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This study investigates the efficacy and effects of Kolb's experiential learning (EL) model and students' scientific field groups on their innovativeness in business development. (1) Humanities and Social Science, and (2) Science and Technology are the scientific field groups. A quasi-experimental quantitative approach with a 2 x 2 factorial design was used in this study. This study's sample encompassed active Faculty of Teacher Training and Education of the University of Mataram enrolling for entrepreneurship courses which were taken using random sampling after commensuration processes. The data collection instrument used to collect data on students' innovativeness is a project-based assessment based on indicators of innovativeness in developing products and digital marketing. The results of the instrument test fulfilled the validity and reliability requirement. All data were analyzed statistically by descriptive statistics and comparative analysis using the ANOVA test, which was preceded by an analysis requirement test. The study results showed an interaction effect of the EL model and students' scientific field on students' innovativeness. In addition, Kolb's EL model also directly affects students' innovativeness, while the scientific field group does not. Nevertheless, the data showed that the Science and Technology group innovates better than the others. The theoretical implication of this study was that EL has a strong theoretical framework for entrepreneurial learning, so it needs to be expanded through further studies.

Giving educational stimulation in early childhood can be given through games. Traditional science-based games make an important contribution to supporting children's development. This study aimed to identify traditional games in Central Lombok Regency that can be played in early childhood and how to play traditional games to improve children's development. This research is survey research conducted at Central Lombok Regency. This research uses observation data collection methods, interviews, and documentation. The subjects of this study were six community leaders or cultural leaders and five teachers. Data analysis used descriptive qualitative analysis. The results showed that there were 28 identified traditional games. After being reviewed and verified based on the criteria for tools and materials used: playground, gender, age of players, number of players, and how to play, 23 traditional games were obtained: fort, bekel, ciwe, cepun, do mi gift, merchandise, long dragon snakes, marbles, playing rope, pese-pese'an, temeong-meong, gobak sodor, trumpets, cingkaleng, manuk brackets, splashing, temong-meong, school stones, playing moon, cupring, segem, playing war and coffee. Traditional games use tools, do not use tools, and use poetry/songs. How to play traditional games each game has steps similar to each others. Based on these criteria, traditional games can indirectly improve child development such as cognitive, language, social-emotional, religious and moral values, physical-motor, and artistic.

The plasminogen receptor, Plg-R KT, is a unique cell surface receptor that is broadly expressed in cells and tissues throughout the body. Plg-R KT localizes plasminogen on cell surfaces and promotes its activation to the broad-spectrum serine protease, plasmin. In this study, we show that overexpression of Plg-R KT protects mice from high fat diet (HFD)-induced adipose and metabolic dysfunction. During the first 10 weeks on the HFD, the body weights of mice that overexpressed Plg-R KT (Plg-R KT -OEX) were lower than those of control mice (CagRosaPlgRKT). After 10 weeks on the HFD, CagRosaPlgRKT and Plg-R KT -OEX mice had similar body weights. However, Plg-R KT -OEX mice showed a more metabolically favourable body composition phenotype. Plg-R KT -OEX mice also showed improved glucose tolerance and increased insulin sensitivity. We found that the improved metabolic functions of Plg-R KT -OEX mice were mechanistically associated with increased energy expenditure and activity, decreased proinflammatory adipose macrophages and decreased inflammation, elevated brown fat thermogenesis, and higher expression of adipose PPARγ and adiponectin. These findings suggest that Plg-R KT signalling promotes healthy adipose function via multiple mechanisms to defend against obesity-associated adverse metabolic phenotypes.

Sepsis is a lethal syndrome characterized by systemic inflammation and abnormal coagulation. Despite therapeutic advances, sepsis mortality remains substantially high. Herein, we investigated the role of the plasminogen/plasmin (Plg/Pla) system during sepsis. Plasma levels of Plg were significantly lower in mice subjected to severe compared with nonsevere sepsis, whereas systemic levels of IL-6, a marker of sepsis severity, were higher in severe sepsis. Plg levels correlated negatively with IL-6 in both septic mice and patients, whereas plasminogen activator inhibitor-1 levels correlated positively with IL-6. Plg deficiency render mice susceptible to nonsevere sepsis induced by cecal ligation and puncture (CLP), resulting in greater numbers of neutrophils and M1 macrophages, liver fibrin(ogen) deposition, lower efferocytosis, and increased IL-6 and neutrophil extracellular trap (NET) release associated with organ damage. Conversely, inflammatory features, fibrin(ogen), and organ damage were substantially reduced, and efferocytosis was increased by exogenous Pla given during CLP- and LPS-induced endotoxemia. Plg or Pla protected mice from sepsis-induced lethality and enhanced the protective effect of antibiotics. Mechanistically, Plg/Pla-afforded protection was associated with regulation of NET release, requiring Pla-protease activity and lysine binding sites. Plg/Pla are important host-protective players during sepsis, controlling local and systemic inflammation and collateral organ damage.

The plasminogen activation system regulates the activity of the serine protease, plasmin. The role of plasminogen receptors in cancer progression is being increasingly appreciated as key players in modulation of the tumor microenvironment. The interaction of plasminogen with cells to promote plasminogen activation requires the presence of proteins exposing C-terminal lysines on the cell surface. Plg-R KT is a structurally unique plasminogen receptor because it is an integral membrane protein that is synthesized with and binds plasminogen via a C-terminal lysine exposed on the cell surface. Here, we have investigated the expression of Plg-R KT in human breast tumors and human breast cancer cell lines. Breast cancer progression tissue microarrays were probed with anti-Plg-R KT mAB and we found that Plg-R KT is widely expressed in human breast tumors, that its expression is increased in tumors that have spread to draining lymph nodes and distant organs, and that Plg-R KT expression is most pronounced in hormone receptor (HR)-positive tumors. Plg-R KT was detected by Western blotting in human breast cancer cell lines. By flow cytometry, Plg-R KT cell surface expression was highest on the most aggressive tumor cell line. Future studies are warranted to address the functions of Plg-R KT in breast cancer.

Machine intelligence can convert raw clinical data into an informational source that helps make decisions and predictions. As a result, cardiovascular diseases are more likely to be addressed as early as possible before affecting the lifespan. Artificial intelligence has taken research on disease diagnosis and identification to another level. Despite several methods and models coming into existence, there is a possibility of improving the classification or forecast accuracy. By selecting the connected combination of models and features, we can improve accuracy. To achieve a better solution, we have proposed a reliable ensemble model in this paper. The proposed model produced results of 96.75% on the cardiovascular disease dataset obtained from the Mendeley Data Center, 93.39% on the comprehensive dataset collected from IEEE DataPort, and 88.24% on data collected from the Cleveland dataset. With this proposed model, we can achieve the safety and health security of an individual., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2022 Bhanu Prakash Doppala et al.)

Background: Plg-R KT , a unique transmembrane plasminogen receptor, enhances the activation of plasminogen to plasmin, and localizes the proteolytic activity of plasmin on the cell surface., Objectives: We investigated the role of Plg-R KT in adipose function, metabolic homeostasis, and obesity., Methods: We used adipose tissue (AT) sections from bariatric surgery patients and from high fat diet (HFD)-induced obese mice together with immunofluorescence and real-time polymerase chain reaction to study adipose expression of Plg-R KT . Mice genetically deficient in Plg-R KT and littermate controls fed a HFD or control low fat diet (LFD) were used to determine the role of Plg-R KT in insulin resistance, glucose tolerance, type 2 diabetes, and associated mechanisms including adipose inflammation, fibrosis, and ectopic lipid storage. The role of Plg-R KT in adipogenesis was determined using 3T3-L1 preadipocytes and primary cultures established from Plg-R KT -deficient and littermate control mice., Results: Plg-R KT was highly expressed in both human and mouse AT, and its levels dramatically increased during adipogenesis. Plg-R KT -deficient mice, when fed a HFD, gained more weight, developed more hepatic steatosis, and were more insulin resistant/glucose intolerant than HFD-fed wild-type littermates. Mechanistically, these metabolic defects were linked with increased AT inflammation, AT macrophage and T-cell accumulation, adipose and hepatic fibrosis, and decreased insulin signaling in the AT and liver. Moreover, Plg-R KT regulated the expression of PPARγ and other adipogenic molecules, suggesting a novel role for Plg-R KT in the adipogenic program., Conclusions: Plg-R KT coordinately regulates multiple aspects of adipose function that are important to maintain efficient metabolic homeostasis., (© 2021 International Society on Thrombosis and Haemostasis.)