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Search Results: 1 - 10 of 163663 matches for " James B. Hannah "
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Dystextia: An Early Sign of Pregnancy-Associated Meningioma  [PDF]
James B. Hannah, Phillip Kissel, Bianca Russell, Jo Ellen Hose
Open Journal of Modern Neurosurgery (OJMN) , 2014, DOI: 10.4236/ojmn.2014.42015
Abstract: Objective: The authors report a case of meningioma causing incomprehensible and excessive text messaging in a postpartum woman. Case Report: We report the case of expressive dystextia related to a postpartum, progesterone receptor-positive meningioma. Growth of meningiomas can accelerate during pregnancy and the postpartum period due to expression of hormone receptors, particularly progesterone. This is the first study describing dystextia related to a brain tumor; previous cases of dystextia are associated with stroke and complex migraine. Here expressive dystextia, the inability to compose syntactically comprehensible text messages, preceded acute neurologic signs by several months, and surgical resection of the meningioma eliminated all neurologic sequelae. Possible genetic etiologies for meningioma are discussed since this patient’s prior thyroid cancer at age 18 suggests a relationship between the two neoplasms. Conclusions: Since text messaging is becoming one of the principal forms of communication in our society and requires both cognitive and motor skills, clinicians should be aware that dystextia may be the initial sign of significant neurologic pathology. We propose that an inquiry about altered text messaging frequency and comprehensibility should be a standard part of the neurologic evaluation.
Population studies of sporadic cerebral amyloid angiopathy and dementia: a systematic review
Hannah AD Keage, Roxanna O Carare, Robert P Friedland, Paul G Ince, Seth Love, James A Nicoll, Stephen B Wharton, Roy O Weller, Carol Brayne
BMC Neurology , 2009, DOI: 10.1186/1471-2377-9-3
Abstract: To identify population-based studies assessing CAA and dementia, a previous systematic review of population-based clinicopathological studies of ageing and dementia was employed. To identify selected-sample studies, PsychInfo (1806–April Week 3 2008), OVID MEDLINE (1950–April Week 2 2008) and Pubmed (searched 21 April 2008) databases were searched using the term "amyloid angiopathy". These databases were also employed to search for any population-based studies not included in the previous systematic review. Studies were included if they reported the prevalence of CAA relative to a dementia classification (clinical or neuropathological).Four population-based studies were identified. They showed that on average 55–59% of those with dementia displayed CAA (of any severity) compared to 28–38% of the non-demented. 37–43% of the demented displayed severe CAA in contrast to 7–24% of the non-demented. There was no overlap in the range of these averages and they were less variable and lower than those reported in 38 selected sample studies (demented v non-demented: 32–100 v 0–77% regardless of severity; 0–50 v 0–11% for severe only).CAA prevalence in populations is consistently higher in the demented as compared to the non-demented. This supports a significant role for CAA in the pathogenesis of dementia.Alzheimer's disease (AD) is the most common type of dementia and is characterised pathologically by the intraneuronal accumulation of neurofibrillary tangles (NFT) containing tau and ubiquitin, and by the extracellular accumulation of amyloid-β (Aβ) in brain tissue and in artery walls as cerebral amyloid angiopathy (CAA). Many studies have correlated the severity of dementia in AD with the number and distribution of NFTs, the number of plaques of insoluble Aβ, and the levels of soluble Aβ in the brain [as reviewed by [1]]. Relatively few studies, however, have investigated the relationship between dementia and the key pathological change of CAA.CAA is the deposition of the a
Microhomology-Mediated Mechanisms Underlie Non-Recurrent Disease-Causing Microdeletions of the FOXL2 Gene or Its Regulatory Domain
Hannah Verdin,Barbara D'haene,Diane Beysen,Yana Novikova,Bj?rn Menten,Tom Sante,Pablo Lapunzina,Julian Nevado,Claudia M. B. Carvalho,James R. Lupski,Elfride De Baere
PLOS Genetics , 2013, DOI: 10.1371/journal.pgen.1003358
Abstract: Genomic disorders are often caused by recurrent copy number variations (CNVs), with nonallelic homologous recombination (NAHR) as the underlying mechanism. Recently, several microhomology-mediated repair mechanisms—such as microhomology-mediated end-joining (MMEJ), fork stalling and template switching (FoSTeS), microhomology-mediated break-induced replication (MMBIR), serial replication slippage (SRS), and break-induced SRS (BISRS)—were described in the etiology of non-recurrent CNVs in human disease. In addition, their formation may be stimulated by genomic architectural features. It is, however, largely unexplored to what extent these mechanisms contribute to rare, locus-specific pathogenic CNVs. Here, fine-mapping of 42 microdeletions of the FOXL2 locus, encompassing FOXL2 (32) or its regulatory domain (10), serves as a model for rare, locus-specific CNVs implicated in genetic disease. These deletions lead to blepharophimosis syndrome (BPES), a developmental condition affecting the eyelids and the ovary. For breakpoint mapping we used targeted array-based comparative genomic hybridization (aCGH), quantitative PCR (qPCR), long-range PCR, and Sanger sequencing of the junction products. Microhomology, ranging from 1 bp to 66 bp, was found in 91.7% of 24 characterized breakpoint junctions, being significantly enriched in comparison with a random control sample. Our results show that microhomology-mediated repair mechanisms underlie at least 50% of these microdeletions. Moreover, genomic architectural features, like sequence motifs, non-B DNA conformations, and repetitive elements, were found in all breakpoint regions. In conclusion, the majority of these microdeletions result from microhomology-mediated mechanisms like MMEJ, FoSTeS, MMBIR, SRS, or BISRS. Moreover, we hypothesize that the genomic architecture might drive their formation by increasing the susceptibility for DNA breakage or promote replication fork stalling. Finally, our locus-centered study, elucidating the etiology of a large set of rare microdeletions involved in a monogenic disorder, can serve as a model for other clustered, non-recurrent microdeletions in genetic disease.
A Hybrid Likelihood Model for Sequence-Based Disease Association Studies
Yun-Ching Chen,Hannah Carter,Jennifer Parla,Melissa Kramer,Fernando S. Goes,Mehdi Pirooznia,Peter P. Zandi,W. Richard McCombie,James B. Potash,Rachel Karchin
PLOS Genetics , 2013, DOI: 10.1371/journal.pgen.1003224
Abstract: In the past few years, case-control studies of common diseases have shifted their focus from single genes to whole exomes. New sequencing technologies now routinely detect hundreds of thousands of sequence variants in a single study, many of which are rare or even novel. The limitation of classical single-marker association analysis for rare variants has been a challenge in such studies. A new generation of statistical methods for case-control association studies has been developed to meet this challenge. A common approach to association analysis of rare variants is the burden-style collapsing methods to combine rare variant data within individuals across or within genes. Here, we propose a new hybrid likelihood model that combines a burden test with a test of the position distribution of variants. In extensive simulations and on empirical data from the Dallas Heart Study, the new model demonstrates consistently good power, in particular when applied to a gene set (e.g., multiple candidate genes with shared biological function or pathway), when rare variants cluster in key functional regions of a gene, and when protective variants are present. When applied to data from an ongoing sequencing study of bipolar disorder (191 cases, 107 controls), the model identifies seven gene sets with nominal p-values0.05, of which one MAPK signaling pathway (KEGG) reaches trend-level significance after correcting for multiple testing.
Marcus Recht: Der sympathische Vampir. Visualisierungen von M nnlichkeiten in der TV-Serie Buffy. Frankfurt am Main u.a.: Campus Verlag 2011.
Hannah B?lling
querelles-net , 2012,
Abstract: Marcus Recht leistet als einer der ersten deutschsprachigen Autoren eine ausführliche Analyse der besonderen Darstellung alternativer Geschlechtlichkeit in der TV-Serie Buffy. Mit Hilfe ausführlicher wissenschaftlicher Methodik zeigt Recht auf, dass die Serie sowohl soziale Konstrukte analysiert, widerspiegelt und karikiert als auch eine alternative Geschlechtlichkeit etabliert, welche die m nnlichen Vampire in einen zur Zeit der Serienausstrahlung g nzlich neuen Gender-Kontext stellt. Viele weitere klassische filmsoziologische Theorien zu Gender-Konstruktion und -Darstellung werden kritisch aufgegriffen und in die Analyse einbezogen. Eine gute Grundlage für Einsteiger/-innen als auch für Kenner/-innen des Feldes, um sich mit dem wissenschaftlichen Potential des popkulturellen Feldes auseinanderzusetzen. As one of the first German-language authors, Marcus Recht presents an elaborate analysis of the extraordinary depiction of alternative sexuality in the TV show Buffy. Using extensive scientific methodology, Recht demonstrates that the show both analyzes, reflects, and caricatures social constructs and establishes an alternative sexuality, which puts the male vampires into a gender context that was completely new at the time when the show was broadcast. Furthermore, the author addresses many other classic film-sociological theories on gender construction and representation and incorporates them into the analysis. A good foundational work for beginners as well as for experts in the field, who want to examine the scientific potential of the pop-cultural field.
Triage of high-risk surgical patients for intensive care
Julia B Sobol, Hannah Wunsch
Critical Care , 2011, DOI: 10.1186/cc9999
Abstract: Postoperative outcomes are a result of the complex interplay between the exact general surgical procedure performed, the previous health of the patient, and specific intra- and postoperative events. Outcomes may also be influenced by aspects of the particular healthcare system, such as the surgical procedure volume at different hospitals [3], as well as care options, such as the availability and suitable use of intensive care beds. Appropriate triage of patients to intensive care postoperatively may have a large impact on outcomes after non-cardiac surgery. This chapter reviews the patient factors and scoring systems developed to help with triage, describes current ICU triage recommendations for postsurgical patients, and identifies potential ways to improve evaluation and management of high-risk postoperative patients.Predictors of postoperative outcomes may be divided into three categories: Known preoperative risk factors; the risk associated with the specific surgical procedure; and the unique aspects of each operative case that may contribute to a particular patient being at high risk for complications or death after surgery.Many preoperative risk factors can help distinguish which patients are most likely to experience poor post-operative outcomes. In particular, preoperative comorbidities are well-established as predictors of both morbidity and mortality after surgery and can be measured in different ways (Table 1). Perhaps the best known is the American Society of Anesthesiologists' (ASA) physical status classification system. This is a widely used preoperative scoring system that describes the overall health of the patient and burden of comorbidities. The score is ideal in being simple to apply and requiring no laboratory data; however, it is also subject to substantial interobserver variation in score assignment [4]. Despite this inherent subjectivity, the ASA classification has been recognized as a helpful predictor of potential postoperative morbidity and
Dysfunctional KEAP1–NRF2 Interaction in Non-Small-Cell Lung Cancer
Anju Singh,Vikas Misra,Rajesh K Thimmulappa,Hannah Lee,Stephen Ames,Mohammad O Hoque,James G Herman,Stephen B Baylin,David Sidransky,Edward Gabrielson,Malcolm V Brock,Shyam Biswal
PLOS Medicine , 2006, DOI: 10.1371/journal.pmed.0030420
Abstract: Background Nuclear factor erythroid-2 related factor 2 (NRF2) is a redox-sensitive transcription factor that positively regulates the expression of genes encoding antioxidants, xenobiotic detoxification enzymes, and drug efflux pumps, and confers cytoprotection against oxidative stress and xenobiotics in normal cells. Kelch-like ECH-associated protein 1 (KEAP1) negatively regulates NRF2 activity by targeting it to proteasomal degradation. Increased expression of cellular antioxidants and xenobiotic detoxification enzymes has been implicated in resistance of tumor cells against chemotherapeutic drugs. Methods and Findings Here we report a systematic analysis of the KEAP1 genomic locus in lung cancer patients and cell lines that revealed deletion, insertion, and missense mutations in functionally important domains of KEAP1 and a very high percentage of loss of heterozygosity at 19p13.2, suggesting that biallelic inactivation of KEAP1 in lung cancer is a common event. Sequencing of KEAP1 in 12 cell lines and 54 non-small-cell lung cancer (NSCLC) samples revealed somatic mutations in KEAP1 in a total of six cell lines and ten tumors at a frequency of 50% and 19%, respectively. All the mutations were within highly conserved amino acid residues located in the Kelch or intervening region domain of the KEAP1 protein, suggesting that these mutations would likely abolish KEAP1 repressor activity. Evaluation of loss of heterozygosity at 19p13.2 revealed allelic losses in 61% of the NSCLC cell lines and 41% of the tumor samples. Decreased KEAP1 activity in cancer cells induced greater nuclear accumulation of NRF2, causing enhanced transcriptional induction of antioxidants, xenobiotic metabolism enzymes, and drug efflux pumps. Conclusions This is the first study to our knowledge to demonstrate that biallelic inactivation of KEAP1 is a frequent genetic alteration in NSCLC. Loss of KEAP1 function leading to constitutive activation of NRF2-mediated gene expression in cancer suggests that tumor cells manipulate the NRF2 pathway for their survival against chemotherapeutic agents.
Differential Modulation of Retinal Degeneration by Ccl2 and Cx3cr1 Chemokine Signalling
Ulrich F. O. Luhmann, Clemens A. Lange, Scott Robbie, Peter M. G. Munro, Jill A. Cowing, Hannah E. J. Armer, Vy Luong, Livia S. Carvalho, Robert E. MacLaren, Frederick W. Fitzke, James W. B. Bainbridge, Robin R. Ali
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035551
Abstract: Microglia and macrophages are recruited to sites of retinal degeneration where local cytokines and chemokines determine protective or neurotoxic microglia responses. Defining the role of Ccl2-Ccr2 and Cx3cl1-Cx3cr1 signalling for retinal pathology is of particular interest because of its potential role in age-related macular degeneration (AMD). Ccl2, Ccr2, and Cx3cr1 signalling defects impair macrophage trafficking, but have, in several conflicting studies, been reported to show different degrees of age-related retinal degeneration. Ccl2/Cx3cr1 double knockout (CCDKO) mice show an early onset retinal degeneration and have been suggested as a model for AMD. In order to understand phenotypic discrepancies in different chemokine knockout lines and to study how defects in Ccl2 and/or Cx3cr1 signalling contribute to the described early onset retinal degeneration, we defined primary and secondary pathological events in CCDKO mice. To control for genetic background variability, we compared the original phenotype with that of single Ccl2, Cx3cr1 and Ccl2/Cx3cr1 double knockout mice obtained from backcrosses of CCDKO with C57Bl/6 mice. We found that the primary pathological event in CCDKO mice develops in the inferior outer nuclear layer independently of light around postnatal day P14. RPE and vascular lesions develop secondarily with increasing penetrance with age and are clinically similar to retinal telangiectasia not to choroidal neovascularisation. Furthermore, we provide evidence that a third autosomal recessive gene causes the degeneration in CCDKO mice and in all affected re-derived lines and subsequently demonstrated co-segregation of the naturally occurring RD8 mutation in the Crb1 gene. By comparing CCDKO mice with re-derived CCl2?/?/Crb1Rd8/RD8, Cx3cr1?/?/Crb1Rd8/RD8 and CCl2?/?/Cx3cr1?/?/Crb1Rd8/RD8 mice, we observed a differential modulation of the retinal phenotype by genetic background and both chemokine signalling pathways. These findings indicate that CCDKO mice are not a model of AMD, but a model for an inherited retinal degeneration that is differentially modulated by Ccl2-Ccr2 and Cx3cl1-Cx3cr1 chemokine signalling.
Admissibility of the Defendant’s Criminal Records at Trial  [PDF]
James B. Jacobs
Beijing Law Review (BLR) , 2013, DOI: 10.4236/blr.2013.43015
Abstract:

The jury trial, which is a hallmark of the Anglo-American adversary system, requires close attention to the evidence that it is permissible for the lay jurors to hear. No evidentiary issue has proved more contentious than the admissibility of witnesses’, especially defendants’, prior criminal history because of concern that the lay jurors might prejudicially infer present guilt from past criminality. This article explains the complex evidentiary rules for admitting criminal history to prove guilt and to impeach witness credibility. It suggests that inquisitorial trial procedure, which historically has been unconcerned that judges know about the defendant’s prior criminal history while they are determining present guilt may have to restrict admissibility of such evidence as lay juries become more common.

Effect of Signature Card on Disposition of Joint Bank Account upon Death of Co-Owner under New York Banking Law  [PDF]
James B. Biagi
Beijing Law Review (BLR) , 2014, DOI: 10.4236/blr.2014.54024
Abstract: It is a common practice for people to open a bank account in the name of one or more owners (a/k/a co-owners) and not just in the name of a single person alone. It is also common for an individual to be added to the ownership of an existing account once it has been established. Oftentimes spouses, friends, family or business associates decide for various reasons, both financial and personal, to establish a joint bank account and hold it as co-owners. Furthermore, as the population ages, it has become a common practice for elderly individuals to place another person’s name on a bank account, effectively creating a joint account arrangement for a once individually held account. As is often the case when multiple parties share in a financial transaction, disputes can arise as to the disposition of the funds held in such an account, either during life or at death. In order to address this issue, New York, a major world financial center, has put in place specific legislation to address the disposition of a joint bank account governed by the laws of that State. In this article, the author discusses New York Banking Law §675 and its application to the transfer of funds held in a joint account at the death of a co-owner, paying particular attention to the effect of the account’s signature card on the issue.
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