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Buies Creek, NC, United States

Campbell University is a coeducational, Baptist university in the U.S. state of North Carolina. Its main campus is located in the community of Buies Creek; its law school moved from Buies Creek to a new campus in the state capital of Raleigh in 2009. Campbell has an approximately equal number of male and female students. The school consciously promotes the awareness and application of Christian principles. It is a university of the liberal arts and science, offering both theory and vocational education and hosting several professional schools. Wikipedia.


Extended-spectrum β-lactamase-producing Escherichia coli (ESBLEC) are emerging pathogens causing urinary tract infections (UTIs) in community patients worldwide. Treatment for community-acquired ESBLEC UTIs, especially in the outpatient setting, may be problematic because many of the strains are resistant to the traditional oral therapies. Fosfomycin is an oral agent that is approved for the treatment of uncomplicated UTIs caused by Enterococcus faecalis and E. coli. Data evaluating the clinical efficacy of fosfomycin for the treatment of community-acquired ESBLEC lower UTIs are limited. Three studies evaluating fosfomycin in the treatment of ESBLEC lower UTIs have been conducted. Clinical success was documented in >78% of patients. From the available data, it seems that fosfomycin may be an effective and reasonable treatment option for outpatient management of community-acquired ESBLEC UTIs, excluding pyelonephritis. Fosfomycin is a very attractive agent because it is available orally, has limited drug interactions, has a favorable adverse event profile, and would be very cost effective considering the potential complications of inadequate treatment and the high cost associated with parenteral therapies. Limitations to the clinical use of fosfomycin may include optimal dose and duration not being established, fosfomycin not often being included on culture and sensitivity reports and emerging resistance. Source


Woodis C.B.,Campbell University | Woodis C.B.,Duke University
Annals of Pharmacotherapy | Year: 2014

Objective: To evaluate the evidence investigating the use of selective serotonin reuptake inhibitors (SSRIs) for the treatment of irritable bowel syndrome (IBS). Data Sources: A literature search was performed using PubMed (1950 through February 2014) for the MeSH terms serotonin reuptake inhibitor and irritable bowel syndrome; subterms of identified MeSH terms (ie, explosion) were also evaluated. EMBASE (1947 to February 2014) was searched using similar search terms. References from identified articles were checked and an updated Cochrane Database review was performed. Study Selection and Data Extraction: All identified English-language peer-reviewed publications were evaluated. Articles (excluding meeting abstracts) specifically addressing SSRIs for the treatment of IBS were reviewed. The literature review was limited to randomized controlled trials (RCTs) conducted in human subjects. Data Synthesis: Fluoxetine, citalopram, and paroxetine have been studied for the treatment of IBS symptoms. Fluoxetine significantly improves abdominal pain, bloating, and stool consistency after 12 weeks of therapy, but these data contradict the findings of another 6-week study. Citalopram decreases abdominal discomfort after 6 to 12 weeks of treatment, but multiple studies have not shown an improvement in adequate relief of most IBS symptoms. Overall well-being was improved after 12 weeks of paroxetine use; however, IBS-related symptoms and social/work functioning were not improved. Conclusions: Available data evaluating the use of SSRIs in the treatment of IBS-related symptoms are conflicting. Additional larger RCTs lasting more than 12 weeks are needed to determine the place in therapy for SSRIs in the treatment of IBS-related symptoms. © The Author(s) 2014. Source


Hollingworth W.,Campbell University
Journal of clinical oncology : official journal of the American Society of Clinical Oncology | Year: 2013

Patients with cancer have a high prevalence of distress. We evaluated whether distress monitoring and needs assessment using the Distress Thermometer and Problem List (DT&PL) improved patient outcomes. We conducted an unblinded, two-arm, parallel randomized controlled trial at two sites among patients starting radiotherapy or chemotherapy. The intervention group completed the DT&PL, rating distress and discussing sources of distress with a trained radiographer/nurse. No specific triage algorithms were followed. The control group received usual care. The main outcome measure was psychological distress (Profile of Mood States [POMS], short form) up to 12 months; secondary outcomes were quality of life (European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire C30) and health care costs. Of 220 patients randomly assigned, 112 patients were allocated to the DT&PL. Ninety-five percent completed the primary outcome at 12 months. The DT&PL took 25 minutes; one third of patients had high levels of distress, and most reported physical (84%) or emotional (56%) problems. There was no evidence of an effect of the DT&PL on adjusted POMS scores over follow-up (difference between groups, -1.84; 95% CI, -5.69 to 2.01; P = .35) or in secondary outcomes. The DT&PL cost £19 ($28) per patient and did not lower subsequent health care costs. Few patients (< 3%) in either arm of the trial were referred to a clinical psychologist. Patients with cancer have a high prevalence of distress. Needs assessment can be performed quickly and inexpensively. However, the DT&PL was not cost effective in improving patient mood states. It is important to explore the reasons for this so that oncology units can design better services to support patients. Source


Khu K.,Campbell University
Cell Death and Differentiation | Year: 2016

The acetyltransferase Tip60/Kat5 acetylates both histone and non-histone proteins, and is involved in a variety of biological processes. By acetylating p53, Tip60 controls p53-dependent transcriptional activity and so is implicated as a tumor suppressor. However, many breast cancers with low Tip60 also show p53 mutation, implying that Tip60 has a tumor suppressor function independent of its acetylation of p53. Here, we show in a p53-null mouse model of sporadic invasive breast adenocarcinoma that heterozygosity for Tip60 deletion promotes mammary tumorigenesis. Low Tip60 reduces DNA repair in normal and tumor mammary epithelial cells, both under resting conditions and following genotoxic stress. We demonstrate that Tip60 controls homologous recombination (HR)-directed DNA repair, and that Tip60 levels correlate inversely with a gene expression signature associated with defective HR-directed DNA repair. In human breast cancer data sets, Tip60 mRNA is downregulated, with low Tip60 levels correlating with p53 mutations in basal-like breast cancers. Our findings indicate that Tip60 is a novel breast tumor suppressor gene whose loss results in genomic instability leading to cancer formation.Cell Death and Differentiation advance online publication, 26 February 2016; doi:10.1038/cdd.2015.173. © 2016 Macmillan Publishers Limited Source


Hall J.M.,Campbell University | Korach K.S.,U.S. National Institutes of Health
Molecular Carcinogenesis | Year: 2013

The majority of ovarian cancers over-express the estrogen receptor (ERα) and grow in response to estrogens. We previously demonstrated that ER induction of the chemokine CXCL12 (stromal cell-derived factor-1) is required for estradiol (E2)-stimulated proliferation of human ovarian carcinoma cells. In the current study, we report that known "endocrine disrupting chemicals" (EDCs) display mitogenic activities in ovarian cancer cells via their ability to activate the ER and upregulate CXCL12 expression. Notably, the EDCs genistein, bisphenol A and HPTE stimulated both cell proliferation and induction of CXCL12 mRNA and protein in a manner comparable to estradiol. The effects were completely attenuated by the ER antagonist ICI 182,780, revealing that observed activities of these agents were receptor-mediated. In cell proliferation assays, the mitogenic effects of estradiol and EDCs were obviated by siRNAs targeting CXCL12 and restored upon addition of exogenous CXCL12. Furthermore, an inhibitor to the CXCL12 receptor CXCR4 completely attenuated growth-stimulatory effects of E2 and EDCs. These studies highlight a potential role of EDCs possessing estrogenic activities in the etiology of ovarian cancer. Moreover, they suggest that the ER-CXCL12-CXCR4 signaling axis may represent a promising target for development of therapeutics for ER+ ovarian cancers. © 2012 Wiley Periodicals, Inc. Source

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