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  • 1
    Online Resource
    Online Resource
    Predicting Imminent Suicidal Thoughts and Nonfatal Attempts: The Role of Complexity
    SAGE Publications ; 2019
    In:  Clinical Psychological Science Vol. 7, No. 5 ( 2019-09), p. 941-957
    Details
    In: Clinical Psychological Science, SAGE Publications, Vol. 7, No. 5 ( 2019-09), p. 941-957
    Abstract: For decades, our ability to predict suicidal thoughts and behaviors (STBs) has been at near-chance levels. The objective of this study was to advance prediction by addressing two major methodological constraints pervasive in past research: (a) the reliance on long follow-ups and (b) the application of simple conceptualizations of risk. Participants were 1,021 high-risk suicidal and/or self-injuring individuals recruited worldwide. Assessments occurred at baseline and 3, 14, and 28 days after baseline using a range of implicit and self-report measures. Retention was high across all time points ( 〉 90%). Risk algorithms were derived and compared with univariate analyses at each follow-up. Results indicated that short-term prediction alone did not improve prediction for attempts, even using commonly cited “warning signs”; however, a small set of factors did provide fair-to-good short-term prediction of ideation. Machine learning produced considerable improvements for both outcomes across follow-ups. Results underscore the importance of complexity in the conceptualization of STBs.
    Type of Medium: Online Resource
    ISSN: 2167-7026 , 2167-7034
    URL: Article
    DOI: 10.1177/2167702619838464
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2019
    detail.hit.zdb_id: 2682220-9
    SSG: 5,2
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  • 2
    Online Resource
    Online Resource
    Genome-wide association study and functional validation implicates JADE1 in tauopathy
    Springer Science and Business Media LLC ; 2022
    In:  Acta Neuropathologica Vol. 143, No. 1 ( 2022-01), p. 33-53
    Details
    In: Acta Neuropathologica, Springer Science and Business Media LLC, Vol. 143, No. 1 ( 2022-01), p. 33-53
    Type of Medium: Online Resource
    ISSN: 0001-6322 , 1432-0533
    URL: Article
    DOI: 10.1007/s00401-021-02379-z
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 1458410-4
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  • 3
    Online Resource
    Online Resource
    Streaming Detection for Evaluation of Indeterminate Sonographic Breast Masses: A Pilot Study
    American Roentgen Ray Society ; 2006
    In:  American Journal of Roentgenology Vol. 186, No. 5 ( 2006-05), p. 1335-1341
    Details
    In: American Journal of Roentgenology, American Roentgen Ray Society, Vol. 186, No. 5 ( 2006-05), p. 1335-1341
    Type of Medium: Online Resource
    ISSN: 0361-803X , 1546-3141
    URL: Article
    DOI: 10.2214/AJR.05.0005
    RVK:
    XA 20300
    RVK:
    XA 10000
    Language: English
    Publisher: American Roentgen Ray Society
    Publication Date: 2006
    detail.hit.zdb_id: 2012224-X
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  • 4
    Online Resource
    Online Resource
    Core curriculum for peroral endoscopic myotomy (POEM)
    Elsevier BV ; 2021
    In:  Gastrointestinal Endoscopy Vol. 93, No. 3 ( 2021-03), p. 539-543
    Details
    In: Gastrointestinal Endoscopy, Elsevier BV, Vol. 93, No. 3 ( 2021-03), p. 539-543
    Type of Medium: Online Resource
    ISSN: 0016-5107
    URL: Article
    DOI: 10.1016/j.gie.2020.10.026
    RVK:
    XA 44545
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2006253-9
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  • 5
    Online Resource
    Online Resource
    CRISPR-Cas9 In Vivo Gene Editing for Transthyretin Amyloidosis
    Massachusetts Medical Society ; 2021
    In:  New England Journal of Medicine Vol. 385, No. 6 ( 2021-08-05), p. 493-502
    Details
    In: New England Journal of Medicine, Massachusetts Medical Society, Vol. 385, No. 6 ( 2021-08-05), p. 493-502
    Type of Medium: Online Resource
    ISSN: 0028-4793 , 1533-4406
    URL: Article
    DOI: 10.1056/NEJMoa2107454
    RVK:
    XA 10000
    Language: English
    Publisher: Massachusetts Medical Society
    Publication Date: 2021
    detail.hit.zdb_id: 1468837-2
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  • 6
    Online Resource
    Online Resource
    Abstract 139: Renal Afferent Nerve Sensitivity and the Pathophysiology of Salt-sensitive Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Hypertension Vol. 66, No. suppl_1 ( 2015-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 66, No. suppl_1 ( 2015-09)
    Abstract: Aim: Altered renal afferent nerve responsiveness contributes to hypertension in the Spontaneously Hypertensive rat. We hypothesized that increased salt-intake differentially impacts the renal afferent nerve sensitivity in salt-resistant vs salt-sensitive rats. Methods: Groups of naïve Sprague-Dawley (SD), Dahl Salt-Resistant (DSR), Dahl Salt-Sensitive (DSS) or SD rats receiving a s.c. norepinephrine (NE:600ng/min) infusion were fed a 0.4% (NS) or 8% NaCl (HS) diet for 14 (SD) or 21 days (DSR & DSS). Following HS intake MAP and plasma NE content were determined. Via a renal pelvis preparation afferent nerve activity was assessed as NE-evoked (6250 pmol) substance P (SP) release (N=5/gp). Results: Salt-resistant phenotypes (SD & DSR) remain normotensive and exhibit HS-evoked suppression of plasma NE and increased renal afferent nerve release of substance P. In contrast in salt-sensitive phenotypes (DSS and NE infused SD) a high salt diet evoked hypertension, increased plasma NE and abolished sodium evoked increased responsiveness of the renal afferent release of substance P. Significance symbols: *p 〈 0.05 vs. resp. NS gp; τ p 〈 0.05 vs. resp. SD Naïve gp. value. Conclusion: These data support a role of the afferent renal nerves in blood pressure regulation during high salt-intake. Increased responsiveness of the renal afferent nerves contributes to the maintenance of normotension in a salt-resistant rat phenotype. Conversely, our data suggest that in salt-sensitive phenotypes excess release of NE triggers impaired activation of the renal afferent nerves, a factor we postulate contributes to the development of salt-sensitive hypertension.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.66.suppl_1.139
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2094210-2
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  • 7
    Online Resource
    Online Resource
    Abstract 121: Afferent Renal Nerve Chemo- and Mechanosensitive Responses and the Modulation of Sodium Homeostasis and Blood Pressure
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Hypertension Vol. 68, No. suppl_1 ( 2016-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 68, No. suppl_1 ( 2016-09)
    Abstract: Aim: We hypothesize that challenges to sodium homeostasis differentially activate chemo- vs. mechanosensitive afferent renal nerves to evoke sympathoinhibition, sodium homeostasis and normotension in the Sprague-Dawley (SD) rat. Methods: Conscious SD rats, post sham (S) or afferent renal nerve ablation (Renal-CAP; capsaicin 33 mM) underwent IV volume expansion (VE; 5% BW) or IV sodium loading (1M NaCl Infusion – constant infusion volume) and HR, MAP, natriuresis and PVN neuronal activation (c-Fos expression) were assessed (N=4/gp). Naïve SD rats were fed a 0.6% (NS) or 4% NaCl (HS) diet for 21 days and afferent renal nerve activity was assessed as norepinephrine (NE) (1250 pmol) and NaCl-evoked (450mM) substance P (SP) release in a renal pelvic assay (N=4/gp). Radiotelemetered SD rats post S or Renal-CAP immediately prior a 0.6% (NS) or 4% NaCl (HS) diet underwent continuous MAP monitoring. On day-21 plasma and renal NE content was assessed (N=5/group). Results: Renal-CAP attenuated the natriuretic and PVN parvocellular responses to IV VE (peak UNaV [μeq/min]; S 43±4 vs Renal-CAP 26±6, P 〈 0.05, PVN Medial Parvocellular neuronal activation [c-fos positive cells]; S 49±6 vs Renal-CAP 22±5 P 〈 0.05) and evoked increased MAP (MAP 90min post-VE [mmHg] S 118±3 vs Renal-CAP 132±4, P 〈 0.05). In contrast Renal-CAP did not alter the natriuresis to IV 1M NaCl (UNaV [μeq/min]; S 21±4 vs Renal-CAP 21±3) or increase MAP. In naïve SD rats HS-intake did not alter MAP and suppressed plasma and renal NE (P 〈 0.05). HS intake increased NE, but not NaCl, mediated afferent renal nerve activity (NE-evoked peak ΔSP [ng/ml); NS 14±2, HS 22±3, P 〈 0.05, NaCl-evoked peak ΔSP [ng/ml]; NS 17±3, HS 16±2). Renal-CAP immediately prior to a HS-intake persistently increased MAP (Day 21 MAP [mmHg] S HS 106±4, Renal-CAP HS 123±5, P 〈 0.05) and attenuated HS-evoked global and renal sympathoinhibition (P 〈 0.05). Conclusion: The mechanosensitive afferent renal nerves mediate acute natriuresis and blood pressure regulation via activation of PVN sympathoinhibitory neurons. During HS intake the afferent renal nerves counter the development of salt-sensitive hypertension via a mechanism involving increased mechano but not chemosensitive afferent nerve responsiveness to potentiate sympathoinhibition.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.68.suppl_1.121
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2094210-2
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  • 8
    Online Resource
    Online Resource
    Sympathetic regulation of NCC in norepinephrine-evoked salt-sensitive hypertension in Sprague-Dawley rats
    American Physiological Society ; 2019
    In:  American Journal of Physiology-Renal Physiology Vol. 317, No. 6 ( 2019-12-01), p. F1623-F1636
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 317, No. 6 ( 2019-12-01), p. F1623-F1636
    Abstract: Salt sensitivity of blood pressure is characterized by inappropriate sympathoexcitation and renal Na + reabsorption during high salt intake. In salt-resistant animal models, exogenous norepinephrine (NE) infusion promotes salt-sensitive hypertension and prevents dietary Na + -evoked suppression of the Na + -Cl − cotransporter (NCC). Studies of the adrenergic signaling pathways that modulate NCC activity during NE infusion have yielded conflicting results implicating α 1 - and/or β-adrenoceptors and a downstream kinase network that phosphorylates and activates NCC, including with no lysine kinases (WNKs), STE20/SPS1-related proline-alanine-rich kinase (SPAK), and oxidative stress response 1 (OxSR1). In the present study, we used selective adrenoceptor antagonism in NE-infused male Sprague-Dawley rats to investigate the differential roles of α 1 - and β-adrenoceptors in sympathetically mediated NCC regulation. NE infusion evoked salt-sensitive hypertension and prevented dietary Na + -evoked suppression of NCC mRNA, protein expression, phosphorylation, and in vivo activity. Impaired NCC suppression during high salt intake in NE-infused rats was paralleled by impaired suppression of WNK1 and OxSR1 expression and SPAK/OxSR1 phosphorylation and a failure to increase WNK4 expression. Antagonism of α 1 -adrenoceptors before high salt intake or after the establishment of salt-sensitive hypertension restored dietary Na + -evoked suppression of NCC, resulted in downregulation of WNK4, SPAK, and OxSR1, and abolished the salt-sensitive component of hypertension. In contrast, β-adrenoceptor antagonism attenuated NE-evoked hypertension independently of dietary Na + intake and did not restore high salt-evoked suppression of NCC. These findings suggest that a selective, reversible, α 1 -adenoceptor-gated WNK/SPAK/OxSR1 NE-activated signaling pathway prevents dietary Na + -evoked NCC suppression, promoting the development and maintenance of salt-sensitive hypertension.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00264.2019
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1477287-5
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  • 9
    Online Resource
    Online Resource
    Clinical Genetic Testing for Patients With Autism Spectrum Disorders
    American Academy of Pediatrics (AAP) ; 2010
    In:  Pediatrics Vol. 125, No. 4 ( 2010-04-01), p. e727-e735
    Details
    In: Pediatrics, American Academy of Pediatrics (AAP), Vol. 125, No. 4 ( 2010-04-01), p. e727-e735
    Abstract: Multiple lines of evidence indicate a strong genetic contribution to autism spectrum disorders (ASDs). Current guidelines for clinical genetic testing recommend a G-banded karyotype to detect chromosomal abnormalities and fragile X DNA testing, but guidelines for chromosomal microarray analysis have not been established. PATIENTS AND METHODS: A cohort of 933 patients received clinical genetic testing for a diagnosis of ASD between January 2006 and December 2008. Clinical genetic testing included G-banded karyotype, fragile X testing, and chromosomal microarray (CMA) to test for submicroscopic genomic deletions and duplications. Diagnostic yield of clinically significant genetic changes was compared. RESULTS: Karyotype yielded abnormal results in 19 of 852 patients (2.23% [95% confidence interval (CI): 1.73%–2.73%]), fragile X testing was abnormal in 4 of 861 (0.46% [95% CI: 0.36%–0.56%] ), and CMA identified deletions or duplications in 154 of 848 patients (18.2% [95% CI: 14.76%–21.64%]). CMA results for 59 of 848 patients (7.0% [95% CI: 5.5%–8.5%] ) were considered abnormal, which includes variants associated with known genomic disorders or variants of possible significance. CMA results were normal in 10 of 852 patients (1.2%) with abnormal karyotype due to balanced rearrangements or unidentified marker chromosome. CMA with whole-genome coverage and CMA with targeted genomic regions detected clinically relevant copy-number changes in 7.3% (51 of 697) and 5.3% (8 of 151) of patients, respectively, both higher than karyotype. With the exception of recurrent deletion and duplication of chromosome 16p11.2 and 15q13.2q13.3, most copy-number changes were unique or identified in only a small subset of patients. CONCLUSIONS: CMA had the highest detection rate among clinically available genetic tests for patients with ASD. Interpretation of microarray data is complicated by the presence of both novel and recurrent copy-number variants of unknown significance. Despite these limitations, CMA should be considered as part of the initial diagnostic evaluation of patients with ASD.
    Type of Medium: Online Resource
    ISSN: 0031-4005 , 1098-4275
    URL: Article
    DOI: 10.1542/peds.2009-1684
    Language: English
    Publisher: American Academy of Pediatrics (AAP)
    Publication Date: 2010
    detail.hit.zdb_id: 1477004-0
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  • 10
    Online Resource
    Online Resource
    Norepinephrine-evoked salt-sensitive hypertension requires impaired renal sodium chloride cotransporter activity in Sprague-Dawley rats
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 310, No. 2 ( 2016-01-15), p. R115-R124
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 310, No. 2 ( 2016-01-15), p. R115-R124
    Abstract: Recent studies have implicated a role of norepinephrine (NE) in the activation of the sodium chloride cotransporter (NCC) to drive the development of salt-sensitive hypertension. However, the interaction between NE and increased salt intake on blood pressure remains to be fully elucidated. This study examined the impact of a continuous NE infusion on sodium homeostasis and blood pressure in conscious Sprague-Dawley rats challenged with a normal (NS; 0.6% NaCl) or high-salt (HS; 8% NaCl) diet for 14 days. Naïve and saline-infused Sprague-Dawley rats remained normotensive when placed on HS and exhibited dietary sodium-evoked suppression of peak natriuresis to hydrochlorothiazide. NE infusion resulted in the development of hypertension, which was exacerbated by HS, demonstrating the development of the salt sensitivity of blood pressure [MAP (mmHg) NE+NS: 151 ± 3 vs. NE+HS: 172 ± 4; P 〈 0.05]. In these salt-sensitive animals, increased NE prevented dietary sodium-evoked suppression of peak natriuresis to hydrochlorothiazide, suggesting impaired NCC activity contributes to the development of salt sensitivity [peak natriuresis to hydrochlorothiazide (μeq/min) Naïve+NS: 9.4 ± 0.2 vs. Naïve+HS: 7 ± 0.1; P 〈 0.05; NE+NS: 11.1 ± 1.1; NE+HS: 10.8 ± 0.4). NE infusion did not alter NCC expression in animals maintained on NS; however, dietary sodium-evoked suppression of NCC expression was prevented in animals challenged with NE. Chronic NCC antagonism abolished the salt-sensitive component of NE-mediated hypertension, while chronic ANG II type 1 receptor antagonism significantly attenuated NE-evoked hypertension without restoring NCC function. These data demonstrate that increased levels of NE prevent dietary sodium-evoked suppression of the NCC, via an ANG II-independent mechanism, to stimulate the development of salt-sensitive hypertension.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00514.2014
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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