bluuebunny/crossref_metadata_2025_split huggingface dataset:
Marriage and Cohabitation Outcomes After Pregnancy Loss
Authors: Gold Katherine J. , Sen Ananda , Hayward Rodney A. 
Published: April 2010

OBJECTIVE:The goal was to evaluate marriage and cohabitation outcomes for couples who experienced a live birth or fetal death at any gestational age.METHODS:For married and cohabitating women who experienced live births, miscarriages, or stillbirths, we conducted a survival analysis (median follow-up period: 7.8 years), by using data from the National Survey of Family Growth, to examine the association between birth outcomes and subsequent relationship survival. The Cox proportional-hazards models controlled for multiple independent risk factors known to affect relationship outcomes. The main outcome measure was the proportion of intact marriages or cohabitations over time.RESULTS:Of 7770 eligible pregnancies, 82% ended in live births, 16% in miscarriages, and 2% in stillbirths. With controlling for known risk factors, women who experienced miscarriages (hazard ratio: 1.22 [95% confidence interval: 1.08–1.38]; P = .001) or stillbirths (hazard ratio: 1.40 [95% confidence interval: 1.10–1.79]; P = .007) had a significantly greater hazard of their relationship ending, compared with women whose pregnancies ended in live births.CONCLUSIONS:This is the first national study to establish that parental relationships have a higher risk of dissolving after miscarriage or stillbirth, compared with live birth. Given the frequency of pregnancy loss, these findings might have significant societal implications if causally related.
An automated approach to the Electric Network Frequency (ENF) criterion - Theory and practice
Authors: Cooper Alan J. 
Published: April 2010

A relatively recent forensic technique developed to help establish the authenticity of audio and video recordings is the Electric Network Frequency (ENF) criterion. This paper confirms the applicability of the ENF criterion for use in mainland UK and describes an automated approach to matching ENF estimates taken from a questioned recording to a database of ENF values. It will be shown that the automated approach has the added advantage of producing statistical data capable of indicating the strength of the match. Consideration has been given to the robust extraction of ENF signals from evidential recordings and the resulting system and signal processing procedures outlined have been used successfully by the Metropolitan Police Forensic Audio Laboratory in London to extract and match ENF data from evidential recordings to an ENF database.
Designing, Implementing, and Evaluating an Online Resource for Professional Legal Communication Skills
Authors: Hafner Christoph A 
Published: April 2010

The ability to use language effectively is an essential part of legal training and has been identified as an area of concern for Hong Kong law students (Redmond and Roper 2001). In order to become proficient members of the legal discourse community, law students must develop an understanding of conventional writing forms, processes and practices as well as patterns of legal reasoning and problem-solving. Although lawyers in the main agree that competence in legal English is crucial to professional competency, legal professionals also take the view that efforts to enhance such competence should be remedial in nature rather than targeted at the specific communication needs of lawyers (Hong Kong Bar Association 2001). In addition, many practitioners of legal education and training see language skills development as falling outside their area of expertise and responsibility. As a consequence, time and resources allocated to the important task of enhancing English for legal purposes are minimal. In view of these constraints, creating computer-mediated online resources for the development of English language skills becomes a particularly attractive option. Students are able to access material in their own time, work at their own pace, learn ‘just-in-time’ for the real-world tasks that they are working on, and it is the students who are in charge of the learning process. This thesis reports on a collaborative project, involving a small team of legal academics and language professionals, to develop such online resources Awarding Institution: Macquarie University Date of award: April 2009
Sitagliptin (MK0431) Inhibition of Dipeptidyl Peptidase IV Decreases Nonobese Diabetic Mouse CD4+ T-Cell Migration Through Incretin-Dependent and -Independent Pathways
Authors: Kim Su-Jin , Nian Cuilan , McIntosh Christopher H.S. 
Published: April 2010

OBJECTIVETreatment of NOD mice with the dipeptidyl peptidase-IV (DPP-IV) inhibitor sitagliptin preserved islet transplants through a pathway involving modulation of splenic CD4+ T-cell migration. In the current study, effects of sitagliptin on migration of additional subsets of CD4+ T-cells were examined and underlying molecular mechanisms were further defined.RESEARCH DESIGN AND METHODSEffects of sitagliptin on migration of NOD mouse splenic, thymic, and lymph node CD4+ T-cells were determined. Signaling modules involved in DPP-IV-, Sitagliptin- and incretin-mediated modulation of CD4+ T-cell migration were studied using Western blot and Rac1 and nuclear factor-κB (NF-κB) activity assays.RESULTSMigration of splenic and lymph node CD4+ T-cells of diabetic NOD mice was reduced by sitagliptin treatment. In vitro treatment of splenic, but not thymic or lymph node CD4+ T-cells, from nondiabetic NOD mice with soluble (s) DPP-IV increased migration. Sitagliptin abolished sDPP-IV effects on splenic CD4+ T-cell migration, whereas incretins decreased migration of lymph node, but not splenic, CD4+ T-cells. Splenic CD4+ T-cells demonstrating increased in vitro migration in response to sDPP-IV and lymph node CD4+ T-cells that were nonresponsive to incretins selectively infiltrated islets of NOD mice, after injection. Sitagliptin decreases migration of splenic CD4+ T-cells through a pathway involving Rac1/vasodilator-stimulated phosphoprotein, whereas its inhibitory effects on the migration of lymph node CD4+ T-cells involve incretin-activation of the NF-κB pathway.CONCLUSIONSBenefits of sitagliptin treatment in diabetic NOD mice may be mediated through selective effects on subpopulations of T-cells that are related to autoimmunity.
Association of Testosterone and Sex Hormone–Binding Globulin With Metabolic Syndrome and Insulin Resistance in Men
Authors: Li Chaoyang , Ford Earl S. , Li Benyi , Giles Wayne H. , Liu Simin 
Published: April 2010

OBJECTIVE
We sought to assess the associations of testosterones and sex hormone–binding globulin (SHBG) with metabolic syndrome and insulin resistance in men.

RESEARCH DESIGN AND METHODS
We defined metabolic syndrome according to the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Among men aged ≥20 years who participated in the Third National Health and Nutrition Examination Survey (n = 1,226), the Cox proportional hazards model was used to estimate the prevalence ratio and 95% CI of metabolic syndrome according to circulating concentrations of testosterones and SHBG.

RESULTS
After adjustment for age, race/ethnicity, smoking status, alcohol intake, physical activity level, LDL cholesterol, C-reactive protein, and insulin resistance, men in the first quartile (lowest) (prevalence ratio 2.16 [95% CI 1.53–3.06]) and second quartile of total testosterone (2.51 [1.86–3.37]) were more likely to have metabolic syndrome than men in the fourth quartile (highest, referent group) (P &lt; 0.001 for linear trend). Similarly, men in the first quartile of SHBG (2.17 [1.32–3.56]) were more likely to have metabolic syndrome than men in the fourth quartile (P = 0.02 for linear trend). No significant associations of calculated free testosterone (P = 0.31 for linear trend) and bioavailable testosterone (P = 0.11 for linear trend) with metabolic syndrome were detected after adjustment for all possible confounders.

CONCLUSIONS
Low concentrations of total testosterone and SHBG were strongly associated with increased likelihood of having metabolic syndrome, independent of traditional cardiovascular risk factors and insulin resistance.
The Importance of Caloric Restriction in the Early Improvements in Insulin Sensitivity After Roux-en-Y Gastric Bypass Surgery
Authors: Isbell James M. , Tamboli Robyn A. , Hansen Erik N. , Saliba Jabbar , Dunn Julia P. , Phillips Sharon E. , Marks-Shulman Pamela A. , Abumrad Naji N. 
Published: April 2010

OBJECTIVEMany of the metabolic benefits of Roux-en-Y gastric bypass (RYGB) occur before weight loss. In this study we investigated the influence of caloric restriction on the improvements in the metabolic responses that occur within the 1st week after RYGB.RESEARCH METHODS AND DESIGNA mixed meal was administered to nine subjects before and after RYGB (average 4 ± 0.5 days) and to nine matched, obese subjects before and after 4 days of the post-RYGB diet.RESULTSWeight loss in both groups was minimal; the RYGB subjects lost 1.4 ± 5.3 kg (P = 0.46) vs. 2.2 ± 1.0 kg (P = 0.004) in the calorically restricted group. Insulin resistance (homeostasis model assessment of insulin resistance) improved with both RYGB (5.0 ± 3.1 to 3.3 ± 2.1; P = 0.03) and caloric restriction (4.8 ± 4.1 to 3.6 ± 4.1; P = 0.004). The insulin response to a mixed meal was blunted in both the RYGB and caloric restriction groups (113 ± 67 to 65 ± 33 and 85 ± 59 to 65 ± 56 nmol · l−1 · min−1, respectively; P &lt; 0.05) without a change in the glucose response. Glucagon-like peptide 1 levels increased (9.2 ± 8.6 to 12.2 ± 5.5 pg · l−1 · min−1; P = 0.04) and peaked higher (45.2 ± 37.3 to 84.8 ± 33.0 pg/ml; P = 0.01) in response to a mixed meal after RYGB, but incretin responses were not altered after caloric restriction.CONCLUSIONSThese data suggest that an improvement in insulin resistance in the 1st week after RYGB is primarily due to caloric restriction, and the enhanced incretin response after RYGB does not improve postprandial glucose homeostasis during this time.
Antidepressant Use Before and After the Diagnosis of Type 2 Diabetes
Authors: Kivimäki Mika , Tabák Adam G. , Lawlor Debbie A. , Batty G. David , Singh-Manoux Archana , Jokela Markus , Virtanen Marianna , Salo Paula , Oksanen Tuula , Pentti Jaana , Witte Daniel R. , Vahtera Jussi 
Published: April 2010

OBJECTIVE
To examine antidepressant use before and after the diagnosis of diabetes.

RESEARCH DESIGN AND METHODS
This study was a longitudinal analysis of diabetic and nondiabetic groups selected from a prospective cohort study of 151,618 men and women in Finland (the Finnish Public Sector Study, 1995–2005). We analyzed the use of antidepressants in those 493 individuals who developed type 2 diabetes and their 2,450 matched nondiabetic control subjects for each year during a period covering 4 years before and 4 years after the diagnosis. For comparison, we undertook a corresponding analysis on 748 individuals who developed cancer and their 3,730 matched control subjects.

RESULTS
In multilevel longitudinal models, the odds ratio for antidepressant use in those who developed diabetes was 2.00 (95% CI 1.57–2.55) times greater than that in nondiabetic subjects. The relative difference in antidepressant use between these groups was similar before and after the diabetes diagnosis except for a temporary peak in antidepressant use at the year of the diagnosis (OR 2.66 [95% CI 1.94–3.65]). In incident cancer case subjects, antidepressant use substantially increased after the cancer diagnosis, demonstrating that our analysis was sensitive for detecting long-term changes in antidepressant trajectories when they existed.

CONCLUSIONS
Awareness of the diagnosis of type 2 diabetes may temporarily increase the risk of depressive symptoms. Further research is needed to determine whether more prevalent use of antidepressants noted before the diagnosis of diabetes relates to effects of depression, side effects of antidepressant use, or a common causal pathway for depression and diabetes.
Maternal Family History of Diabetes Is Associated With a Reduced Risk of Cardiovascular Disease in Women With Type 2 Diabetes
Authors: Bruce David G. , Van Minnen Kylie , Davis Wendy A. , Mudhar Jaspreet , Perret Michael , Subawickrama Dayani P. , Venkitachalam Stephanie , Ravine David , Davis Timothy M.E. 
Published: April 2010

OBJECTIVE
To investigate whether parental family history of diabetes influences cardiovascular outcomes in type 2 diabetes.

RESEARCH DESIGN AND METHODS
We studied 1,294 type 2 diabetic patients (mean age 64.1 years, 51.2% female) recruited to a community-based cohort study from 1993 to 1996 and followed until mid-2006. A data linkage system assessed all-cause and cardiac mortality, incident myocardial infarction, and stroke. Cox proportional hazards modeling was used to determine the influence of maternal or paternal family history on these outcomes.

RESULTS
A maternal family history of diabetes was reported by 20.4% of the cohort, 8.3% reported paternal family history, and 2.0% reported both parents affected. Maternal and paternal family history was associated with earlier age of diabetes onset, and maternal family history was associated with worse glycemic control. For all patients, maternal family history was significantly associated with reduced risk of all-cause mortality and cardiac mortality. When analyzed by sex, maternal family history had no effect on male patients, whereas female patients with diabetic mothers had significantly reduced hazard ratios for death from all causes (0.63 [95% CI 0.41–0.96]; P = 0.033), for death from cardiac causes (0.32 [0.14–0.72]; P = 0.006), and for first myocardial infarction (0.45 [0.26–0.76]; P = 0.003). Paternal family history status was not associated with these outcomes.

CONCLUSIONS
A maternal family history of diabetes confers relative protection against cardiovascular disease in female patients but not in male patients with type 2 diabetes. Paternal family history is associated with risks equivalent to those without a family history of diabetes. Some of the clinical heterogeneity of type 2 diabetes is related to maternal transmission effects with differential impact on male and female patients.
Cytokine Secretion Is Distinct from Secretion of Cytotoxic Granules in NK Cells
Authors: Reefman Esther , Kay Jason G. , Wood Stephanie M. , Offenhäuser Carolin , Brown Darren L. , Roy Sandrine , Stanley Amanda C. , Low Pei Ching , Manderson Anthony P. , Stow Jennifer L. 
Published: April 2010

Abstract
NK cells are renowned for their ability to kill virally infected or transformed host cells by release of cytotoxic granules containing granzymes and perforin. NK cells also have important regulatory capabilities chiefly mediated by secretion of cytokines, such as IFN-γ and TNF. The secretory pathway for the release of cytokines in NK cells is unknown. In this study, we show localization and trafficking of IFN-γ and TNF in human NK cells in compartments and vesicles that do not overlap with perforin or other late endosome granule markers. Cytokines in post-Golgi compartments colocalized with markers of the recycling endosome (RE). REs are functionally required for cytokine release because inactivation of REs or mutation of RE-associated proteins Rab11 and vesicle-associated membrane protein-3 blocked cytokine surface delivery and release. In contrast, REs are not needed for release of perforin from preformed granules but may be involved at earlier stages of granule maturation. These findings suggest a new role for REs in orchestrating secretion in NK cells. We show that the cytokines IFN-γ and TNF are trafficked and secreted via a different pathway than perforin. Although perforin granules are released in a polarized fashion at lytic synapses, distinct carriers transport both IFN-γ and TNF to points all over the cell surface, including within the synapse, for nonpolarized release.
Differential but Direct Abolishment of Human Regulatory T Cell Suppressive Capacity by Various TLR2 Ligands
Authors: Oberg Hans-Heinrich , Ly Thi Thuy Hoa , Ussat Sandra , Meyer Tim , Kabelitz Dieter , Wesch Daniela 
Published: April 2010

Abstract
CD4+CD25high regulatory T cells (Tregs) control cellular immune responses and maintain peripheral tolerance. We investigated whether TLR2 ligands are able to abrogate Treg-induced suppression in humans based on different reports about effects of triacylated lipopeptide Pam3CSK4 in mice. Pretreatment of human Tregs with a mixture of TLR2 ligands Pam2CSK4, FSL-1, and Pam3CSK4 reduced the Treg-mediated suppression of CD4+CD25− responder T cells in the majority of the analyzed donors. Differential effects of individual TLR2 ligands are explained by usage of different TLR2 heterodimers in the recognition of Pam2CSK4, FSL-1, and Pam3CSK4. In contrast to the murine system, TLR2 ligand-mediated abrogation of human Treg function was not associated with a downregulation of FoxP3 transcription factor. Furthermore, our results excluded an effect of TLR2 ligands on granzyme A/B release by human Tregs as a potential mechanism to abolish Treg-mediated suppression. Our data suggest that a downregulation of p27Kip1 and restoration of Akt phosphorylation in human Tregs pretreated with TLR2 ligands result in a reversal of suppression on responder T cells. Moreover, our data indicate that a mixture of TLR2 ligands can be used to modulate human Treg activity.
Plasma Cells and Nonplasma B Cells Express Differing IgE Repertoires in Allergic Sensitization
Authors: Rogosch Tobias , Kerzel Sebastian , Sikula Larisa , Gentil Katrin , Liebetruth Michael , Schlingmann Karl-Peter , Maier Rolf F. , Zemlin Michael 
Published: April 2010

AbstractThe selection of allergen-specific B cells into the plasma cell (PC) pool is a critical step in the immune dysregulation that leads to the production of IgE in allergic diseases. We sought to characterize the murine IgE repertoire. In particular, we questioned whether the IgE repertoire of plasmablasts (PBs)/PCs differs from the IgE repertoire of non-PCs. Therefore, we sorted splenocytes from OVA-sensitized BALB/c mice into CD138pos (PBs/PCs) and CD19pos/CD138neg (non-PCs) B cell fractions. Using reverse transcription PCR, we amplified, cloned, and sequenced IgE mRNA transcripts and analyzed the Ig H chain repertoire. As a reference, we characterized the IgM repertoire of the same animals. Compared to IgM, the IgE sequences contained a significantly higher level of somatic mutations and displayed an oligoclonal expansion with clonotype restriction. Interestingly, we found two phenotypically distinct IgE-producing B cell subpopulations that differed in their repertoire of H chain transcripts; IgE transcripts from PBs/PCs showed significantly more signs of Ag-driven selection than transcripts from non-PCs, including 1) a higher number of somatic mutations, 2) increased clustering of replacement mutations in the CDRs, and 3) biased third CDR of the heavy Ig chain composition. In conclusion, PBs/PCs and non-PCs from OVA-sensitized mice express distinct IgE repertoires, suggesting that 1) the repertoire of IgE-expressing PBs/PCs represents a highly biased selection from the global B cell repertoire and 2) Ag-driven affinity maturation is a major force that selects IgE-producing B cells into the CD138pos PC pool.
Hypertonicity-Induced Expression of Monocyte Chemoattractant Protein-1 through a Novel Cis-Acting Element and MAPK Signaling Pathways
Authors: Kojima Ryoji , Taniguchi Hajime , Tsuzuki Aya , Nakamura Kanako , Sakakura Yumi , Ito Mikio 
Published: April 2010

Abstract
MCP1 is upregulated by various stimuli, including LPS, high glucose, and hyperosmolality. However, the molecular mechanisms of transcriptional regulation of the MCP1 gene under hyperosmolar conditions are poorly understood. Treatment of NRK52E cells with NaCl or mannitol resulted in significant elevation of MCP1 mRNA and protein in a time- and dose-dependent manner. Treatment with a p38MAPK inhibitor (SB203580), an ERK inhibitor (PD98059), or an MEK inhibitor (U0126), suppressed the increase in MCP1 expression caused by hypertonic NaCl, whereas a JNK inhibitor (SP600125) and an AP1 inhibitor (curcumin) failed to attenuate MCP1 mRNA expression by NaCl. In the 5′-flanking region of the MCP1 gene, there is a sequence motif similar to the consensus TonE/ORE as well as the consensus C/E binding protein (BP), NF-κB, and AP1/Sp1 sites. Luciferase activity in cells transfected with reporter constructs containing a putative TonE/ORE element (MCP1-TonE/ORE) enhanced reporter gene expression under hypertonic stress. Results of electrophoretic gel mobility shift assay showed a slow migration of the MCP1-TonE/ORE probe, representing the binding of TonEBP/OREBP/NFAT5 to this enhancer element. These results indicate that the 5′-flanking region of MCP1 contains a hypertonicity-sensitive cis-acting element, MCP1-TonE/ORE, as a novel element in the MCP1 gene. Furthermore, p38MAPK and MEK–ERK pathways appear to be, at least in part, involved in hypertonic stress-mediated regulation of MCP1 expression through the MCP1-TonE/ORE.
A Threonine-Based Targeting Signal in the Human CD1d Cytoplasmic Tail Controls Its Functional Expression
Authors: Liu Jianyun , Shaji Daniel , Cho Sungyoo , Du Wenjun , Gervay-Hague Jacquelyn , Brutkiewicz Randy R. 
Published: April 2010

Abstract
CD1d molecules are MHC class I-like molecules that present lipids to a unique subpopulation of T cells called NKT cells. The cytoplasmic tail of human CD1d possesses a tyrosine-based endosomal targeting motif (YXXZ). As such, these molecules traffic through the endocytic pathway, where it is believed that they are loaded with the antigenic lipid that stimulates NKT cells. In the current study, it was found that the T322 residue in the human CD1d tail is a major signal controlling transport to the cell surface and thus its functional expression. Mimicking the phosphorylation of this residue or removal of the entire cytoplasmic tail negates its ability to regulate CD1d trafficking, resulting in lysosomal targeting and degradation. These results demonstrate an important role of a heretofore unknown signal in the cytoplasmic tail of CD1d that may have relevance to other type I integral membrane proteins that traverse through the endocytic pathway.
SHIP Influences Signals from CD48 and MHC Class I Ligands That Regulate NK Cell Homeostasis, Effector Function, and Repertoire Formation
Authors: Fortenbery Nicole R. , Paraiso Kim H. T. , Taniguchi Masaru , Brooks Colin , Ibrahim Leina , Kerr William G. 
Published: April 2010

Abstract
Previously, we showed that 2B4 is a dominant inhibitory receptor in SHIP-deficient NK cells that prevents efficient cytolysis of complex targets. We show in this study that 2B4 deficiency restores homeostatic control and cytolytic function to SHIP-deficient NK cells. However, 2B4−/−SHIP−/− NK cells still exhibit a profound disruption of their NK receptor repertoire and are compromised for induction of IFN-γ by several NK-activating receptors, including NKp46, NK.1.1, and NKG2D. In addition, we find that 2B4−/− NK cells have an extensively disrupted repertoire, including a supernormal frequency of NKp46+ NK cells. Consequently IFN-γ is induced on a much higher percentage of 2B4−/− NK cells following engagement of NKp46. We also find that both SHIP and 2B4 are required to prevent expression of Ly49B, a myeloid lineage MHC class I receptor not normally expressed by the NK lineage. Finally, when SHIP-deficient NK cells are on an H-2d background, they exhibit supernormal levels of Ly49A and possess normal cytolytic function against MHC-matched tumor targets and enhanced cytolysis of MHC mismatched tumor targets. However, despite normal or elevated cytolytic function, H2d SHIP−/− NK cells exhibit poor induction of IFN-γ like their H2b+ or 2B4−/− counterparts, demonstrating a uniform requirement for SHIP in induction of IFN-γ downstream of key NK activating receptors. These findings reveal a complex interplay of SHIP, 2B4, and MHC in the regulation of homeostasis, effector function, and repertoire formation in the NK cell lineage.