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Setting: Côte d'Ivoire is a country with a high incidence of TB. The control of TB infection is focused on high-risk patients but has limited implementation., Objective: Cost-benefit analysis of TB infection (TBI) screening of household contacts in Côte d'Ivoire to evaluate economic implications of the implementation of interferon-gamma release assays (IGRAs) and the tuberculin skin test (TST)., Design: We compared the effectiveness of QuantiFERON-TB Gold Plus (QuantiFERON) with the TST using an economic model previously evaluated in medium TB incidence settings. Principal outcomes relating to TBI screening, as well as the lifetime costs and benefits of the patient cohort, were captured using a decision tree, followed by a Markov model., Results: QuantiFERON proved to be both more effective and less costly than TST. Compared to QuantiFERON, TST use leads to an approximate 33% increase in the lifetime risk of developing active TB., Conclusions: For household contacts of active TB cases in Côte d'Ivoire, QuantiFERON is cost-effective when compared with TST. R shiny interactive interface enables model customisation for different scenarios, settings, risk groups and TBI screening methods. Further research should be conducted in similar settings to generalise the results., Competing Interests: Competing interests: Data collection and scientific writing for this study was partially supported by QIAGEN. QIAGEN had no role in the study design, data analysis, or interpretation of results. Authors have no other conflicts of interests to declare., (© 2024 The Authors.)

RB1-inducible coiled-coil 1 (RB1CC1) is a novel molecule implicated in the regulation of RB1 (retinoblastoma 1) expression. However, information about the RB1CC1 gene is limited and its function remains somewhat obscure. The present study analyzes the expression and promoter activities of RB1CC1 in developing murine and human tissues. Rb1cc1 was abundantly expressed from an early stage of the mouse embryo throughout development. Immunohistochemical analyses revealed that Rb1cc1 was ubiquitous in the mouse, rather than in the human embryo, especially in the musculoskeletal system, heart and neural tissues. Promoter activity was highest in a region located about 300 bp immediately upstream of exon 1 in both the mouse and human RB1CC1 genes, suggesting that this region is a core promoter. The promoter activity of RB1CC1 was generally higher in mice than in humans, and suppressive with intron 1, especially in humans. These results suggested that more Rb1cc1 is expressed throughout developing murine than in human tissues, and that RB1CC1 expression is controlled more stringently by modification at intron 1 in humans than in mice.

We established a cell line (hPTC) from the tissue of papillary thyroid cancer surgically excised from a 27-year-old female patient. Synthesis of cAMP by the hPTC cells was stimulated by TSH. This cell line has continued to divide as a monolayer in a tissue culture for three years. We assessed growth regulation of the hPTC cells by protein tyrosine kinase and cAMP-dependent protein kinase by measuring the DNA content of the hPTC cells in 24-well plates with 3,5-diaminobenzoic acid after incubation in various growth factors. Basic fibroblast growth factor (FGF), epidermal growth factor (EGF), and insulin-like growth factor-1 (IGF-1), all of which bind to their respective receptors with tyrosine kinase activity, stimulated DNA synthesis in the hPTC cells. Neutralizing antibodies to basic FGF and EGF suppressed the growth stimulation by basic FGF and EGF, respectively. Genistein, a specific protein tyrosine kinase inhibitor, inhibited proliferation of the hPTC cells. On the other hand, thyrotropin, dibutyryl cAMP (dBC) and forskolin inhibited proliferation. KT5720, a specific cAMP-dependent protein kinase inhibitor, restored the growth of the hPTC cells even in the presence of dBC. This study shows that stimulation of the protein tyrosine kinase activity by basic FGF, EGF, and IGF-1 promoted DNA replication by the human thyroid cancer cell line. However, activation of the cAMP-dependent protein kinase inhibited proliferation of this cell line.