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Antimicrobial resistance (AMR) and environmental degradation represent two of the most pressing and existential threats to global public health. The intersection of microplastic (MP) pollution and AMR is particularly alarming, as the pervasive presence of MPs could significantly hinder efforts to combat AMR. However, the precise effects of MPs on the dissemination and genetic mechanisms underlying AMR in bacterial populations remain inadequately understood.

In this study, we employed the Simonsen end-point conjugation assay to assess the impact of four commonly encountered MPs on the transfer of clinically relevant plasmids. The scope of plasmid transfer, exemplified by the pA/C_MCR-8 plasmid, across diverse bacterial communities was confirmed through cell sorting and 16S rRNA gene amplicon sequencing. Our results demonstrate that exposure to these four ubiquitous MPs significantly enhances the conjugation rates of four clinically significant AMR plasmids, with an up to 200-fold increase in transfer frequency compared to non-exposed controls. Moreover, we observed a clear concentration-dependent relationship, wherein higher MP concentrations were associated with elevated plasmid transfer rates.

Additionally, our findings indicate that MPs stimulate the expression of plasmid-borne conjugative genes as well as genes involved in the SOS response, including recA, lexA, dinB, and dinD. High-throughput sequencing of the broad transmission dynamics of plasmid pA/C_MCR-8 revealed its distribution across two dominant bacterial phyla: Pseudomonadota (50.0%-95.0%) and Bacillota (0.4%-2.0%).

These results definitively establish a connection between two critical global health crises—AMR and environmental degradation via MPs. To effectively address the growing threat of AMR, it is imperative that we not only focus on antimicrobial stewardship but also consider the broader environmental context, including plastic production and waste management.

To address the limitations in color purity of donor-acceptor (D-A) type thermally activated delayed fluorescence (TADF) emitters, Hatakeyama introduced multiresonance (MR) molecules in 2016.

Fig. 3(b) illustrates the Fourier Transform Infrared (FTIR) spectra of BC@TNS, BC, and TNS. For BC, the peak at 1120 cm⁻¹ was attributed to the carbonyl (C=O) stretch of carbonyl groups, while the bands observed at 2916, 1581, and 1456 cm⁻¹ correspond to the stretching vibrations of C-H bonds, C-C/C=C bonds, and -CH₃ groups, respectively [45, 46]. In the case of TNS, the bands at 3400, 1630, 900, and 500 cm⁻¹ were ascribed to the O-H stretching, H-O-H bending, Ti-O stretching in a four-coordinated Ti environment, and the vibrational modes associated with the [TiO₆] octahedral unit, respectively [47, 48]. The FTIR spectrum of BC@TNS displayed the characteristic bands from both TNS (3400, 1630, 900, 500 cm⁻¹) and BC (2927, 1581 cm⁻¹), thereby confirming the successful synthesis of the composite material.

Esophageal Cancer (EC): A Global and Regional Health Challenge

Esophageal cancer (EC) is a prevalent malignancy of the digestive tract, characterized by its high aggressiveness. Globally, EC ranks as the seventh most common cancer in incidence and the sixth leading cause of cancer-related mortality【1,2】. Among its subtypes, esophageal squamous cell carcinoma (ESCC) predominates in Asia, accounting for approximately 70% of cases, with China alone bearing a significant burden. Recent epidemiological data reveal that in China, there were 224,000 new EC cases, ranking it as the seventh most frequently diagnosed cancer. Meanwhile, EC caused 188,000 deaths, placing it as the fifth leading cause of cancer mortality【3】. Notably, more than 90% of cases exhibit the histopathological features of ESCC【4,5】.

Histologically, ESCC originates from the epithelial cells lining the upper two-thirds of the esophagus and shares similarities with head and neck cancers. In contrast, esophageal adenocarcinoma (EAC), arising from glandular cells in the lower third of the esophagus, is typically associated with the metaplastic transformation of Barrett's esophagus and bears histological resemblance to gastric cancer. Key risk factors for both subtypes include various forms of tobacco use, alcohol consumption, hot beverages, and nutritional deficiencies【6】.

Challenges in Detection and Treatment

Early-stage ESCC is primarily treated through surgical intervention, while advanced stages (II and III) often necessitate adjuvant radiotherapy and chemotherapy, which have been shown to improve patient outcomes compared to surgery alone. However, most ESCC cases are diagnosed at advanced stages (III or IV), when therapeutic options are limited and survival rates are dismal【7】.

Currently, robust diagnostic biomarkers for ESCC are lacking. Identifying reliable markers for early detection and integrating them into clinical practice is critical to enabling personalized treatment strategies and advancing therapeutic development. Although innovations such as immunotherapy and neoadjuvant therapy have yielded promising results in the treatment of EC, significant limitations remain. For instance, a subset of patients exhibits resistance to chemoradiotherapy, resulting in suboptimal therapeutic outcomes. Furthermore, these treatments are often accompanied by adverse effects, including nausea, vomiting, and myelosuppression.

Future Directions

The development of novel therapeutic strategies for ESCC remains an urgent and formidable challenge. Enhancing diagnostic precision and tailoring treatment to individual patients are essential goals. Addressing these issues will pave the way for more effective and less toxic interventions, ultimately improving prognosis and quality of life for patients with ESCC.