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Loma Linda University

EducationLoma Linda, California, United States
About: Loma Linda University is a education organization based out in Loma Linda, California, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 9220 authors who have published 13485 publications receiving 447094 citations. The organization is also known as: University of Loma Linda.


Papers
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Journal ArticleDOI
TL;DR: Although each individual maternal stress is characterized by up- or down-regulation of specific genes in the placenta, functional analysis reveals some patterns of gene expression common to the several forms of stress.
Abstract: Successful placental development is crucial for optimal growth, development, maturation and survival of the embryo/fetus into adulthood. Numerous epidemiologic and experimental studies have demonstrated the profound influence of intrauterine environment on life, and the diseases to which one is subject as an adult. For the most part, these invidious influences, whether maternal hypoxia, protein or caloric deficiency or excess, and others, represent types of maternal stress. In the present review, we examine certain aspects of gene expression in the placenta as a consequence of maternal stressors. To examine these issues in a controlled manner, and in a species in which the genome has been sequenced, most of these reported studies have been performed in the mouse. Although each individual maternal stress is characterized by up- or down-regulation of specific genes in the placenta, functional analysis reveals some patterns of gene expression common to the several forms of stress. Of critical importance, these genes include those involved in DNA methylation and histone modification, cell cycle regulation, and related global pathways of great relevance to epigenesis and the developmental origins of adult health and disease.

135 citations

Journal ArticleDOI
TL;DR: It is concluded that long‐term fluoride exposure from drinking water containing ≥4.32 ppm increases the risk of overall fractures as well as hip fractures, and drinking water was the only major source of fluoride exposure in the study populations.
Abstract: Findings on the risk of bone fractures associated with long-term fluoride exposure from drinking water have been contradictory. The purpose of this study was to determine the prevalence of bone fracture, including hip fracture, in six Chinese populations with water fluoride concentrations ranging from 0.25 to 7.97 parts per million (ppm). A total of 8266 male and female subjects > or =50 years of age were enrolled. Parameters evaluated included fluoride exposure, prevalence of bone fractures, demographics, medical history, physical activity, cigarette smoking, and alcohol consumption. The results confirmed that drinking water was the only major source of fluoride exposure in the study populations. A U-shaped pattern was detected for the relationship between the prevalence of bone fracture and water fluoride level. The prevalence of overall bone fracture was lowest in the population of 1.00-1.06 ppm fluoride in drinking water, which was significantly lower (p or =4.32 and or =4.32 ppm increases the risk of overall fractures as well as hip fractures. Water fluoride levels at 1.00-1.06 ppm decrease the risk of overall fractures relative to negligible fluoride in water; however, there does not appear to be similar protective benefits for the risk of hip fractures.

135 citations

Journal ArticleDOI
TL;DR: The ADA Caries Classification System (CCS) as discussed by the authors was developed by the American Dental Association (ADA) to classify the location, site of origin, extent, and when possible, activity level of caries lesions consistently over time.
Abstract: Background The caries lesion, the most commonly observed sign of dental caries disease, is the cumulative result of an imbalance in the dynamic demineralization and remineralization process that causes a net mineral loss over time. A classification system to categorize the location, site of origin, extent, and when possible, activity level of caries lesions consistently over time is necessary to determine which clinical treatments and therapeutic interventions are appropriate to control and treat these lesions. Methods In 2008, the American Dental Association (ADA) convened a group of experts to develop an easy-to-implement caries classification system. The ADA Council on Scientific Affairs subsequently compiled information from these discussions to create the ADA Caries Classification System (CCS) presented in this article. Conclusions The ADA CCS offers clinicians the capability to capture the spectrum of caries disease presentations ranging from clinically unaffected (sound) tooth structure to noncavitated initial lesions to extensively cavitated advanced lesions. The ADA CCS supports a broad range of clinical management options necessary to treat both noncavitated and cavitated caries lesions. Practical Implications The ADA CCS is available for implementation in clinical practice to evaluate its usability, reliability, and validity. Feedback from clinical practitioners and researchers will allow system improvement. Use of the ADA CCS will offer standardized data that can be used to improve the scientific rationale for the treatment of all stages of caries disease.

135 citations

Journal ArticleDOI
TL;DR: These results serve as a benchmark for the time course of recurrence following initially successful ablation of supraventricular tachycardia in children and are likely to be a guide for future research on radiofrequency ablation in children.

135 citations

Journal ArticleDOI
TL;DR: Results indicate that gingipains from P. gingivalis can alter cell adhesion molecules and induce endothelial cell death, which could have implications for the pathogenicity of this organism.
Abstract: The presence of Porphyromonas gingivalis in the periodontal pocket and the high levels of gingipain activity detected in gingival crevicular fluid could implicate a role for gingipains in the destruction of the highly vascular periodontal tissue. To explore the effects of these proteases on endothelial cells, we exposed bovine coronary artery endothelial cells and human microvascular endothelial cells to gingipain-active extracellular protein preparations and/or purified gingipains from P. gingivalis. Treated cells exhibited a rapid loss of cell adhesion properties that was followed by apoptotic cell death. Cleavage of N- and VE-cadherin and integrin β1 was observed in immunoblots of cell lysates. There was a direct correlation between the kinetics of cleavage of N- and VE-cadherin and loss of cell adhesion properties. Loss of cell adhesion, as well as N- and VE-cadherin and integrin β1 cleavage, could be inhibited or significantly delayed by preincubation of P. gingivalis W83 gingipain-active extracellular extracts with the cysteine protease inhibitor Nα-p-tosyl-l-lysine chloromethylketone. Furthermore, purified gingipains also induced endothelial cell detachment and apoptosis. Apoptosis-associated events, including annexin V positivity, caspase-3 activation, and cleavage of the caspase substrates poly(ADP-ribose) polymerase and topoisomerase I (Topo I), were observed in endothelial cells after detachment. All of the effects observed were correlated with the different levels of cysteine-dependent proteolytic activity of the extracts tested. Taken together, these results indicate that gingipains from P. gingivalis can alter cell adhesion molecules and induce endothelial cell death, which could have implications for the pathogenicity of this organism.

134 citations


Authors

Showing all 9287 results

NameH-indexPapersCitations
Bruce L. Miller1631153115975
Jonathan I. Epstein138112180975
Tony L. Yaksh12380660898
David M. Livingston11831258142
William B. Isaacs11752158187
Alan W. Partin11171054213
David N. Herndon108122754888
Edward R. Laws10572239822
David C. Bellinger9845235449
Pedram Argani9737235607
Michael W. Steffes9634143260
Gary K. Steinberg9452931259
Michael S. Gazzaniga9237235305
David J. Baylink9042529109
Jesse B. Jupiter9054326480
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202332
202267
2021904
2020823
2019727
2018638