Combining Fuzzy MCDM with BSC Approach in Performance Evaluation of Iranian Private Banking Sector

The objective of this study is to construct an approach based on multiple criteria decision making (MCDM) and balanced scorecard (BSC) for evaluating performance for three nongovernmental Iranian's banks. Following the literature relating to banking performance and BSC concepts, experts and managers select 21 indexes for evaluation. Furthermore, fuzzy analytic hierarchy process (FAHP) calculated the relative weights of each chosen index in order to tolerate vagueness and ambiguity of information, and three MCDM analytical tools (TOPSIS, VIKOR, and ELECTRE) were adopted to rank the banking performance. The results indicate that a customer “” has the most significant BSC perspectives and the customer satisfaction “1” is the most major index in banking sector. This proposed fuzzy MCDM method combined with BSC approach is a comprehensive and up-to-date model that can be a useful and effective assessment tool

Evaluation of Neurofibromatosis Gene Expression in Non-Hereditary Breast Cancer

Background: Breast cancer is the most common cause of death in women. Studies have shown that changes in neurofibromatosis gene expression can cause breast cancer. The aim of this study was to investigate the change of neurofibromatosis type 1 gene expression in non-hereditary breast cancer using real time PCR. Materials and Methods: In this study, 160 tissue samples were collected from patients following ethical principles. After lysis of tissues, extraction of RNA and synthesis of cDNA was performed. The amount of gene expression changes was investigated. Results: The results showed that the level of NF1 gene expression was dependent on the stages of the disease and as the stages progress, the level of expression of this gene showed a significant decrease. Conclusion: The use of gene biomarkers can help to diagnose and treat diseases faster. Along with examining other candidate genes, using NF1 gene expression analysis in breast cancer patients can be a suitable option for diagnosing the stages of disease progression

Nomophobia and Its Association with Sleep Quality, Communication Skills, and Stress Among Nursing Students: A Cross-sectional Study

Background:Nomophobia, the fear of being without mobile phone connectivity, is increasingly prevalent among university students, particularly nursing students who face rigorous academic and clinical demands.Objectives:This study examines the prevalence of nomophobia and its associations with sleep quality, communication skills, and perceived stress in nursing students to inform targeted interventions for their well-being and professional competencies.Methods:A cross-sectional study was conducted from March to May 2025 with 208 undergraduate nursing students from two universities in Kashan, Iran, using stratified sampling. Participants completed validated Persian versions of the Nomophobia Questionnaire (NMP-Q), Pittsburgh Sleep Quality Index (PSQI), Communication Skills Attitude Scale (CSAS), and Stress Index in Nursing Students (SINS). Data were collected via paper-based questionnaires during class and clinical sessions. Descriptive statistics, Pearson correlations, hierarchical regression, and Bayesian regression with a Jeffreys-Zellner-Siow (JZS) prior were used to analyze relationships between nomophobia and study variables, controlling for demographics. The sample size was calculated using G*Power, targeting a minimum of 200 participants for adequate power.Results:The mean NMP-Q score indicated moderate-to-high nomophobia levels. Participants reported poor sleep quality (mean PSQI = 7.91) and elevated stress (mean SINS = 82.38). Nomophobia was positively correlated with poor sleep quality (R = 0.42, P < 0.001) and stress (R = 0.51, P < 0.001), and negatively correlated with positive communication attitudes (R = -0.26, P < 0.001). Hierarchical regression showed that stress (β = 0.39, P < 0.001) and poor sleep quality (β = 0.28, P < 0.001) were the strongest predictors of nomophobia, with positive communication attitudes offering a protective effect (β = -0.16, P = 0.014). Bayesian analysis confirmed these findings (BF10 = 142.6). Daily smartphone use was not significant after controlling for psychosocial variables. The cross-sectional design limits causal inference.Conclusions:Nomophobia is prevalent among nursing students and significantly associated with poor sleep quality and high stress, while positive communication attitudes mitigate its impact. These findings suggest the possibility of interventions targeting stress management, sleep hygiene, and communication skills to reduce nomophobia. Future longitudinal studies should explore causality and evaluate intervention efficacy to support nursing students’ well-being

Plasminogen : a pleiotropic inflammatory regulator in radiation-induced wound formation and wound repair

The plasminogen activator (PA) system plays important roles in many physiological and pathological processes, including inflammation and wound healing. Plasmin, the central component of the PA system, is a broad-spectrum serine protease that is derived from its inactive precursor form, plasminogen. The first aim of this thesis was to study the role of plasminogen in the formation of radiation-induced wounds, which are an inflammatory side effect of radiotherapy. The second aim was to investigate the molecular mechanisms behind the potentiating effect of plasminogen in the healing of radiation-induced wounds. The third aim was to explore the therapeutic potential of plasminogen in the healing of radiation-induced wounds. Radiation therapy in cancer patients is often limited by side effects such as radiation-induced skin damage (radiodermatitis). The mechanisms behind the formation of radiodermatitis are not fully elucidated, and there are no effective preventive therapies for clinical use. In this study, we show that irradiation of skin in WT (wild-type) mice induces plasminogen accumulation, which is followed by activation of TGF-β (transforming growth factor-beta) signaling and the development of inflammation that leads to skin damage. However, plasminogen-deficient mice and mice lacking PAs were mostly resistant to radiodermatitis. Moreover, treatment with a plasminogen inhibitor, tranexamic acid, decreases radiodermatitis in WT mice and prevented radiodermatitis in heterozygous mice. Thus, plasmin is required for the formation of radiodermatitis, and inhibition of plasminogen activation might be a novel treatment strategy to reduce or prevent radiodermatitis in patients undergoing radiotherapy. Wound healing consists of partially overlapping inflammatory, proliferation, and tissue remodeling phases, and failure to terminate inflammation leads to the formation of chronic wounds. Previous studies by our group have shown that plasminogen is transported to acute wounds by inflammatory cells where it potentiates inflammation and enhances wound healing. Here, we report that plasminogen-deficient mice, which have delayed wound healing, have extensive fibrin and neutrophil depositions in the wounded area long after re-epithelialization, indicating inefficient debridement and chronic inflammation. The delayed formation of granulation tissue suggests that fibroblast function is also impaired in the absence of plasminogen. Therefore, in addition to its role in the activation of inflammation, plasminogen is also crucial for the resolution of inflammation and the activation of the proliferation phase. Importantly, supplementation of plasminogen-deficient mice with human plasminogen leads to a restored healing capacity that is comparable to that in WT mice. Therefore, plasminogen might be an important future therapeutic agent for treatment of wounds. In radiation-induced wounds, inflammation often cannot resolve and the wounds become chronic and fibrotic. Currently, there is no gold standard for the treatment of radiation-induced wounds. In this study, we have shown that radiation-induced wounds treated with plasminogen healed faster than placebo-treated wounds, had diminished inflammation and granulation tissue formation, and had enhanced re-epithelialization and collagen maturation. Transcriptome analysis showed that plasminogen has a pleiotropic effect on gene expression during wound healing, influencing the expression of 33 genes out of the 84 genes studied. In particular, plasminogen decreased the expression of 11 pro-inflammatory genes early in the healing process. Later, plasminogen decreased WNT (Wingless/Integrated) and TGF-β signaling, as well as the expression of 5 growth factors and 13 factors involved in granulation tissue formation. From the genes downregulated by plasminogen, 19 genes are known to be involved in fibrosis. These results show that in radiation-induced wounds with excessive inflammation and tissue formation plasminogen is able to direct the healing process to a normal outcome without the risk for developing fibrosis. This makes plasminogen an attractive drug candidate for treating radiodermatitis in cancer patients. Taken together, our results indicate that plasminogen is a pleiotropic inflammatory regulator involved in radiation-induced wound formation as well as in wound repair

Plasminogen : a pleiotropic inflammatory regulator in radiation-induced wound formation and wound repair

The plasminogen activator (PA) system plays important roles in many physiological and pathological processes, including inflammation and wound healing. Plasmin, the central component of the PA system, is a broad-spectrum serine protease that is derived from its inactive precursor form, plasminogen. The first aim of this thesis was to study the role of plasminogen in the formation of radiation-induced wounds, which are an inflammatory side effect of radiotherapy. The second aim was to investigate the molecular mechanisms behind the potentiating effect of plasminogen in the healing of radiation-induced wounds. The third aim was to explore the therapeutic potential of plasminogen in the healing of radiation-induced wounds. Radiation therapy in cancer patients is often limited by side effects such as radiation-induced skin damage (radiodermatitis). The mechanisms behind the formation of radiodermatitis are not fully elucidated, and there are no effective preventive therapies for clinical use. In this study, we show that irradiation of skin in WT (wild-type) mice induces plasminogen accumulation, which is followed by activation of TGF-β (transforming growth factor-beta) signaling and the development of inflammation that leads to skin damage. However, plasminogen-deficient mice and mice lacking PAs were mostly resistant to radiodermatitis. Moreover, treatment with a plasminogen inhibitor, tranexamic acid, decreases radiodermatitis in WT mice and prevented radiodermatitis in heterozygous mice. Thus, plasmin is required for the formation of radiodermatitis, and inhibition of plasminogen activation might be a novel treatment strategy to reduce or prevent radiodermatitis in patients undergoing radiotherapy. Wound healing consists of partially overlapping inflammatory, proliferation, and tissue remodeling phases, and failure to terminate inflammation leads to the formation of chronic wounds. Previous studies by our group have shown that plasminogen is transported to acute wounds by inflammatory cells where it potentiates inflammation and enhances wound healing. Here, we report that plasminogen-deficient mice, which have delayed wound healing, have extensive fibrin and neutrophil depositions in the wounded area long after re-epithelialization, indicating inefficient debridement and chronic inflammation. The delayed formation of granulation tissue suggests that fibroblast function is also impaired in the absence of plasminogen. Therefore, in addition to its role in the activation of inflammation, plasminogen is also crucial for the resolution of inflammation and the activation of the proliferation phase. Importantly, supplementation of plasminogen-deficient mice with human plasminogen leads to a restored healing capacity that is comparable to that in WT mice. Therefore, plasminogen might be an important future therapeutic agent for treatment of wounds. In radiation-induced wounds, inflammation often cannot resolve and the wounds become chronic and fibrotic. Currently, there is no gold standard for the treatment of radiation-induced wounds. In this study, we have shown that radiation-induced wounds treated with plasminogen healed faster than placebo-treated wounds, had diminished inflammation and granulation tissue formation, and had enhanced re-epithelialization and collagen maturation. Transcriptome analysis showed that plasminogen has a pleiotropic effect on gene expression during wound healing, influencing the expression of 33 genes out of the 84 genes studied. In particular, plasminogen decreased the expression of 11 pro-inflammatory genes early in the healing process. Later, plasminogen decreased WNT (Wingless/Integrated) and TGF-β signaling, as well as the expression of 5 growth factors and 13 factors involved in granulation tissue formation. From the genes downregulated by plasminogen, 19 genes are known to be involved in fibrosis. These results show that in radiation-induced wounds with excessive inflammation and tissue formation plasminogen is able to direct the healing process to a normal outcome without the risk for developing fibrosis. This makes plasminogen an attractive drug candidate for treating radiodermatitis in cancer patients. Taken together, our results indicate that plasminogen is a pleiotropic inflammatory regulator involved in radiation-induced wound formation as well as in wound repair

Plasminogen : a pleiotropic inflammatory regulator in radiation-induced wound formation and wound repair

The plasminogen activator (PA) system plays important roles in many physiological and pathological processes, including inflammation and wound healing. Plasmin, the central component of the PA system, is a broad-spectrum serine protease that is derived from its inactive precursor form, plasminogen. The first aim of this thesis was to study the role of plasminogen in the formation of radiation-induced wounds, which are an inflammatory side effect of radiotherapy. The second aim was to investigate the molecular mechanisms behind the potentiating effect of plasminogen in the healing of radiation-induced wounds. The third aim was to explore the therapeutic potential of plasminogen in the healing of radiation-induced wounds. Radiation therapy in cancer patients is often limited by side effects such as radiation-induced skin damage (radiodermatitis). The mechanisms behind the formation of radiodermatitis are not fully elucidated, and there are no effective preventive therapies for clinical use. In this study, we show that irradiation of skin in WT (wild-type) mice induces plasminogen accumulation, which is followed by activation of TGF-β (transforming growth factor-beta) signaling and the development of inflammation that leads to skin damage. However, plasminogen-deficient mice and mice lacking PAs were mostly resistant to radiodermatitis. Moreover, treatment with a plasminogen inhibitor, tranexamic acid, decreases radiodermatitis in WT mice and prevented radiodermatitis in heterozygous mice. Thus, plasmin is required for the formation of radiodermatitis, and inhibition of plasminogen activation might be a novel treatment strategy to reduce or prevent radiodermatitis in patients undergoing radiotherapy. Wound healing consists of partially overlapping inflammatory, proliferation, and tissue remodeling phases, and failure to terminate inflammation leads to the formation of chronic wounds. Previous studies by our group have shown that plasminogen is transported to acute wounds by inflammatory cells where it potentiates inflammation and enhances wound healing. Here, we report that plasminogen-deficient mice, which have delayed wound healing, have extensive fibrin and neutrophil depositions in the wounded area long after re-epithelialization, indicating inefficient debridement and chronic inflammation. The delayed formation of granulation tissue suggests that fibroblast function is also impaired in the absence of plasminogen. Therefore, in addition to its role in the activation of inflammation, plasminogen is also crucial for the resolution of inflammation and the activation of the proliferation phase. Importantly, supplementation of plasminogen-deficient mice with human plasminogen leads to a restored healing capacity that is comparable to that in WT mice. Therefore, plasminogen might be an important future therapeutic agent for treatment of wounds. In radiation-induced wounds, inflammation often cannot resolve and the wounds become chronic and fibrotic. Currently, there is no gold standard for the treatment of radiation-induced wounds. In this study, we have shown that radiation-induced wounds treated with plasminogen healed faster than placebo-treated wounds, had diminished inflammation and granulation tissue formation, and had enhanced re-epithelialization and collagen maturation. Transcriptome analysis showed that plasminogen has a pleiotropic effect on gene expression during wound healing, influencing the expression of 33 genes out of the 84 genes studied. In particular, plasminogen decreased the expression of 11 pro-inflammatory genes early in the healing process. Later, plasminogen decreased WNT (Wingless/Integrated) and TGF-β signaling, as well as the expression of 5 growth factors and 13 factors involved in granulation tissue formation. From the genes downregulated by plasminogen, 19 genes are known to be involved in fibrosis. These results show that in radiation-induced wounds with excessive inflammation and tissue formation plasminogen is able to direct the healing process to a normal outcome without the risk for developing fibrosis. This makes plasminogen an attractive drug candidate for treating radiodermatitis in cancer patients. Taken together, our results indicate that plasminogen is a pleiotropic inflammatory regulator involved in radiation-induced wound formation as well as in wound repair

Row Data Day 0_2.fq.gz

Row data for mRNA sequensing of sample from radiation wounds before treatment

Row Data Day 0-1fq.gz

Row data for mRNA sequensing of sample from radiation wounds before treatment

Row Data Day 20-PBS_1.fq.gz

Row data for mRNA sequensing of sample from radiation wounds treated with PBS for 20 days