University Park is the postal address used by Pennsylvania State University for its flagship campus in State College and adjacent College Township, Pennsylvania. It is not an incorporated community but exists as a postal address, with the accompanying zip code of 16802, for ease of mail delivery and to distinguish on-campus from off-campus addresses. Almost all of University Park sits within the borough of State College; the northeastern part of campus is within College Township. The campus post office was designated "University Park, Pennsylvania" in 1953 by Penn State president Milton Eisenhower, after what was then Pennsylvania State College was upgraded to university status.University Park sits within the State College Metropolitan Statistical Area , which encompasses all of Centre County, Pennsylvania. The ZCTA for ZIP code 16802 had a population of 12,764 at the 2010 census.The campus is served by the Penn State University Police.Federally, the University Park campus is part of Pennsylvania's 5th congressional district, represented by Republican Glenn "G.T." Thompson, elected in 2008. Wikipedia.
Ultaigh S.N.,Park University
Arthritis research & therapy | Year: 2011
The aim of this study was to examine the effect of blocking Toll-like receptor 2 (TLR2) in rheumatoid arthritis (RA) synovial cells. RA synovial tissue biopsies, obtained under direct visualization at arthroscopy, were established as synovial explant cultures ex vivo or snap frozen for immunohistology. Mononuclear cell cultures were isolated from peripheral blood and synovial fluid of RA patients. Cultures were incubated with the TLR1/2 ligand, Pam3CSK4 (200 ng, 1 and 10 μg/ml), an anti-TLR2 antibody (OPN301, 1 μg/ml) or an immunoglobulin G (IgG) (1 μg/ml) matched control. The comparative effect of OPN301 and adalimumab (anti-tumour necrosis factor alpha) on spontaneous release of proinflammatory cytokines from RA synovial explants was determined using quantitative cytokine MSD multiplex assays or ELISA. OPN301 penetration into RA synovial tissue explants cultures was assessed by immunohistology. Pam3CSK4 significantly upregulated interleukin (IL)-6 and IL-8 in RA peripheral blood mononuclear cells (PBMCs), RA synovial fluid mononuclear cells (SFMCs) and RA synovial explant cultures (P < 0.05). OPN301 significantly decreased Pam3CSK4-induced cytokine production of tumour necrosis factor alpha (TNF-α), IL-1β, IL-6, interferon (IFN)-γ and IL-8 compared to IgG control in RA PBMCs and SFMCs cultures (all P < 0.05). OPN301 penetration of RA synovial tissue cultures was detected in the lining layer and perivascular regions. OPN301 significantly decreased spontaneous cytokine production of TNF-α, IL-1β, IFN-γ and IL-8 from RA synovial tissue explant cultures (all P < 0.05). Importantly, the inhibitory effect of OPN on spontaneous cytokine secretion was comparable to inhibition by anti-TNFα monoclonal antibody adalimumab. These findings further support targeting TLR2 as a potential therapeutic agent for the treatment of RA.
Ledwidge M.T.,Park University
European journal of heart failure | Year: 2013
Previous studies have demonstrated poor sensitivity of guideline weight monitoring in predicting clinical deterioration of heart failure (HF). This study aimed to evaluate patterns of remotely transmitted daily weights in a high-risk HF population and also to compare guideline weight monitoring and an individualized weight monitoring algorithm. Consenting, consecutive, high-risk patients were provided with a mobile phone-based remote weight telemonitoring device. We aimed to evaluate population vs. individual weight variability, weight patterns pre- and post-events of clinical deterioration of HF, and to compare guideline weight thresholds with the HeartPhone algorithm in terms of sensitivity and specificity for such events. Of 87 patients recruited and followed for an average of 23.9 ± 12 weeks, 19 patients experienced 28 evaluable episodes of clinical deterioration of HF. Following a post-discharge decline, the population average weight remained stable for the follow-up period, yet the 7-day moving average of individual patients exceeded 2 kg in three-quarters of patients. Significant increases in weight were observed up to 4 days before HF events. The HeartPhone algorithm was significantly more sensitive (82%) in predicting HF events than guideline weight thresholds of 2 kg over 2-3 days (21%) and a 'rule of thumb' threshold of 1.36 kg over 1 day (46%). An individualized approach to weight monitoring in HF with the HeartPhone algorithm improved prediction of HF deterioration. Further evaluation of HeartPhone with and without other biomarkers of HF deterioration is warranted.
Molloy E.S.,Park University
Cleveland Clinic Journal of Medicine | Year: 2011
Progressive multifocal leukoencephalopathy (PML), a rare, typically fatal, opportunistic infection caused by the JC virus, is becoming relevant to physicians in multiple specialties, including those who prescribe biologic agents for the treatment of autoimmune disorders. Reports of PML have led to US Food and Drug Administration alerts and warning letters regarding four immunosuppressive agents in recent years (natalizumab, rituximab, efalizumab, and mycophenolate mofetil). Consequently, informed clinical decisionmaking requires understanding the risk of PML associated with these therapies. An estimate of the relative frequency of PML associated with specifi c rheumatic conditions has been generated. Systemic lupus erythematosus appears to be associated with susceptibility to PML that cannot be fully explained by the intensity of immunosuppressive therapy. Further, the use of rituximab in patients with rheumatic disease has raised concerns. However, defi nitive attribution of cause is precluded by the limitations of the currently available data. All patients with rheumatic disease, regardless of the intensity of their current immunosuppressive therapy, should be considered potentially at risk of PML. With an evolving understanding of a greater clinical heterogeneity of PML, advances in diagnostic methods, and signifi cant implications for therapy, PML should be considered in the differential diagnosis of neurologic manifestations of rheumatic diseases.
Molloy E.S.,Park University |
Calabrese L.H.,Cleveland Clinic
Arthritis and Rheumatism | Year: 2012
Objective To evaluate the association of progressive multifocal leukoencephalopathy (PML) with immunosuppressive therapy for autoimmune rheumatic diseases (ARDs). Methods A Freedom of Information Act request was submitted for all cases of PML within the Food and Drug Administration Adverse Event Reporting System database. ARD cases were selected for further analysis. Results A total of 34 confirmed cases of PML in the setting of ARDs were identified: 17 had systemic lupus erythematosus, 10 had rheumatoid arthritis, 4 had vasculitis, and 3 had dermatomyositis. Fifteen of these patients were treated with one or more biologic agents: 14 received rituximab (RTX), 6 received anti-tumor necrosis factor (anti-TNF) therapy (5 treated with anti-TNF agent prior to RTX). Four RTX-treated patients were not receiving additional immunosuppressive therapy at the time of PML onset, other than an antimalarial drug and/or low-dose glucocorticoids; all others who were receiving a biologic agent were also receiving one or more synthetic disease-modifying agents. All but 1 patient receiving a biologic agent had at least 1 potential confounding factor for the diagnosis of PML. The remaining 19 confirmed cases of PML among ARD patients were treated with synthetic disease-modifying antirheumatic drugs only, 14 of whom had received an alkylating agent. Conclusion PML has been reported in patients with ARD treated with various immunosuppressive agents. The limitations of this study preclude definitive attribution of causality. While the paucity of confirmed cases recently exposed to anti-TNF therapy suggests a causal relationship is unlikely, a specific signal is emerging with regard to rituximab and PML. Although this is a rare adverse event associated with RTX therapy, the devastating nature of PML mandates continued vigilance, particularly in patients with current or prior exposure to an alkylating agent. Copyright © 2012 by the American College of Rheumatology.
Duffy M.J.,Park University
Medical Principles and Practice | Year: 2013
Tumor markers are playing an increasingly important role in cancer detection and management. These laboratory-based tests are potentially useful in screening for early malignancy, aiding cancer diagnosis, determining prognosis, surveillance following curative surgery for cancer, up front predicting drug response or resistance, and monitoring therapy in advanced disease. Clinically useful markers include fecal occult blood testing in screening for early colorectal cancer, carcinoembryonic antigen in the management of patients with colorectal cancer, both α-fetoprotein and human chorionic gonadotrophin in the management of patients with non-seminomatous germ cell tumors, CA 125 for monitoring therapy in patients with ovarian cancer, estrogen receptors for predicting response to hormone therapy in breast cancer, human epidermal growth factor receptor 2 for the identification of women with breast cancer likely to respond to trastuzumab (Herceptin) and KRAS mutational status for identifying patients with advanced colorectal cancer likely to benefit from treatment with the anti-epidermal growth factor receptor antibodies, cetuximab and panitumumab. Although widely used, the value of prostate-specific antigen screening in reducing mortality from prostate cancer is unclear. Copyright © 2012 S. Karger AG, Basel.