
Abstract: This essay explores the central importance of human interest and aspiration in learning. In an age when our educational institutions and ministries of education seem to be preoccupied with defining and measuring the “outcomes” of schooling, there is a great need to reconsider what we are doing in curriculum studies and refocus at least some of our energy on helping young people develop and sustain their interests. I use an autobiographical account of my interest in playing guitar and how this is related to my formative school experiences to develop my argument. The article also reviews literature tracing educational research and writing that focuses on the role of interest in learning.
Figuring out what works: a need for more and better studies on the relationship between ICU organization and outcomes
Allan Garland
Critical Care , 2010, DOI: 10.1186/cc8843
Abstract: In the previous issue of Critical Care, Billington and colleagues [1] presented an intriguing study assessing differences in intensive care unit (ICU) outcomes and resource use according to the base specialty of intensivists. While certain to be controversial, this type of research is important, and we need much more of it. But, first, details about the study itself.This retrospective statistical analysis used data from three medical-surgical ICUs in Calgary, Alberta. All are closed ICUs, with house staff, and a single intensivist in charge for each block of time. Multivariable regression was used to evaluate the association of outcomes and resource use with the specialty training of their 26 intensivists. Specialties were divided into three groups: (a) internal medicine, (b) internal medicine and pulmonary subspecialty, or (c) all others, representing anesthesia, surgery, and emergency medicine.While not perfect, their analysis is appropriate, adjusting for the type and severity of illness and a number of other potentially confounding variables and using methods to deal with the intrinsically clustered data. They found some differences according to intensivist specialty, most prominent of which was that adjusted ICU mortality was significantly lower for patients under the care of those trained in internal medicine and pulmonary medicine. However, when all of their data were considered, the association between the intensivists' base specialty and outcomes was not very robust. As the authors indicate, these findings cannot be assumed to represent a causal pathway, and without additional studies they cannot be taken as either definitive or generalizable. However, it is completely plausible that such differences exist.Variations in care and outcomes not related to patient or illness characteristics have been found throughout the health care system. Differences have been found at the level of geographic region [2], hospital [3], physician specialty, and individual physi
Clinical and laboratory characteristics of drug-induced vasculitic syndromes
Allan Wiik
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1805
Abstract: The differential diagnosis between drug-induced and idiopathic vasculitic conditions may be difficult in the individual patient. Because the mere withdrawal of the offending drug in the former situation is usually sufficient to attain complete remission of clinical symptoms, the distinction between these syndromes is very important. Failure to recognize a relationship with a drug can lead to fatal organ damage.The report by Branka Bonaci-Nikolic and coworkers [1] included in this issue of Arthritis Research and Therapy is a good example of clinical research aimed at identifying details that can aid in distinguishing between seemingly related syndromes, such as idiopathic vasculitides (IVs) and drug-induced vasculitides (DIVs). The clinical importance of recognizing patients with DIV is great because withdrawal of the offending drug usually leads to resolution of the syndrome without further therapy, whereas the IVs must always be treated with immunosuppressive and anti-inflammatory drugs, and sometimes even with plasmapheresis.The study included 72 consecutive patients who had been found to be positive for antineutrophil cytoplasmic antibodies (ANCAs) directed at proteinase-3 or myeloperoxidase. Twenty-nine of these patients suffered from Wegener's granulomatosis, 23 from microscopic polyangiitis, four from Churg–Strauss syndrome, and 16 from a DIV caused by either propylthiouracil or methimazol. All sera were additionally studied for presence of antinuclear antibodies (ANAs), antihistone and anticardiolipin antibodies, cryoglobulins, complement factors C3 and C4, C-reactive protein and α1-antitrypsin.Cutaneous vasculitis was found to be most common in the DIV patients, being present in 63%, whereas it was found in only 25% of the IV patients. In contrast, renal vasculitis was seen in 75% of the IV patients but only in 19% of the DIV patients. Four of the DIV patients presented with symptoms compatible with an IV-like syndrome (one Wegener's granulomatosis, three mi
Vaccinia tricks Toll
Rachel Allan
Genome Biology , 2000, DOI: 10.1186/gb-2000-1-6-reports0079
Abstract: A search of the vaccinia virus sequences identified two potential TLR homologs, A46R and A52R. Subsequent cloning confirmed that these proteins each contained a putative TIR domain, although they lacked a further conserved set of amino acids known to be important for TLR signaling. The viral homologs could therefore inhibit Toll signaling by competing for a TIR-dependent substrate while failing to recruit downstream components. To explore this possibility, the authors used a reporter gene system to study the effects of A46R and A52R on the Toll-like IL-1 receptor pathway. Expression of A46R and A52R in human cells was found to inhibit NFκB activation following IL-1 stimulation but had no effect on an unrelated pathway. Inhibition was more profound for the A52R protein. A52R was subsequently coexpressed with high levels of various IL-1 signaling intermediates in an attempt to pinpoint its action within the signaling pathway. Upstream components, including MyD88, failed to compensate for the action of A52R, whereas overexpression of downstream IRAK restored NFκB activation. These results indicate that A52R acts at the level of MyD88, consistent with its predicted TIR-dependent mechanism. Similar experiments performed on the IL-8 and TLR-4 systems confirmed that A52R could inhibit multiple TIR-dependent pathways.The authors conclude that A46R and A52R can effectively inhibit TIR-dependent signaling pathways. These proteins may therefore be useful for defining the importance of TIR-dependent pathways in the host immune response.The ancient origin of Toll pathways is reflected by their occurrence throughout multicellular organisms - from plants to insects and mammals. Studies of Drosophila Toll proteins have provided valuable insights into the role of these innate pattern-recognition receptors. Thus, we now know that binding of Toll receptors by microbial products such as lipopolysaccharide leads to the activation of appropriate immune defense mechanisms in the host. Clo
DAP12 and dendritic cells
Rachel Allan
Genome Biology , 2000, DOI: 10.1186/gb-2000-1-6-reports0080
Abstract: Knock-in mice expressing a non-functional DAP12 mutant were generated using standard homologous recombination and embryonic stem cell techniques. Reverse-transcriptase-coupled-PCR (RT-PCR) confirmed that these mice were homozygous for the mutant gene, and that the integrity of flanking genes was maintained. DAP12 mutant mice developed normally, with no significant alteration in the levels of lymphoid and myeloid cell subsets in their peripheral blood. The lytic capacity of their NK cells was assessed by killing assays in vitro. Lysis mediated specifically by the DAP12-associated NK receptor Ly49D was severely impaired, although alternative killing systems (dependent on other transmembrane adaptors) remained intact. It has previously been suggested that activating receptors such as Ly49D and Ly49H might regulate the expression of their inhibitory isoforms. Flow cytometric analysis of NK cells from DAP12 mutant mice revealed a normal inhibitory receptor repertoire, however, indicating that NK cell differentiation was not affected. The most significant effects of DAP12 deficiency were apparent in dendritic cell populations. Although no detectable changes in dendritic cell populations in lymphoid organs were observed, immunohistochemical staining of lympho-epithelial tissues revealed striking abnormal accumulations of dendritic cells in the mucosa of the small intestine, the dermis of buccal epithelia and the dermis of the skin. No gross deficiencies were observed in the phenotype of DAP12-deficient dendritic cells, their migratory capacity or their ability to stimulate allogeneic CD4 T cells, but they were unable to prime hapten-specific CD8 T cells in a contact-sensitivity test.A related paper describing the failure of DAP12-deficient mice to develop autoimmunity appeared in the same issue of Immunity and is available to subscribers.The authors conclude that DAP12 must have a critical role in myeloid dendritic cell/pre-dendritic cell differentiation and/or activation,
Autoantibodies in vasculitis
Allan Wiik
Arthritis Research & Therapy , 2003, DOI: 10.1186/ar758
Abstract: 'Vasculitis' is the term used for inflammatory diseases that involve blood vessel walls and the surrounding interstitium. Vasculitis may affect large, medium and small sized arteries, arterioles, capillaries, venules and veins [1]. Only the vasculitides that involve arterioles, capillaries and venules give rise to production of autoantibodies, which can serve as practical surrogate markers of the condition in question. Hence, the primary focus of the present review is on autoantibodies that are characteristically found in small vessel vasculitides [2].The lack of a unified terminology and classification for the various vasculitic conditions in the 1980s led to several attempts to set up a clinically applicable nomenclature. The American College of Rheumatology proposed classification criteria for some primary vasculitides and advocated the use of somewhat complicated diagnostic algorithms for establishing a precise diagnosis for each condition [3], but one clinically important vasculitic condition, namely microscopic polyangiitis [4], had been left out. A simplified nomenclature for primary vasculitic conditions, each one defined by their most common clinical, histological and immunological characteristics, was proposed by an ad hoc expert committee in 1994 [1]. This so-called Chapel Hill terminology has been widely accepted because of its simplicity and ease of use in clinical work up and is therefore used in this review.The antineutrophil cytoplasmic antibodies (ANCAs) directed at proteinase-3 (PR3) and myeloperoxidase (MPO) were discussed at length at the Chapel Hill Conference. That they are very characteristic markers of systemic Wegener's granulomatosis (WG), Churg–Strauss syndrome and microscopic polyangiitis (as well as limited forms of these conditions, such as renal-limited necrotizing and crescentic glomerulonephritis [NCGN]) was recognized, but it was not proposed that they be included in the criteria for these conditions.The varying presentations of sma
What you should know about PR3-ANCA: An introduction
Allan Wiik
Arthritis Research & Therapy , 2000, DOI: 10.1186/ar96
Abstract: Autoantibodies to human neutrophilic granulocytes (ANCA), described in the early 1960s, were initially demonstrated in patients with rheumatoid arthritis, autoimmune neutropenia, and ulcerative colitis (reviewed in [1]). The initial observations were by indirect immunofluorescence, in which the antibodies stained mainly the nuclear or perinuclear part of human neutrophils and monocytes, and the antibodies were therefore named `granulocyte-specific antinuclear antibodies'. In the early 1980s, indirect immunofluorescence studies revealed autoantibodies to neutrophil cytoplasmic granules, visible as a distinct, speckled pattern of staining in the cytoplasm (Fig. 1). These antibodies were found in sera from patients with Wegener's granulomatosis, especially those who had active systemic vasculitis [2]. These particular autoantibodies were named `classic anti-neutrophil cytoplasm antibodies' (C-ANCA) [3]. They were subsequently found to target conformational epitopes on a novel elastinolytic serine protease in azurophil granules, proteinase 3 (PR3), which was encoded by a gene on chromosome 19 [4]. PR3 can catabolize a number of human proteins, such as proteoglycans, elastin, and all four subclasses of IgG including the PR3-ANCA/PR3 complex. The latter activity suggests that PR3-ANCA is an inefficient inhibitor of the PR3 enzyme activity [5]. The circulating neutrophils of certain healthy individuals may constitutively express PR3 on their cell surface, and it has been hypothesized that this genetic trait may predispose to small-vessel vasculitis if self-tolerance to PR3 is overcome [6].In most laboratories, screening for ANCA is done by use of an internationally agreed indirect immunofluorescence technique using human buffy-coat cells as substrate [7]. Sera positive for C-ANCA are further tested by direct enzyme immunoassay (EIA) to reveal their specificity for either purified PR3 or myeloperoxidase (MPO) as target antigen, both of which can give rise to a C-ANCA staini
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