Empirical research on the financing of small and medium-sized enterprises (SMEs) has focused mainly on theoretical approaches related to hierarchical order and, to a lesser extent, on trade-off theory. However, the financial literature has recently revealed that the life-cycle stages of SMEs influence their financial choices, which may explain why business financing evolves over time. Thus, this paper used a panel data approach to study the impact of life cycle phases on the capital structure of 70 Tunisian industrial SMEs during the period from 2013 to 2016. We found that Tunisian SMEs tended to use debt more intensively in the short term, while long-term debt was rarely used. We also found that the life cycle theory is perfectly adapted to describe the financial behavior adopted by Tunisian SMEs, which tend to use debt (regardless of maturity) during the early life cycle phases. Once SMEs age and mature, other sources of funding take over (mainly self-financing and even an IPO). Contribution/ Originality:This study is one of very few to investigate the influence of life cycle phases on the capital structure for Tunisian SMEs. The paper's primary contribution is that each source of funding is often adapted to a specific moment in the life cycle of the SME. 1.In Tunisia and according to the National Institute of Statistics (NIS), is considered an SME, any company whose workforce varies between 6 and 199 employees.In addition, there is another definition of SME eligible for intervention by the Industrial Promotion and Decentralization Fund (IPDF), which defines SMEs in the industrial and service sector as those with a total investment not exceeding 10 million dinars (including working capital).
Purpose/Aim: Many genes have been associated with primary open-angle glaucoma (POAG). Knowing exactly where they are expressed in the eye helps to unravel POAG pathology and to select optimal targets for intervention. We investigated whether RNA in situ hybridization (RNA-ISH) is a convenient technique to obtain detailed pan-ocular expression data of these genes. We tested this for four diverse candidate POAG genes, selected because of unclear ocular distribution (F5 and Dusp1) and relevance for potential new therapies (Tnf, Tgfβr3). Optn, a POAG gene with well-known ocular expression pattern served as control. Methods: We made a list of candidate glaucoma genes reported in genetic studies. A table of their ocular expression at the tissue level was compiled using publicly available microarray data (the ocular tissue database). To add cellular detail we performed RNA-ISH for Optn, Tnf, Tgfβr3, F5, and Dusp1 on eyes of healthy, 2-month-old, pigmented, and albino mice. Results: Expression of the Optn control matched with published immunohistochemistry data. Ocular expression of Tnf was generally low, with patches of higher Tnf expression, superficially in the corneal epithelium. F5 had a restricted expression pattern with high expression in the nonpigmented ciliary body epithelium and moderate expression in the peripapillary region. Tgfβr3 and Dusp1 showed ubiquitous expression. Conclusions: RNA-ISH is a suitable technique to determine the ocular expression pattern of POAG genes, adding meaningful cellular detail to existing microarray expression data. For instance, the high expression of F5 in the nonpigmented ciliary body epithelium suggests a role of this gene in aqueous humor dynamics and intraocular pressure. In addition, the ubiquitous expression of Tgfβr3 has implications for designing TGF-β-related glaucoma therapies, with respect to side effects. Creating pan-ocular expression maps of POAG genes with RNA-ISH will help to identify POAG pathways in specific cell types and to select targets for drug development.
Endometrial cancer (EC) is the most common gynaecological tumor in developed countries and its incidence is increasing. Approximately 80% of newly diagnosed EC cases are estrogen-dependent. Type 1 17β-hydroxysteroid dehydrogenase (17β-HSD-1) is the enzyme that catalyzes the final step in estrogen biosynthesis by reducing the weak estrogen estrone (E1) to the potent estrogen 17β-estradiol (E2), and previous studies showed that this enzyme is implicated in the local E2 generation in EC. In the present study we employed a recently developed orthotopic and estrogen-dependent xenograft mouse model of EC to show that pharmacological inhibition of the 17β-HSD-1 enzyme inhibits disease development. Tumors were induced in one uterine horn of athymic nude mice by intra-uterine injection of the well-differentiated human endometrial adenocarcinoma Ishikawa cell line that was modified to express 17β-HSD-1 in levels comparable to humans and, in addition, the luciferase and green fluorescent protein reporter genes. After tumor engraftment, controlled estrogen exposure was achieved using subcutaneous MedRod implants that released either E1 or placebo. A subgroup of the E1 supplemented mice received daily gavage of FP4643, a well characterized 17β-HSD-1 inhibitor. Bioluminescence imaging (BLI) was used to measure tumor growth non-invasively. At sacrifice, mice receiving E1 and treated with the FP4643 inhibitor showed a significant reduction in tumor growth by approximately 65% compared to mice receiving E1 alone. Tumors exhibited metastatic spread to the peritoneum, to the lymphovascular space (LVI) and to the thoracic cavity. Metastatic spread and LVI were both reduced in the inhibitor treated group. Transcriptional profiling of tumors indicated that FP4643 treatment reduced the oncogenic potential at the mRNA level. In conclusion, we show that the FP4643 inhibition represents a potential promising novel endocrine treatment for EC Citation Format: Sofia Xanthoulea, Gonda Konings, Niina Saarinen, Bert Delvoux, Loes Kooreman, Pasi Koskimies, Merja Häkkinen, Seppo Auriola, Elisabetta d'Avanzo, Youssef Walid, Frank Verhaegen, Natasja Lieuwes, Florian Caiment, Roy Kruitwagen, Andrea Romano. Pharmacological inhibition of 17β-hydroxysteroid dehydrogenase impairs endometrial cancer growth in an orthotopic xenograft mouse model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2931.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.