Protein S-nitrosylation (SNO), emerging as an important posttranslational modification, involves covalent addition of nitric oxide (NO) to the sulfur atom of cysteine in proteins. Accumulated evidence suggests that protein SNO plays crucial roles in pathophysiological mechanisms in cancer, which is attracting great attention. However, there are still controversies about whether S-nitrosylated proteins act as oncogenic proteins or tumor suppressors in cancer. In this review, we provide an overview of the early and latest evidence regarding the underlying mechanism and dual roles of SNO in cancer, in an effort to clarify its contribution in tumor progression. It has been well established that S-nitrosylated proteins restrain tumor progression in several types of cancer, while they have exhibited activities in promoting cell proliferation and inhibiting apoptosis in some other kinds of cancer. Interestingly, emerging evidence also has highlighted both its anti-cancer and pro-tumorigenic roles in several other cancer diseases. Finally, current limitations and future research prospects are presented. The overview of targeting SNO in cancer will provide new opportunities for drug development through in-depth exploration of SNO-mediated signaling pathways.

This paper analyses a model of private value auctions with symmetric risk-neutral bidders, where bidders' private values of an indivisible good are fuzzy. The auction is studied as a game with incomplete information. Fuzzy random variables, their quantile functions, and expressions for expectations through quantile functions are used. An explicit expression for the solution is found. Also, expected bidders' payments are studied.

Income and population growth are key determinants of housing demand, while land use regulations are designed to affect housing supply. Previous studies of housing price determinants focus either on specific regulations in particular cities/regions, or on selective subsets of major cities and regulations. This study examines the impact of land use regulations on housing prices from 1989 to 2006 in an unusually large sample of 250 major US cities. Aside from factors that are commonly associated with housing demand (income, population growth and density), housing prices are found to be associated with local cost-increasing land use regulations (approval delays) and with statewide regulations. Since statewide regulations factor prominently into the results, specific examples of the impact of different types of land use regulations are provided for 5 cities in the state of Washington. The estimated increase in housing prices associated with regulations is, on average (over 250 cities), substantially larger than the effects of income and population growth. While the estimated dollar costs associated with regulations may be sizable at times, the results are remarkably consistent with previous studies that were based on smaller cross sections.

In the past, investing in housing has served as an engine of growth for many economies as it is widely recognized that poor housing conditions can have significant negative impacts on human health, education, and economic opportunities. To assess the housing-related quality of life, indicators such as housing quality, housing environment, and cost burdens can be applied. However, recent studies indicate that materials used for construction are critical. Permanent materials, as opposed to temporary materials, typically offer a range of benefits in terms of durability, low maintenance, improved energy efficiency, increased property value, and better safety. The ultimate aim is to identify the key drivers of housing conditions in Cambodia, with a particular focus on materials and water quality, and the legal status of housing. To find the empirical relationship between economic, socio-economic, and demographic variables on the one hand, and variables measuring housing and living conditions in Cambodia on the other, the analysis employs Ordinary Least Squares and Methods-of-Moments regression modeling. Results indicate that high employment rates and entrepreneurship increase home ownership, and improve the quality of drinking water available. Furthermore, in addition to employment and entrepreneurship, the higher-performing construction materials can also be empirically explained by a bigger labor force and variables capturing the wider macroeconomic environment.

Tripartite motif-containing (TRIM) proteins consist of over 80 proteins, the majority of which exhibit E3 ubiquitin ligase activity. E3 ligases have a critical role in various cellular processes by specifically recognizing and ubiquitinating substrate proteins to promote their proteasomal degradation or alter their activities. Numerous studies have indicated that TRIMs are involved in carcinogenesis through various mechanisms. However, the regulatory mechanisms delimitating TRIMs’ function as E3 ligases has not yet been specifically addressed in a previous review article. In this review, we focus on recent advancements in understanding how certain TRIMs function solely as E3 ligases during cancer cell proliferation, apoptosis, and metastasis. We comprehensively summarize the target proteins of TRIMs involved in disordered signaling pathways such as Wnt/β-catenin, PI3K/AKT, NF-κB, p53, ERK, and STAT3, as well as those regulating the cell cycle and glycolysis. Following ubiquitination modification by TRIM E3 ligases, these target proteins either undergo proteasome-mediating degradation, maintain steady levels, or get activated/inactivated. This review provides a foundation for the development of E3 ligase-based cancer treatments.

 In the past, researchers investigated the immune response acting against mycobacterial antigens in tuberculosis (TB). Several ELISA tests have been conducted for the diagnosis of tuberculosis. Other researchers manipulated 16 kDa antigen from Mycobacterium Tuberculosis to develop a tuberculosis diagnostic test while some others studied the subspecies of M. tuberculosis. In the present study, we explored the possibilities of detecting 16 kDa protein derived from M. tuberculosis, on an interdigitated electrode (IDE). Measurements with Electrochemical impedance spectroscopy and current-volt systems were demonstrated using antibody as the probe.  Further, the involvement of gold nanoparticle for the signal-enhancement and high-performance are evidenced. The specificity in the serum containing samples is used to show the clinical relevancy. 16 kDa antigen used in this experiment is highly reliable for TB diagnosis as it largely expresses and can be implemented in other sensing system.

Breast cancer, as a malignant tumor with easy metastasis and poor prognosis, threatens the health of women around the world. Increasing studies have shown that the Bcl-2 family of apoptosis-related proteins is often expressed abnormally in breast cancer. The Bcl-2 homology 3 (BH3) mimetic peptide can bind and neutralize Bcl-2, preventing its binding to the apoptosis "effector" proteins Bak and Bax, thereby promoting the apoptosis process. However, there is a lack of effective intracellular delivery system for BH3 to exert its biological activity. Therefore, this study utilized an activatable supercharged polypeptide (ASCP) tumor-targeted delivery platform based on pH and protease response to achieve the targeted release of BH3 at the tumor site. Ultimately, intracellular delivery of BH3 was achieved and induced apoptosis of breast tumor cells, preventing the development of breast cancer.

Metadherin (MTDH), also known as LYRIC or AEG-1, is an oncogene that enhances tumor progression, metastasis, drug resistance, and immune escape in various cancers by modulating multiple oncogenic pathways, including NF-κB, PI3K/AKT, Wnt/β-catenin, MAPK, and AMPK. Due to the unknown of the complete structure of MTDH, the deep mechanisms of MTDH and selective inhibitors targeting MTDH remain to be explored. The Protein-Protein interaction (PPI) with the Staphylococcal nuclease domain containing 1 (SND1) is a crucial mechanism underlying the function of MTDH. Current studies have demonstrated that inhibitors, including antisense oligonucleotides, peptides, and small molecules targeting MTDH or MTDH-SND1 interactions, provide novel strategies to inhibit the oncogenetic effects of MTDH. This review summarizes and discusses the structure, function, and regulation of MTDH in cancers, providing the potential therapeutic perspectives of MTDH or MTDH-SND1 PPI for drug discovery.

Objective: The DSS was utilized to construct colitis model of mouse. The colitis mice were colonized with gut microbiota. The effects of gut microbial metabolites on colitis were studied. The mechanisms of gut microbial metabolites to improve intestinal immunity were also further explored. Methods: The male BALB/c mice were selected to construct colitis mouse model with DSS and colonized with gut microbiota. The content of short-chain fatty acids in intestinal metabolites of mice during modeling were detected with GC-MS. After the mice were sacrificed, the colon tissue was stained to observe the colitis in different groups of mice. The contents of IL-22 and IL-17 in colon tissue was determined with ELISA method. To study the mechanism of relieving colitis, qRT-PCR and western blotting were used to study the horizontal of Ffar2 gene and pSTAT3 and pAKT in colon tissue, respectively. The congenital lymphocytes were isolated and purified, and the migration ability of the congenital lymphocytes was examined by cell scratch plane migration test. Results: The colonization of the gut microbiota had significant effects on the contents of short-chain fatty acids in the intestinal metabolites of colitis mice, of which the effect on the content of acetic acid and butyric acid was more significant. The colonization of gut microbiota could effectively relieve colitis in mice and effectively promote the secretion of IL-22 in colon tissue. Studying the remission mechanism indicated that colonization of gut microbiota with colitis could effectively promote the expression of Ffar2 gene in colon tissue and increase the expression of pSTAT3 and pAKT protein. The migration ability of the lymphocyte was significantly upregulated in the model group compared with the other groups, demonstrating that DSS can effectively activate the lymphocyte; The migration of congenital lymphocyte in the experimental group was significantly alleviated than that in the model group, but it was up-regulated than that in the positive control group, and the colonic tissue of the positive control group was similar to that of the normal group. Conclusion: The short-chain fatty acids in the intestinal flora metabolites can promote the gene expression of the metabolite-sensitive receptor Ffar2. The effective combination of short-chain fatty acids and Ffar2 receptors can promote the phosphorylation of STAT3 and AKT proteins, effectively promote the secretion of IL-22 in intestinal ILC3 cells, alleviate colitis in mice, and thereby improve their intestinal immune function.

Although docetaxel treatment yields a high survival rate for prostate cancer (PCa), resistance eventually develops in many patients. Understanding the underlying mechanisms of docetaxel resistance is essential for improving treatment strategies. Cytokines, which play a role in cell signaling and immune responses, have been implicated in drug resistance mechanisms. The study revealed that interleukin-8 (IL-8) was consistently overexpressed in both docetaxel-resistant PCa cell lines. Thus, the expression levels of cytokines released from docetaxel-sensitive (PC-3- and DU-145) and resistant (PC-3/R-DU-145/R) PCa cells were compared. IL-8 was found to be commonly expressed in resistant cell lines. This finding led to the hypothesis that IL-8 could play a key role in mediating PCa cell resistance to docetaxel. IL-8 siRNA treatment increased docetaxel sensitivity in both resistant cells. To demonstrate the mechanism of IL-8-related resistance, MDR1 expression was evaluated. After IL-8 siRNA treatment MDR1 expression was reduced in both resistant cells suggesting that IL-8 regulates the docetaxel resistance of PCa cells via modulation of multidrug resistance 1 (MDR1). By expanding the knowledge of the cytokines and their effect mechanisms, novel approaches can be developed for the treatment of docetaxel-resistant prostate cancer. Further investigations into the role of IL-8 in docetaxel resistance could offer valuable insights into the development of effective treatment strategies for PCa patients.

Foreign direct investment (FDI) is widely viewed as a key driving force behind China’s exceptional growth performance in the last four decades. This paper investigates several questions posed by China’s success in capturing gains from FDI. What explains that success? Can other countries replicate it, or is it unique to China? What lessons are from China for other countries? China indeed has advantages in attracting FDI such as huge market and cheap labor, the well-designed policy and strategy, however, seem to play more important role in the successful story. Our empirical estimates support on four hypotheses: FDI and GDP growth in China positively interact each other; FDI is helpful to China’s technological progress, FDI promotes China’s industrial development, and FDI stimulates China’s manufactured exports.

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.

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.

The UK fully legalised open market share repurchases in 1981, and to our knowledge no study has investigated the business cycle’s influence on repurchase decision-making. We address this aspect and investigate the period 1985-2014. This is relevant as the business cycle factors impact the firm-specific variables such as cash flow, profitability, dividends and capital structure, and these factors traditionally influence repurchase decisions. This forms the paper’s theoretical intuition, and the empirical objectives test the business cycle’s influence on the decision to undertake a repurchase, and also its influence on repurchases values. The results find that the business cycle influences both the decision of undertaking repurchases and repurchases’ values, and this influence has aggregately remained positively associated with economic prosperity. Thus, the frequency of repurchase announcements by British firms is more probable during prosperous economic circumstances. The results also reveal that the repurchase-business cycle relationship witnessed a structural break in 1996:Q2, and the real difference following this break is the increase in the business cycle’s influence on the decision regarding repurchase values. The paper thus contributes to existing literature by directly testing the UK’s repurchase-business cycle relationship, and providing detailed empirical evidences that business cycle conditions strongly impact the repurchase decision-making.

Liquidity and its associated issues are one of dominant strands in the market microstructure. In this study, microblogging-based behavioral perspective on economic unrest is linked to the market liquidity. The concept of liquidity is examined in terms of price dispersion relative to the quantity traded. The analysis contains the quantification of multiple linear regression, Gaussian distribution technique, and vector error correction methodology. In the economic stability period, the investor’s mood, either in positive manner or pessimistic context, had an influential role on the price impact volume-based liquidity. Meantime, the probability was higher for occurrence of price impact volume-based liquidity in response to the sentiment indicators. In the economic unrest environments, the positive bias investor’s mood was not vigorous enough to influence the dispersion of asset’s prices and trading quantity. Most importantly, the negative bias investor’s emotion was linked to increase the dispersion of asset’s prices relative to the quantity traded. Investors with a lower amount of trading quantity had declined the liquidity in the market. Additionally, there was a higher probability for occurrence of illiquidity in the pessimistic market periods. However, changes in past sentiment series were not associated with changes in pervious liquidity series, either in short run or long run. The findings may be potentially applicable to manage the behavioral perspective of liquidity risk.

The purpose of this research is to investigate how globalization affects innovation in Vietnam’s small and medium sized enterprises (SMEs). Utilizing Probit model and the data from Vietnam’s SMEs Survey during the period 2005-2015, the research examines the micro and macro effects of globalization on the innovation of these businesses. The main results show that at macro level, globalization is negatively correlated with innovation. However, at micro level, increasing competition pressure and knowledge transfer due to globalization are positively correlated with innovation of Vietnam’s SMEs.

We assess the impact of the Strategic Economic Plan on Singapore’s long-term GDP per capita. To our knowledge, we are the first to evaluate the effect of the 1991 plan on Singapore’s successful growth trajectory using methodologies aimed at causal identification. In other words, this article applies the Synthetic Control method and World Bank data from 1970 to 2018. We estimate an average increase of 6,641.71 US$ in Singapore’s GDP per capita. Results remain robust to placebo and leave-one-out tests and the Synthetic Difference-in-Differences method.

This paper investigates the impacts of COVID-19 on women’s employment and gender disparity with a longitudinal dataset spanning the pandemic. We exploit the regional intensities of social vulnerability and temporal variation to implement the difference-in-differences (DID) estimation. The results indicate that the pandemic and its associated lockdowns generate a significant and negative impact on women’s employment but not on men’s employment. Moreover, a counterfactual analysis using pre-pandemic data further supports the causal nature of the documented relationships. The evidence suggests that economic downturns caused by public health emergencies, unlike previous economic recessions, have a greater impact on women, and differentiated policies should be designed.

This study simultaneously tests Wagner’s law on one hand and Keynes proposition on the other hand related both government spending and output in Ivory Coast that experiencing long run economic growth and widened deficit. That challenges the country’s fiscal sustainability. With annual data from 1980 to 2020, results show that Wagner’s law holds, the elasticity of government spending to output is greater than one. There is bidirectional causality between government size and output validating Keynesian idea that public expenditure is an exogenous factor and a policy instrument for increasing national income. Wagner law and public deficit can justify Ivorian over-indebtedness.

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.