Comparison of Surface Water Quality and Yields from Organically and Conventionally Produced Sweet Corn Plots with Conservation and Conventional Tillage.

Organic agricultural systems are often assumed to be more sustainable than conventional farming, yet there has been little work comparing surface water quality from organic and conventional production, especially under the same cropping sequence. Our objective was to compare nutrient and sediment losses, as well as sweet corn ( L. var. ) yield, from organic and conventional production with conventional and conservation tillage. The experiment was located in the Appalachian Mountains of North Carolina. Four treatments, replicated four times, had been in place for over 18 yr and consisted of conventional tillage (chisel plow and disk) with conventional production (CT/Conven), conservation no-till with conventional production (NT/Conven), conventional tillage with organic production (CT/Org), and conservation no-till with organic production (NT/Org). Water quality (surface flow volume; nitrogen, phosphorus, and sediment concentrations) and sweet corn yield data were collected in 2011 and 2012. Sediment and sediment-attached nutrient losses were influenced by tillage and cropping system in 2011, due to higher rainfall, and tillage in 2012. Soluble nutrients were affected by the nutrient source and rate, which are a function of the cropping system. Sweet corn marketable yields were greater in conventional systems due to high weed competition and reduced total nitrogen availability in organic treatments. When comparing treatment efficiency (yield kg ha /nutrient loss kg ha ), the NT/Conven treatment had the greatest sweet corn yield per unit of nutrient and sediment loss. Other treatment ratios were similar to each other; thus, it appears the most sustainably productive treatment was NT/Conven.

Some antiphospholipid antibodies bind to hemostasis and fibrinolysis proteases and promote thrombosis.

It is generally accepted that the major autoantigen for antiphospholipid antibodies (aPL) is beta(2)glycoprotein I (beta(2)GPI). Interestingly, some aPL bind to beta(2)GPI and the homologous enzymatic domains of several proteases involved in hemostasis and fibrinolysis, and correspondingly hinder anticoagulant regulation and resolution of clots. These findings are consistent with several early findings of aPL and provide a new perspective about some aPL in terms of their binding specificities and related functional properties in promoting thrombosis. In addition, homologous enzymatic domains of the involved proteases share conformation epitope(s) with beta(2)GPI, thus providing a possible structural basis for some non-mutually exclusive mechanisms of aPL-mediated thrombosis.

High-order quantum resonances observed in a periodically kicked Bose-Einstein condensate.

We have observed high-order quantum resonances in a realization of the quantum delta-kicked rotor, using Bose-condensed Na atoms subjected to a pulsed standing wave of laser light. These resonances occur for pulse intervals that are rational fractions of the Talbot time, and are characterized by ballistic momentum transfer to the atoms. The condensate's narrow momentum distribution not only permits the observation of the quantum resonances at 3/4 and 1/3 of the Talbot time, but also allows us to study scaling laws for the resonance width in quasimomentum and pulse interval.

Polymorphisms of human CD19 gene: possible association with susceptibility to systemic lupus erythematosus in Japanese.

CD19 regulates the signaling for B lymphocyte development, activation and proliferation. In mice, CD19 deficiency and overexpression were shown to result in hypogammaglobulinemia and autoantibody production, respectively. In the present study, we screened for the polymorphisms of CD19, and examined the detected polymorphisms for the association with rheumatoid arthritis (RA), Crohn's disease and systemic lupus erythematosus (SLE). Two SNPs, c.705G>T (P235P and IVS14-30C>T, were decreased (P = 0.0096 and P = 0.028, respectively), in SLE. A GT repeat polymorphism, c.*132(GT)(12-18), was detected within the 3'-untranslated region, and individuals with > or =15 times repeat was significantly increased in the independent two groups of Japanese SLE patients (P = 0.011 and P = 0.035, respectively); the overall difference between total SLE and controls was striking (P = 0.0061). No association was observed for RA and Crohn's disease. In addition, no variations other than the common polymorphisms were detected in four patients with common variable immunodeficiency, the phenotype of which resembles CD19 deficient mice. In Caucasian SLE families, this GT repeat polymorphism was rare. CD19 mRNA level in the isolated peripheral blood B lymphocytes was lower in individuals possessing (GT)(15-18) alleles compared with those without these alleles, both in controls and in SLE patients; however, the difference did not reach statistical significance. These results suggested that either the slight reduction in the CD19 mRNA level associated with the elongation of GT repeat, or an allele of another locus in linkage disequilibrium with CD19 (GT)(15-18), may be associated with susceptibility to SLE in Japanese.

Identification of anti-thrombin antibodies in the antiphospholipid syndrome that interfere with the inactivation of thrombin by antithrombin.

The combined presence of anti-phospholipid (PL) Ab, including lupus anticoagulants (LAC) and/or anticardiolipin Ab (aCL), and thrombosis is recognized as the antiphospholipid syndrome (APS). LAC are detected as an inhibitory effect on PL-restricted in vitro blood coagulation tests, and are comprised mainly of Ab against beta(2) glycoprotein I and prothrombin (PT). Recently, anti-PT Ab (aPT) were found to be associated with thrombosis by some investigators, although this is not confirmed by others. Considering that aPT are heterogeneous in patients and that PT is converted into thrombin, we hypothesize that certain aPT in patients may bind to thrombin, and that some of such anti-thrombin Ab may interfere with thrombin-antithrombin (AT) interaction and thus reduce the AT inactivation of thrombin. To test this hypothesis, we searched for anti-thrombin Ab in APS patients and then studied those found for their effects on the AT inactivation of thrombin. The results revealed that most, but not all, aPT-positive patient plasma samples contained anti-thrombin Ab. To study the functional significance of these Ab, we identified six patient-derived mAb that bound to both PT and thrombin. Of these mAb, three could reduce the AT inactivation of thrombin, whereas others had minimal effect. These findings indicate that some aPT in patients react with thrombin, and that some of such anti-thrombin Ab could inhibit feedback regulation of thrombin. Because the latter anti-thrombin Ab are likely to promote clotting, it will be important to develop specific assays for such Ab and study their roles in thrombosis in APS patients.

Analysis of the association of HLA-DRB1, TNFalpha promoter and TNFR2 (TNFRSF1B) polymorphisms with SLE using transmission disequilibrium test.

A number of studies reported associations of HLA-DRB1, TNFalpha (TNF) promoter and TNF receptor II (TNFR2, TNFRSF1B) polymorphisms with systemic lupus erythematosus (SLE), however, the results have often been inconsistent. Such lack of consistency could partly derive from the population admixture involved in the case-control study. To avoid such a problem, polymorphisms in these genes were analyzed using transmission disequilibrium test (TDT) in Caucasian SLE families. Ninety-one Caucasian SLE family samples recruited in southern California were analyzed for the association with HLA-DRB1, TNF promoter positions at -1031, -863, -857 and -308, and TNFR2-196M/R polymorphisms. Significant transmission was observed for HLA-DRB1*1501, but not for HLA-DRB1*0301, nor for TNF haplotype that codes for -308A. Interestingly, TNF haplotype coding for -1031C, -863A, -857C showed a tendency of preferential nontransmission in the patients without lupus nephritis and in those with malar rash. No transmission distortion was observed for TNFR2-196R allele. These findings confirmed the association of HLA-DRB1*1501, but did not replicate that of the HLA-DRB1*0301, TNFA-308A and TNFR2-196R with SLE in this population. In addition, a possible disease-protective role for TNF haplotype coding for -1031C, -863A, -857C was suggested.

Genetics and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex, multifactorial autoimmune disease. Genetic factors are believed to contribute to its pathogenesis. There have been numerous recent advances in the study of murine and human lupus genetics. In well-defined, experimental, transgenic or gene-knockout mouse models, the development of lupus-like disease has implicated specific genes and pathways in the disease pathogenesis. Linkage analyses have mapped multiple susceptibility loci and disease suppressive loci using inbred strains of mice that spontaneously develop lupus-like disease. Elegant genetic dissection has demonstrated that a component phenotype of SLE is displayed by each congenic strain carrying a single susceptibility locus on a resistant genetic background, whereas polycongenic strains exhibit fatal lupus nephritis. These studies suggest that genes in separate pathways can interact to augment or suppress the initiation and progression of systemic autoimmunity. In association studies of human lupus, the contributions of the MHC loci, Fcg receptors, various cytokines, components of the complement cascade, and proteins involved in apoptosis have been explored. Most recently, linkage analyses have been performed and provide many chromosomal regions for further exploration for susceptibility genes. Studies to identify the genes in the susceptibility regions are underway. An understanding of the genes involved in the development of lupus should provide targets for more focused therapy in lupus.

Consumers face higher costs as health plans seek to control drug spending.

Faced with relentless growth in pharmaceutical spending during the 1990s, health plans in recent years have tried to rein in costs by negotiating lower drug prices, encouraging more cost-conscious physician prescribing patterns and moderating the volume and mix of drugs demanded by consumers. Because of limited success with these strategies, plans have moved rapidly to three-tier benefit packages that offer broader drug choices but shift more costs to consumers. The move to three-tier pharmacy benefits appears to have slowed drug-spending growth for some plans--at least for the short term--but raises questions about the cost and quality of pharmaceutical care for consumers. Based on interviews with health plan executives in the 12 nationally representative communities the Center for Studying Health System Change (HSC) visits every two years, this Issue Brief examines plans' strategies to contain drug spending and the possible consequences for consumers.

Genetics and systemic lupus erythematosus.

Systemic lupus erythematosus is a complex, multifactorial, autoimmune disease. Genetic factors are believed to contribute to its pathogenesis. There have been numerous recent advances in the study of both murine and human lupus genetics. In murine lupus, congenic strains of three susceptibility loci have been developed. Transgenic and knock-out mice models of candidate genes now exist. In association studies of human lupus, the contributions of the MHC loci, Fcgamma receptors, various cytokines, components of the complement cascade, and proteins involved in apoptosis have been explored. Most recently, linkage analyses have been performed and provide numerous regions for further exploration for susceptibility genes. Studies to identify the genes in the susceptibility regions are underway. An understanding of the genes involved in the development of lupus should provide targets for more focused therapy.

Health plan competition in local markets.

OBJECTIVE: To examine the structure of local health insurance markets and the strategies health plans were using to respond to competitive pressures in local markets in 1996/1997. DATA SOURCES/STUDY SETTING: Community Tracking Study site visits conducted between May 1996 and April 1997 in 12 U.S. markets selected to be nationally representative. STUDY DESIGN: In each site, 36 to 60 interviews on local health system change were conducted with healthcare industry informants representing health plans, providers, and purchasers. DATA COLLECTION/EXTRACTION METHOD: Relevant data for this article were abstracted from standardized protocols administered to multiple respondents in each site. PRINCIPAL FINDINGS: Although the competitive threat from national plans was pervasive, local plans in most sites continued to retain strong, often dominant, positions in historically concentrated markets. In all sites, in response to purchaser pressures for stable premiums and provider choice, and the threat of entry and to plans were using three strategies to increase market share and market power: (1) consolidation/geographic expansion, (2) price competition, and (3) product line/segment diversification that focused on broad networks and open-access products. In most markets, in response to the demand for provider choice, the trend was away from ownership and exclusive arrangements with providers. CONCLUSIONS: Although local plans were moving to become full-service regional players, there was uncertainty about the abilities of all plans to sustain growth strategies at the expense of margins and organizational stability, and to effectively manage care with broad networks.

Validity and reliability of retrospective assessment of disease activity and flare in observational cohorts of lupus patients.

BACKGROUND: The use of validated retrospective tools to assess disease activity in an observational cohort of patients would allow researchers the flexibility to analyze unique exploratory questions. Valid, reliable tools exist for assessing disease activity and flare for Systemic Lupus Erythematosus (SLE) patients. However, these tools have been designed for use in structured settings. Many of these populations under study are subject to strict inclusion, exclusion criteria and disease management protocols. The ability to apply these tools to populations not subject to such control would allow researchers to explore questions about unique populations, new treatment applications or predictors of clinical outcomes. This study sought to establish the reliability and validity of retrospective medical record abstraction of SLE disease activity and flare instruments by two rheumatologists. METHODS: From university rheumatology outpatient clinics, 22 patients were randomly selected to establish intra-rater reliability and 26 patients were selected to establish inter-rater reliability. Two rheumatologists using a Physician Global Assessment (PGA), the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and the Safety of Estrogens in Lupus Erythematosus-National Assessment (SELENA) flare tool retrospectively abstracted patient charts. Agreement between the tools was evaluated to assess validity. RESULTS: The mean patient age was 39 y; 96% were female, 54% Caucasian, 27% Hispanic, 19% Asian; median PGA was 1.4 (on a 0-3 scale) and median SLEDAI score was 4 (range 0-27). Intra-rater reliability for PGA, SLEDAI and the SELENA flare tool was 0.88, 0.87 and 0.52, respectively. Inter-rater reliability for PGA, SLEDAI, and SELENA flare was 0.79, 0.75, and 0. 50, respectively. To assess validity, the tools were compared against each other to assess agreement. From the parent study sample (n=54 patients), the disease activity measures, PGA and SLEDAI demonstrated adequate agreement (r=0.60). However, the SELENA flare tool demonstrated poor agreement with either PGA-defined flare or SLEDAI-defined flare (weighted kappa, 0.29 and 0.40 respectively). PGA-defined and SLEDAI-defined flare also demonstrated poor agreement (weighted kappa, 0.35). CONCLUSIONS: These data suggest that investigators can reliably reproduce patient disease activity through retrospective chart abstraction using PGA and SLEDAI. Assessing flare is a more difficult concept. The validity of assessing flare at a specific patient-visit is poor. Retrospective assessment of patient flare risk over a specified time period is conceptually more valid and avoids difficulties assessing timing and duration of flare. As there have been no similar published prospective analyses of validity using the SELENA flare tool, it is not clear if this problem was unique to the method of retrospective chart abstraction, the nature of non-protocol study patient visits, the tool itself or a combination of all three aspects.

PARP alleles within the linked chromosomal region are associated with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by various autoantibodies that recognize autoantigens displayed on the surface of cells undergoing apoptosis. The genetic contribution to SLE susceptibility has been widely recognized. We previously reported evidence for linkage to SLE of the human chromosome 1q41-q42 region and have now narrowed it from 15 to 5 cM in an extended sample using multipoint linkage analysis. Candidate genes within this region include (a) PARP, poly(ADP-ribose) polymerase, encoding a zinc-finger DNA-binding protein that is involved in DNA repair and apoptosis; (b) TGFB2, encoding a transforming growth factor that regulates cellular interactions and responses; and (c) HLX1, encoding a homeobox protein that may regulate T-cell development. Using a multiallelic, transmission-disequilibrium test (TDT), we found overall skewing of transmission of PARP alleles to affected offspring in 124 families (P = 0.00008), preferential transmission of a PARP allele to affected offspring (P = 0.0003), and lack of transmission to unaffected offspring (P = 0.004). Similar TDT analyses of TGFB2 and HLX1 polymorphisms yielded no evidence for association with SLE. These results suggest that PARP may be (or is close to) the susceptibility gene within the chromosome 1q41-q42 region linked to SLE.

Managed care and physicians' provision of charity care.

CONTEXT: Health system changes may be affecting the ability of physicians to provide care with little or no compensation from patients who are uninsured and under-insured and may result in decreased access to physicians for uninsured persons. OBJECTIVE: To examine the association between managed care and physicians' provision of charity care. DESIGN: The 1996-1997 Community Tracking Study physician survey. SETTING AND PARTICIPANTS: A nationally representative sample of 10881 physicians from 60 randomly selected communities. MAIN OUTCOME MEASURE: The number of hours in the month prior to the interview that the physician provided care for free or at reduced fees because of the financial need of the patient. RESULTS: Overall, 77.3% of respondents provided an average of 10.3 hours of charity care per month [corrected]. Physicians who derive at least 85% of their practice revenue from managed care plans were considerably less likely to provide charity care and spend fewer hours providing charity care than physicians with little involvement in managed care plans (P = .01). In addition, physicians who practice in areas with high managed care penetration provided fewer hours of charity care than physicians in other areas, regardless of their own level of involvement with managed care (P<.01). Differences in charity care provision were also shown for other important factors, including ownership of the practice and practice arrangements (more charity care occurred in solo and 2-physician practices; P<.01). CONCLUSION: Physicians involved with managed care plans and those who practice in areas with high managed care penetration tend to provide less charity care.

Rheumatoid arthritis: current clinical and research directions.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by synovitis and joint erosions. It affects approximately 1% of the adult population in a female/male ratio ranging from 2:1 to 4:1. RA is an insidious disease, typically having an onset of symmetric joint swelling and reaching a peak incidence in the fourth and fifth decades. Extraarticular manifestations include pulmonary, ocular, and vascular disease. The etiology of RA remains unknown. Attempts to discover infectious causes have proven unsuccessful, although environmental influences may trigger a response leading to the development of this autoimmune disease. Genetic associations have been identified, particularly with the major histocompatibility complex class II antigens. Furthermore, twin studies have shown a 30%-50% concordance rate for monozygotic twins. Approximately 70%-80% of patients with RA have rheumatoid factor present in the blood, although its role remains unclear. Hormonal status may influence RA. The majority of RA patients are women, and in 75% of them, the disease improves during pregnancy. RA has significant financial and social implications associated with treatment costs, lost wages, disability, and increased mortality. Mainstays of medical therapy have included nonsteroidal anti-inflammatory and immunosuppressive agents, such as prednisone and methotrexate. Recent advances in the treatment of RA include specific inhibitors of cyclooxygenase II, T cells, blood vessels, cytokines (such as tumor necrosis factor-alpha [TNF-alpha] or interleukin-1 [IL-1]), and adhesion molecules. Additional studies are ongoing with combination interventions. It is anticipated that a better understanding of the basic pathophysiologic mechanisms critical in RA pathogenesis will provide more precise and efficacious therapy.

A Disordered Eating Response Team's Effect on Nutrition Practices in College Athletes.

The disordered eating response team developed a protocol for assessment and intervention for athletes who are identified as at risk for disordered eating. Team members included the team physician, athletic trainers, a dietitian with knowledge of sports nutrition, and a psychologist. Team members also developed education programs for coaches and athletic trainers, athletes, and dining services personnel regarding eating to support health and athletic performance. During the first year of the program, 12 athletes were referred to the disordered eating program. Evaluations from the education programs indicated that they were well received by all participants. Information considered to be most useful by the athletes included: high-carbohydrate vs high-fat foods (98%), timing of food intake (88%), and fluid needs (68%). Topics about which the athletes requested more information included: increasing lean body mass (70%) and foods to eat while traveling (55%). In response to the program(s), the athletes reported increasing intake of carbohydrate foods (100%), decreasing intake of caffeine-containing beverages (68%), and increasing dietary intake of iron and calcium (78% females). Our programs have improved athletes' knowledge of nutrition to support health and performance and have provided intervention for athletes at risk for disordered eating.