ECU Health (formerly Vidant Health) is a not-for-profit, 1,447-bed hospital system that serves more than 1.4 million people in 29 Eastern North Carolina counties. The health system is made up of nine hospitals and more than 12,000 employees. ECU Health also includes wellness centers, home health and hospice services, a dedicated children's hospital, rehab facilities, pain management and wound healing centers and specialized cancer care. Their flagship hospital, ECU Health Medical Center, is a level I trauma center and serves as the teaching hospital for the Brody School of Medicine at East Carolina University in Greenville.ECU Health is the largest private employer in Eastern North Carolina.All nine ECU Health hospitals have achieved The Gold Seal of Approval for quality care by The Joint Commission, the leading accreditor of healthcare organizations in America.In 2002, the organization implemented a program in which diabetes educators regularly visit rural clinics to improve glycemic control in African-American patients.ECU Health changed their name from University Health Systems of Eastern Carolina in January 2012 to Vidant Health.On January 3, 2022, Vidant Health announced that they would be rebranding as ECU Health. In the announcement, they indicated that it would take several months for the branding to be noticeable to the public.
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An estimated 250 million people are chronically infected with hepatitis B virus (HBV), with more than 800,000 deaths related to HBV.1 Although the prevalence of HBV has been decreasing, reactivation remains a cause for concern.2 Reactivation is defined by the resurgence of HBV DNA and/or HBV surface antigen (HBsAg) seroreversion in patients with resolved HBV or an increase in HBV viral load in chronic hepatitis.3 Anti-tumor necrosis factor (TNF) therapies have been shown to place patients at a risk for HBV reactivation.4.
Background:Adherence is increasingly understood as a complex concept and is affected by many factors. Among rural patients with cancer, adherence behavior can be affected by increased psychosocial and physical distress as well as economic burden. This study explored facilitators and barriers to medication adherence to oral chemotherapeutic agents (OCAs) from the perspective of both rural patients with cancer and their cancer care providers. Methods:This study was conducted in a regional Cancer Center in North Carolina. Data for the cancer care providers (N = 10) were collected (January-February 2016), and data for the patients with cancer (N = 25) were collected (March-June 2016). Qualitative interviews were conducted with patients with cancer currently taking OCAs, and interviews/focus groups were conducted with cancer care providers. Data analysis was conducted using the immersion crystallization approach. Results:The results of this qualitative study provide valuable insights into the attitudes of both cancer care providers and patients with cancer and their perceptions of adherence barriers and facilitators. The main barriers to adherence were costs associated with treatment, side effect management, comorbidities and concomitant treatments, limited health literacy, lack of social support, and patient-provider communication. Facilitators to adherence include education and follow-up, social support networks, and adherence strategies. Conclusion:Better communication, education/information, and social support were identified as facilitators of adherence in this study. It is critical to develop tailored strategies such as self-management behaviors, adherence strategies, and effective communication that can improve medication adherence and empower patients and their caregivers in their treatment management.
e15095 Background: RNA-binding proteins (RBPs) play a crucial role in orchestrating the function of RNAs. The regulation of RBPs is critical in various biological processes, including tumorigenesis. The PUF (Pumilio/FBF) RBPs are of particular interest due to their function in stem cells and tumor-initiating cells. Its has been shown that PUF proteins inhibit the translation of target genes by binding to a regulatory element (PBE) in the 3’ untranslated regions (3’UTRs) of their target mRNA. PUF proteins are required to maintain normal stem cells and potentially inhibit the formation of tumor-initiating cells by repressing the expression of oncogenes. Bioinformatics analysis has identified many oncogenes as potential targets of PUF, and pilot studies have confirmed that ERK, p38, JAK2, RUNX2, and RET mRNAs specifically interact with PUF protein. The objective of this study is to investigate the function of human PUF proteins in the initiation and progression of cancer cells. Methods: In worms (C. elegans), 100 % PUF mutants form tumors. Bioinformatics were performed to identify PUF target genes, it specifically binds UGUAnAUA sequences on target mRNA 3'UTRs. Yeast three-hybrid assay were performed to test the physical interaction between PUF protein and its target mRNA. The novel function of human PUF proteins in the initiation and progression of cancer cells was investigated using CRISPR/Cas9 knockout cancer cell lines and western Blot/IHC was done to determine their expression. Results: The results of the study showed that PUF proteins play a crucial role in inhibiting the formation of tumor-initiating cells. Loss of PUF function and activation of ERK signaling were found to promote the formation of these cells. Bioinformatics analysis revealed that many oncogenes are potential targets for PUF repression. The study also demonstrated that PUF represses the expression of ERK and p38 mRNAs via their 3’UTRs. These findings suggest that PUF may have therapeutic potential as a target for cancer treatment. Conclusions: In worms and human cells, normal PUF proteins promote the cell proliferation of stem cells, however, stem cells begin to differentiate, PUF proteins are required to complete differentiation. Therefore, in the differentiating cells, PUF mutation cannot complete differentiation, instead, return to undifferentiating cells, resulting in tumors. Bioinformatics and biochemical analyses revealed that many PUF repressing targets (~ > 30%) are oncogene and some labs including us found that PUF knockdown enhanced oncogene expression. PUF can be a potential biomarker, as low PUF expression may initiate tumors. Therapeutically, conditional PUF expression in tumor-initiating cells may suppress tumor progression by suppressing oncogene.
Gastrojejunostomy is performed in the treatment of many diseases, from bariatric surgery to malignancy. The Billroth II reconstruction is one such procedure whereby the greater curvature of the stomach is attached by an end-to-side anastomosis with the jejunum. Despite this alteration, peristalsis continues in an organized manner with antegrade propulsion of enteric contents. The most common complication following gastrojejunostomy is anastomotic leak; however adhesions, strictures, and intussusception also occur with varying degrees of frequency. Intussusception occurs due to primary or secondary causes referred to as a “ lead point. ” This pathologic lead point has a variety of causes including diverticula, polyps, strictures, and benign or malignant neoplasms. 1 In-tussusception most commonly occurs at junctions be-tween freely mobile segments of bowel and those that are fi xed by the retroperitoneum or other structures. 3 However, prior surgery may also be responsible for triggering intussusception due to adhesions, enterocutaneous fi stu-las, and anastomotic sutures or staples may all function as lead points. Gastric intussusception is uncommon and only has been reported after surgical intervention on the stomach. Among the reported cases of JGI, none have identi fi ed pathologic lesions within the affected segments. 2 The exact cause of this disruption remains unknown, presenting a dif fi cult obstacle to overcome in
