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Background Sickle cell disease (SCD), a chronic hemolytic disorder, results in cumulative end-organ damage affecting major organs such as the cardiovascular, renal, and central nervous systems. Effects of modifiable risk factors, such as blood pressure (BP), on the development of end-organ complications in SCD have not been well studied, particularly among the pediatric population. Relative hypertension in patients with SCD increases their risks of stroke, cardiovascular complications, and death. The primary hypothesis of this study was that abnormal BP patterns are common among patients with SCD and they impact end-organ complications. Methods Patients with SCD (HbSS, HbSβ0) were enrolled from the Children's Hospital at Montefiore (N = 100). For each patient, demographic data were collected, biochemical variables in urine and blood samples were analyzed, BP was determined with ambulatory blood pressure monitoring (ABPM), and an echocardiogram was performed. The prevalence of abnormalities in BP parameters was defined, and their relationships with measures of SCD severity and end-organ damage were assessed. Results Sufficient ABPM data were available for 67 patients. Enrolled children were 13 ± 4 years (40% were males). Assessment of diurnal variation demonstrated that 81% of patients had abnormal systolic nocturnal dipping and 61% had abnormal diastolic nocturnal dipping. Abnormalities in the diurnal pattern were associated with reticulocytosis and hyperfiltration. Microalbuminuria was present in 19% (n = 13) of patients, of which 77% (n = 10) were females (p = 0.014). Diastolic load and abnormal nocturnal dipping were associated with hyperfiltration but not with microalbuminuria. Conclusions BP abnormalities detected with ABPM in SCD patients are prevalent and perhaps are a risk factor for end-organ complications. Further studies are required to identify the mechanisms underlying these relationships and their longitudinal changes.

Purpose To describe severe acute corneal hydrops in a patient with previously undiagnosed keratoconus, in which anterior segment optical coherence tomography (AS-OCT) revealed a protruding ridge of tissue on either side of Descemet membrane (DM) break, treated successfully with ultrathin Descemet-stripping automated endothelial keratoplasty (UT-DSAEK). Methods A case report. Results A 32-year-old man presented with severe corneal hydrops in OS. He was treated conservatively with hypertonic saline. Serial AS-OCT revealed persistent edema and haze overlying a break in DM, with a ridge of protruding tissue on either side. Based on these findings, UT-DSAEK was performed. Intraoperatively, the ridge of tissue remained firmly adhered after DM removal and was felt to possibly represent posterior stroma. The patient's uncorrected visual acuity improved to 20/80. Literature review revealed 1 case with similar AS-OCT findings who underwent penetrating keratoplasty; histopathology was reported to show Descemet scrolls on either side of the break, but our analysis of this and other reports suggest that an additional layer of tissue is contained within the scroll along with DM. Conclusions This case demonstrates severe corneal hydrops in the setting of keratoconus, in which AS-OCT revealed a ridge of protruding tissue on either side of a break in DM. UT-DSAEK led to resolution of corneal edema and improvement in stromal haze and visual acuity. Further research is required to determine the precise role of endothelial keratoplasty and potential role of posterior stromal rupture in some cases of acute corneal hydrops.

BACKGROUND: Longitudinal changes in body mass index (BMI) among overweight and obese children with chronic kidney disease (CKD) are not well characterized. We studied longitudinal trajectories and correlates of these trajectories, as results may identify opportunities to optimize health outcomes. METHODS: Longitudinal changes in age-sex-specific BMI z-scores over 1851 person-years of follow-up were assessed in 524 participants of the Chronic Kidney Disease in Children Study. A total of 353 participants were categorized as normal (BMI > 5th to < 85th percentile), 56 overweight (BMI ≥ 85th to 95th percentile) and 115 obese (BMI ≥ 95th percentile) based on the average of three BMI measurements during the first year of follow-up. Studied covariates included age, sex, race, CKD etiology, corticosteroid usage, household income, and maternal education. RESULTS: In unadjusted analysis, BMI z-scores decreased over time in elevated BMI groups (overweight: mean = −0.06 standard deviations (SD) per year, 95% CI: −0.11, −0.01; obese: mean = −0.04 SD per year, 95% CI: −0.07, −0.01). Among obese children, only age was associated with change in BMI z-score; children < 6 years had a mean decrease of 0.19 SD during follow-up (95% CI: −0.30, −0.09). Socioeconomic factors were not associated with change in BMI. CONCLUSION: Overweight and obese children with CKD demonstrated a significant annual decline in BMI, though the absolute change was modest. Among obese children, only age < 6 years was associated with significant decline in BMI. Persistence of elevated BMI in older children and adolescents with CKD underscores the need for early prevention and effective intervention.

The causes of macroscopic and microscopic hematuria overlap; both are often caused by urinary tract infections or urethral/bladder irritation. Coexistent hypertension and proteinuria should prompt investigation for glomerular disease. The most common glomerulonephritis in children is postinfectious glomerulonephritis. In most patients, and especially with isolated microscopic hematuria, the diagnostic workup reveals no clear underlying cause. In those cases whereby a diagnosis is made, the most common causes of persistent microscopic hematuria are thin basement membrane nephropathy, immunoglobulin A nephropathy, or idiopathic hypercalciuria. Treatment and long-term prognosis varies with the underlying disease.

Preeclampsia, which disproportionately affects Black women, is a leading cause of preterm delivery and risk for future hypertension and chronic kidney disease (CKD). Apolipoprotein L1 (APOL1) kidney risk alleles, common among Black individuals, contribute substantially to CKD disparities. Given the strong link between preeclampsia and CKD, we investigated whether maternal and fetal APOL1 risk alleles can jointly influence preeclampsia risk, and explored potential modifiers of the association between APOL1 and preeclampsia.Nested case-control study.426 Black mother-infant pairs (275 African Americans and 151 Haitians) from the Boston Birth Cohort.Maternal and fetal APOL1 risk alleles.Preeclampsia.Logistic regression models with adjustment for demographic characteristics were applied to analyze associations between fetal and maternal APOL1 risk alleles and risk of preeclampsia and to investigate the effects of modification by maternal country of origin.Fetal APOL1 risk alleles tended to be associated with an increased risk of preeclampsia, which was not statistically significant in the total genotyped population. However, this association was modified by maternal country of origin (P0.05 for interaction tests): fetal APOL1 risk alleles were significantly associated with an increased risk of preeclampsia among African Americans under recessive (odds ratio [OR], 3.6 [95% CI, 1.3-9.7]; P=0.01) and additive (OR, 1.7 [95% CI, 1.1-2.6]; P=0.01) genetic models but not in Haitian Americans. Also, maternal-fetal genotype discordance at the APOL1 locus was associated with a 2.6-fold higher risk of preeclampsia (P0.001) in African Americans.Limited sample size in stratified analyses; self-reported maternal country of origin; pre-pregnancy estimated glomerular filtration rate (eGFR) and proteinuria data in mothers were not collected; unmeasured confounding social and/or environmental factors; no replication study.This study supports the hypothesis that fetal APOL1 kidney risk alleles are associated with increased risk for preeclampsia in a recessive mode of inheritance in African Americans and suggests that maternal-fetal genotype discordance is also associated with this risk. These conclusions underscore the need to better understand maternal-fetal interaction and their genetic and environmental factors as contributors to ethnic disparities in preeclampsia.

Inmates serving life-without-parole (LWOP) have been described as having “nothing to lose” by virtue of their sentence, leading to an assumption that they are more prone to disciplinary violations. This study refutes such an argument and is consistent with research demonstrating that LWOP inmates do not pose a disproportional risk for disciplinary misconduct. Results from our study comparing LWOP with parole-eligible, life-sentenced (LWP) inmates revealed neither significant differences in the total violation count nor the time to commission of an act of disciplinary misconduct. Trajectories of misconduct showed slightly higher prevalence of misconduct among LWOP inmates, a pattern of declining prevalence during the first 18 months of confinement, and a convergence with LWP inmates thereafter. The failure of assumptions of high violence risk for LWOP inmates has important public policy and correctional implications.

Black Americans are at increased risk for preeclampsia. Genetic variants in apolipoprotein L1 (APOL1) account for much of the increased risk for kidney disease in blacks. APOL1 is expressed in human placenta and transgenic mice expressing APOL1 develop preeclampsia. We evaluated the role of APOL1 variants in human preeclampsia. We determined maternal and fetal APOL1 genotypes in black women with preeclampsia in two populations. At Einstein Montefiore Center (EMC) Affiliated Hospitals, we studied 121 pregnancies in black women with preeclampsia. At University of Tennessee Health Science Center (UTHSC), we studied 93 pregnancies in black women with preeclampsia and 793 pregnancies without preeclampsia. We measured serum markers of preeclampsia soluble fms-like tyrosine kinase 1 (sFlt-1), placental growth factor (PlGF), and soluble endoglin (sEng). Fetal APOL1 high-risk (HR) genotype was associated with preeclampsia, with odds ratios at EMC and UTHSC of 1.84 (95% CI 1.11, 2.93) and 1.92 (95% CI 1.05, 3.49), respectively. Maternal APOL1 HR genotype was not associated with preeclampsia. Mothers with the fetal APOL1 HR genotype had more cerebral or visual disturbances (63% versus 37%, p = 0.04). In addition, fetal APOL1 HR genotype was associated with a higher sFLT-1/PlGF ratio at birth (p = 0.04). Fetal APOL1 high-risk genotype increases the risk for preeclampsia, likely by adversely affecting placental function. Further research is needed to assess whether APOL1 genetic testing can predict preeclampsia and improve pregnancy outcomes.

• This study investigated the progression of misconduct for serious and violent juveniles receiving a blended sentence.

Background: Acute kidney injury (AKI) in preterm neonates is becoming an increasingly recognized morbidity in the neonatal intensive care unit neonatal intensive care unit (NICU), yet its epidemiol...

Until 2008, genetic risk of kidney disease was underestimated in association with complex kidney phenotypes unlike Mendelian forms of kidney disease such as focal segmental glomerulosclerosis (FSGS) and IgA nephropathy. With identification of the chromosome 22q12 locus and the gene, APOL1, genetic risk now accounts for 70% of the excess risk for end stage renal disease (ESRD) and FSGS among African Americans1–3. There are 3 single nucleotide polymorphisms (SNPs) in APOL1, that comprise the G1 (terminal exon with two SNPs: rs73885319 and rs609101) and G2 (six base pair deletion: rs71785313) haplotypes. The development of variants in APOL1 are likely due to changes approximately 60,000 years ago for protection against trypanosomal infection (sleeping sickness) on the African continent. Carriers of 2 risk alleles are at high-risk of progression to ESRD in a recessive pattern. Among African Americans in the US, it is estimated that 12–14% carry 2 high-risk alleles, yet less than 15 out of 100 with high risk alleles are predicted to develop ESRD4. Moreover, APOL1 high-risk variants are virtually nonexistent in other ethnicities5. Unravelling the epidemiology and biology of APOL1 is complex as the gene exists only in humans and higher order primates, penetrance is not 100%, and interaction with the genes and/or environment is necessary to develop kidney disease. In this review, we will highlight the specific studies focused on the epidemiology in children and young adults impacting lifetime risk, and the recent studies on the biology of APOL1 leading to kidney disease.

Purpose: To report a case of atypical keratitis caused by Rothia dentocariosa.Methods: Retrospective case review.Results: A 49 year-old woman of South Asian descent presented with a non-discrete co...

We present a study of the interplay among electric charging rate, capacitance, salt removal, and mass transport in "flow-through electrode" capacitive deionization (CDI) systems. We develop two models describing coupled transport and electro-adsorption/desorption which capture salt removal dynamics. The first model is a simplified, unsteady zero-dimensional volume-averaged model which identifies dimensionless parameters and figures of merits associated with cell performance. The second model is a higher fidelity area-averaged model which captures both spatial and temporal responses of charging. We further conducted an experimental study of these dynamics and considered two salt transport regimes: (1) advection-limited regime and (2) dispersion-limited regime. We use these data to validate models. The study shows that, in the advection-limited regime, differential charge efficiency determines the salt adsorption at the early stage of the deionization process. Subsequently, charging transitions to a quasi-steady state where salt removal rate is proportional to applied current scaled by the inlet flow rate. In the dispersion-dominated regime, differential charge efficiency, cell volume, and diffusion rates govern adsorption dynamics and flow rate has little effect. In both regimes, the interplay among mass transport rate, differential charge efficiency, cell capacitance, and (electric) charging current governs salt removal in flow-through electrode CDI.

This study is the first to investigate the progression of serious disciplinary infractions among an imprisoned female sample. Findings from a trajectory analysis over a three-year time span revealed a three-class model with stable-limited, early-onset, and delayed-onset groups, clearly highlighting the heterogeneous nature of the female inmate population. After the classification of groups, a multinomial logistic regression was relied on to identify predictors of group membership relative to a group of “innocents” who had not committed any serious disciplinary infraction during the study period. Results from a multivariate analysis indicate that expected associations among predictors, such as age and mental health need, and disciplinary violations generally held for the rule-violating classes, especially the stable-limited group, which makes up the bulk of rule violators. These patterns and correlates are consistent with those identified in previous studies examining male inmates and pooled samples of male and female inmates.

Congenital abnormalities of the kidney and urinary tract (CAKUT) are one of the leading congenital defects to be identified on prenatal ultrasound. CAKUT represent a broad spectrum of abnormalities, from transient hydronephrosis to severe bilateral renal agenesis. CAKUT are a major contributor to chronic and end stage kidney disease (CKD/ESKD) in children. Prenatal imaging is useful to identify CAKUT, but will not detect all defects. Both genetic abnormalities and the fetal environment contribute to CAKUT. Monogenic gene mutations identified in human CAKUT have advanced our understanding of molecular mechanisms of renal development. Low nephron number and solitary kidneys are associated with increased risk of adult onset CKD and ESKD. Premature and low birth weight infants represent a high risk population for low nephron number. Additional research is needed to identify biomarkers and appropriate follow-up of premature and low birth weight infants into adulthood.

Background Understanding the relationship between clinical and patient-reported outcomes (PROs) will help support clinical care and future clinical trial design of novel therapies for focal segmental glomerulosclerosis (FSGS). Methods FSGS patients ≥8 years of age enrolled in the Nephrotic Syndrome Study Network completed Patient-Reported Outcomes Measurement Information System PRO measures of health-related quality of life (HRQoL) (children: global health, mobility, fatigue, pain interference, depression, anxiety, stress and peer relationships; adults: physical functioning, fatigue, pain interference, sleep impairment, mental health, depression, anxiety and social satisfaction) at baseline and during longitudinal follow-up for a maximum of 5 years. Linear mixed-effects models were used to determine which demographic, clinical and laboratory features were associated with PROs for each of the eight children and eight adults studied. Results There were 45 children and 114 adult FSGS patients enrolled that had at least one PRO assessment and 519 patient visits. Multivariable analyses among children found that edema was associated with global health (−7.6 points, P = 0.02) and mobility (−4.2, P = 0.02), the number of reported symptoms was associated with worse depression (−2.7 per symptom, P = 0.009) and anxiety (−2.3, P = 0.02) and the number of emergency room (ER) visits in the prior 6 months was associated with worse mobility (−2.8 per visit, P Conclusions PROs provide important information about HRQoL for persons with FSGS that is not captured solely by the examination of laboratory-based markers of disease. However, it is critical that instruments capture the patient experience and FSGS clinical trials may benefit from a disease-specific instrument more sensitive to within-patient changes.

BACKGROUND: We evaluated the epidemiology of fluid balance (FB) over the first postnatal week and its impact on outcomes in a multi-center cohort of premature neonates from the AWAKEN study. METHODS: Retrospective analysis of infants

BACKGROUND: The relationship between muscle strength and chronic kidney disease (CKD) in children is unknown. This study aims to quantify the association between grip strength (GS) and kidney function and to explore factors associated with grip strength in children and adolescents with CKD. METHODS: We included 411 children (699 GS assessments) of the Chronic Kidney Disease in Children (CKiD) study. They were matched by age, sex, and height to a healthy control from the National Health and Nutrition Examination Survey to quantify the relationship between GS and CKD. Linear mixed models were used to identify factors associated with GS among CKD patients. RESULTS: Median GS z-score was − 0.72 (IQR − 1.39, 0.11) among CKD patients with CKD stages 2 through 5 having significantly lower GS than CKD stage 1. Compared with healthy controls, CKiD participants had a decreased GS z-score (− 0.53 SD lower, 95% CI − 0.67 to − 0.39) independent of race/ethnicity and body mass index. Factors associated with reduced GS included longer duration of CKD, pre-pubertal status, delayed puberty, neuropsychiatric comorbidities, need of feeding support, need for alkali therapy, and hemoglobin level. Decreased GS was also associated with both a lower frequency and intensity of physical activity. CONCLUSIONS: CKD is associated with impaired muscle strength in children independent of growth retardation and BMI. Exposure to CKD for a prolonged time is associated with impaired muscle strength. Potential mediators of the impact of CKD on muscle strength include growth retardation, acidosis, poor nutritional status, and low physical activity. Additional studies are needed to assess the efficacy of interventions targeted at these risk factors.

Arthrogryposis, renal dysfunction, and cholestasis syndrome is a rare autosomal recessive disorder caused by mutations in the VPS33B and VIPAR genes. Most cases are fatal within the first year of life. Here we describe one of the two oldest patients with arthrogryposis, renal dysfunction, and cholestasis syndrome. This is a 12-year-old Hispanic female, from a non-consanguineous parents, diagnosed with an incomplete phenotype of arthrogryposis, renal dysfunction, and cholestasis syndrome with arthrogryposis and renal tubular dysfunction but without cholestasis. At 11 years of age, she was found to have impaired renal function, nephrotic-range proteinuria, Fanconi syndrome, and distal renal tubular acidosis. She also had hypercalciuria, nephrogenic diabetes insipidus, and small kidneys by renal ultrasound. Genetic analysis using whole exome sequencing showed a mutation and a partial deletion in the VPS33B gene. Further studies showed that the mother has a partial deletion in the VPS33B gene. Her medication regimen includes potassium citrate and enalapril.

BACKGROUND AND OBJECTIVES: Studies of adults have demonstrated an association between metabolic acidosis, as measured by low serum bicarbonate levels, and CKD progression. We evaluated this relationship in children using data from the Chronic Kidney Disease in Children study. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: The relationship between serum bicarbonate and a composite end point, defined as 50% decline in eGFR or KRT, was described using parametric and semiparametric survival methods. Analyses were stratified by underlying nonglomerular and glomerular diagnoses, and adjusted for demographic characteristics, eGFR, proteinuria, anemia, phosphate, hypertension, and alkali therapy. RESULTS: Six hundred and three participants with nonglomerular disease contributed 2673 person-years of follow-up, and 255 with a glomerular diagnosis contributed 808 person-years of follow-up. At baseline, 39% (237 of 603) of participants with nonglomerular disease had a bicarbonate level of ≤22 meq/L and 36% (85 of 237) of those participants reported alkali therapy treatment. In participants with glomerular disease, 31% (79 of 255) had a bicarbonate of ≤22 meq/L, 18% (14 of 79) of those participants reported alkali therapy treatment. In adjusted longitudinal analyses, compared with participants with a bicarbonate level >22 meq/L, hazard ratios associated with a bicarbonate level of

Homicide in prison is rare, and undermines institutional security. Only three studies have addressed characteristics of perpetrators or victims, their motives, and circumstances of the crime. This study expanded the literature by exploring features of the homicide, and characteristics of 18 perpetrators and 14 victims of homicide during a 30-year period. Findings revealed the prison killer is an older, gang-affiliated inmate or career criminal serving a lengthy sentence for a previous murder and other violent crimes. Homicide victims, despite older age, could generally not be characterized as weak or vulnerable. Implications for theory, prison management, and future research are explored.

The kidney is a highly polarized epithelial organ that develops from undifferentiated mesenchyme, although the mechanisms that regulate the development of renal epithelial polarity are incompletely understood. Partitioning-defective 1 (Par1) proteins have been implicated in cell polarity and epithelial morphogenesis; however, the role of these proteins in the developing kidney has not been established. Therefore, we studied the contribution of Par1a/b to renal epithelial development. We examined the renal phenotype of newborn compound mutant mice carrying only one allele of Par1a or Par1b. Loss of three out of four Par1a/b alleles resulted in severe renal hypoplasia, associated with impaired ureteric bud branching. Compared with kidneys of newborn control littermates, kidneys of newborn mutant mice exhibited dilated proximal tubules and immature glomeruli, and the renal proximal tubular epithelia lacked proper localization of adhesion complexes. Furthermore, Par1a/b mutants expressed low levels of renal Notch ligand Jag1, activated Notch2, and Notch effecter Hes1. Together, these data demonstrate that Par1a/b has a key role in glomerular and proximal tubule development, likely via modulation of Notch signaling.

Introduction Nursing is one of the top occupations suffering musculoskeletal disorders, especially low back pain (LBP). Nursing staff also experience short and disturbed sleep. Although there is a known relationship between pain and sleep, the specific associations between different aspects of LBP (e.g., duration, frequency, intensity) and sleep have not been studied. The objective of this study is to examine different aspects of LBP and their cross-sectional associations with sleep among nursing staff. Methods Online Qualtrics surveys were distributed among nurses and nursing assistants at a community hospital in the northeast U.S. LBP was assessed in terms of duration, frequency, intensity, and intensity change from before to after the work shift. Sleep duration and disturbances were assessed with validated scales. Results Among the 541 participants (94% female; age 43±13y), more than a third reported short sleep duration (≤6hrs/day; 38%) or sleep disturbances (38%), and more than half (60%) reported LBP in the past 6 months. Among those with LBP, 82% had ongoing pain for at least 6 months; 44% had ongoing pain for at least half the days in the past 6 months; 39% had LBP intensity ≥4 out of 10; and 79% reported post-shift LBP intensity increased of at least 1 level. Short sleep duration was associated with ongoing LBP for at least half the days in the past 6 months, intensity ≥4, and post-shift LBP intensity increase. Sleep disturbances were associated with prevalent LBP and intensity ≥4. Conclusion Nursing staff reported a high prevalence of LBP as well as short and disturbed sleep. Overall, poor sleep was associated with higher LBP prevalence, frequency, intensity, and post-shift increase. Future longitudinal studies are needed to clarify the causal directions of these relationships. Workplace interventions should address the widespread problems of LBP and sleep deficiency of nursing staff. Support Drs. Yuan Zhang and Jeanne F. Duffy were supported by NIH grant R01 AG044416.

Renal tubule epithelial cells are high-energy demanding polarized epithelial cells. Liver kinase B1 (LKB1) is a key regulator of polarity, proliferation, and cell metabolism in epithelial cells, but the function of LKB1 in the kidney is unclear. Our unbiased gene expression studies of human control and CKD kidney samples identified lower expression of LKB1 and regulatory proteins in CKD. Mice with distal tubule epithelial-specific Lkb1 deletion (Ksp-Cre/Lkb1(flox/flox)) exhibited progressive kidney disease characterized by flattened dedifferentiated tubule epithelial cells, interstitial matrix accumulation, and dilated cystic-appearing tubules. Expression of epithelial polarity markers β-catenin and E-cadherin was not altered even at later stages. However, expression levels of key regulators of metabolism, AMP-activated protein kinase (Ampk), peroxisome proliferative activated receptor gamma coactivator 1-α (Ppargc1a), and Ppara, were significantly lower than those in controls and correlated with fibrosis development. Loss of Lkb1 in cultured epithelial cells resulted in energy depletion, apoptosis, less fatty acid oxidation and glycolysis, and a profibrotic phenotype. Treatment of Lkb1-deficient cells with an AMP-activated protein kinase (AMPK) agonist (A769662) or a peroxisome proliferative activated receptor alpha agonist (fenofibrate) restored the fatty oxidation defect and reduced apoptosis. In conclusion, we show that loss of LKB1 in renal tubular epithelial cells has an important role in kidney disease development by influencing intracellular metabolism.

SummaryThe kidney has a tremendous capacity to regenerate following injury, but factors that govern this response are still largely unknown. We isolated cells from mouse kidneys with high proliferative and multi-lineage differentiation capacity. These cells expressed a high level of Sox9. In regenerating kidneys, Sox9 expression was induced early, and 89% of proliferating cells were Sox9 positive. In vitro, Sox9-positive cells showed unlimited proliferation and multi-lineage differentiation capacity. Using an inducible Sox9 Cre line and lineage-tagging methods, we show that Sox9-positive cells can generate new daughter cells, contributing to the regeneration of proximal tubule, loop of Henle, and distal tubule segments but not to collecting duct and glomerular cells. Furthermore, inducible deletion of Sox9 resulted in reduced epithelial proliferation, more severe injury, and fibrosis development. In summary, we demonstrate that, in the kidney, Sox9-positive cells show progenitor-like properties in vitro and contribute to epithelial regeneration following injury in vivo.

A B S T R A C T Objective: To assess patients’ satisfaction and the intermediate and long-term patterns of symptom progression following uterine artery fibroid embolization (UAE). Study design: Intermediate (2–6 years) and long-term (9–14 years) follow-up questionnaire survey to women who underwent UAE during the period 1996–2000, at a tertiary referral centre. Results: The mean (SD) age of women at the time of embolization was 43 (5.58) years. A total of 142/197 (72.1%) women had the embolization in view of heavy menstrual periods, while 87/197 (44%) indicated a desire to retain fertility. 160/197 (81.7%) women who completed Q1 reported an improvement in menstrual symptoms compared to 41/80 (51.2%) for Q2 [p < 0.01]. The majority indicated they would recommend the procedure to a friend (Q1: 165 (83.8%), Q2: 62/80 (77.5%)) [p = 0.75]. 23/80 (28.8%) required further surgical treatment following UAE, and within the latter group, only 7/23 (30.4%) were satisfied with the embolization. 22/80 (27.5%) tried for a pregnancy following the procedure, and of these 3/22 (13.6%) had a live birth. The mean (SD) age at the menopause for women who returned Q2 was 49.1 (4.91) years. Conclusions: The majority of women were satisfied with the embolization and noted an improvement in menstrual symptoms. However, this improvement diminished over time following the embolization, and over a quarter of women required further surgical intervention. Findings from this study may provide useful information in counselling women undergoing UAE and help guide clinicians in their patient selection criteria when discussing the procedure.

Richard Burgess, in his Studies in Eusebian and post-Eusebian chronology, argues convincingly for the existence of a hitherto unknown Antiochene continuation of Eusebius' Chronicle. While Burgess does much to advance understanding of fourth-century historiography, his conclusion that this effort derives from a pro-Nicene author is less convincing than his other arguments. Internal evidence in the fragments themselves, and circumstances surrounding the life of the fourth-century bishop Eusebius of Emesa, point to that prelate as the likely author of the source identified by Burgess.

This study investigated prison homicide perpetrators through the lens of the career criminal perspective. Prison homicide, while a rare event, has critical implications for the prison environment. Despite its importance as a form of institutional violence that must be addressed, only four studies in the past five decades have explored the characteristics of homicide perpetrators/victims, the motives, and circumstances of the crime. The goal of the current study was to develop a better understanding of prison homicide by examining 54 perpetrators who committed 37 inmate homicides over 40 years in a mid-Western state prison system. Results showed that prison homicides typically involved a younger male inmate perpetrator, acting independently, murdering an older inmate, in his cell, by stabbing or beating the victim during an altercation. Perpetrators, in comparison with victims and prisoners in general, had a record indicating more prior community homicides, elevated institutional risk scores, and higher rates of serious and assaultive prison misconduct, all indicative of prior community and prison maladjustment. Consistent with career criminal research, prison homicide perpetrators constitute a small but distinct subset of habitually deviant criminals that perpetrate high rates of criminal and violent behavior regardless of context.

Quidditch is a fast growing, physically intense, mixed-gender full-contact sport. Originally adapted from Harry Potter novels, quidditch was first played in 2005 in the USA but is now played worldwide. It is essential to elucidate patterns of injury for the safety and growth of the sport of quidditch. It also provides a unique opportunity to study injury patterns in mixed-gender full-contact sport, an area of increasing importance with the developing culture of transition from single-gender to mixed-gender sports.The purpose of this investigation was to examine the types of injuries sustained while playing quidditch in terms of their incidence, anatomical distribution and severity, and gender distribution.An anonymous self-reporting questionnaire was distributed to all active quidditch players in the UK. Data collection included player demographics, type of injury, mechanism of injury, player position, experience and treatment required, relating to the previous 12 months.A total of 348 participants of 684 eligible athletes responded to the questionnaire representing a 50.87% response rate. There were 315 injuries reported by 180 athletes in total, with an overall incidence of 4.06 injuries per 1,000 hours. A statistically significantly different rate of concussion was observed with female athletes sustaining more concussion than males (p=0.006). The overall rate of concussion was 0.651/1000hrs in males and 1.163/1000hrs in females (0.877/1000 hours overall).This study provides the first quantitative description of injury rates in quidditch. The overall injury rates are no higher than those reported in other recreational contact sports. Female athletes were found to have a higher rate of concussion, which needs further investigation. These findings are relevant to players concerned about safety in quidditch and to governing bodies regarding governance of the sport.3b.