Explore the vast range of titles available.

There are challenges Jordanian Islamic banks face in maintaining and enhancing their competitive advantage in a rapidly evolving and increasingly competitive market. This paper aims to examine the factors that affect Jordanian Islamic banks towards competitive advantage, in addition to examining the roles of strategic intelligence and organizational creativity in enhancing Jordanian Islamic banks' competitiveness. However, this paper relied on the descriptive analytical approach, and the study population included general manager, department manager, branch manager, head of department based on Banks structures and annual reports from 2018 to the end of 2023. A stratified random sample was used, approximately 243 questionnaires were examined. The results indicated that organizational creativity and strategic intelligence play a crucial role in building competitive advantage. Also, organizational creativity contributes to achieving superiority by creating an innovative organizational environment, while strategic intelligence reflects the ability to make smart decisions that enhance competitive effectiveness. This paper also demonstrated the importance of managing and harnessing information effectively in order to enhance strategic intelligence. However, this paper contributes to the understanding of success factors in Islamic banking and provides actionable insights for managers navigating the complexities of the banking sector, emphasizing the importance of innovation, differentiation, and strategic decision-making for sustained growth and competitiveness.

The induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. Here, we report that the removal of the special AT-rich binding protein 2 (SATB2), a nuclear protein known to bind matrix attachment regions, is a key event in initiating myogenic differentiation. The deletion of myoblast SATB2 in vitro initiates chromatin remodeling and accelerates differentiation, which is dependent on the caspase 7-mediated cleavage of SATB2. A genome-wide analysis indicates that SATB2 binding within chromatin loops and near anchor points influences both loop and sub-TAD domain formation. Consequently, the chromatin changes that occur with the removal of SATB2 lead to the derepression of differentiation-inducing factors while also limiting the expression of genes that inhibit this cell fate change. Taken together, this study demonstrates that the temporal control of the SATB2 protein is critical in shaping the chromatin environment and coordinating the myogenic differentiation program.

Muscle atrophy derived from excessive proteolysis is a hallmark of numerous disease conditions. Accordingly, the negative consequences of skeletal muscle protein breakdown often overshadow the critical nature of proteolytic systems in maintaining normal cellular function. Here, we discuss the major cellular proteolysis machinery—the ubiquitin/proteosome system, the autophagy/lysosomal system, and caspase-mediated protein cleavage—and the critical role of these protein machines in establishing and preserving muscle health. We examine how ordered degradation modifies (1) the spatiotemporal expression of myogenic regulatory factors during myoblast differentiation, (2) membrane fusion during myotube formation, (3) sarcomere remodeling and muscle growth following physical stress, and (4) energy homeostasis during nutrient deprivation. Finally, we review the origin and etiology of a number of myopathies and how these devastating conditions arise from inborn errors in proteolysis.

Heart failure (HF) is a rising global cardiovascular epidemic driven by aging and chronic inflammation. As elderly populations continue to increase, precision treatments for age-related cardiac decline are urgently needed. Here we report that cardiac and blood expression of IGFBP7 is robustly increased in patients with chronic HF and in an HF mouse model. In a pressure overload mouse HF model, Igfbp7 deficiency attenuated cardiac dysfunction by reducing cardiac inflammatory injury, tissue fibrosis and cellular senescence. IGFBP7 promoted cardiac senescence by stimulating IGF-1R/IRS/AKT-dependent suppression of FOXO3a, preventing DNA repair and reactive oxygen species (ROS) detoxification, thereby accelerating the progression of HF. In vivo, AAV9-shRNA-mediated cardiac myocyte Igfbp7 knockdown indicated that myocardial IGFBP7 directly regulates pathological cardiac remodeling. Moreover, antibody-mediated IGFBP7 neutralization in vivo reversed IGFBP7-induced suppression of FOXO3a, restored DNA repair and ROS detoxification signals and attenuated pressure-overload-induced HF in mice. Consequently, selectively targeting IGFBP7-regulated senescence pathways may have broad therapeutic potential for HF.

Transient DNA strand break formation has been identified as an effective means to enhance gene expression in living cells. In the muscle lineage, cell differentiation is contingent upon the induction of caspase-mediated DNA strand breaks, which act to establish the terminal gene expression program. This coordinated DNA nicking is rapidly resolved, suggesting that myoblasts may deploy DNA repair machinery to stabilize the genome and entrench the differentiated phenotype. Here, we identify the base excision repair pathway component XRCC1 as an indispensable mediator of muscle differentiation. Caspase-triggered XRCC1 repair foci form rapidly within differentiating myonuclei, and then dissipate as the maturation program proceeds. Skeletal myoblast deletion of Xrcc1 does not have an impact on cell growth, yet leads to perinatal lethality, with sustained DNA damage and impaired myofiber development. Together, these results demonstrate that XRCC1 manages a temporally responsive DNA repair process to advance the muscle differentiation program.

Energy consumption of wireless network communication is still a big issue and a lot of research papers have proposed many solutions to increase node life time. The WMN architecture is made up of a fixed and mobile component, whereas the wireless mesh networks (WMNs) are multi-hop wireless networks with instant deployment, self-healing, self-organization and self-configuration features. The reduction in the distance by a factor of two can result in at least four times more powerful signals at the receiver. This paper presents suggestions that the links are more reliable without the increase in power of the transmitter in individual nodes. As a result, the present simulations networks are nine mobile nodes for considering coverage issues of the service area. The analytic results show that the link power node for direct communication between two nodes with long distance consuming more power than it is cleared. The improvement in the network performance for maintaining is available and this solution can be used to implement mobility in such case with low power region for the wireless mesh networks.

[This corrects the article DOI: 10.1186/s13395-016-0086-6.].

Induction of lineage-specific gene programs are strongly influenced by alterations in local chromatin architecture. However, key players that impact this genome reorganization remain largely unknown. Here, we report that removal of special AT-rich binding protein 2 (SATB2), a nuclear protein that binds matrix attachment regions, is a key event in initiating myogenic differentiation. Deletion of SATB2 in muscle cell culture models and in vivo, accelerates differentiation and depletes the muscle progenitor pool, respectively. Genome wide analysis indicates that SATB2 binding is both repressive and inductive, as loss of SATB2 leads to expression of differentiation regulatory factors and inhibition of genes that impair this process. Finally, we noted that the differentiation-specific decline in SATB2 protein is dependent on a caspase 7-mediated cleavage event. Taken together, this study demonstrates that temporal control of SATB2 protein is critical for shaping the chromatin environment and coordinating the myogenic differentiation program.

Aim: The aim of this study is, to calculate the publications published in PubMed Indexed journals by authors participated as the first or as a participatory author associated with Colleges of Applied Medical Sciences, affiliated with universities of Saudi Arabia. Methods: The data was retrieved and collected from the PubMed/Medline database to tabulate in Microsoft Excel 2010 year and subject wise, annual growth of publications, a pattern of authorship and frequency of journals from the period 2009 - 2018. Results: This study showed that n=1652; 165.2 per annum and 75 articles per university were published during the period of 2009 - 2018. The year 2018 produced n=431; 183.4% higher than the year 2009. King Saud University place its share in research and produced n=785; 47.5% articles followed by Qassim University with n=109; 6.6% articles. While eight universities contributed in n=460; 27.8% articles as minimum 53 and maximum 80 articles as a participator in research productivity. A multi-authorship is visible in this study as a majority, which contributes n=1519; 92% articles. Subject Physiotherapy takes attention of researcher and they produced n=209; 12.6% articles. Another 12 subjects participated in n=1130; 68.6% articles. Saudi Journal of Biological Sciences facilitated in the publication of n=36; 2.1% articles out of 1151 journals which indexed in PubMed database. Conclusion: Significant participation of authors and institutes in the production of publications published in PubMed Indexed journals reveals the culture of research pertained in the colleges affiliated with 22 universities of Saudi Arabia. Every year they produced qualitative and quantitative manuscripts which strengthen the objectives of policymakers in the development of the research environment among academics.