Chemotherapy is a well-established method for treating cancer, but it has limited effectiveness due to its high dosage and harmful side effects. To address this issue, researchers have explored the use of photothermal agent nanoparticles as carriers for precise drug release in vivo. In this study, three different sizes of polydopamine nanoparticles (PDA-1, PDA-2, and PDA-3) were synthesized and evaluated. PDA-2 was selected for its optimal size, encapsulation rate, and drug loading rate. The release of the drug from PDA-2@TAX was tested at different pH and NIR laser irradiation levels. The results showed that PDA-2@TAX released more readily in an acidic environment and exhibited a high photothermal conversion efficiency when exposed to an 808 nm laser. In vitro experiments on ovarian cancer cells demonstrated that PDA-2@TAX effectively inhibited cell proliferation, highlighting its potential for synergistic chemotherapy-photothermal treatment.

Environmental protection, which is beneficial for the present and the future, has become a global consensus, and environmental information disclosure (EID) is an effective way to realize and fulfill enterprise environmental responsibility. Although some scholars have studied the impact of EID on firms, there is less empirical evidence on the impact of EID on investors. In this study, we examine the impact of EID on enterprise investment value based on signaling theory using a time-varying difference-in-differences model and extract two channels of this effect. The study shows that the implementation of EID helps to enhance the value of enterprise investment. This enhancement will vary according to the location, the industry pollution type, and the nature of the enterprise: EID has a remarkable enhancement effect on the investment value of the eastern region, heavily polluted enterprises, and non-state-owned enterprises. To investigate the channel of EID\'s effect on enterprise investment value, we use the moderating effect model to analyze and find that enterprises with low tax ratios and small financing constraints can significantly enhance the effect of EID on investment value.

As a primary source of added sugars in the US diet, sugar-sweetened beverage (SSB) consumption is presumed to contribute to obesity prevalence and poor oral health. We systematically synthesized and quantified evidence from US-based natural experiments concerning the impact of SSB taxes on beverage prices, sales, purchases, and consumption.
A keyword and reference search was performed in PubMed, Web of Science, Cochrane Library, Scopus, and EconLit from the inception of an electronic bibliographic database to Oct 31, 2022. Meta-analysis was conducted to estimate the pooled effect of soda taxes on SSB consumption, prices, passthrough rate, and purchases.
Twenty-six natural experiments, all adopting a difference-in-differences approach, were included. Studies assessed soda taxes in Berkeley, Oakland, and San Francisco in California, Philadelphia in Pennsylvania, Boulder in Colorado, Seattle in Washington, and Cook County in Illinois. Tax rates ranged from 1 to 2 ¢/oz. The imposition of the soda tax was associated with a 1.06 ¢/oz. (95% confidence interval [CI] = 0.90, 1.22) increase in SSB prices and a 27.3% (95% CI = 19.3, 35.4%) decrease in SSB purchases. The soda tax passthrough rate was 79.7% (95% CI = 65.8, 93.6%). A 1 ¢/oz. increase in soda tax rate was associated with increased prices of SSBs by 0.84 ¢/oz (95% CI = 0.33, 1.35).
Soda taxes could be effective policy leverage to nudge people toward purchasing and consuming fewer SSBs. Future research should examine evidence-based classifications of SSBs, targeted use of revenues generated by taxes to reduce health and income disparities, and the feasibility of redesigning the soda tax to improve efficiency.

Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that causes adult T-cell leukemia/lymphoma (ATL). HTLV-1 encodes Tax protein that activates transcription from viral long terminal repeats (LTR). Multiple cofactors are involved in the regulation of HTLV-1 transcription via association with Tax. Yes-associated protein (YAP), which is the key effector of Hippo pathway, is elevated and activated in ATL cells. In this study, we reported that YAP protein suppressed Tax activation of HTLV-1 5\' LTR but not 3\' LTR. The activation of the 5\' LTR by Tax was potentiated when YAP was depleted. Moreover, overexpression of YAP repressed HTLV-1 plus-strand viral gene expression and virion production, whereas compromising YAP by RNA inference augmented the expression of HTLV-1 protein. As mechanisms of YAP-mediated viral transcription inhibition, we found that YAP interacted with Tax, and prevented the association between Tax and p300. It finally led to the inhibition of recruitment of Tax to the Tax-responsive element in the 5\' LTR of HTLV-1. Taken together, our results demonstrate the negative regulatory function of YAP in Tax activation of HTLV-1 transcription. It may achieve sufficient transcriptional repression to maintain persistent infection and long-term latency of HTLV-1 in the host cells.

Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus; whereas HTLV-1 mainly persists in the infected host cell as a provirus, it also causes a malignancy called adult T-cell leukemia/lymphoma (ATLL) in about 5% of infection. HTLV-1 replication is in most cases silent in vivo and viral de novo infection rarely occurs; HTLV-1 rather relies on clonal proliferation of infected T cells for viral propagation as it multiplies the number of the provirus copies. It is mechanistically elusive how leukemic clones emerge during the course of HTLV-1 infection in vivo and eventually cause the onset of ATLL. This review summarizes our current understanding of HTLV-1 persistence and oncogenesis, with the incorporation of recent cutting-edge discoveries obtained by high-throughput sequencing.

Taraxasterol (TAX), one of the active components in Dandelion, demonstrated strong antitumor properties in several cancers. However, the effect and underlying mechanism of TAX in non-small cell lung cancer (NSCLC) is unclear. In this study, we showed that TAX inhibited the proliferation of cells by inducing S-phase cell cycle arrest and prevented cell migration by interfering epithelial-mesenchymal transition (EMT) in Lewis lung cancer (LLC) cells and lung carcinoma SPC-A1 cells. The pharmacological network analysis predicted that induction of apoptosis might be the potential mechanism of TAX-mediated cell deaths. Further in vitro experiments showed that TAX could significantly induce cancer cell apoptosis as verified by increased pro-apoptotic molecules including Bax, caspase-9, and PARP1 downregulated anti-apoptotic protein Bcl-2; and decreased mitochondrial potential. The LLC subcutaneous tumor model demonstrated that TAX inhibited tumor growth by induction of apoptosis and inhibition of proliferation in vivo, which is consistent with the in vitro data. Importantly, TAX administration downregulated the proportion of Treg cells and upregulated CD107a+ NK cells in the tumor microenvironment in the tumor model. Together, these data reveal that TAX performs its antitumor effect by inducing apoptosis and modulating the tumor microenvironment, providing evidence that TAX could serve as a potential natural drug for lung cancer therapy.

UNASSIGNED: Contrary to most developed economies, Hong Kong has reduced and eliminated taxes on beer and wine over the last 15 years and observed increasing alcohol consumption.
UNASSIGNED: We applied econometric epidemiological modelling to assess the impact of reverting ad valorem taxation to pre-2008 levels (20% on wine and 40% on beer) on consumption and health outcomes. We used 15 years of industry sales and pricing data (2004-2018) to derive 25 own-price and cross-price elasticity estimates. We applied risk functions from the World Health Organization 2018 Global Status Report to assess the impact on 25 alcohol-attributable conditions.
UNASSIGNED: An estimated 616 deaths (91.3% in men) were attributable to alcohol in 2018. Raising taxes to pre-2008 levels is estimated to reduce consumption of pure alcohol consumption by 8.0%, 15.9%, and 31.1%; and reduce alcohol-attributable deaths by 11.6%, 21.8%, and 40.2% assuming 25%, 50% and 100% pass through rates of taxes to consumers. The largest projected decreases in alcohol-attributable mortality in absolute numbers are alcohol abuse, alcohol dependence, and alcoholic psychoses (wholly alcohol-attributable disorders). The largest absolute number of new alcohol-attributable cases in 2018 were hypertension, alcohol dependence and alcohol abuse; which are estimated to be reduced by 31.3%, 34.2%, and 34.3% respectively by raising taxes to pre-2008 levels. The alcohol-attributable health burden and absolute reductions in health harms are far greater in men.
UNASSIGNED: Reversing the 2008 alcohol tax reductions is potentially effective in averting the alcohol-attributable health burden and thus mitigate against the avoidable harms of alcohol-related disease.
UNASSIGNED: Health and Medical Research Fund, Food and Health Bureau of the Hong Kong SAR, China [03170067].

Chimeric antigen receptor (CAR) T cells have been successfully used in the therapy of B cell leukemia and lymphoma, but still have many challenges in their use for treating T cell malignancies, such as the lack of unique tumor antigens, their limitation of T cell expansion, and the need for third party donors or genome editing. Therefore, we need to find novel targets for CAR T cell therapy to overcome these challenges. Here, we found that both adult T-cell leukemia/lymphoma (ATLL) patients and ATLL cells had increased CCR8 expression but did not express CD7. Moreover, targeting CCR8 in T cells did not impair T cell expansion in vitro. Importantly, anti-CCR8 CAR T cells exhibited antitumor effects on ATLL- and other CCR8-expressing T-ALL cells in vitro and in vivo, and prolonged the survival of ATLL and Jurkat tumor-bearing mouse models. In conclusion, these collective results show that anti-CCR8 CAR T cells possess strong antitumor activity and represent a promising therapeutic approach for ATLL and CCR8+ tumors.

Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy caused by human T-cell leukemia virus type 1 (HTLV-1) infection. HTLV-1 exerts its oncogenic functions by interacting with signaling pathways involved in cell proliferation and transformation. Dysregulation of the Hippo/YAP pathway is associated with multiple cancers, including virus-induced malignancies. In the present study, we observe that expression of YAP, which is the key effector of Hippo signaling, is elevated in ATL cells by the action of the HTLV-1 Tax protein. YAP transcriptional activity is remarkably enhanced in HTLV-1-infected cells and ATL patients. In addition, Tax activates the YAP protein via a mechanism involving the NF-κB/p65 pathway. As a mechanism for this cross talk between the Hippo and NF-κB pathways, we found that p65 abrogates the interaction between YAP and LATS1, leading to suppression of YAP phosphorylation, inhibition of ubiquitination-dependent degradation of YAP, and YAP nuclear accumulation. Finally, knockdown of YAP suppresses the proliferation of ATL cells in vitro and tumor formation in ATL-engrafted mice. Taken together, our results suggest that p65-induced YAP activation is essential for ATL pathogenesis and implicate YAP as a potential therapeutic target for ATL treatment.

The control and prevention of public health emergencies can face severe challenges, especially financial and material challenges during the coronavirus disease 2019 (COVID-19). Enabling and ensuring smooth financial and material flows across levels, within the country, and across countries are essentially important to preparedness for global health emergencies, which cannot easily be achieved without being facilitated by preferential tax policies. China\'s preferential tax policy practice developed at early stages of the COVID-19 pandemic could be useful experiences which can be adapted to unique contexts of other countries, so different stakeholders including citizens could be effectively motivated and involved in the fight against the COVID-19 pandemic. However, we should see that these policies are temporary and issued as an afterthought. There is still much to learn about how epidemic responders and policy-makers can make the most of each other\'s expertise to fit into the wider information architecture of epidemic response.