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Toxoplasmosis is one of the most common zoonotic diseases in the world. Felines excrete Toxoplasma gondii oocysts, which play a key role in the transmission of this protozoon. Pathological diagnoses were performed on four carcasses of captive tigers collected from 2019 to 2021 in China, and T. gondii was surveyed using serology, molecular analysis, and aetiology. Striated muscle samples of the tigers (n = 4) were bioassayed in mice. DNA derived from T. gondii tachyzoites was isolated and characterized using PCR–RFLP. The pathological diagnoses revealed that ageing, declined immune function, liver, and kidney failures caused the deaths in the tigers examined. A modified agglutination test (cut–off: 1:25) revealed that IgG antibodies to T. gondii were 100% (4/4) in the captive tigers. Two viable T. gondii strains (TgTigerCHn3 and TgTigerCHn4) were isolated from tiger striated muscles and seeded on the Vero cell culture for further propagation. The genotypes of TgTigerCHn3 and TgTigerCHn4 were ToxoDB#20 and ToxoDB#2, respectively. The two strains were avirulent for Swiss mice, which matched the ROP18 and ROP5 gene alleles of TgtigerCHn3 (3/4) and TgtigerCHn4 (3/3). Few brain tissue cysts (0–213) were observed in the mice after inoculation with TgTigerCHn3 and TgTigerCHn4. This is the first documented isolation of T. gondii ToxoDB#20 and ToxoDB#2 from tigers. The results provide additional direct evidence of tiger as intermediate hosts for T. gondii. Tigers in the zoos may potentially transmit T. gondii to other animals and humans. [Display omitted] • Two viable T. gondii strains were isolated from two tigers. • The higher T. gondii detection rate was striated muscle digestive fluid by PCR. [ABSTRACT FROM AUTHOR]

Abstract Marsupials are highly susceptible to Toxoplasma gondii infection. Here, we report T. gondii infection in four kangaroos from a zoo in China. Kangaroos were imported into China in 2000 and were since bred in zoo. In 2017–2018, four kangaroos died due to respiratory system disease or injury. The bodies were submitted to the laboratory to test for T. gondii infection. Antibodies to T. gondii were found in 75% (3/4) of the kangaroos via the modified agglutination test with the cut-off 1:25. Cysts were observed in the histopathological sections of tongue and diaphragm or squashes of fresh myocardium in two kangaroos. These cysts were confirmed as T. gondii by immunohistochemical staining and molecular biological analysis. One viable T. gondii strain was isolated from one kangaroo and designated as TgRooCHn1. DNA from T. gondii tachyzoites obtained from cell culture was characterized by 10 PCR-RFLP markers and the virulence genes ROP5 and ROP18. The genotype of this isolate did not match with any known genotypes; it was designated as ToxoDB#292. The virulence of TgRooCHn1 (104 tachyzoites) was non-lethal to mice, and it formed tissue cysts. To our knowledge, the present study is the first isolation of ToxoDB#292 strain from kangaroo. Improvemets for captive settings were initiated, including greater attention being paied to birds and stray cats, fed frozen meat for carnivores. Graphical abstract Image 1 Highlights • T. gondii infection in kangaroo was confirmed by serological and molecular analysis, histopathology, and bioassay in mice. • One viable T. gondii strain (ToxoDB#292) was isolated from one kangaroo. • The virulence of TgRooCHn1 in mice was low and it formed tissue cysts. [ABSTRACT FROM AUTHOR]

T-2 toxin, a type A trichothecene, is a secondary metabolite produced by Fusarium poae , Fusarium sporotrichioides , and Fusarium tricinctum. As the most toxic trichothecenes, T-2 toxin causes severe damage to multiple organs, especially to liver. However, the contamination of T-2 toxin covers a wide range of plants, including nuts, grains, fruits and herbs globally. And due to chemical stability of T-2 toxin, it is difficult to be completely removed from the food and feeds, which poses a great threat to human and animal health. Liver is the major detoxifying organ which also makes it the main target of T-2 toxin. After being absorbed by intestine, the first pass effect will reduce the level of T-2 toxin in blood indicating that liver is the main metabolic site of T-2 toxin in vivo. In this review, updated researches on the hepatotoxicity of T-2 toxin were summarized. The metabolic characteristic of T-2 toxin in vivo was introduced. The main hepatotoxic mechanisms of T-2 toxin are oxidative stress, mitochondrial damage, deoxyribonucleic acid (DNA) methylation, autophagy and apoptosis. The remission of the hepatotoxicity induced by T-2 toxin was also studied in this review followed by new findings on the detoxification of hepatotoxicity induced by T-2 toxin. The review aimed to offer a comprehensive view and proposes new perspectives in the field of hepatotoxicity induced by T-2 toxin. Liver, as the major detoxifying and metabolism organ, is the main target of T-2 toxin toxicity. The hepatotoxicity induced by T-2 toxin can cause histological alterations in cell structure, the loss of live function, energy metabolism disorder and bile acids metabolism disorder that involve the activation of oxidative stress, mitochondrial damage, abnormal DNA methylation, autophagy and apoptosis. The detoxifications of T-2 toxin induced hepatotoxicity are physical absorption, biological detoxification, nutrition intervention and multi-component detoxifying agents. [Display omitted] • T-2 toxin accumulates in liver and causes hepatotoxicity. • CYPs play an important role in metabolizing T-2 toxin into its derivatives. • T-2 toxin causes the disorder of liver energy metabolism and bile acids metabolism. • T-2 cause hepatic mitochondrial damage, DNA methylation, apoptosis, autophagy, etc. • Physical, microbial and nutrition intervention reduce hepatotoxicity of T-2 toxin. [ABSTRACT FROM AUTHOR]

The deployment of sophisticated and costly large-capacity wind turbines continues to rise. It is urgent for precise real-time simulation to accurately identify and address potential problems. However, the existing solutions, which joint various simulation platforms, suffer from the disadvantages of complex architecture and high cost. This paper proposes a CPU-FPGA heterogeneous computing-based real-time simulation platform for detailed wind turbine model (DWTM). DWTM encompasses the turbine model (covering the inflow wind, aerodynamic, and mechanical dynamic), the electrical model (covering the electromagnetic transient), and the control system. The real-time operating system is introduced to guarantee the real-time performance of the turbine model and control system in the CPU. FPGA is used to perform real-time electrical model calculation. Furthermore, a general FPGA solver for electromagnetic transients is designed. It can accommodate various circuit topologies without the need for recompiling the FPGA code. Finally, the real-time simulation performance and accuracy are verified. The coupled dynamics between the turbine and electrical models are investigated under multiple power grid and wind conditions. • The CPU-FPGA heterogeneous computing platform for the real-time simulation of detailed wind turbine model is developed. • A general FPGA solver is designed and developed for various circuit topologies. • The coupling phenomena between power grid faults and mechanical component vibrations are analyzed comprehensively under multiple power grid conditions and wind conditions. [ABSTRACT FROM AUTHOR]

Deoxynivalenol (DON) is the most common mycotoxin contaminant in food and feed. DON accumulation in food chain severely threatens human and animal health due to the toxic effects on the reproduction system. However, the underlying mechanism of DON on male reproductive dysfunction is still in debate and there is little information about whether DON triggers testicular ferroptosis. In this study, male C57BL/6 mice were divided into 4 groups and treated by oral gavage with 0, 0.5, 1.0, 2.0 mg/kg BW DON for 28 days. Firstly, we proved that male reproduction dysfunction was induced by DON through assessing testicular histopathology, serum testosterone level as well as blood-testis barrier integrity. Then, we verified ferroptosis occurred in DON-induced testicular dysfunction model through disrupting iron homeostasis, increasing lipid peroxidation and inhibiting system Xc−/Gpx4 axis. Notably, the present data showed DON reduced antioxidant capacity via blocking Nrf2 pathway to lead to the further weakness of ferroptosis resistance. Altogether, these results indicated that DON caused mice testicular ferroptosis associated with inhibiting Nrf2/System Xc-/GPx4 axis, which provided that maintaining testicular iron homeostasis and activating Nrf2 pathway may be a potential target for alleviating testicular toxicity of DON in the future. DON is the most frequently detected trichothecene mycotoxin in cereal commodities. DON exposure disrupted testicular morphology, inhibited serum testosterone content and induced blood-testis barrier disorder. DON exposure destroyed the iron ion imbalance homeostasis and increased of lipid peroxidation and inhibition of cysteine/glutamate antiporter, all of which were involved in the process of ferroptsis. Moreover, Nrf2 signaling pathway was blocked after DON treatment. This study provides new insights showing that DON induced testicular injury by regulating the Nrf2/System Xc−/GPX4 axis to trigger ferroptosis. [Display omitted] [ABSTRACT FROM AUTHOR]

Toxoplasmosis is one of the most common foodborne diseases in the world. The objective of this study was to determine Toxoplasma gondii infection in lambs from Henan province, China. A total of 166 lamb hearts were collected from 2017 to 2019. T. gondii infection was determined by the Modified Agglutination Test (MAT) using heart juice of lambs. 11 isolates (TgSheepCHn3 - TgSheepCHn13) were obtained from samples with MAT titers ≥1:100. The rate of T. gondii isolation increased with antibody titer against T. gondii (P < 0.05). No isolate was obtained from samples with titer 1:25 and 1:50, suggesting the cut-off titer for MAT is better set at 1:100. With cut-off value of 1:100, IgG antibodies to T. gondii were found in 25.3% (42/166) of the lambs by MAT. T. gondii parasite was not found in IHC and HE-stained tissue sections of lamb hearts (0/166). Sixty-seven heart tissues with ≥1:25 MAT titers were subjected to acid pepsin digestion and detected T. gondii by PCR. Only 7.5% (5/67) of DNA amplified products were found in heart tissues by the primer TOX5/TOX8. Brain tissue cysts were observed in all mice infected with the 11 isolates at day 60 post infection, suggesting these isolates are non-lethal to mice. PCR-RFLP analysis revealed that 7 isolates belonged to ToxoDB#2, 4 isolates belonged to ToxoDB#4. This is the first isolation of ToxoDB#2 and ToxoDB#4 from lambs in China. Interestingly, none of these isolates belongs to the ToxoDB#9 that is common in China. Our results suggest that the genetic diversity and population structure of T. gondii from China maybe more abundant and magical than previous speculation. • A total of 25.3% (42/166) lambs showed sera conversion of T. gondii antibodies (cut-off titer for MAT: 1:100). • 11 viable T. gondii isolates were obtained from lambs, ToxoDB genotype #2 and #4 were identified. • The rate of isolation T. gondii increased with antibody titer against T. gondii in lamb (P < 0.05). [ABSTRACT FROM AUTHOR]