Legislative History in Ohio: Myths and Realities

In this article I will explore what seems to be a prevailing formal view about Ohio legislative history, and the contradictory signals expressed by the Ohio Revised Code and the courts, particularly the Ohio Supreme Court. In Part Two, I consider the prevailing assumptions about legislative history in Ohio. In Part Three, I examine the reality of judicial use of legislative history in Ohio; Part Four describes the Ohio Legislative Service Commission and its non-partisan legislative staff. Part Five compares federal and Ohio legislative history, and argues that Ohio\u27s legislative process and history are rooted in its political culture. In Part Six, I look at the accessibility of Ohio legislative history and the identities of the lawyers who have used Ohio legislative history in their arguments before courts. When I conclude, I hope to have convinced you to view these things through altered lenses and to consider a different possibility: there is legislative history in Ohio after all

Comparison of PREDICTS atherosclerosis biomarker changes after initiation of new treatments in patients with SLE

Objective Patients with SLE have an increased risk ofatherosclerosis (ATH) that is not adequately explainedby traditional risk factors. We previously described thePredictors of Risk for Elevated Flares, Damage Progression,and Increased Cardiovascular disease in PaTients withSLE (PREDICTS) atherosclerosis-risk panel, which includesproinflammatory HDL (piHDL), leptin, soluble tumournecrosis factor-like weak inducer of apoptosis (sTWEAK)and homocysteine, as well as age and diabetes. A highPREDICTS score confers 28-fold increased odds forfuture atherosclerosis in SLE. The aim of this study is todetermine whether PREDICTS biomarkers are modifiable bycommon lupus therapies.Methods This prospective observational study includedSLE subjects started on new lupus treatments. Leptin,sTWEAK, homocysteine and antioxidant function of HDLwere measured at baseline (prior to drug initiation), 6weeks and 12 weeks.Results 16 subjects started mycophenolate (MMF), 18azathioprine (AZA) and 25 hydroxychloroquine (HCQ).In MMF-treated subjects, HDL function progressivelyimproved from 2.23 ± 1.32 at baseline to 1.37±0.81at 6 weeks (p=0.02) and 0.93±0.54 at 12 weeks(p=0.009). sTWEAK levels also improved in MMF-treatedsubjects from 477.5±447.1 to 290.3±204.6 pg/mLafter 12 weeks (p=0.04), but leptin and homocysteinelevels were not significantly changed. In HCQ-treatedsubjects, only HDL function improved from 1.80±1.29 atbaseline to 1.03±0.74 after 12 weeks (p=0.05). Therewere no changes in the AZA group. MMF treatmentwas still associated with significant improvements inHDL function after accounting for potential confounderssuch as total prednisone dose and changes in diseaseactivity. Overall, the mean number of high-risk PREDICTSbiomarkers at week 12 significantly decreased in theentire group of patients started on a new lupus therapy(2.1±0.9 to 1.8±0.9, p=0.02) and in the MMF-treatedgroup (2.4±0.8 vs 1.8±0.9, p=0.003), but not in theAZA or HCQ groups. In multivariate analysis, the odds ofhaving a high PREDICTS atherosclerosis risk score at 12weeks were lower with MMF treatment (OR 0.002, 95%CI 0.000 to 0.55, p=0.03).Conclusions 12 weeks of MMF therapy improves theoverall PREDICTS atherosclerosis biomarker profile.Further studies will determine whether biomarkerchanges reflect decreases in future cardiovascularevents

Altered lipoprotein metabolism in chronic inflammatory states: proinflammatory high-density lipoprotein and accelerated atherosclerosis in systemic lupus erythematosus and rheumatoid arthritis

In this review, the authors discuss the formation and structure of high-density lipoproteins (HDLs) and how those particles are altered in inflammatory or stress states to lose their capacity for reverse cholesterol transport and for antioxidant activity. In addition, abnormal HDLs can become proinflammatory (piHDLs) and actually contribute to oxidative damage. The assay by which piHDLs are identified involves studying the ability of test HDLs to prevent oxidation of low-density lipoproteins. Finally, the authors discuss the potential role of piHDLs (found in some 45% of patients with systemic lupus erythematosus and 20% of patients with rheumatoid arthritis) in the accelerated atherosclerosis associated with some chronic rheumatic diseases

High plasma leptin levels confer increased risk of atherosclerosis in women with systemic lupus erythematosus, and are associated with inflammatory oxidised lipids.

BackgroundPatients with systemic lupus erythematosus (SLE) are at increased risk of atherosclerosis, even after accounting for traditional risk factors. High levels of leptin and low levels of adiponectin are associated with both atherosclerosis and immunomodulatory functions in the general population.ObjectiveTo examine the association between these adipokines and subclinical atherosclerosis in SLE, and also with other known inflammatory biomarkers of atherosclerosis.MethodsCarotid ultrasonography was performed in 250 women with SLE and 122 controls. Plasma leptin and adiponectin levels were measured. Lipoprotein a (Lp(a)), oxidised phospholipids on apoB100 (OxPL/apoB100), paraoxonase, apoA-1 and inflammatory high-density lipoprotein (HDL) function were also assessed.ResultsLeptin levels were significantly higher in patients with SLE than in controls (23.7±28.0 vs 13.3±12.9 ng/ml, p<0.001). Leptin was also higher in the 43 patients with SLE with plaque than without plaque (36.4±32.3 vs 20.9±26.4 ng/ml, p=0.002). After multivariate analysis, the only significant factors associated with plaque in SLE were leptin levels in the highest quartile (≥29.5 ng/ml) (OR=2.8, p=0.03), proinflammatory HDL (piHDL) (OR=12.8, p<0.001), age (OR=1.1, p<0.001), tobacco use (OR=7.7, p=0.03) and hypertension (OR=3.0, p=0.01). Adiponectin levels were not significantly associated with plaque in our cohort. A significant correlation between leptin and piHDL function (p<0.001), Lp(a) (p=0.01) and OxPL/apoB100 (p=0.02) was also present.ConclusionsHigh leptin levels greatly increase the risk of subclinical atherosclerosis in SLE, and are also associated with an increase in inflammatory biomarkers of atherosclerosis such as piHDL, Lp(a) and OxPL/apoB100. High leptin levels may help to identify patients with SLE at risk of atherosclerosis

The Grizzly, August 31, 2006

Rebirth of Zack\u27s • Internet Outage on Campus • Changes to Parking on Campus • Class of 2010 Moves In • Sex at Ursinus • Getting to Know Ursinus • Local Dining Delights • Experiencing the Journey • Opinions: Save the Moderates; Opinions Editors Opinions on Opinions; Election Projections • Talent and Experience Lead Bears Into 2006 Season • Field Hockey Looks to Continue Dominance in CChttps://digitalcommons.ursinus.edu/grizzlynews/1715/thumbnail.jp

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Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146328/1/hep30137_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146328/2/hep30137.pd

Update on Prevention, Diagnosis, and Treatment of Chronic Hepatitis B: AASLD 2018 Hepatitis B Guidance

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/145507/1/cld728.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/145507/2/cld728_am.pd

Serologic features of cohorts with variable genetic risk for systemic lupus erythematosus

Abstract Background Systemic lupus erythematosus (SLE) is an autoimmune disease with genetic, hormonal, and environmental influences. In Western Europe and North America, individuals of West African descent have a 3–4 fold greater incidence of SLE than Caucasians. Paradoxically, West Africans in sub-Saharan Africa appear to have a low incidence of SLE, and some studies suggest a milder disease with less nephritis. In this study, we analyzed sera from African American female SLE patients and four other cohorts, one with SLE and others with varying degrees of risk for SLE in order to identify serologic factors that might correlate with risk of or protection against SLE. Methods Our cohorts included West African women with previous malaria infection assumed to be protected from development of SLE, clinically unaffected sisters of SLE patients with high risk of developing SLE, healthy African American women with intermediate risk, healthy Caucasian women with low risk of developing SLE, and women with a diagnosis of SLE. We developed a lupus risk index (LRI) based on titers of IgM and IgG anti-double stranded DNA antibodies and levels of C1q. Results The risk index was highest in SLE patients; second highest in unaffected sisters of SLE patients; third highest in healthy African-American women and lowest in healthy Caucasian women and malaria-exposed West African women. Conclusion This risk index may be useful in early interventions to prevent SLE. In addition, it suggests new therapeutic approaches for the treatment of SLE.https://deepblue.lib.umich.edu/bitstream/2027.42/143866/1/10020_2018_Article_19.pd

Refining the value of secretory phospholipase A2 as a predictor of acute chest syndrome in sickle cell disease: results of a feasibility study (PROACTIVE)

Acute chest syndrome (ACS) is defined as fever, respiratory symptoms and a new pulmonary infiltrate in an individual with sickle cell disease (SCD). Nearly half of ACS episodes occur in SCD patients already hospitalized, potentially permitting pre-emptive therapy in high-risk patients. Simple transfusion of red blood cells may abort ACS if given to patients hospitalized for pain who develop fever and elevated levels of secretory phospholipase A2 (sPLA2). In a feasibility study (PROACTIVE; ClinicalTrials.gov NCT00951808), patients hospitalized for pain who developed fever and elevated sPLA2 were eligible for randomization to transfusion or observation; all others were enrolled in an observational arm. Of 237 enrolled, only 10 were randomized; one of the four to receive transfusion had delayed treatment. Of 233 subjects receiving standard care, 22 developed ACS. A threshold level of sPLA2 ≥ 48 ng/ml gave optimal sensitivity (73%), specificity (71%) and accuracy (71%), but a positive predictive value of only 24%. The predictive value of sPLA2 was improved in adults and patients with chest or back pain, lower haemoglobin concentration and higher white blood cell counts; and those receiving less than two-thirds maintenance fluids. The hurdles identified in PROACTIVE should facilitate design of a larger, definitive, phase 3 randomized controlled trial