Nursing Students’ Clinical Confidence In Caring Tuberculosis: Indonesian Version Of The U.S Tuberculosis Curriculum Consortium Survey Using Rasch Analysis

Background: Nursing students who are prepared in clinical practicums to comprehend the knowledge, reflect their beliefs about tuberculosis instruction, and perceive their abilities in caring for tuberculosis patients are also at risk. Nursing students’ clinical confidence in caring for tuberculosis patients is essential to be assessed. Knowledge, beliefs, and clinical confidence, as unidimensional constructs based on Bandura’s theory of self-efficacy, had been used in the US National Tuberculosis Curriculum Consortium (NTCC) survey for nursing students. This study's objective was to investigate the Indonesian version of the NTCC survey among nursing students' experiences caring for tuberculosis patients.   Methods: A quantitative study with cross-sectional using an online survey among 250 students 1st to 3rd-yearrd year students in one faculty of nursing in Banten, Indonesia. Prior to data collection, NTCC surveys were translated backward and forward, reviewed by experts, and tested in a pilot project.   Results: Internal consistency using Rasch analysis on each subscale showed good results and gave strong evidence that three subscales are unidimensional. There was an item separation index and reliability score, in that order: knowledge about tuberculosis (8.68 and 0.99), beliefs regarding tuberculosis instructions (6.50 and 0.98), and clinical confidence in caring for tuberculosis patients (6.29 and 0.98).   Conclusion: The Indonesian version of the NTCC survey has excellent internal consistency. This instrument might be improved since the original instrument is 13 years old and there is a cultural gap between the US and Indonesia. Moreover, this instrument might be needed for improving tuberculosis teaching in the nursing curriculum in Indonesia

The Role of Molecular Imaging in the Diagnosis and Management of Neuropsychiatric Disorders

Neuropsychiatric disorders are becoming a major socioeconomic burden to modern society. In recent years, a dramatic expansion of tools has facilitated the study of the molecular basis of neuropsychiatric disorders. Molecular imaging has enabled the noninvasive characterization and quantification of biological processes at the cellular, tissue, and organism levels in intact living subjects. This technology has revolutionized the practice of medicine and has become critical to quality health care. New advances in research on molecular imaging hold promise for personalized medicine in neuropsychiatric disorders, with adjusted therapeutic doses, predictable responses, reduced adverse drug reactions, early diagnosis, and personal health planning. In this paper, we discuss the development of radiotracers for imaging dopaminergic, serotonergic, and noradrenergic systems and β-amyloid plaques. We will underline the role of molecular imaging technologies in various neuropsychiatric disorders, describe their unique strengths and limitations, and suggest future directions in the diagnosis and management of neuropsychiatric disorders

Application of Rat In Situ Single-pass Intestinal Perfusion in the Evaluation of Presystemic Extraction of Indinavir Under Different Perfusion Rates

Background/PurposeFirst-pass effect has been an important concern for oral pharmaceuticals. An in vivo system was developed for measuring different concentrations of pharmaceuticals in the portal vein and hepatic vein (via the inferior vena cava) for delineating presystemic metabolism under different perfusion rates by using indinavir as an exemplary agent.MethodsAn in situ single-pass intestinal perfusion technique was modified from previous studies to concomitantly obtain portal and hepatic venous bloods. Portal and hepatic venous samples were simultaneously taken from rats at appropriate time points using the perfusion model of 1 mg/mL indinavir at flow rates of 0.05, 0.1, 0.5 and 1.0 mL/min. The indinavir concentrations were assayed by binary-gradient high-pressure liquid chromatography with UV detection.ResultsThe mean indinavir concentrations in portal vein concentration−time profiles at different perfusion times under various flow rates were all higher than those obtained for hepatic veins. At flow rates of 0.5 and 1.0 mL/min, in particular, the area under the curve (AUC) and maximal concentration (C max) of indinavir absorption were significantly different between portal veins and hepatic veins (p < 0.05), indicating considerable hepatic involvement in the presystemic extraction of indinavir. The system also has potential for use when estimating the hepatic extraction ratio (E H) and hepatic clearance (Cl H).ConclusionThis in vivo approach could provide another useful tool for improving our basic understanding of the absorption kinetics and hepatic metabolism of pharmaceuticals under development and facilitating the clinical application of such

The Inhibitory Effect of Ellagic Acid on Cell Growth of Ovarian Carcinoma Cells

Ellagic acid (EA) is able to inhibit the growth of several cancer cells; however, its effect on human ovarian carcinoma cells has not yet been investigated. Ovarian carcinoma ES-2 and PA-1 cells were treated with EA (10~100 μM) and assessed for viability, cell cycle, apoptosis, anoikis, autophagy, and chemosensitivity to doxorubicin and their molecular mechanisms. EA inhibited cell proliferation in a dose- and time-dependent manner by arresting both cell lines at the G1 phase of the cell cycle, which were from elevating p53 and Cip1/p21 and decreasing cyclin D1 and E levels. EA also induced caspase-3-mediated apoptosis by increasing the Bax : Bcl-2 ratio and restored anoikis in both cell lines. The enhancement of apoptosis and/or inhibition of autophagy in these cells by EA assisted the chemotherapy efficacy. The results indicated that EA is a potential novel chemoprevention and treatment assistant agent for human ovarian carcinoma

Pulmonary IL- 33 orchestrates innate immune cells to mediate respiratory syncytial virus- evoked airway hyperreactivity and eosinophilia

BackgroundRespiratory syncytial virus (RSV) infection is epidemiologically linked to asthma. During RSV infection, IL- 33 is elevated and promotes immune cell activation, leading to the development of asthma. However, which immune cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia remained to be clarified. We aimed to elucidate the individual roles of IL- 33- activated innate immune cells, including ILC2s and ST2+ myeloid cells, in RSV infection- triggered pathophysiology.MethodsThe role of IL- 33/ILC2 axis in RSV- induced AHR inflammation and eosinophilia were evaluated in the IL- 33- deficient and YetCre- 13 Rosa- DTA mice. Myeloid- specific, IL- 33- deficient or ST2- deficient mice were employed to examine the role of IL- 33 and ST2 signaling in myeloid cells.ResultsWe found that IL- 33- activated ILC2s were crucial for the development of AHR and airway inflammation, during RSV infection. ILC2- derived IL- 13 was sufficient for RSV- driven AHR, since reconstitution of wild- type ILC2 rescued RSV- driven AHR in IL- 13- deficient mice. Meanwhile, myeloid cell- derived IL- 33 was required for airway inflammation, ST2+ myeloid cells contributed to exacerbation of airway inflammation, suggesting the importance of IL- 33 signaling in these cells. Local and peripheral eosinophilia is linked to both ILC2 and myeloid IL- 33 signaling.ConclusionsThis study highlights the importance of IL- 33- activated ILC2s in mediating RSV- triggered AHR and eosinophilia. In addition, IL- 33 signaling in myeloid cells is crucial for airway inflammation.Respiratory syncytial virus induces ILC2 to produce IL- 5 and IL- 13 through IL- 33, which is crucial for the development of airway hyperreactivity and airway inflammation. Myeloid cell- derived IL- 33 and suppression of tumorigenicity 2- positive myeloid cells contribute to cytokine production and cellular inflammation in airway. Both ILC2 and myeloid cell IL- 33 signaling contribute to local and peripheral eosinophilia.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154896/1/all14091.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154896/2/all14091-sup-0001-Supinfo.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154896/3/all14091_am.pd

EBV-encoded small RNA1 and nonresolving inflammation in rheumatoid arthritis

AbstractRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by perpetuated inflammation in multiple joints. To date, there is no cure for RA, and the causal factor for non-resolving inflammation in RA remains unclear. In this study, we initially observed expression of Epstein–Barr virus-encoded small RNA1 (EBER1) in the synovial tissue of all five patients who showed nonresolving RA inflammation. By contrast, EBER1 was detected in the synovial tissue of only one out of seven patients with advanced osteoarthritis (OA; p < 0.01, Fisher’s exact test). To confirm this finding, we conducted a second study on synovial tissue samples taken from 23 patients with nonresolving RA inflammation and 13 patients with OA. All synovial samples from patients with nonresolving inflammation of RA showed positive expression of EBER1 (23/23, 100%), whereas none of the synovial samples from patients with OA showed expression of EBER1 (0/13, 0%; p < 0.001, by Fisher’s exact test). In vitro, transfection of RA synovial fibroblasts with EBER1 induced the production of interleukin-6. Taken together, these data strongly suggest that nonresolving RA inflammation is strongly related to the presence of EBER1, which might be, at least partially, responsible for synovial fibroblast interleukin-6 production