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Plastic pollution is a rapidly worsening environmental problem, especially in oceanic habitats. Environmental pollution with microplastic particles is also causing food consumed by humans to be increasingly polluted, including table salts. Therefore, we present the first study which focuses only on table salt products purchased in Taiwan which we examined for the presence of microplastics. We used Fourier transform infrared spectroscopy to identify the polymer type of each particle. Within 4.4 kg of salt, we detected 43 microplastic particles which averages to 9.77 microplastic particles/kg. The identified polymer types were, in descending abundance, polypropylene, polyethylene, polystyrene, polyester, polyetherimide, polyethylene terephthalate, and polyoxymethylene. We combined our novel results with those of previous studies to provide the first global review of microplastic contamination of table salts. We found that 94% of salt products tested worldwide contained microplastics, with 3 out of 27 polymer types (polyethylene terephthalate, polypropylene, polyethylene) accounting for the majority of all particles. Averaging over seven separate studies, table salts contain a mean of 140.2 microplastic particles/kg. With a mean annual salt consumption of ~3.75 kg/year, humans therefore annually ingest several hundred microplastic particles from salt alone.

Background Post-transplant malignancy is major morbidity complicated in kidney transplantation (KT). In Korea, a few studies have investigated the sex- and age-dependent risk for post-transplant malignancy among KT recipients on a large scale. Methods We utilized a national health insurance database in Korea to investigate the relative risk of post-transplant malignancy in 12,634 KT recipients between 2007 and 2017. The same number of patients with acute appendicitis was included as a control group. The relative risk of malignancy was estimated using a multivariable-adjusted Cox model, and interaction analysis was performed to investigate age- and sex-predominant patterns. Results KT recipients had an overall 1.8-fold higher risk for post-transplant malignancy with an increased risk for 14 of 29 cancer types, among which Kaposi’s sarcoma, non-Hodgkin’s lymphoma, kidney, uterus, and bladder/urinary tract cancers were most prominent. Although the overall risk for post-transplant malignancy was similar between male and female KT recipients, head and neck cancer had a higher risk among male KT recipients, whereas non-Hodgkin’s lymphoma and bladder/urinary tract cancer had a higher risk among female KT recipients. Overall, the young (< 50 years) KT recipients had a higher risk for post-transplant malignancy than older ones (≥ 50 years), whose pattern was most prominent in non-Hodgkin’s lymphoma. In contrast, breast and nonmelanoma skin cancer showed a higher risk among older KT recipients. Conclusion KT recipients had an increased risk for a wide range of cancer types, some of which showed differential risk patterns with age and sex. Our result suggests that focused screening for predominant post-transplant malignancies may be an effective strategy for selected KT recipients.

Research reflects the importance of understanding the motivational variables of ethical consumer behavior. However, existing research has been limited to more narrowly construed factors that show an obvious link with ethics. Currently, empirical work on motivational factors relevant to orientations working across context is scarce. To address this gap, this project investigated ethical consumption from the perspective of person orientation (PO) and thing orientation (TO), both of which presumably motivate individual differences. For this purpose, three main studies were conducted by using correlational and experimental approaches to assess the relationships among PO, TO, and ethical consumer behavior. Across the three studies, the current research provides strong evidence for PO as a key driver of ethical consumption behavior. In contrast, the role of TO was inconsistent. Moderating effects of gender were also somewhat apparent. The findings suggest that individual orientations are important motivational variables for better understanding ethical consumers and that future researchers should further investigate PO/TO in this context.

The anti-cancer effects of metformin, the most widely used drug for type 2 diabetes, alone or in combination with ionizing radiation were studied with MCF-7 human breast cancer cells and FSaII mouse fibrosarcoma cells. Clinically achievable concentrations of metformin caused significant clonogenic death in cancer cells. Importantly, metformin was preferentially cytotoxic to cancer stem cells relative to non-cancer stem cells. Metformin increased the radiosensitivity of cancer cells in vitro and significantly enhanced the radiation-induced growth delay of FSaII tumors (s.c.) in the legs of C3H mice. Both metformin and ionizing radiation activated AMPK leading to inactivation of mTOR and suppression of its downstream effectors such as S6K1 and 4EBP1, a crucial signaling pathway for proliferation and survival of cancer cells, in vitro as well as in the in vivo tumors. Conclusion: Metformin kills and radiosensitizes cancer cells and eradicates radioresistant cancer stem cells by activating AMPK and suppressing mTOR.

The trapping of pathogenic ligands can potentially be used to prevent signal transduction mediated by catabolic factor expression in osteoarthritis (OA). Although vaspin is known to function as a pathogenic ligand and represents a novel adipokine, little is known about its function and the impact of its nebulization-based administration in OA. Here we provide a report on the function of vaspin in articular chondrocytes and OA model mice. RNA sequencing analysis and ingenuity pathway analysis demonstrated that vaspin upregulation in chondrocytes triggers OA development-related signaling. Vaspin is upregulated in the injured cartilage of patients with OA and DMM (Destabilization of the Medial Meniscus) mice, and its overexpression induces catabolic factor expression in vitro under OA-mimicked conditions. Col2a1–vaspin Tg (Transgenic) animals showed extensive cartilage degradation, whereas vaspin −/− (knockout) mice exhibited decreased OA development. Furthermore, in silico and biochemical analyses showed that vaspin activates the p38 and JNK signaling pathways to regulate AP-1-driven catabolic factor production and cartilage breakdown. Finally, we identified and characterized a vaspin-targeting nanobody, vas nanobody, and showed that intraarticularly injected vas nanobody could effectively block the vaspin–AP-1 axis to treat OA in DMM mice. Together, our results suggest that blockade of the vaspin–AP-1 axis could be an effective therapeutic approach for preventing OA development. Vaspin blockade offers new hope for osteoarthritis treatment Osteoarthritis (OA) is a common joint disease that causes pain and stiffness. This study explores the role of a protein called vaspin in OA. Researchers collected cartilage samples from humans and mice to study vaspin’s effects. They found that vaspin levels were higher in damaged cartilage, suggesting it may worsen OA. To test this, they used mice genetically modified to produce more or less vaspin. Mice with more vaspin had worse OA symptoms, while those with less had milder symptoms. The team also developed a small antibody called a nanobody to block vaspin. When injected into mice with OA, this nanobody reduced cartilage damage and pain without causing side effects. The study concludes that targeting vaspin could be a promising new approach for treating OA. Future research may focus on developing nanobody treatments for human use. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Bromodomains are epigenetic readers that modulate gene expression linked to inflammation and cartilage degeneration. Emerging evidence suggests their dysregulation plays a pivotal role in osteoarthritis (OA) pathogenesis, making them promising therapeutic targets. We evaluated the therapeutic efficacy of a novel carboxamide derivative bromodomain inhibitor (NCD) as a potentially safer alternative for preventing OA progression. The inhibitory effects of NCD were assessed through both in vitro and in vivo models. In vitro , mouse primary chondrocytes were stimulated with IL-1β, and the effects of NCD treatment were analyzed using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. In vivo , destabilization of the medial meniscus (DMM) surgery was performed in 12-week-old male C57BL/6 mice, followed by either oral administration or intra-articular (IA) NCD injection. Cartilage integrity was assessed by histology. We analyzed changes in the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways to elucidate the mechanism of NCD. NCD treatment significantly suppressed IL-1β-induced expression of matrix metalloproteinases (Mmp3 and Mmp13) and cyclooxygenase-2 (Cox2) in mouse chondrocytes. In the DMM mouse model, both oral IA administration of NCD alleviated OA-related cartilage destruction. Mechanistically, NCD inhibited IκB degradation and reduced Erk and Jnk phosphorylation, indicating suppression of the NF-κB and MAPK signaling pathways. This study demonstrates that targeting bromodomains with a novel carboxamide-based inhibitor effectively attenuates OA cartilage destruction by suppressing these signaling pathways. These findings support the therapeutic potential of epigenetic modulation in mitigating OA pathogenesis.

Research on neuronal and astroglial markers for predicting outcomes in aquaporin-4 antibody-seropositive neuromyelitis optica spectrum disorders (NMOSD) remains limited. We aimed to evaluate the prognostic value of blood biomarkers for neuronal and astroglial damage in NMOSD compared with multiple sclerosis (MS). Patients with NMOSD and MS were prospectively recruited, and baseline serum levels of neurofilament light (sNfL) and glial fibrillary acidic protein (sGFAP) were measured. The correlations between these biomarkers and neurological disability (Expanded Disability Status Scale, EDSS) and cognitive function (iPad-based processing speed test, PST) were analyzed at baseline and two years later. In this cohort of 41 NMOSD and 92 MS patients, blood biomarkers demonstrated distinct patterns of association with current and future outcomes. In NMOSD, sGFAP was consistently linked to neurological disability and cognitive impairment over time, reflecting astrocytopathy with minimal silent neurodegeneration. In MS, sGFAP did not correlate with baseline EDSS but showed associations with future scores. Notably, sNfL was more strongly associated with future PST scores than baseline scores ( p  = 0.005), suggesting ongoing neurodegeneration. These results underscore that blood biomarkers are predictive of both current and future outcomes in NMOSD and MS, with differing patterns reflecting the unique pathogenesis of each disease.

Osteoarthritis (OA) is an age-related degenerative disease for which an effective disease-modifying therapy is not available. Natural compounds derived from plants have been traditionally used in the clinic to treat OA. Over the years, many studies have explored the treatment of OA using natural extracts. Although various active natural extracts with broad application prospects have been discovered, single compounds are more important for clinical trials than total natural extracts. Moreover, although natural extracts exhibit minimal safety issues, the cytotoxicity and function of all single compounds in a total extract remain unclear. Therefore, understanding single compounds with the ability to inhibit catabolic factor expression is essential for developing therapeutic agents for OA. This review describes effective single compounds recently obtained from natural extracts and the possibility of developing therapeutic agents against OA using these compounds.

Metformin, the most widely prescribed drug for treatment of type 2 diabetes, has been shown to exert significant anticancer effects. Hyperthermia has been known to kill cancer cells and enhance the efficacy of various anti-cancer drugs and radiotherapy. We investigated the combined effects of metformin and hyperthermia against MCF-7 and MDA-MB-231 human breast cancer cell, and MIA PaCa-2 human pancreatic cancer cells. Incubation of breast cancer cells with 0.5-10 mM metformin for 48 h caused significant clonogenic cell death. Culturing breast cancer cells with 30 µM metformin, clinically relevant plasma concentration of metformin, significantly reduced the survival of cancer cells. Importantly, metformin was preferentially cytotoxic to CD44(high)/CD24(low) cells of MCF-7 cells and, CD44(high)/CD24(high) cells of MIA PaCa-2 cells, which are known to be cancer stem cells (CSCs) of MCF-7 cells and MIA PaCa-2 cells, respectively. Heating at 42°C for 1 h was slightly toxic to both cancer cells and CSCs, and it markedly enhanced the efficacy of metformin to kill cancer cells and CSCs. Metformin has been reported to activate AMPK, thereby suppressing mTOR, which plays an important role for protein synthesis, cell cycle progression, and cell survival. For the first time, we show that hyperthermia activates AMPK and inactivates mTOR and its downstream effector S6K. Furthermore, hyperthermia potentiated the effect of metformin to activate AMPK and inactivate mTOR and S6K. Cell proliferation was markedly suppressed by metformin or combination of metformin and hyperthermia, which could be attributed to activation of AMPK leading to inactivation of mTOR. It is conclude that the effects of metformin against cancer cells including CSCs can be markedly enhanced by hyperthermia.

Background and Objectives: To assess whether country-level changes in major cardiometabolic risk factors were associated with concurrent changes in age-standardized death rates (ASDR) from ischaemic heart disease (IHD) and stroke between 2000 and 2015. Materials and Methods: We conducted a multinational ecological analysis using harmonized data from WHO, NCD-RisC, and the World Bank across 157 countries (n = 157). Absolute changes in systolic blood pressure, obesity, diabetes, and total cholesterol were standardized to z-scores. Linear regression models examined change–change associations, adjusting for income group and behavioral factors. Income-stratified and quartile-based analyses were performed. Results: Between 2000 and 2015, IHD and stroke mortality declined, while obesity and diabetes increased. In adjusted models, change in total cholesterol showed the most consistent association with change in IHD ASDR (β = 13.09, 95% CIs = 4.58–21.60, p = 0.003), whereas the other risk factors did not show consistent independent associations. Significant associations were confined to high- and upper middle-income countries, where change in total cholesterol was associated with IHD mortality. Conclusions: Changes in total cholesterol showed the most consistent correspondence with concurrent changes in IHD mortality at the country level, whereas other cardiometabolic risk factors showed less consistent patterns. These patterns were observed mainly in high- and upper–middle-income countries, suggesting heterogeneity by socioeconomic context.