139 research outputs found

    Justice on the Tennessee Frontier: The Williamson County Circuit Court 1810-1820

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    This Note examines the history of one early nineteenth-century circuit court and the caliber of its bench and bar. To analyze the workings of that court, this Note applies the analytical framework adopted by Friedman, Blume, and other historians to the raw data provided by a study of the Williamson County Circuit Court records. In each of several substantive areas for which the court\u27s records provide information, the Note first considers Friedman\u27s generalizations about nineteenth-century law and then interprets the Williamson County data in the light of those generalizations and the results of other case studies. This Note proceeds on the theory that the records of the Williamson County Circuit Court reveal substantive decision making representative of all newly established nineteenth-century judicial systems struggling for existence and order. It suggests possible explanations for those findings that do not comport with the results of previous studies in other areas. But this Note concludes that in Tennessee, as elsewhere, it was the strength of the American justice system that helped tame the frontier, rather than the frontier that tamed the law

    Judicial Panel: Tennessee Legal Reform from a Judicial Standpoint

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    A transcript of the judicial panel discussion held at the Belmont University College of Law Symposium, Tennessee Legal Reform

    Polymorphism in the IGF-I gene: clinical relevance for short children born small fos gestational age (SGA)

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    Low birth weight is associated with an increased risk in adult life of type 2 diabetes, hypertension and cardiovascular disease (CVD). The fetal insulin hypothesis postulates that genes involving insulin resistance could effect birth weight and disease in later life (Hattersley, 1999). Besides insulin, there is extensive evidence that insulin-like growth factor-I and -II (IGF-I, IGF-II) play an important role in fetal growth. We hypothesized that minor genetic variation in the IGF-I gene could influence pre- and postnatal growth. Three microsatellite markers located in the IGF-I gene in 124 short children (height &amp;lt; −1.88 SDS) who were born small for gestational age (SGA) and their parents were studied. SGA was defined as both a birth weight and birth length below −1.88 SDS for gestational age. Two polymorphic markers showed transmission disequilibrium. Allele 191 of the IGF1.PCR1 marker was transmitted more frequently from parent to child (χ2 = 4.8 and p = 0.02) and allele 198 of the 737/738 marker was transmitted less frequently from parent to child (χ = 4.5 and p = 0.03). Children carrying the 191-allele had significantly lower IGF-1 levels than children not carrying this allele (−1.1 SDS vs.− 0.05 SDS; p = 0.03). Also, head circumference SDS remained smaller in children with allele 191 compared to children without allele 191 (−2.1 SDS vs. −0.9 SDS; p = 0.003). Our results show that genetically determined low IGF-I levels may lead to a reduction in birth weight, length and head circumference and to persistent short stature and small head circumference in later life (proportionate small). Since low IGF-I levels are associated with type 2 diabetes and CVD, we propose that the IGF-I gene may provide a link between low birth weight and such diseases in later life.</jats:p

    Recent Cases

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    Constitutional Law-First Amendment-School Authorities May Prohibit High School Student\u27s Distribution of Sex Questionnaire to Prevent Possible Psychological Harm to Other Students Robert Edward Banta Plaintiff, editor of a high school publication,\u27 brought suit in federal court seeking an order compelling defendant school officials to allow the student publication to distribute a sex questionnaire,to students in the high school and to publish the results. Plaintiff claimed that defendants had not shown that the planned distribution would disrupt school activities and that, therefore, defendants\u27prohibition of the questionnaire violated 42 U.S.C. § 19831 and the first and fourteenth amendments. Pointing to potential psychological harm to students, defendants argued that the state\u27s interest in protecting the students\u27 emotional well-being outweighed plaintiffs interest in distributing the questionnaire. The trial court held that defendants could prohibit distribution of the questionnaire to ninth-and tenth-grade students but not to eleventh- and twelfth-grade students. On appeal to the United States Court of Appeals for the Second Circuit, held, reversed in part\u27 and remanded with instructions to dismiss the complaint. If school officials reasonably believe that distribution on school grounds of a high school student\u27s questionnaire soliciting information about the sexual habits of his fellow students might cause psychological harm to other students, then prohibition of the questionnaire does not violate the right to freedom of expression of the student seeking to distribute the questionnaire. Trachtman v. Anker, 563 F.2d 512 (2d Cir. 1977). Corporations--Freeze-Out Mergers--The Delaware Supreme Court Requires Majority Shareholder Proof of a Valid Business Purpose As a Component of Entire Fairness in Freeze-Out Merger Challenges Oby T. Brewer, III Recent declines in stock market averages\u27 accompanied by costly disclosure requirements imposed under the federal securities laws have prompted many companies to reconsider their positions as publicly held corporations. In response to the resulting minimal benefits of public ownership, many controlling shareholders now seek to increase their control and participation in a corporation\u27s future profits by going private.\u27 One means of going private is the freeze-out merger, by which a parent company forces the liquidation of minority interests in a publicly held subsidiary through a merger of the subsidiary with the parent. By complying with applicable state merger statutes, the parent may eliminate the minority\u27s shares by tendering a cash-out price, which the minority either must accept or have appraised judicially. The merger statutes thus represent a legislative compromise between total majority control and the single vote veto available to the minority at common law. Criminal Procedure--Prosecutorial Immunity-Federal Prosecutor Is Not Absolutely Immune From Suit for Alleged Perjury Cornelia Anne Clark Plaintiffs\u27 brought a civil action in tort charging that defendant federal prosecutor\u27s alleged perjury at a hearing incident to a grand jury investigation of plaintiffs\u27 activities\u27 violated their constitutional rights. On motion to dismiss, defendant contended that he enjoyed absolute quasi-judicial immunity because he had been acting at the hearing in his official capacity as a special federal prosecutor. The district court\u27 denied the motion, holding that the doctrine of quasi-judicial immunity does not apply when the prosecutor is alleged to have committed perjury. On interlocutory appeal to the United States Court of Appeals for the District of Columbia Circuit, held, affirmed. Because a federal prosecutor\u27s perjury during a court hearing incident and prior to a grand jury investigation falls within his investigative duty rather than his advocatory duty,the prosecutor is entitled only to a qualified immunity.\u27 Briggs v.Goodwin, No. 75-1642 (D.C. Cir. Sept. 21, 1977). Securities Law--Rule 10b-5-Defense of In Pari Delicto Bars Private Damage Action Brought Against Tipper by Tippee Who Fails to Disclose Before Trading Terry Currie Tippees\u27 brought a private action for damages under section 10(b) of the Securities Exchange Act of 1934 and rule 10b-53 charging that defendant tippers disseminated false and misleading material inside information in advising plaintiffs of an imminent merger between two corporations that would result in appreciated stock values.\u27 In reliance on this information, plaintiffs purchased stock in one of the corporations and subsequently incurred substantial losses on the stock when the proposed merger did not occur. Defendants moved for summary judgment, claiming that the doctrine of in pari delicto barred plaintiffs\u27 recovery because plaintiffs also had violated rule 10b-5 by failing to make full disclosure of the inside information before trading on the open market.\u27 The district court granted the tippers\u27 motion for summary judgment. On appeal to the United States Court of Appeals for the Third Circuit, held, affirmed. When a tippee violates rule 10b-5 by failing to make full disclosure to the investing public of material inside information prior to trading on the open market, the defense of in pari delicto bars a rule 10b-5 private damage action by the tippee against the tipper. Torts--Negligence--Child Has Cause of Action for Preconception Medical Malpractice Douglas William Ey, Jr. Plaintiff, claiming that she suffered permanent physical injuries\u27 as a result of defendants\u27 conduct prior to her conception,sought to recover damages in a negligence action.2 In 1965 plaintiffs mother,who had Rh negative blood, was given two transfusions of incompatible Rh positive blood in defendant hospital where defendant physician was director of laboratories.\u27 Plaintiff\u27s mother did not discover that these transfusions had sensitized her blood until shortly before plaintiffs birth in 1973. Defendants moved to dis-miss for failure to state a cause of action, arguing that because plaintiff had not been conceived at the time of the alleged negligent conduct, defendants owed no duty of care to plaintiff. The trial court granted defendants\u27 motion, but the Illinois Appellate Court reversed and remanded the case for further proceedings. On appeal to the Supreme Court of Illinois, held, affirmed. A child injured by the negligent acts of a physician and a hospital committed against his mother prior to his conception has a cause of action based on negligence. Renslow v. Mennonite Hospital, 367 N.E.2d 1250 (Ill.1977)

    Global change pressures on soils from land use and management

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    Soils are subject to varying degrees of direct or indirect human disturbance, constituting a major global change driver. Factoring out natural from direct and indirect human influence is not always straightforward, but some human activities have clear impacts. These include land-use change, land management and land degradation (erosion, compaction, sealing and salinization). The intensity of land use also exerts a great impact on soils, and soils are also subject to indirect impacts arising from human activity, such as acid deposition (sulphur and nitrogen) and heavy metal pollution. In this critical review, we report the state-of-the-art understanding of these global change pressures on soils, identify knowledge gaps and research challenges and highlight actions and policies to minimize adverse environmental impacts arising from these global change drivers. Soils are central to considerations of what constitutes sustainable intensification. Therefore, ensuring that vulnerable and high environmental value soils are considered when protecting important habitats and ecosystems, will help to reduce the pressure on land from global change drivers. To ensure that soils are protected as part of wider environmental efforts, a global soil resilience programme should be considered, to monitor, recover or sustain soil fertility and function, and to enhance the ecosystem services provided by soils. Soils cannot, and should not, be considered in isolation of the ecosystems that they underpin and vice versa. The role of soils in supporting ecosystems and natural capital needs greater recognition. The lasting legacy of the International Year of Soils in 2015 should be to put soils at the centre of policy supporting environmental protection and sustainable development

    Genetic Determinants of Circulating Sphingolipid Concentrations in European Populations

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    Sphingolipids have essential roles as structural components of cell membranes and in cell signalling, and disruption of their metabolism causes several diseases, with diverse neurological, psychiatric, and metabolic consequences. Increasingly, variants within a few of the genes that encode enzymes involved in sphingolipid metabolism are being associated with complex disease phenotypes. Direct experimental evidence supports a role of specific sphingolipid species in several common complex chronic disease processes including atherosclerotic plaque formation, myocardial infarction (MI), cardiomyopathy, pancreatic beta-cell failure, insulin resistance, and type 2 diabetes mellitus. Therefore, sphingolipids represent novel and important intermediate phenotypes for genetic analysis, yet little is known about the major genetic variants that influence their circulating levels in the general population. We performed a genome-wide association study (GWAS) between 318,237 single-nucleotide polymorphisms (SNPs) and levels of circulating sphingomyelin (SM), dihydrosphingomyelin (Dih-SM), ceramide (Cer), and glucosylceramide (GluCer) single lipid species (33 traits); and 43 matched metabolite ratios measured in 4,400 subjects from five diverse European populations. Associated variants (32) in five genomic regions were identified with genome-wide significant corrected p-values ranging down to 9.08 x 10(-66). The strongest associations were observed in or near 7 genes functionally involved in ceramide biosynthesis and trafficking: SPTLC3, LASS4, SGPP1, ATP10D, and FADS1-3. Variants in 3 loci (ATP10D, FADS3, and SPTLC3) associate with MI in a series of three German MI studies. An additional 70 variants across 23 candidate genes involved in sphingolipid-metabolizing pathways also demonstrate association (p = 10(-4) or less). Circulating concentrations of several key components in sphingolipid metabolism are thus under strong genetic control, and variants in these loci can be tested for a role in the development of common cardiovascular, metabolic, neurological, and psychiatric diseases

    The therapeutic effect of clinical trials: understanding placebo response rates in clinical trials – A secondary analysis

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    BACKGROUND AND PURPOSE: Placebo response rates in clinical trials vary considerably and are observed frequently. For new drugs it can be difficult to prove effectiveness superior to placebo. It is unclear what contributes to improvement in the placebo groups. We wanted to clarify, what elements of clinical trials determine placebo variability. METHODS: We analysed a representative sample of 141 published long-term trials (randomized, double-blind, placebo-controlled; duration > 12 weeks) to find out what study characteristics predict placebo response rates in various diseases. Correlational and regression analyses with study characteristics and placebo response rates were carried out. RESULTS: We found a high and significant correlation between placebo and treatment response rate across diseases (r = .78; p < .001). A multiple regression model explained 79% of the variance in placebo variability (F = 59.7; p < 0.0001). Significant predictors are, among others, the duration of the study (beta = .31), the quality of the study (beta = .18), the fact whether a study is a prevention trial (beta = .44), whether dropouts have been documented (beta = -.20), or whether additional treatments have been documented (beta = -.17). Healing rates with placebo are lower in the following diagnoses; neoplasms (beta = -.21), nervous diseases (beta = -.10), substance abuse (beta = -.14). Without prevention trials the amount of variance explained is 42%. CONCLUSION: Medication response rates and placebo response rates in clinical trials are highly correlated. Trial characteristics can explain some portion of the variance in placebo healing rates in RCTs. Placebo response in trials is only partially due to methodological artefacts and only partially dependent on the diagnoses treated

    No evidence for association between tau gene haplotypic variants and susceptibility to Creutzfeldt-Jakob disease

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    Contains fulltext : 52965.pdf ( ) (Open Access)BACKGROUND: A polymorphism at codon 129 of the prion protein gene (PRNP) is the only well-known genetic risk factor for Creutzfeldt-Jakob disease (CJD). However, there is increasing evidence that other loci outside the PRNP open reading frame might play a role in CJD aetiology as well. METHODS: We studied tau protein gene (MAPT) haplotypic variations in a population of sporadic and variant CJD patients. We tested 6 MAPT haplotype tagging SNPs (htSNPs) in a Dutch population-based sample of sporadic CJD (sCJD) patients and a cognitively normal control group of similar age distribution. We genotyped the same polymorphisms in two other sample groups of sCJD cases from Italy and the UK. In addition, we compared MAPT haplotypes between sCJD and variant CJD (vCJD) patients. RESULTS: Single locus and haplotype analyses did not detect any significant difference between sCJD cases and controls. When we compared MAPT haplotypes between sCJD and variant CJD (vCJD) patients, we found that two of them were represented differently (H1f: 8% in sCJD versus 2% in vCJD; H1j:1% in sCJD versus 7% in vCJD). However, these two haplotypes were rare in both groups of patients, and taking the small sample sizes into account, we cannot exclude that the differences are due to chance. None of the p-values remained statistically significant after applying a multiple testing correction. CONCLUSION: Our study shows no evidence for an association between MAPT gene variations and sCJD, and some weak evidence for an association to vCJD

    A new polygenic score for refractive error improves detection of children at risk of high myopia but not the prediction of those at risk of myopic macular degeneration.

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    BackgroundHigh myopia (HM), defined as a spherical equivalent refractive error (SER) ≤ -6.00 diopters (D), is a leading cause of sight impairment, through myopic macular degeneration (MMD). We aimed to derive an improved polygenic score (PGS) for predicting children at risk of HM and to test if a PGS is predictive of MMD after accounting for SER.MethodsThe PGS was derived from genome-wide association studies in participants of UK Biobank, CREAM Consortium, and Genetic Epidemiology Research on Adult Health and Aging. MMD severity was quantified by a deep learning algorithm. Prediction of HM was quantified as the area under the receiver operating curve (AUROC). Prediction of severe MMD was assessed by logistic regression.FindingsIn independent samples of European, African, South Asian and East Asian ancestry, the PGS explained 19% (95% confidence interval 17-21%), 2% (1-3%), 8% (7-10%) and 6% (3-9%) of the variation in SER, respectively. The AUROC for HM in these samples was 0.78 (0.75-0.81), 0.58 (0.53-0.64), 0.71 (0.69-0.74) and 0.67 (0.62-0.72), respectively. The PGS was not associated with the risk of MMD after accounting for SER: OR = 1.07 (0.92-1.24).InterpretationPerformance of the PGS approached the level required for clinical utility in Europeans but not in other ancestries. A PGS for refractive error was not predictive of MMD risk once SER was accounted for.FundingSupported by the Welsh Government and Fight for Sight (24WG201)

    Genome-wide meta-analysis associates HLA-DQA1/DRB1 and LPA and lifestyle factors with human longevity

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    Genomic analysis of longevity offers the potential to illuminate the biology of human aging. Here, using genome-wide association meta-analysis of 606,059 parents' survival, we discover two regions associated with longevity (HLA-DQA1/DRB1 and LPA). We also validate previous suggestions that APOE, CHRNA3/5, CDKN2A/B, SH2B3 and FOXO3A influence longevity. Next we show that giving up smoking, educational attainment, openness to new experience and high-density lipoprotein (HDL) cholesterol levels are most positively genetically correlated with lifespan while susceptibility to coronary artery disease (CAD), cigarettes smoked per day, lung cancer, insulin resistance and body fat are most negatively correlated. We suggest that the effect of education on lifespan is principally mediated through smoking while the effect of obesity appears to act via CAD. Using instrumental variables, we suggest that an increase of one body mass index unit reduces lifespan by 7 months while 1 year of education adds 11 months to expected lifespan
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