Fibrous microplastics in the environment: Sources, occurrence, impacts, and mitigation strategies.

Fibrous microplastics (FMPs), a unique class of microplastics, are increasingly recognized as a significant environmental threat due to their ubiquitous presence and potential risks to ecological and human health. This review provides a comprehensive overview of FMPs, including their sources, prevalence in various environmental media, and potential impacts. FMPs, which can be found in over 90 % of certain environmental samples, originate from a diverse range of sources, including synthetic textiles, landfill waste, industrial emissions, and atmospheric deposition. These persistent pollutants pose a threat to both terrestrial and marine ecosystems. Their insidious presence can lead to ingestion by organisms, potentially disrupting ecosystems and posing risks to human health. Addressing the challenge of FMPs requires a multi-faceted approach. Reducing the production and use of synthetic fibers, implementing effective waste management practices, and developing new technologies to remove FMPs from wastewater and the broader environment are all crucial components of the solution. However, further research is essential to fully understand the long-term implications of FMPs on ecosystems and human health, laying the foundation for the development of robust and effective mitigation strategies.

Seaweeds as a major source of dietary microplastics exposure in East Asia.

Microplastics (MPs) occurrence in marine ecosystems is well known, but their accumulation in seaweeds and subsequent human exposure remain understudied. This research quantifies MPs presence in two commonly consumed seaweeds, kelp (Saccharina japonica) and nori (Pyropia yezoensis), in East Asia, revealing widespread contamination dominated by microfibers (<500 µm). Based on dietary patterns, human uptake through seaweed consumption was estimated and quantified. Notably, Chinese people consume an estimated 17,034 MPs/person/year through seaweed consumption, representing 13.1% of their total annual MPs intake. This seaweeds-derived exposure surpasses all other dietary sources, contributing up to 45.5% of overall MPs intake. The highest intake was in South Korea, followed by North Korea, China, and Japan. This research identifies seaweeds as a major, previously overlooked route of dietary MPs exposure. These findings are crucial for comprehensive risk assessments of seaweed consumption and the development of mitigation strategies, particularly for populations in East Asian countries.

Repair mechanism of radiation-induced salivary gland injury by hypoxia-pretreated human urine-derived stem cell exosomes.

OBJECTIVE: To explore the protective effect of human urine-derived stem cell exosomes (hUSC-Exos) on radiation-induced salivary gland (SG) injuries in Sprague Dawley rats. METHODS: Fresh adult urine was collected, and primary hUSCs were isolated and identified. The hUSCs were hypoxia-pretreated with 1% oxygen for 24 h and then transferred to a normoxic culture environment for 24 h. The hUSC-Exos were collected and identified for exosomes. A radiation-induced injury model was established in the rats, and exosomes were introduced by local injection in the SG and tail vein. The submandibular gland was excised for morphological observation 1 week later. Immunohistochemical detection of the glandular tissue was conducted by α-smooth muscle actin (a-SMA), stem cell growth factor receptor (c-Kit) staining, and periodic acid-Schiff staining. Qualitative polymerase chain reaction and western blot analysis were adopted to detect the gene and protein expression of Wnt3a, GSK3ß, and Axin. RESULTS: In both the normoxic and hypoxic hUSC-Exo groups, microvesicular structures with bilayer membranes of approximately 80 nm in diameter were detected, and the expressions of CD9 and CD63 were detected by nanoflow cytometry. Compared with the control group, in the radiation-induced injury model group, the expression of a-SMA was significantly higher, the expression of c-Kit was significantly lower, and the expressions of Wnt3a, GSK3ß, and Axin were significantly upregulated; the differences were statistically significant (p < 0.05). Compared with the model group, in the normoxic and hypoxic hUSC-Exo groups, the expression of a-SMA was significantly decreased, the expression of c-Kit was significantly increased, and the expressions of Wnt3a, GSK3ß, and Axin were significantly upregulated; the differences were statistically significant (p < 0.05). CONCLUSION: Hypoxia-pretreated hUSC-Exos could repair radiation-induced SG injuries by activating the Wnt3a/GSK3ß pathway to suppress the expressions of a-SMA and c-Kit.

Efficacy and Safety of Scarpa Fascia Preservation During Abdominoplasty: A Systematic Review and Meta-analysis.

INTRODUCTION: Scarpa fascia preservation might be a promising approach to reduce seroma and other complications after abdominoplasty. However, the results remained controversial. We conducted a systematic review and meta-analysis to evaluate the efficacy and safety of scarpa fascia preservation in patients with abdominoplasty. METHODS: PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials and clinical controlled trials assessing the effect of scarpa fascia preservation versus control (without scarpa fascia) during abdominoplasty were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcomes were seroma and hematoma/bleeding. Meta-analysis was performed using random-effect model. RESULTS: Four studies involving 630 patients were included in the meta-analysis. Overall, compared with the control group, scarpa fascia preservation was associated with a significant reduced seroma (OR 0.16; 95% CI 0.06-0.43; P = 0.0004), time until drain removal (std. mean difference = -0.92; 95% CI -1.31 to -0.54; P<0.00001;), drain output (std. mean difference = -0.92; 95% CI -1.38 to -0.45; P = 0.0001), and hospital stay (std. mean difference = -0.93; 95% CI -1.48 to -0.39; P = 0.0008), but it failed to alter hematoma/bleeding (OR 0.46; 95% CI 0.09-2.38; P = 0.36), infection (OR 0.38; 95% CI 0.11-1.25; P = 0.11), and suture rupture (OR 0.67; 95% CI 0.12-3.73; P = 0.65) in patients with abdominoplasty. CONCLUSIONS: Scarpa fascia preservation was associated with a significant decreased seroma, time until drain removal, drain output, and hospital stay, but could not change hematoma/bleeding, infection and suture rupture following abdominoplasty. Scarpa fascia preservation should be recommended during abdominoplasty. LEVEL OF EVIDENCE II: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

The Comparison of Etomidate and Propofol Anesthesia in Patients Undergoing Gastrointestinal Endoscopy: A Systematic Review and Meta-Analysis.

INTRODUCTION: Etomidate and propofol played an important role in the sedation of patients undergoing gastrointestinal endoscopy. We conducted a systematic review and meta-analysis to compare their efficacy and safety. MATERIALS AND METHODS: PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases were systematically searched. Randomized controlled trials assessing the effect of etomidate versus propofol for the anesthesia of patients undergoing gastrointestinal endoscopy were included. Two investigators independently searched articles, extracted data, and assessed the quality of included studies. The primary outcomes were anesthesia duration and recovery time. Meta-analysis was performed using random-effect model. RESULTS: Six randomized controlled trials involving 1115 patients were included in the meta-analysis. Overall, compared with propofol, etomidate resulted in comparable anesthesia duration [standard mean difference (Std. MD)=-0.03; 95% confidence interval (CI), -0.16 to 0.10; P=0.66], recovery time (Std. MD=0.25; 95% CI, -0.42 to 0.92; P=0.47), mean arterial pressure at intubation (Std. MD=0.44; 95% CI, -0.26 to 1.15; P=0.21), heart pulse at intubation (Std. MD=0.93; 95% CI, -0.69 to 2.55; P=0.26), SPO2 at intubation (Std. MD=-0.52; 95% CI, -1.04 to 0.01; P=0.05), patient satisfaction [odds risk (OR)=0.42; 95% CI, 0.11-1.66; P=0.22], hypotension (OR=0.14; 95% CI, 0.02-1.22; P=0.07), changes of heart rate (OR=0.97; 95% CI, 0.61-1.53; P=0.88), nausea-vomiting (OR=2.02; 95% CI, 0.73-5.57; P=0.17), and the reduction in apnea or hyoxemia (OR=0.39; 95% CI, 0.24-0.64; P=0.0002), and injection pain (OR=0.03; 95% CI, 0.01-0.08; P<0.00001), but the increase in myoclonus (OR=8.54; 95% CI, 3.14-23.20; P<0.0001). CONCLUSIONS: Between etomidate and propofol, no significant difference was revealed regarding anesthesia duration, recovery time, mean arterial pressure at intubation, heart pulse at intubation, SPO2 at intubation, patient satisfaction, hypotension, changes of heart rate and nausea-vomiting. Compared with propofol, etomidate showed reduced apnea or hyoxemia, and injection pain, but with an increased myoclonus.

Bufalin inhibits pancreatic cancer by inducing cell cycle arrest via the c-Myc/NF-κB pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Bufalin, a cardiotonic steroid isolated from toad venom (bufo gargarizans Cantor or B. melanotictus Schneider), has widely demonstrated antitumor effects and exhibits potential antitumor activity in various human cancer cells lines. AIMS OF THE STUDY: The main characteristic of cancers including pancreatic cancer is the ability of uncontrolled proliferation. The aim of this study is to clarify the underlying mechanism by which bufalin inhibits pancreatic cancer cell proliferation. MATERIALS AND METHODS: The effect of bufalin on the suppression of tumor growth in vivo was studied in a bioluminescent mouse model generated using the pancreatic cancer cell line BxPC3-luc2 and the cytotoxicity was evaluated in BcPc3 and Sw1990 cells with MTT. Flow cytometry and western blotting analyses were utilized to detect the effect of bufalin on the cell cycle and to detect the cell cycle-related proteins, respectively. Then, a luciferase reporter assay was applied to screen the activity of potent transcription factors following bufalin exposure and their expression was detected by western blotting. RESULTS: Bufalin suppressed tumor growth in a bioluminescence mouse model generated using BxPC3-luc2 cells and inhibited cell proliferation in vitro through inducing cell cycle arrest at S phase. Bufalin treatment inhibited cyclin D1 and cyclin E1 expression and therefore increased expression of p27, a regulatory molecular that controls cell cycle transition from S to G2 phase. Furthermore, luciferase reporter screening studies revealed that bufalin inhibited the expression and activity of the transcription factors c-Myc and NF-κB, which might cause cell cycle arrest at S phase and the inhibition of cell proliferation. CONCLUSIONS: Taken together, our results indicate that bufalin can inhibit pancreatic cancer by targeting c-Myc, thus suggesting that the mechanism of c-Myc regulation by bufalin might be worthy of further study regarding its potential as a therapeutic target for pancreatic cancer treatment.

Inhibition of P38 MAPK Downregulates the Expression of IL-1ß to Protect Lung from Acute Injury in Intestinal Ischemia Reperfusion Rats.

Acute lung injury (ALI) induced by intestinal ischemia/reperfusion (II/R) has high incidence and mortality, in which IL-1ß was essential for the full development of ALI. However, the detailed regulating mechanism for this phenomenon remains to be unclear. The purpose of this study was to investigate whether inhibition of P38 MAPK could downregulate the expression of IL-1ß to protect lung from acute injury in II/R rats. Here, we found that the level of pulmonary edema at 16 hours after operation (hpo) was obviously enhanced compared to that in 8hpo and sham groups. Immunofluorescent staining demonstrated that IL-1ß and P38 MAPK were detected in lung tissues. And rats with II/R have the highest translation level for IL-1ß and phosphorylation of P38 MAPK in lung tissues at 16hpo compared with 8hpo and sham groups. Moreover, administration of SB239063, an inhibitor of P38 α and ß, could effectively downregulate the expressions of IL-1ß and protects lung tissues from injury in II/R rats. Our findings indicate that the inhibition of P38 α and ß may downregulate the expression of IL-1ß to protect lung from acute injury in II/R, which could be used as a potential target for reducing ALI induced by II/R in the future clinical trial.