The microbiota is present in many parts of the human body and plays essential roles. The most typical case is the occurrence and development of cancer. Pancreatic cancer (PC), one of the most aggressive and lethal types of cancer, has recently attracted the attention of researchers. Recent research has revealed that the microbiota regulates PC carcinogenesis via an altered immune response. Specifically, the microbiota, in several sites, including the oral cavity, gastrointestinal tract, and pancreatic tissue, along with the numerous small molecules and metabolites it produces, influences cancer progression and treatment by activating oncogenic signaling, enhancing oncogenic metabolic pathways, altering cancer cell proliferation, and triggering chronic inflammation that suppresses tumor immunity. Diagnostics and treatments based on or in combination with the microbiota offer novel insights to improve efficiency compared with existing therapies.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant cancers. It is characterized by stromal richness, lack of blood supply and special metabolic reprogramming in the tumor microenvironment, which is difficult to treat and easy to metastase. Great efforts have been made to develop new drugs which can pass through the stroma and are more effective than traditional chemotherapeutics, such as ferroptosis inducers–Erastin and RSL-3. As current anti-angiogenic therapy drugs alone are suboptimal for PDAC, novel vascular disruption agents in combination with ferroptosis inducers might provide a possible solution. Here, we designed human platelet vesicles (PVs) to camouflage RSL-3 to enhance drug uptake rate by tumor cells and circulation time in vivo, deteriorating the tumor vessels and resulting in tumor embolism to cut the nutrient supply as well as causing cell death due to excessive lipid peroxidation. The RSL-3@PVs can also cause the classic ferroptosis-related change of mitochondrial morphology, with changes in cellular redox levels. Besides that, RSL-3@PVs has been proved to have great biological safety profile in vitro and in vivo. This study demonstrates the promising potential of integrating PVs and RSL-3 as a combination therapy for improving the outcome of PDAC.

Obesity is often regarded as a factor that promotes tumorigenesis, but the role of obesity in promoting hepatocellular carcinoma (HCC) is still controversial. We compared the trend change of 14 obesity-related genes in the formation and development of HCC in normal, adjacent, and HCC tissues. Mendelian randomization (MR) analysis was used to verify the relationship between obesity and HCC occurrence. Metabolism of cobalamin-associated A (MMAA) was discovered as an obesity- and metabolism-differential gene, and its function in HCC was tested in vitro and in vivo. Finally, we explored how obese female patients with an originally high expression of female estrogen receptor (ESR1) directly upregulated MMAA to interfere with the progression of HCC. Fourteen obesity-related genes were downregulated in adjacent and tumoral tissues compared with normal liver tissues, which indicated that obesity may be inversely related to the occurrence of HCC and was consistent with the results of MR analysis. We also discovered that MMAA is a metabolic gene closely related to the occurrence and development of HCC by mining the TCGA database, and it functioned an anti-tumor-promoting role in HCC by damaging the mitochondrial function and preserving the redox balance. We further verified that obese females with a high expression of ESR1 can regulate MMAA to protect HCC from progression. This study elucidates that obesity might be a protective factor for female HCC patients, as they originally highly expressed ESR1, which could upregulate MMAA to suppress tumor growth and participate in metabolic reprogramming.

Adhesive materials have become popular biomaterials in the field of biomedical and tissue engineering. In our previous work, we presented a new material - gelatin o-nitrosobenzaldehyde (gelatin-NB) - which is mainly used for tissue regeneration and has been validated in animal models of corneal injury and inflammatory bowel disease. This is a novel hydrogel formed by modifying biological gelatin with o-nitrosobenzaldehyde (NB). Gelatin-NB was synthesized by activating the carboxyl group of NB-COOH and reacting with gelatin through 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride (EDC) and N-hydroxysuccinimide (NHS). The obtained compound was purified to generate the final product, which can be stably stored for at least 18 months. NB has a strong adhesion to -NH2 on the tissue, which can form many C = N bonds, thus increasing the adhesion of gelatin-NB to the tissue interface. The preparation process comprises steps for the synthesis of the NB-COOH group, modification of the group, synthesis of gelatin-NB, and purification of the compound. The goal is to describe the specific synthesis process of gelatin-NB in detail and to demonstrate the application of gelatin-NB to damage repair. Moreover, the protocol is presented to further strengthen and expand the nature of the material produced by the scientific community for more applicable scenarios.

AIM: This study evaluated the effect of the presence of air bubbles in a drainage tube on its pressure difference and analyzed the relationship between air bubble volume, tube diameter, drainage fluid viscosity, and pressure difference. Accordingly, it provides a theoretical basis for optimizing drainage treatment and preventing obstruction in clinical practice.METHODS: A custom-designed experimental device was used to measure the pressure difference in medical-grade silicone drainage tubes. Tubes with various diameters (3 and 6 mm), air bubble volumes (0, 0.1, 0.2, and 0.3 mL), and drainage fluids (low and high viscosities) were used. The pressure difference between the two ends of each drainage tube was measured using a pressure sensor and calculated. A rotational viscometer was used to measure the viscosity of each drainage fluid. Differences in the pressure difference under different conditions of air bubbles, air bubble volumes, tube diameters, and drainage fluid viscosities were compared.RESULTS: The presence of air bubbles in each drainage tube significantly increased the pressure difference, with the pressure difference being higher compared to that under the bubble-free condition (0.591 ± 0.069 vs. 0.830 ± 0.039 kPa, p < 0.01). In addition, the pressure difference progressively increased with increasing air bubble volume, with the maximum increase occurring at a bubble volume of 0.3 mL (0.951 ± 0.039 kPa). The pressure difference was negatively correlated with the tube diameter, with higher pressure difference observed at smaller diameters, and the differences between the values of the different diameter groups were statistically significant (p < 0.01). The pressure difference was positively correlated with the viscosity of the drainage fluid, with a higher pressure difference observed at a higher viscosity. The enhancing effect of air bubbles on the pressure difference was more pronounced in more viscous fluids (p < 0.0001).CONCLUSIONS: This study showed that the presence of air bubbles in a drainage tube significantly increases the outflow pressure difference, and this effect is enhanced by increasing the bubble volume, decreasing the tube diameter, and increasing the drainage fluid viscosity. These findings reveal that the hydrodynamic factors associated with air bubbles can theoretically contribute to a poor outflow. Therefore, they provide a preliminary in vitro basis for exploring the rational selection of drainage tube diameter, early detection of air bubble-related obstructions, and development of targeted interventions in future clinical practice.