Vascular endothelial growth factor (VEGF) plays a significant role as a pro-angiogenic and pro-permeability factor within the kidney. Bevacizumab is a pharmaceutical monoclonal anti-VEGF antibody that inhibits the growth of new blood vessels, which blocks blood supply and thereby restricts tumor growth. Thus, we conducted a nationwide study to explore the risk of chronic kidney disease (CKD) development in Taiwan residents after bevacizumab therapy. We drew data from the extensive National Health Insurance Research Database (NHIRD), which encompasses data from >99% of Taiwan’s population from 1995 onwards. Individuals who received bevacizumab between 2012–2018 were identified as the bevacizumab cohort, with the index date set at the first usage. We randomly selected dates within the study period for the control group to serve as index dates. We excluded patients with a history of CKD prior to the index date or those <20 years old. In both cohorts, patients’ propensity scores matched in a 1:1 ratio based on sex, age, index year, income, urbanization level, comorbidities, and medications. We found patients treated with bevacizumab had a significantly higher risk of contracting CKD than patients without bevacizumab (adjusted hazard ratio = 1.35, 95% confidence interval = 1.35–1.73). The risk of CKD was 1.35-fold higher in participants with bevacizumab treatment than those in the control group. These findings suggest that close monitoring of CKD development after bevacizumab administration is needed.

To explore whether the p17 protein of oncolytic avian reovirus (ARV) mediates cell migration and invadopodia formation, we applied several molecular biological approaches for studying the involved cellular factors and signal pathways. We found that ARV p17 activates the p53/phosphatase and tensin homolog (PTEN) pathway to suppress the focal adhesion kinase (FAK)/Src signaling and downstream signal molecules, thus inhibiting cell migration and the formation of invadopodia in murine melanoma cancer cell line (B16-F10). Importantly, p17-induced formation of invadopodia could be reversed in cells transfected with the mutant PTEN_C124A. p17 protein was found to significantly reduce the expression levels of tyrosine kinase substrate 5 (TKs5), Rab40b, non-catalytic region of tyrosine kinase adaptor protein 1 (NCK1), and matrix metalloproteinases (MMP9), suggesting that TKs5 and Rab40b were transcriptionally downregulated by p17. Furthermore, we found that p17 suppresses the formation of the TKs5/NCK1 complex. Coexpression of TKs5 and Rab40b in B16-F10 cancer cells reversed p17-modulated suppression of the formation of invadopodia. This work provides new insights into p17-modulated suppression of invadopodia formation by activating the p53/PTEN pathway, suppressing the FAK/Src pathway, and inhibiting the formation of the TKs5/NCK1 complex.

RNA interference (RNAi) is a biological process in which RNA molecules are involved in sequence-specific suppression of gene expression, via small RNA triggers derived from double-stranded RNA that can target specific genes; it is a natural process that plays a role in both the regulation of protein synthesis and in immunity. Discovery of RNAi by Fire and Mello in 1998 had a profound impact on unraveling novel aspects of eukaryotic biology. RNA interference (RNAi) has proven to be an immensely useful tool for studying gene function and validation of potential drug targets in almost all organisms. A great advance in parasitic protozoa was achieved by the experimental demonstration of RNAi in Trypanosoma brucei, and in other protists such as Leishmania braziliensis, Entamoeba histolytica and Giardia lamblia/intestinalis. These organisms exhibit numerous differences beyond the core 'dicer' and 'slicer' activities, thereby expanding knowledge of the evolutionary diversification of this pathway in eukaryotes. When present, RNAi has led to new technologies for engineering powerful and facile knockdowns in gene expression, revolutionizing biomedical research and opening clinical potentialities. In this review, we discuss the distribution of RNAi pathways, their biological roles, and experimental applications in protozoan parasites.

Anisakis pegreffii (Nematoda: Anisakidae) is a marine parasitic nematode responsible for anisakiasis, a zoonotic disease acquired through the consumption of raw or undercooked fish. With the rising popularity of dishes such as sushi and sashimi, the risk of infection has grown, prompting the need for effective food-safety measures. This study investigates the nematocidal effects of commercial wasabi substitute paste (WSP) and its bioactive compound, allyl isothiocyanate (AITC), on third-stage larvae (L3) of A. pegreffii , and explores their associated stress-response mechanisms. WSP at 1 g/mL and 2 g/mL significantly reduced larval viability, with hazard rates of 3.1% and 3.8% per minute and mean lethal times of 45 and 30 minutes, respectively ( p < 0.0001). AITC, tested at a 10-fold dilution, exhibited stronger activity, inducing 50% mortality in 16 minutes with a hazard rate of 13.45%/min. Expression analyses revealed that WSP robustly upregulated HSP70 mRNA and protein in a time-dependent manner, whereas AITC caused only a modest increase in HSP70 mRNA without a significant protein-level rise over the same exposure window. Conversely, HSP90 expression showed early, transient upregulation followed by suppression or downregulation, suggesting differential regulation of heat shock pathways under chemical stress. These findings demonstrate that WSP and AITC exert potent, rapid nematocidal effects on A. pegreffii larvae and elicit distinctive molecular stress responses. The data support the potential of wasabi-derived compounds as safe, natural agents for reducing anisakiasis risk in raw seafood consumption.

Background/Objectives: Low-density lipoprotein cholesterol (LDL-C) remains central to atherosclerotic cardiovascular disease prevention, but in obesity it may not fully reflect atherogenic particle burden because cholesterol content per particle can vary. We examined whether central adiposity is more consistently associated with apolipoprotein B (ApoB)-related atherogenic phenotypes than with elevated LDL-C in Taiwanese adults. Methods: Cross-sectional analyses used data from the nationally representative Taiwan Survey on Hypertension, Hyperglycemia, and Hyperlipidemia. Waist circumference (WC) analyses included 6771 adults (3162 men and 3609 women), and 6061 of these participants (2975 men and 3086 women) had available body mass index (BMI) data for BMI-based analyses. Survey-weighted, sex-specific multivariable logistic regression was performed. High LDL-C and high ApoB were defined as ≥130 mg/dL, and dysapolipoproteinemia as an ApoB/ApoA-I ratio ≥ 75th percentile. Results: Increasing BMI and WC were associated with higher triglycerides, ApoB, and ApoB/ApoA-I ratios, whereas LDL-C gradients were less consistent. Among women, WC ≥ 90 cm was associated with high ApoB (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.4–3.7) and dysapolipoproteinemia (OR, 1.6; 95% CI, 1.2–2.2), but not with high LDL-C. Among men, WC 90–100 cm and ≥100 cm were associated with dysapolipoproteinemia (OR, 1.6; 95% CI, 1.3–1.9; and OR, 2.0; 95% CI, 1.4–2.8, respectively), whereas associations with high LDL-C were not significant. Conclusions: In this cross-sectional dataset, central adiposity showed a pattern of more consistent associations with ApoB-related phenotypes than with high LDL-C, particularly for the ApoB/ApoA-I ratio; however, no formal statistical test directly compared effect sizes across lipid outcomes, and higher WC was not significantly associated with high ApoB in men. These findings are descriptive and hypothesis-generating and require confirmation in contemporary prospective cohorts before clinical implementation.