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Institution

National University of Health Sciences

EducationLombard, Illinois, United States
About: National University of Health Sciences is a education organization based out in Lombard, Illinois, United States. It is known for research contribution in the topics: Chiropractic & Health care. The organization has 611 authors who have published 614 publications receiving 15825 citations. The organization is also known as: National College of Chiropractic.


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Journal ArticleDOI
TL;DR: Changes in serum T( 3) levels in patients with chronic congestive heart failure are caused by alterations in thyroid hormone metabolism suggesting that patients may benefit from T(3) replacement in this setting.
Abstract: Thyroid hormone has many effects on the heart and vascular system.1 Many of the clinical manifestations of hyperthyroidism are due to the ability of thyroid hormone to alter cardiovascular hemodynamics.2 The hemodynamic effects of hypothyroidism are opposite to those of hyperthyroidism, although the clinical manifestations are less obvious. This review will integrate what is known about the mechanisms of thyroid hormone action on the heart2–5 with recent observations from both experimental and clinical studies of hyperthyroidism and hypothyroidism. We will also address the potential role of thyroid hormone treatment in patients with acute or chronic cardiac disease. Effects of . . .

1,862 citations

Journal ArticleDOI
TL;DR: Experimental strategies that selectively target HMGB1 and TLR4 effectively reverse and prevent activation of innate immunity and significantly attenuate damage in diverse models of sterile and infection-induced threat.
Abstract: A key question in immunology concerns how sterile injury activates innate immunity to mediate damaging inflammation in the absence of foreign invaders. The discovery that HMGB1, a ubiquitous nuclear protein, mediates the activation of innate immune responses led directly to the understanding that HMGB1 plays a critical role at the intersection of the host inflammatory response to sterile and infectious threat. HMGB1 is actively released by stimulation of the innate immune system with exogenous pathogen-derived molecules and is passively released by ischemia or cell injury in the absence of invasion. Established molecular mechanisms of HMGB1 binding and signaling through TLR4 reveal signaling pathways that mediate cytokine release and tissue damage. Experimental strategies that selectively target HMGB1 and TLR4 effectively reverse and prevent activation of innate immunity and significantly attenuate damage in diverse models of sterile and infection-induced threat.

1,227 citations

Journal ArticleDOI
TL;DR: The process used to write a narrative review of the literature for publication in a peer-reviewed journal is described and step by step instructions for how to conduct andwrite a narrative overview utilizing a 'best-evidence synthesis' approach are discussed.

1,174 citations

Journal ArticleDOI
TL;DR: A review of COVID-19 in pregnancy, bringing together the various factors integral to the understanding of pathophysiology and susceptibility, diagnostic challenges with real-time reverse transcriptase polymerase chain reaction (RT-PCR) assays, therapeutic controversies, intrauterine transmission and maternal-fetal complications.

865 citations

Journal ArticleDOI
05 Jan 2016-JAMA
TL;DR: There was significant excess familial risk for cancer overall and for specific types of cancer, including prostate, melanoma, breast, ovary, and uterus, in this long-term follow-up study among Nordic twins.
Abstract: Importance Estimates of familial cancer risk from population-based studies are essential components of cancer risk prediction. Objective To estimate familial risk and heritability of cancer types in a large twin cohort. Design, Setting, and Participants Prospective study of 80 309 monozygotic and 123 382 same-sex dizygotic twin individuals (N = 203 691) within the population-based registers of Denmark, Finland, Norway, and Sweden. Twins were followed up a median of 32 years between 1943 and 2010. There were 50 990 individuals who died of any cause, and 3804 who emigrated and were lost to follow-up. Exposures Shared environmental and heritable risk factors among pairs of twins. Main Outcomes and Measures The main outcome was incident cancer. Time-to-event analyses were used to estimate familial risk (risk of cancer in an individual given a twin’s development of cancer) and heritability (proportion of variance in cancer risk due to interindividual genetic differences) with follow-up via cancer registries. Statistical models adjusted for age and follow-up time, and accounted for censoring and competing risk of death. Results A total of 27 156 incident cancers were diagnosed in 23 980 individuals, translating to a cumulative incidence of 32%. Cancer was diagnosed in both twins among 1383 monozygotic (2766 individuals) and 1933 dizygotic (2866 individuals) pairs. Of these, 38% of monozygotic and 26% of dizygotic pairs were diagnosed with the same cancer type. There was an excess cancer risk in twins whose co-twin was diagnosed with cancer, with estimated cumulative risks that were an absolute 5% (95% CI, 4%-6%) higher in dizygotic (37%; 95% CI, 36%-38%) and an absolute 14% (95% CI, 12%-16%) higher in monozygotic twins (46%; 95% CI, 44%-48%) whose twin also developed cancer compared with the cumulative risk in the overall cohort (32%). For most cancer types, there were significant familial risks and the cumulative risks were higher in monozygotic than dizygotic twins. Heritability of cancer overall was 33% (95% CI, 30%-37%). Significant heritability was observed for the cancer types of skin melanoma (58%; 95% CI, 43%-73%), prostate (57%; 95% CI, 51%-63%), nonmelanoma skin (43%; 95% CI, 26%-59%), ovary (39%; 95% CI, 23%-55%), kidney (38%; 95% CI, 21%-55%), breast (31%; 95% CI, 11%-51%), and corpus uteri (27%; 95% CI, 11%-43%). Conclusions and Relevance In this long-term follow-up study among Nordic twins, there was significant excess familial risk for cancer overall and for specific types of cancer, including prostate, melanoma, breast, ovary, and uterus. This information about hereditary risks of cancers may be helpful in patient education and cancer risk counseling.

623 citations


Authors

Showing all 624 results

NameH-indexPapersCitations
Vivek Sharma1503030136228
Kevin J. Tracey13856182791
Rob M. van Dam9936238939
David Eidelberg8834523915
Haichao Wang8125540235
Markus R. Wenk8129221516
E. Shyong Tai7934337147
Bruce T. Volpe7825622100
Ping Wang6950217507
Naresh Kumar66110620786
Timothy P. Johnson6131213734
Shazib Pervaiz6118822982
Roger C.M. Ho6050421935
A. Mark Richards6035913910
Wee Joo Chng5835914714
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202216
202147
202044
201940
201844
201739