Stay Connected. Manage Your Care.
Access your health information anytime and anywhere, at home or on the go, with MyHealth.
- Message your clinic
- View your lab results
- Schedule your next appointment
- Pay your bill
The MyHealth mobile app from Stanford Health Care puts all your health information at your fingertips and makes managing your health care simple and quick.
Guest Services
24/7
We are available to assist you
whenever you need it. Give us a call at
650-498-3333 or
PHYSICIAN HELPLINE
Have a question? We're here to help! Call 1-866-742-4811
Monday - Friday, 8 a.m. - 5 p.m.
REFER A PATIENT
Fax 650-320-9443
Track your patients' progress and communicate with Stanford providers conveniently and securely.
Abstract
In lymphedema, there is a profound predisposition to infection with bacterial pathogens. It therefore seems appropriate to reconsider our unique functional definition of the lymphatic structures within a circulatory construct. While the lymphatics unquestionably fulfill a vital circulatory function, it seems more appropriate to view this complex network, comprised both of endothelial-lined vessels and of lymphoid tissue, as the nexus between the circulatory and immune systems. Viewed in this fashion, it becomes evident that the complex biology of regional lymphatic disruption is a manifestation of the interplay between these two vital bodily functions. Experimental lymph stasis in murine model has been utilized to effectively demonstrate the pathological attributes of human lymphedema, namely, inflammation, fat deposition, and fibrosis. Large-scale transcriptional corroborates the role of inflammatory mechanisms. The murine studies have set the stage for subsequent translational investigation of human lymphedema. Many of the gene expression pathways invoked by lymphedema are relevant to the inflammatory response and have provided a pragmatic approach to the successful identification of potentially relevant circulating biomarkers for human lymphedema.
View details for DOI 10.1089/lrb.2013.1132
View details for Web of Science ID 000324477300003
View details for PubMedID 24024576