Praziquantel (PZQ) is a drug commonly used to treat some parasitic infections in animals. This study aimed to apply a reliable and simple method to identify important biological metabolites relevant to PZQ in crucian carp (Carassius auratus) to decipher the metabolic pathways and provide a basis for developing new anti-parasite drugs. The experimental group of crucian carp was administered oral PZQ at a dose of 10 mg kg-1 via a stomach feed tube. All biological blood samples were analysed using liquid chromatography electrospray ionization/quadrupole time-of-flight mass spectrometry (LC ESI/Q-TOF MS). MetPA analysis was used to identify relevant pathways for PZQ in crucian carp. Thirty-five potential metabolic pathways were revealed by MetPA network software. Furthermore, the chemical structures of the related metabolites and pathways were identified by comparison with data obtained from free online databases. Forty-four significantly differentially abundant endogenous metabolites were found in the PZQ-treated crucian carp. The changes in metabolomic profiles and pathways induced by PZQ played a role in inhibiting pathogenesis.Studies have indicated that formaldehyde and low temperature are considered to be the factors associated with several respiratory diseases. However, the effect of co-exposure to formaldehyde and low temperature on allergic asthma, and the potential mechanisms, are unknown. In this study, an allergic asthma mouse model was built and mice were exposed to 0.8 mg/m3 formaldehyde and/or subjected to low temperatures of 16 °C. The data showed that exposure to either low temperature or formaldehyde did not induce a significant aggravation on allergic asthma. However, simultaneous exposure to formaldehyde and low temperature was shown to aggravate mucus hypersecretion and inflammation in the lung, lead to an exacerbation of allergic asthma. After blocking the TRPM8 and TRPA1 ion channels, the levels of inflammatory factors reduced. These results demonstrated that co-exposure to formaldehyde and low temperature exacerbate allergic asthma, and that TRPM8 and TRPA1 are involved in this process.The abundance of cellular fibronectin (c-Fn) for ischemic stroke patients and the narrow time-window ( less then 4.5 h) for the decision to administer the thrombolytic treatment with recombinant tissue plasminogen activator (rtPA) are challenging for the development of a point-of-care (PoC) diagnostic platform. We report a case of stratification of ischemic stroke patients based on a magnetoresistive biosensor platform that quantifies the c-Fn levels in a small volume of serum, within the clinically relevant time-window. Our PoC platform uses different ratios of biofunctionalized magnetic nanoparticles (MNPs) as immunoassay labels to adjust the sensitivity within the clinically relevant ranges for c-Fn (1-4 μg/mL). After optimizing the detection range, resolution, and sensitivity, our device was able to stratify ischemic stroke patients who developed hemorrhagic transformation, the main side-effect of rtPA, from those (both non-treated and treated with rtPA) who did not.CpG oligodeoxynucleotides (CpGs) can induce an anti-tumor immune response, but also uniquely cause direct lymphoma cytotoxicity. To improve the delivery and efficacy of CpGs, we utilized a tri-ethylene modified CpG conjugated gold nanoparticle (tmCpG NP) platform that is compatible with both class B and class C CpGs, to treat various types of lymphoma, including diffuse large B cell lymphoma, high-grade lymphoma, Burkitt’s lymphoma, and mantle cell lymphoma. Both classes of tmCpG NPs reduced viability of human and murine lymphoma cells via apoptosis compared with free CpGs, while having no toxic effects on dendritic cells. TmCpG NPs increased CD19, CD20, and OX40 expression on the lymphoma cells. Overall, we introduced a stable tmCpG NP design that has significant anti-lymphoma effects.A number of publications have reported that cysteamine has significant therapeutic effects on several aspects of Parkinson’s disease (PD)-related pathology but none of these studies have evaluated its impact on pathological forms of α-Synuclein (α-Syn), one of the main hallmarks of PD. We therefore tested the efficacy of cysteamine on the Thy1-α-Syn mouse model which over-expresses full-length human wild-type α-Syn. Two-month (early stage disease) and 6-month old (late stage disease) mice and littermate controls were treated daily with cysteamine (20 mg/kg, i.p.) to assess the protective and restorative properties of this compound. After 6 weeks of treatment, animals were tested using a battery of motor tests. Cysteamine-treated transgenic mice displayed significant improvements in motor performance as compared to saline-treated transgenic littermates. Post-mortem readouts revealed a reduction in fibrillation, phosphorylation and total levels of overexpresed human α-Syn. To determine if such outcomes extended to human cells, the benefits of cysteamine were additionally tested using 6-hydroxydopamine (6-OHDA) treated neurons differentiated from induced pluripotent stem cells (iPSCs) derived from a PD patient harbouring a triplication of the SNCA gene. SNCA neurons treated with cysteamine exhibited significantly more intact/healthy neurites than cells treated with 6-OHDA alone. Additionally, SNCA neurons treated with cysteamine in the absence of 6-OHDA showed a trend towards lower total α-Syn levels. Elenestinib research buy Overall, our in vivo and in vitro findings suggest that cysteamine can act as a disease-modifying molecule by enhancing -the survival of dopaminergic neurons and reducing pathological forms of α-Syn.Lysosomal Storage Diseases (LSD) are genetic diseases causing systemic and nervous system dysfunction. The glia-derived lipid binding protein Apolipoprotein D (ApoD) is required for lysosomal functional integrity in glial and neuronal cells, ensuring cell survival upon oxidative stress or injury. Here we test whether ApoD counteracts the pathogenic consequences of a LSD, Niemann Pick-type-A disease (NPA), where mutations in the acid sphingomyelinase gene result in sphingomyelin accumulation, lysosomal permeabilization and early-onset neurodegeneration. We performed a multivariable analysis of behavioral, cellular and molecular outputs in 12 and 24 week-old male and female NPA model mice, combined with ApoD loss-of-function mutation. Lack of ApoD in NPA mice accelerates cerebellar-dependent motor deficits, enhancing loss of Purkinje neurons. We studied ApoD expression in brain sections from a NPA patient and age-matched control, and the functional consequences of ApoD supplementation in primary human fibroblasts from two independent NPA patients and two control subjects.