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.

This paper investigates the degree of inflation persistence across regions in Portugal by analyzing the Consumer Price Index (CPI) growth rates for NUTS II regions. The study employs the Augmented Dickey-Fuller (ADF) test to determine whether the CPI data for Portugal is stationary or non-stationary. The results of the ADF test reveal that the IPC data for Portugal is non-stationary, indicating that inflation exhibits persistence in the long run. The study further assesses the persistence of inflation by estimating an autoregressive integrated moving average (ARIMA) model for each region. The Ljung-Box test is used to test for autocorrelation in the time series data, and the Hurst exponent is calculated to evaluate the presence of long-term memory in the time series data. The study finds that there is significant autocorrelation in the time series data for all regions, supporting the presence of persistence in inflation at the regional level in Portugal. The Hurst exponent also shows that the time series data for each region exhibits a high degree of persistence in inflation. Finally, the study applies the ARIMA model to each CPI division's data and uses the Ljung-Box test to test for autocorrelation in the time series data. The results show that some CPI divisions exhibited higher levels of persistence compared to others. For example, the "Housing, water, electricity, gas and other fuels" division exhibited high persistence, while the "Communication" division exhibited low persistence. This study contributes to the existing literature by exploring regional inflation persistence in Portugal and its implications for policymaking. The results provide insights into the inflation persistence patterns across regional levels in Portugal, by emphasizing the need to consider regional differences in inflation dynamics when formulating effective policy interventions. Understanding the persistence of inflation is crucial for policymakers to ensure price stability and sustainable economic growth.

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.

Many of Keynes´s ideas and concepts are proven correct in this paper. The demand side, mainly business investments, drives the economy. Business firms steer the business cycle via profit expectations and animal spirits. Injections to and withdrawals from the circular flow of income are multiplied throughout the economy in accordance with Keynes´s multiplier. A sudden and sharp rise in households´ saving rates has a detrimental effect on aggregate demand, in line with Keynes´s paradox of thrift. Finance, not saving in the S=I sense, is the necessary condition for business investments and economic growth to be realized. Keynes´s finance motive thus makes money endogenous, contradicting the textbook result that exogenous money steers aggregate demand, contradicting the mainstream loanable funds theory and putting into question the Keynesian theory of sticky prices as a condition for real growth. However, a crucial omission in Keynes´s productive writings is the lack of an accelerator tying income to investment. Some of his followers such as Paul Samuelson tried to remedy that by developing multiplier-accelerator models. The problem with them is that the accelerator lacks micro foundations, in specific disregarding business confidence. Linking macro accounting identities with empirical national accounts data for five major economies produces the finding that business firms explain more than all aggregate expenditure growth during a 25-year period. Thus, it is concluded that business confidence is the root of the business cycle. Making the accelerator account for business confidence casts new light on the perhaps most well-known Keynesian “truth”: active fiscal policy as a main force stabilizing the business cycle. With business confidence being the endogenous and ubiquitous variable driving the business cycle, it turns out that any exogenous factor has the possibility to affect it. Policy needs to be viewed as a competing factor to the factor(s) driving the cycle in the other, destabilizing direction. The more powerful those factors are (e.g., a deadly virus), the tougher it gets for policy to “win” the competition, turning business confidence around. This leads up to the paper´s main conclusion: the worse the economy, the stronger is the case for active fiscal policy, but the lesser is the chance for it to succeed.

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.