The Impact of Pension Obligations on Firm Decisions.

Employer-sponsored defined benefit pensions are declining in popularity, yet these long-term obligations will influence firm decisions for decades to come. The first chapter models how the tax and other incentives posed by sponsoring a defined benefit pension interact with traditional moral hazard between stockholders and bondholders. While the contracting problems associated with each may be manageable, moral hazards arising from investment risk and from contributing to a pension plan together lead to first-order distortions. The second chapter describes how this dynamic leads to higher borrowing rates among firms with defined benefit pensions. Like traditional corporate bonds, pension debt is a long-term liability that influences default risk and firm value -- two important determinants of bond spreads. Yet pension debt magnifies default risk stemming from agency problems, implying that a ten percentage point increase in unfunded pension liabilities raises defined benefit firms' bond spreads by 23 basis points, while an equivalent increase in standard external leverage increases bond spreads by only 2.6 basis points. Finally, the third chapter looks at how sponsoring a defined benefit pension influenced firm performance in the Great Recession. Many firms with defined benefit pensions experienced dramatic losses in the value of pension assets between 2007 and 2009 that led to high required pension payments. A general concern was that those payments prevented firms from making productive investments that could assist economic recovery. This paper suggests, instead, that pension losses allowed firms to borrow from their pensioners, while the credit crunch prevented those firms from taking on sub-optimally high leverage ratios and investment risk that are usually motivated by costly pensions. Indeed, firms making minimum required contributions from 2000 through 2007 supported leverage ratios that were 4.6 percentage points higher and default premiums that were 22 percent higher than their counterparts with less costly pensions. This wedge did not exist during the Great Recession.PhDEconomicsUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/133288/1/laymarga_1.pd

Predicting the risk of acute kidney injury in primary care: derivation and validation of STRATIFY-AKI

BACKGROUND: Antihypertensives reduce the risk of cardiovascular disease but are also associated with harms including acute kidney injury (AKI). Few data exist to guide clinical decision making regarding these risks. AIM: To develop a prediction model estimating the risk of AKI in people potentially indicated for antihypertensive treatment. DESIGN AND SETTING: Observational cohort study using routine primary care data from the Clinical Practice Research Datalink (CPRD) in England. METHOD: People aged ≥40 years, with at least one blood pressure measurement between 130 mmHg and 179 mmHg were included. Outcomes were admission to hospital or death with AKI within 1, 5, and 10 years. The model was derived with data from CPRD GOLD (n = 1 772 618), using a Fine-Gray competing risks approach, with subsequent recalibration using pseudo-values. External validation used data from CPRD Aurum (n = 3 805 322). RESULTS: The mean age of participants was 59.4 years and 52% were female. The final model consisted of 27 predictors and showed good discrimination at 1, 5, and 10 years (C-statistic for 10-year risk 0.821, 95% confidence interval [CI] = 0.818 to 0.823). There was some overprediction at the highest predicted probabilities (ratio of observed to expected event probability for 10-year risk 0.633, 95% CI = 0.621 to 0.645), affecting patients with the highest risk. Most patients (>95%) had a low 1- to 5-year risk of AKI, and at 10 years only 0.1% of the population had a high AKI and low CVD risk. CONCLUSION: This clinical prediction model enables GPs to accurately identify patients at high risk of AKI, which will aid treatment decisions. As the vast majority of patients were at low risk, such a model may provide useful reassurance that most antihypertensive treatment is safe and appropriate while flagging the few for whom this is not the case

The Effect of Locally Delivered Controlledâ Release Doxycycline or Scaling and Root Planing on Periodontal Maintenance Patients Over 9 Months

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142157/1/jper0022.pd

‘I’m not your mother’: British social realism, neoliberalism and the maternal subject in Sally Wainwright’s Happy Valley (BBC1 2014-2016)

This article examines Sally Wainwright's Happy Valley (BBC1, 2014–2016) in the context of recent feminist attempts to theorise the idea of a maternal subject. Happy Valley, a police series set in an economically disadvantaged community in West Yorkshire, has been seen as expanding the genre of British social realism, in its focus on strong Northern women, by giving it ‘a female voice’ (Gorton, 2016: 73). I argue that its challenge is more substantial. Both the tradition of British social realism on which the series draws, and the neoliberal narratives of the family which formed the discursive context of its production, I argue, are founded on a social imaginary in which the mother is seen as responsible for the production of the selves of others, but cannot herself be a subject. The series itself, however, places at its centre an active, articulate, mobile and angry maternal subject. In so doing, it radically contests both a tradition of British social realism rooted in male nostalgia and more recent neoliberal narratives of maternal guilt and lifestyle choice. It does this through a more fundamental contestation: of the wider cultural narratives about selfhood and the maternal that underpin both. Its reflective maternal subject, whose narrative journey involves acceptance of an irrecoverable loss, anger and guilt as a crucial aspect of subjectivity, and who embodies an ethics of relationality, is a figure impossible in conventional accounts of subject and nation. She can be understood, however, in terms of recent feminist theories of the maternal

Association between antihypertensive treatment and adverse events: systematic review and meta-analysis

Abstract: Objective: To examine the association between antihypertensive treatment and specific adverse events. Design: Systematic review and meta-analysis. Eligibility criteria: Randomised controlled trials of adults receiving antihypertensives compared with placebo or no treatment, more antihypertensive drugs compared with fewer antihypertensive drugs, or higher blood pressure targets compared with lower targets. To avoid small early phase trials, studies were required to have at least 650 patient years of follow-up. Information sources: Searches were conducted in Embase, Medline, CENTRAL, and the Science Citation Index databases from inception until 14 April 2020. Main outcome measures: The primary outcome was falls during trial follow-up. Secondary outcomes were acute kidney injury, fractures, gout, hyperkalaemia, hypokalaemia, hypotension, and syncope. Additional outcomes related to death and major cardiovascular events were extracted. Risk of bias was assessed using the Cochrane risk of bias tool, and random effects meta-analysis was used to pool rate ratios, odds ratios, and hazard ratios across studies, allowing for between study heterogeneity (τ2). Results: Of 15 023 articles screened for inclusion, 58 randomised controlled trials were identified, including 280 638 participants followed up for a median of 3 (interquartile range 2-4) years. Most of the trials (n=40, 69%) had a low risk of bias. Among seven trials reporting data for falls, no evidence was found of an association with antihypertensive treatment (summary risk ratio 1.05, 95% confidence interval 0.89 to 1.24, τ2=0.009). Antihypertensives were associated with an increased risk of acute kidney injury (1.18, 95% confidence interval 1.01 to 1.39, τ2=0.037, n=15), hyperkalaemia (1.89, 1.56 to 2.30, τ2=0.122, n=26), hypotension (1.97, 1.67 to 2.32, τ2=0.132, n=35), and syncope (1.28, 1.03 to 1.59, τ2=0.050, n=16). The heterogeneity between studies assessing acute kidney injury and hyperkalaemia events was reduced when focusing on drugs that affect the renin angiotensin-aldosterone system. Results were robust to sensitivity analyses focusing on adverse events leading to withdrawal from each trial. Antihypertensive treatment was associated with a reduced risk of all cause mortality, cardiovascular death, and stroke, but not of myocardial infarction. Conclusions: This meta-analysis found no evidence to suggest that antihypertensive treatment is associated with falls but found evidence of an association with mild (hyperkalaemia, hypotension) and severe adverse events (acute kidney injury, syncope). These data could be used to inform shared decision making between doctors and patients about initiation and continuation of antihypertensive treatment, especially in patients at high risk of harm because of previous adverse events or poor renal function. Registration: PROSPERO CRD42018116860

Two Multiâ Center Studies Evaluating Locally Delivered Doxycycline Hyclate, Placebo Control, Oral Hygiene, and Scaling and Root Planing in the Treatment of Periodontitis

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142011/1/jper0490.pd

Pathogenetics of alveolar capillary dysplasia with misalignment of pulmonary veins.

Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a lethal lung developmental disorder caused by heterozygous point mutations or genomic deletion copy-number variants (CNVs) of FOXF1 or its upstream enhancer involving fetal lung-expressed long noncoding RNA genes LINC01081 and LINC01082. Using custom-designed array comparative genomic hybridization, Sanger sequencing, whole exome sequencing (WES), and bioinformatic analyses, we studied 22 new unrelated families (20 postnatal and two prenatal) with clinically diagnosed ACDMPV. We describe novel deletion CNVs at the FOXF1 locus in 13 unrelated ACDMPV patients. Together with the previously reported cases, all 31 genomic deletions in 16q24.1, pathogenic for ACDMPV, for which parental origin was determined, arose de novo with 30 of them occurring on the maternally inherited chromosome 16, strongly implicating genomic imprinting of the FOXF1 locus in human lungs. Surprisingly, we have also identified four ACDMPV families with the pathogenic variants in the FOXF1 locus that arose on paternal chromosome 16. Interestingly, a combination of the severe cardiac defects, including hypoplastic left heart, and single umbilical artery were observed only in children with deletion CNVs involving FOXF1 and its upstream enhancer. Our data demonstrate that genomic imprinting at 16q24.1 plays an important role in variable ACDMPV manifestation likely through long-range regulation of FOXF1 expression, and may be also responsible for key phenotypic features of maternal uniparental disomy 16. Moreover, in one family, WES revealed a de novo missense variant in ESRP1, potentially implicating FGF signaling in the etiology of ACDMPV

Racism as a determinant of health: a systematic review and meta-analysis

Despite a growing body of epidemiological evidence in recent years documenting the health impacts of racism, the cumulative evidence base has yet to be synthesized in a comprehensive meta-analysis focused specifically on racism as a determinant of health. This meta-analysis reviewed the literature focusing on the relationship between reported racism and mental and physical health outcomes. Data from 293 studies reported in 333 articles published between 1983 and 2013, and conducted predominately in the U.S., were analysed using random effects models and mean weighted effect sizes. Racism was associated with poorer mental health (negative mental health: r = -.23, 95% CI [-.24,-.21], k = 227; positive mental health: r = -.13, 95% CI [-.16,-.10], k = 113), including depression, anxiety, psychological stress and various other outcomes. Racism was also associated with poorer general health (r = -.13 (95% CI [-.18,-.09], k = 30), and poorer physical health (r = -.09, 95% CI [-.12,-.06], k = 50). Moderation effects were found for some outcomes with regard to study and exposure characteristics. Effect sizes of racism on mental health were stronger in cross-sectional compared with longitudinal data and in non-representative samples compared with representative samples. Age, sex, birthplace and education level did not moderate the effects of racism on health. Ethnicity significantly moderated the effect of racism on negative mental health and physical health: the association between racism and negative mental health was significantly stronger for Asian American and Latino(a) American participants compared with African American participants, and the association between racism and physical health was significantly stronger for Latino(a) American participants compared with African American participants.<br /