University of California, Davis

About: University of California, Davis is a education organization based out in Davis, California, United States. It is known for research contribution in the topics: Population & Gene. The organization has 78770 authors who have published 180033 publications receiving 8064158 citations. The organization is also known as: UC Davis & UCD.

Resilience in Midwestern Families: Selected Findings from the First Decade of a Prospective, Longitudinal Study

Abstract: The authors review findings related to mechanisms of resilience in an ongoing longitudinal study of a cohort of 558 focal youth and their families. The ongoing study began when the cohort of adolescents was in 7th grade. Findings demonstrate that resilience to economic adversity for the parents of the focal adolescents was promoted by marital support, effective problem solving skills, and a sense of mastery. For the cohort of youth, resilience to economic hardship was promoted by support from parents, siblings, and adults outside the family. Resilience to the difficult transitions from childhood to adolescence and from adolescence to early adulthood was especially fostered by nurturant-involved parenting and by less angry or hostile parenting.

Neutrophil extracellular traps produced during inflammation awaken dormant cancer cells in mice.

Abstract: INTRODUCTION Most cancer patients die from cancer that recurs after spreading to a different tissue, rather than from their original tumor. After successful treatment of the original tumor, cancer cells that have disseminated to other sites can undergo dormancy, remaining viable but not proliferating. In breast, prostate, and other cancers, cancer cells can remain dormant and clinically undetectable for years and even decades before recurring, or awakening, as metastatic cancer. Little is known about what might initiate cancer awakening, and this in turn reduces our opportunities to prevent metastasis. RATIONALE Epidemiological studies have suggested that inflammation is linked to a higher risk of breast cancer recurrence after a period of clinical dormancy. Smoking, which causes chronic lung inflammation, is also associated with a higher risk of recurrence. However, whether inflammation can cause awakening is not clear. Inflammatory cells, such as neutrophils, can provide many different signals that promote cancer progression. Neutrophils can kill harmful microorganisms by the release of neutrophil extracellular traps (NETs) into the extracellular space. NETs are scaffolds of DNA with associated cytotoxic proteins and proteases [e.g., neutrophil elastase (NE) and matrix metalloproteinase 9 (MMP9)]. NETs induced by bacteria or by cancer cells can promote metastasis, but the mechanism by which this occurs is not known. In this study, we tested whether NETs formed during lung inflammation could induce awakening. RESULTS We found that sustained experimental lung inflammation—induced by either tobacco smoke exposure or nasal instillation of lipopolysaccharide (LPS)—converted dormant cancer cells to aggressive lung metastases in mice. Both types of sustained inflammation also caused the formation of NETs. Inhibiting NET formation or digesting the NETs’ DNA scaffold prevented conversion of single disseminated cancer cells to growing metastases in mouse models of breast and prostate cancer. The NET DNA bound to the extracellular matrix (ECM) protein laminin, thus bringing two NET-associated proteases, NE and MMP9, to their substrate. This in turn facilitated a sequential cleavage of laminin, first by NE and then by MMP9. The NET-mediated proteolytic remodeling of laminin revealed an epitope that triggered proliferation of dormant cancer cells through integrin activation and FAK/ERK/MLCK/YAP signaling. We generated a blocking antibody against NET-remodeled laminin, and this antibody prevented or reduced tobacco smoke exposure– or LPS-induced inflammation from awakening dormant cancer cells in mice. CONCLUSION Our data implicate NETs and NET-mediated ECM remodeling as critical mediators of inflammation-induced awakening in mouse models of dormancy. We propose that NETs awaken cancer by concentrating neutrophil proteases at the ECM protein laminin, allowing for sequential proteolytic remodeling of laminin and leading to integrin-mediated signaling in the cancer cells. Our findings set the stage for epidemiological studies to test possible links among inflammation or smoking, NETs, and recurrence after dormancy in human patients. If such links can be established, we envision that approaches similar to the ones used in mouse models in our study could be used to target NETs and their downstream effectors to reduce the risk of cancer recurrence in human patients.

The effectiveness of telemental health: A 2013 review

Abstract: Introduction: The effectiveness of any new technology is typically measured in order to determine whether it successfully achieves equal or superior objectives over what is currently offered. Research in telemental health—in this article mainly referring to telepsychiatry and psychological services—has advanced rapidly since 2003, and a new effectiveness review is needed. Materials and Methods: The authors reviewed the published literature to synthesize information on what is and what is not effective related to telemental health. Terms for the search included, but were not limited to, telepsychiatry, effectiveness, mental health, e-health, videoconferencing, telemedicine, cost, access, and international. Results: Telemental health is effective for diagnosis and assessment across many populations (adult, child, geriatric, and ethnic) and for disorders in many settings (emergency, home health) and appears to be comparable to in-person care. In addition, this review has identified new models of car...

Structural evidence for the authenticity of the human retinoblastoma gene.

Abstract: The retinoblastoma (Rb) gene is the prototype for a class of recessive human cancer genes in which loss of activity of both normal alleles is thought to be associated with tumorigenesis. Sixteen of 40 retinoblastomas examined with a complementary DNA probe shown to be the Rb gene had identifiable structural changes of the Rb gene including in some cases homozygous internal deletions with corresponding truncated transcripts. An osteosarcoma also had a homozygous internal deletion with a truncated transcript. In addition, possible hot spots for deletion were identified within the Rb genomic locus. Among those tumors with no identifiable structural changes there was either absence of an Rb transcript or abnormal expression of the Rb transcript. Comparison of the structural changes in the tumor cells and fibroblasts of certain patients provided support for Knudson's two-hit hypothesis for the development of retinoblastoma at the molecular level. The ability to detect germline structural deletions in fibroblasts from some patients with bilateral retinoblastoma also indicates that the isolated gene is useful for diagnostic purposes.