Empiricism and Theorizing in Epidemiology and Social Network Analysis

The connection between theory and data is an iterative one. In principle, each is informed by the other: data provide the basis for theory that in turn generates the need for new information. This circularity is reflected in the notion of abduction, a concept that focuses on the space between induction (generating theory from data) and deduction (testing theory with data). Einstein, in the 1920s, placed scientific creativity in that space. In the field of social network analysis, some remarkable theory has been developed, accompanied by sophisticated tools to develop, extend, and test the theory. At the same time, important empirical data have been generated that provide insight into transmission dynamics. Unfortunately, the connection between them is often tenuous and the iterative loop is frayed. This circumstance may arise both from data deficiencies and from the ease with which data can be created by simulation. But for whatever reason, theory and empirical data often occupy different orbits. Fortunately, the relationship, while frayed, is not broken, to which several recent analyses merging theory and extant data will attest. Their further rapprochement in the field of social network analysis could provide the field with a more creative approach to experimentation and inference

SLE - Practical and theoretical barriers to the prevention of accelerated atherosclerosis in systemic lupus erythematosus

Accelerated atherosclerotic vascular disease (ASVD) is a major cause of death in systemic lupus erythematosus (SLE). Although many authorities are calling for aggressive assessment and management of cardiac risk factors in patients with SLE, both theoretical and practical barriers to this approach exist. It seems that SLE and/or its treatment are themselves strong risk factors for the development of ASVD and it is unclear how much this risk can be decreased by the control of traditional risk factors. Studies from several centers have shown that suboptimal risk factor management and barriers to acceptance of these measures must also be studied further

Epstein–Barr virus and rheumatoid arthritis: is there a link?

Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic, destructive, debilitating arthritis. Its etiology is unknown; it is presumed that environmental factors trigger development in the genetically predisposed. Epstein–Barr virus, a nearly ubiquitous virus in the human population, has generated great interest as a potential trigger. This virus stimulates polyclonal lymphocyte expansion and persists within B lymphocytes for the host's life, inhibited from reactivating by the immune response. In latent and replicating forms, it has immunomodulating actions that could play a role in the development of this autoimmune disease. The evidence linking Epstein–Barr virus and rheumatoid arthritis is reviewed

If everything is ADHD then...teachers\u27 confusion of ADHD with other disorders

The ability of Special Education teachers (SET) and Regular Education teachers (RET) to accurately identify and distinguish the characteristics of Attention Deficit Hyperactivity Disorder (ADHD) from those of other childhood behavior disorders was examined. Both SET and RET teachers were able to identify a majority of ADHD characteristics ; however, both groups were poor in differentiating ADHD characteristics from those of other disorders, with SET showing more incorrect assignment of problem behavior than RET (p\u3c.01). Neither pre-service nor in-service training correlated significantly with the ability to accurately identify ADHD characteristics. The general lack of skill in the discrimination of ADHD from other behavior problems by both SET and RET teachers strongly suggests the need for better pre-service or in-service training

Sand Trends and Habitat Degradation

Scholarship domains: Discovery, Teaching and Learning Author keywords: Sand Movement, Fish Diversity, Kankakee River, Sportfish, Side-scan sona

Using a Computer Simulation in the Research, Training, and Evaluation of School Psychologists

A computer program, School Psychologist Simulation, is described. The program presents users with information and events such as might be encountered in a real school setting regarding schoolchildren referred to the school psychologist; users can practice the skills needed by a school psychologist in the assessment of the case. The participant then submits a report detailing assessment, recommendations, and reasoning for the case in either essay or multiple-choice format. An additional program permits the instructor to customize the material presented to the user by modifying the case material of a specific child and/or by altering the forms displayed to the user in all cases

Altered expression of protein tyrosine phosphatase, non-receptor type 22 isoforms in systemic lupus erythematosus

Introduction: A C-to-T single nucleotide polymorphism (SNP) located at position 1858 of human protein tyrosine phosphatase, non-receptor type 22 (PTPN22) complementary DNA (cDNA) is associated with an increased risk of systemic lupus erythematosus (SLE). How the overall activity of PTPN22 is regulated and how the expression of PTPN22 differs between healthy individuals and patients with lupus are poorly understood. Our objectives were to identify novel alternatively spliced forms of PTPN22 and to examine the expression of PTPN22 isoforms in healthy donors and patients with lupus. Methods: Various human PTPN22 isoforms were identified from the GenBank database or amplified directly from human T cells. The expression of these isoforms in primary T cells and macrophages was examined with real-time polymerase chain reaction. The function of the isoforms was determined with luciferase assays. Blood samples were collected from 49 subjects with SLE and 15 healthy controls. Correlation between the level of PTPN22 isoforms in peripheral blood and clinical features of SLE was examined with statistical analyses. Results: Human PTPN22 was expressed in several isoforms, which differed in their level of expression and subcellular localization. All isoforms except one were functionally interchangeable in regulating NFAT activity. SLE patients expressed higher levels of PTPN22 than healthy individuals and the levels of PTPN22 were negatively correlated with the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SLICC-DI). Conclusions: The overall activity of PTPN22 is determined by the functional balance among all isoforms. The levels of PTPN22 isoforms in peripheral blood could represent a useful biomarker of SLE

Effect of Vitamin D on serum markers of bone turnover in SLE in a randomised controlled trial

© 2019 Author(s). Objective Bone health in SLE is adversely affected by vitamin D deficiency, inflammatory cytokines and glucocorticoid use. We hypothesised that vitamin D supplementation would increase markers of bone formation and decrease markers of bone resorption in SLE subjects. Methods We studied 43 vitamin D-deficient SLE subjects who participated in a 12-week randomised controlled trial of 2000-4000 IU/day vitamin D supplementation versus placebo. Subjects had inactive SLE (SLE Disease Activity Index ≤4) and were taking D, N-terminal propeptide of type 1 collagen (P1NP) and C-telopeptide (CTX). We tested the effect of vitamin D versus placebo on change (δ) in P1NP and δCTX in an intention-to-treat analysis. Secondary analyses evaluated whether vitamin D affected bone turnover among subjects achieving vitamin D repletion (≥30 ng/mL) or currently taking glucocorticoids. Results 28 subjects were randomised to vitamin D and 15 to placebo. Mean age was 39 years and 40% were using glucocorticoids at enrolment. Repletion was achieved by 46% in the vitamin D group versus none in the placebo group. Changes in bone turnover markers were not significantly different in the vitamin D group versus placebo group (median δP1NP -0.2 vitamin D group vs -1.1 placebo group (p=0.83); median δCTX +3.5 vitamin D group vs -37.0 placebo group (p=0.50)). The effect of vitamin D did not differ based on achieving vitamin D repletion or baseline glucocorticoid use. Conclusion Vitamin D supplementation did not affect the 12-week change in bone turnover markers among SLE subjects in this trial