Giving full play to the interaction of multi-dimensional environmental regulation is an important method to accelerate the green transformation of manufacturing enterprises which is a significant way to achieve carbon peaking and carbon neutrality goals. Based on the theory of evolution game, a green transformation strategy evolution game model participated by the government, consumers, and manufacturing enterprises has been constructed. Stability research is conducted based on the behavioral mode of the three parties participating subjects and the paper uses MATLAB for numerical simulation to analyze the impact of environmental regulations of different dimensions on the green transformation of enterprises. The research shows that: (1) When the government adopts a single environmental regulation of carbon emission right transaction or green consumption subsidy, it will not affect the choice of green transformation strategies of the enterprise. (2) When the government adopts a single environmental regulation of environmental protection tax, it only promotes enterprises to choose green transformation strategies under limited conditions. (3) Under the multi-dimensional environmental regulations of the government, by affecting the cost and income of enterprise green technology innovation, consumers’ green consumption behavior, and the manufacturing enterprises choose green transformation as a stable strategy. Therefore, the government should give full play to the role of multi-dimensional environmental regulations in promoting consumers' green consumption and enterprises’ green technology innovation to accelerate the green transformation of manufacturing enterprises.

Stock indexes are used as a barometer of economic health, and fluctuations in these markets can have a substantial influence on the economy. For example, the Covid-19 pandemic caused severe economic disruption, as reflected in stock market indexes. Similarly, Russia's invasion of Ukraine has geopolitical implications that might undermine global trade and economic stability, impacting stock market indexes. Considering these developments, the purpose of this article is to examine the co-movements of the stock markets of Austria (ATX), Poland (WIG), the Czech Republic (PX Prague), Hungary (BUX), Croatia (CROBEX), Serbia (BELEX 15), Romania (BET), and Slovenia (SBI TOP) from February 16, 2018, to February 15, 2023. To achieve the research objectives, the aim is to answer the following research question: i) Have the events of 2020 and 2022 accentuated the co-movements between the stock markets in Central Europe? The results show the presence of 21 shocks between markets (out of a potential 56) during the Tranquil subperiod, with the WIG stock index having a greater predictive influence on the behavior of its peers (4 shocks out of 7 possible). During the Stress subperiod, 45 shocks were confirmed (out of 56 possible). The markets that triggered the most market shocks (7 out of 7 possibilities) were BET, BUX, CROBEX, and SBI TOP. The research question was validated based on the conclusion supplied, as all markets increased their movements, showing a considerable effect of the 2020 and 2022 events on these markets.

The latent transforming growth factor-beta (TGF-β) binding protein 1 (LTBP1) has been implicated in various cellular processes, but its role in triple-negative breast cancer (TNBC) remains unclear. In this study, we investigated the impact of LTBP1 on TNBC progression and its underlying mechanisms. Analysis of online datasets revealed elevated LTBP1 mRNA expression in breast cancer tissues compared to normal adjacent tissues. Kaplan-Meier Plotter analysis indicated that high LTBP1 expression was negatively correlated with relapse-free survival (RFS), distant-metastasis free survival (DMFS), and overall survival (OS) of breast cancer patients. Additionally, LTBP1 mRNA levels were associated with chemotherapy resistance. Functional assays in TNBC cells demonstrated that LTBP1 knockdown suppressed cell proliferation, induced apoptosis, and attenuated migration and invasion. In vivo studies confirmed that LTBP1 knockdown inhibited tumor growth in a xenograft mouse model. Mechanistically, LTBP1 positively correlated with genes involved in signaling regulation and organelle organization, with significant associations to GTPase binding and the RhoA/ROCK pathway. LTBP1 knockdown reduced RhoA activity and phosphorylation of Myosin Light Chain 2 (MLC2), suggesting inhibition of the RhoA/ROCK signaling pathway. Moreover, activation of the RhoA/ROCK pathway partially rescued the effects of LTBP1 knockdown on TNBC cell proliferation, apoptosis, migration, and invasion. In conclusion, our findings suggest that LTBP1 promotes TNBC progression through activation of the RhoA/ROCK signaling pathway, highlighting its potential as a therapeutic target for TNBC.

Spence’s signaling model (Spence, 1973) suggests that education can signal workers’ unobserved ability to employers thereby mitigating discrimination. There have been several studies concerning education’s impact on labor market discrimination against minority or disadvantaged groups. Our approach in this inquiry is unique in that we utilize the data of PhD recipients, a group of people with the highest education attainment, to test Spence’s theory. Another novelty of this paper is that in addition to examining possible discrimination against women and foreign-born, as has been done in previous studies, we further explore possible discrimination against the physically challenged individuals. Our baseline results show conflicting results that Ph.D. education can reduce discrimination against disability and foreign-born but not against gender. Further analysis by the Blinder-Oaxaca Decomposition shows that the wage gaps of gender and disability come more from the unobserved part than the explained part, while the foreign-born wage gap come more from the observable human capital differences. Since prejudice is an unobserved factor and we know that the disadvantaged groups are likely to suffer from prejudice (Oaxaca, 1973; Blinder, 1973; Montes-Rojas et al., 2017; Deshpande and Khanna, 2018), we conjecture that prejudice might be attributable to the unexplained part of the wage gaps. Furthermore, prejudice might be deeply rooted in one’s mind, thus difficult to remove even with the influence of education. Hence, our results reveal that it would be hard for Ph.D. education to eradicate the discrimination against gender and disability, but not against foreign-born.

The paramount prerequisite for effective anti-cancer drugs is their ability to eradicate malignant cells while sparing non-cancer cells. The divergence in properties between malignant and non-cancer cells establishes a "therapeutic window," a critical consideration for achieving desirable treatment outcomes. Central to this is the imperative of a cancer drug's "selectivity and specificity." Taxanes, a pivotal class of successful anti-cancer drugs, continue to serve as the linchpin of cancer treatment due to their efficacy across a spectrum of cancer types. Operating as broad-spectrum chemotherapeutic agents, taxanes exert cytotoxic effects on proliferative cancer cells by binding to and stabilizing microtubules, disrupting mitosis, inducing mitotic catastrophe, and resulting in cell death. The distinct proliferative nature of cancer cells, as opposed to less proliferative non-cancer cells, affords taxanes a measure of specificity and selectivity. Nevertheless, sporadic yet recurring evidence suggests that taxanes also operate through non-mitotic mechanisms. Taxanes' binding and stabilization of microtubules lead to micronucleation and subsequent cell death, impacting both mitotic and non-mitotic cells. Recent discoveries indicate that the flexible and weakened nuclear envelope of malignant cells renders them sensitive to taxane-mediated micronucleation and cell death during various phases of the cell cycle. Conversely, non-cancerous cells typically exhibit a more robust and sturdy nuclear envelope, rendering them more tolerant to taxane-induced nuclear envelope fragmentation and subsequent micronucleation and cell death. The expression levels of nuclear envelope structural proteins, particularly Lamin A/C, emerge as indicators of taxane sensitivity. This evolving understanding underscores that nuclear envelope malleability, in conjunction with a high proliferation rate, is a pivotal determinant of taxane specificity and selectivity against malignant cells. These insights necessitate reconsidering oncological strategies to augment taxane efficacy, overcome resistance, and mitigate side effects.

This paper provides a thorough review of the shifting landscape of economic analysis, spotlighting recent trends and predicting future paths. While traditional economic models remain key for interpreting economic activity, they are being supplemented by fresh methods and cross-disciplinary viewpoints. The increased attention to inequality studies, using advanced statistical techniques and unique data sources, underscores the growing emphasis on fairness and distribution within economic analysis. The incorporation of behavioral elements into economic models also expands our comprehension of economic decision-making and market results. Notably, the emergence of computational economics-integrating artificial intelligence (AI), big data, and machine learning into economic scrutiny-represents a major development. Often referred to as ’smart economics,’ this field employs technology to formulate, address complex economic dilemmas, and perceive economic activity in unconventional ways. Yet, the application of AI and machine learning in economics introduces new hurdles around data privacy, algorithmic bias, and the transparency of model outcomes. The impact of the digital revolution on economic analysis is significant, as the advent of computational economics and the surge of big data are transforming research techniques and policy implications. Concurrently, the advent of the circular economy indicates a radical shift in our perspective on economic sustainability, carrying considerable implications for environmental policy and business tactics.  In the future, it’s anticipated that these trends will further modify the realm of economic analysis, with AI and machine learning integration, emphasis on sustainability and fairness, and the influence of big data becoming more pronounced. As these changes take place, it’s imperative for researchers, policymakers, and practitioners to remain adaptable and flexible, prepared to capitalize on the opportunities and tackle the challenges these trends present.

Approximately 28 million individuals in the United States face the risk of developing precancerous colonic adenomas (polyps) and potentially progressing to colorectal cancer (CRC). While a promising strategy for CRC prevention involves pharmacological intervention, such as cancer chemoprevention or interception, currently, there are no FDA-approved drugs capable of preventing the formation or progression of adenomas to adenocarcinoma. Numerous clinical, epidemiological, and preclinical studies have offered compelling evidence supporting the efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs) in CRC chemoprevention. However, the prolonged use of NSAIDs is not FDA-approved due to potential life-threatening toxicities resulting from cyclooxygenase (COX) inhibition and the depletion of physiological prostaglandins. Despite indications that the COX inhibitory activity of NSAIDs may not be essential for their antineoplastic effects, the absence of a well-defined target impeded the development of derivatives that do not inhibit COX. Earlier research suggests that the inhibition of cyclic guanosine monophosphate phosphodiesterase (cGMP PDE) may be responsible, at least in part, for the antineoplastic activity of the NSAID sulindac. This could potentially offer a novel target for CRC chemoprevention. To identify the cGMP PDE isozyme(s) contributing to the antineoplastic activity of sulindac, we synthesized a chemically diverse library of over 1500 compounds, all sharing the indene scaffold of sulindac. Subsequently, we screened these compounds for their impact on cancer cell growth and PDE inhibitory activity. From this screening, a series of lead compounds emerged. These compounds lacked COX-1 and COX-2 inhibitory activity, surpassing sulindac in potency to inhibit CRC cell growth. Importantly, they demonstrated greater selectivity by not affecting normal cell growth. Through chemical optimization, we identified several development candidates that selectively inhibit PDE5 and/or PDE10. These compounds activate cGMP/PKG signaling, suppressing Wnt/β-catenin transcription. This action counters the growth advantages resulting from APC or CTNNB1 mutations, which are responsible for most human CRCs. This review delves into the scientific literature supporting PDE5 and/or PDE10 as potential targets for CRC chemoprevention or interception. Our findings suggest a promising avenue for developing drugs that may effectively intervene in the progression of colorectal cancer, offering hope for improved preventive strategies in the future.