A case of acute yellow atrophy of the liver R. N. Stiehrn a. A. J. Hockett (The Journ. Of the Am. M. As. 1930.94, no. 25).

R. H. Stiehrn a. A. J. Hockett (The Journ. Of the Am. M. As. 1930.94, no. 25). reporting on the observed case of acute yellow atrophy of the liver, they dwell on the etiology of the disease, symptoms, age and gender of patients. The term acute liver necrosis is considered the most appropriate to the essence of the disease.

Aflatoxicosis in dogs

Aflatoxins are toxic, naturally occurring bisfuranocoumarin compounds produced by certain strains of the moulds Aspergillus flavus, A. parasiticus and A. nomius. Aflatoxin metabolites cause hepatotoxicity by reacting with macromolecules (including DNA and proteins) to cause fatty liver or liver necrosis. Most cases involve dog food or, less commonly, ingestion of mouldy bread. Periodic outbreaks are reported in dogs, most recently at the end of 2020 to early 2021 in the US. Multiple dogs may be involved in incidents and the dogs usually present with gastrointestinal signs, lethargy, melaena and jaundice. Diagnosis is based on a history of possible ingestion and laboratory confirmation of aflatoxin(s) in suspect material. In the liver the typical histological changes are centrilobular necrosis of the liver and bile duct proliferation. Treatment of aflatoxicosis in dogs in supportive, with management of liver failure. Prognosis depends on the severity of liver damage, but mortality rates in dogs with aflatoxicosis are high.

Selenoproteins Protect Against Avian Liver Necrosis by Metabolizing Peroxides and Regulating Receptor Interacting Serine Threonine Kinase 1/Receptor Interacting Serine Threonine Kinase 3/Mixed Lineage Kinase Domain-Like and Mitogen-Activated Protein Kinase Signaling

Liver necroptosis of chicks is induced by selenium (Se)/vitamin E (VE) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms of liver necrosis, a pool of the corn–soy basal diet (10 μg Se/kg; no VE added), a basal diet plus all-rac-α-tocopheryl acetate (50 mg/kg), Se (sodium selenite at 0.3 mg/kg), or both of these nutrients were provided to day-old broiler chicks (n = 40/group) for 6 weeks. High incidences of liver necrosis (30%) of chicks were induced by –SE–VE, starting at day 16. The Se concentration in liver and glutathione peroxidase (GPX) activity were decreased (P < 0.05) by dietary Se deficiency. Meanwhile, Se deficiency elevated malondialdehyde content and decreased superoxide dismutase (SOD) activity in the liver at weeks 2 and 4. Chicks fed with the two Se-deficient diets showed lower (P < 0.05) hepatic mRNA expression of Gpx1, Gpx3, Gpx4, Selenof, Selenoh, Selenok, Selenom, Selenon, Selenoo, Selenop, Selenot, Selenou, Selenow, and Dio1 than those fed with the two Se-supplemented diets. Dietary Se deficiency had elevated (P < 0.05) the expression of SELENOP, but decreased the downregulation (P < 0.05) of GPX1, GPX4, SELENON, and SELENOW in the liver of chicks at two time points. Meanwhile, dietary Se deficiency upregulated (P < 0.05) the abundance of hepatic proteins of p38 mitogen-activated protein kinase, phospho-p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, phospho-c-Jun N-terminal kinase, extracellular signal-regulated kinase, phospho-mitogen-activated protein kinase, receptor-interacting serine-threonine kinase 1 (RIPK1), receptor-interacting serine-threonine kinase 3 (RIPK3), and mixed lineage kinase domain-like (MLKL) at two time points. In conclusion, our data confirmed the differential regulation of dietary Se deficiency on several key selenoproteins, the RIPK1/RIPK3/MLKL, and mitogen-activated protein kinase signaling pathway in chicks and identified new molecular clues for understanding the etiology of nutritional liver necrosis.

The Effect of Different Doses of Mesobuthus eupeus (Scorpionida: Buthidae) Scorpion Venom on the Production of Liver Necrosis in Nmri Mice

Background: Scorpion venom has a variety of different components considerably. Some of these compounds are pro-teins such as Phospholipase A2 which is one of the most important. Use of scorpion venom for the treatment of any disease requires an initial study to determine the therapeutic dose or safe dose. Therefore, due to the necessity of study-ing scorpion venom, it is of special importance to study the effects of its dose response in animal tissues. Methods: To determine the inflammatory effects of scorpion’s venom (Mesobuthus eupeus), 50 Nmri mice with an average weight of 24±7g were selected for investigation in two experiments. In first-round 25 of them were divided into 5 groups and were exposed to different doses of venom injection paralleling the control group. Single-injection of vari-ous doses on 25 mice was performed and results were compared. Results: There was a significant differences between the test and control groups (in most groups). Liver necrosis was one of the important symptoms in this study, the severity of which was measured and statistically analyzed. Conclusion: It was determined that 0.05ppm is a safe dose and sub-lethal doses can use for the investigation of thera-peutic effects of venom on cancer, diabetes, dermatitis, and so on.

Steroid-mediated liver steatosis is CD1d-dependent while steroid-induced liver necrosis, inflammation, and metabolic changes are CD1d-independent: A dichotomy between steatosis and steatohepatitis

Glucocorticoids have been implicated in the pathogenesis of all stages of non-alcoholic fatty liver disease (NAFLD). Natural killer T cells play a role in the pathogenesis of NAFLD and in the response to steroids. The aim of the present study was to determine the role of CD1d in steroid-mediated metabolic derangement and the steroid-protective effect of glycosphingolipids. Methods: Ten groups of mice were studied. Steroids were orally administered to C57BL/6 mice to assess the therapeutic effect of β-glucsylceramide (GC) on the development of steroid-mediated liver damage and metabolic derangements. The role of CD1d in the pathogenesis of steroid-induced liver damage, and in mediating the hepatoprotective effect of GC were studied in CD1d−/− mice. Results: A model of oral administration of steroids was established, resulting in insulin resistance, hyperinsulinemia, hypertriglyceridemia, liver steatosis, and hepatocellular injury. Steroid administration to CD1d−/− mice was associated with hyperglycemia and hypertriglyceridemia. However, CD1d−/− mice were relatively resistant to steroid-induced steatosis. GC treatment alleviated steroid-associated metabolic derangements and liver injury independent of CD1d expression. Conclusion: A steroid-mediated model of NAFLD and metabolic derangements was established in which steroid-mediated steatosis was CD1d-dependent while steroid-induced liver necrosis, inflammation, and metabolic changes were CD1d-independent, further supporting a dichotomy between steatosis and steatohepatitis in NAFLD.

Results of chemoembolization in hepatocellular cancer and metastatic liver damage

Treatment of patients with hepatocellular cancer remains a complex problem in modern oncology. The purpose was to evaluate the effectiveness of chemoembolization in hepatocellular cancer and metastatic liver disease. Results: During and after the procedure, the risk of complications was minimal: in 2 cases (0.25%), liver necrosis and death from cardiovascular insufficiency were recorded after five therapy courses. Eleven patients (23.9%) with a continued tumor growth showed a negative response and were administered symptomatic treatment. Conclusion: In primary hepatocellular cancer and metastatic liver lesions, chemoembolization is one of the priorities in interventional radiology and a stage of complex treatment. This method is low-traumatic due to a minimal toxic effect of the chemotherapy drug. This method is indicated for inoperable liver tumors because a high concentration of an anticancer drug is delivered right to the focus and ensures a prolonged tumor exposure, with minimal risk of complications during and after the procedure. In our observations, complications in the form of necrosis and death occurred in 2 (0.25%) cases.

Loss of BOK Has a Minor Impact on Acetaminophen Overdose-Induced Liver Damage in Mice

Acetaminophen (APAP) is one of the most commonly used analgesic and anti-pyretic drugs, and APAP intoxication is one of the main reasons for liver transplantation following liver failure in the Western world. While APAP poisoning ultimately leads to liver necrosis, various programmed cell death modalities have been implicated, including ER stress-triggered apoptosis. The BCL-2 family member BOK (BCL-2-related ovarian killer) has been described to modulate the unfolded protein response and to promote chemical-induced liver injury. We therefore investigated the impact of the loss of BOK following APAP overdosing in mice. Surprisingly, we observed sex-dependent differences in the activation of the unfolded protein response (UPR) in both wildtype (WT) and Bok-/- mice, with increased activation of JNK in females compared with males. Loss of BOK led to a decrease in JNK activation and a reduced percentage of centrilobular necrosis in both sexes after APAP treatment; however, this protection was more pronounced in Bok-/- females. Nevertheless, serum ALT and AST levels of Bok-/- and WT mice were comparable, indicating that there was no major difference in the overall outcome of liver injury. We conclude that after APAP overdosing, loss of BOK affects initiating signaling steps linked to ER stress, but has a more minor impact on the outcome of liver necrosis. Furthermore, we observed sex-dependent differences that might be worthwhile to investigate.

HISTOPATOLOGI HATI IKAN PATIN YANG DIBERI PAKAN MENGANDUNG TEPUNG KUNYIT

This research was conducted from February to May 2019. The purpose of this study was to determine the network structure of striped catfish fed with turmeric flour before and after being tested with Aeromonas hydrophila. Sampling of histopathological preparations was carried out 2 times, namely at the beginning of maintenance, 30 days of maintenance and 14 days after the challenge test. The observed organ was the liver. The results of histological observations of catfish liver for 30 days of maintenance and fed with turmeric flour were still good. The structure of liver tissue after being challenged in treatment P1, P2 and P3 suffered damage such as hypertrophy, vacuole degeneration and necrosis. The best dose of adding turmeric flour to feed is 0.7 g / kg (P2) with the least damage.Key words: Striped fish, histopathology, liver, necrosis, turmeric flour

Identification of early liver toxicity gene biomarkers using comparative supervised machine learning

Screening agrochemicals and pharmaceuticals for potential liver toxicity is required for regulatory approval and is an expensive and time-consuming process. The identification and utilization of early exposure gene signatures and robust predictive models in regulatory toxicity testing has the potential to reduce time and costs substantially. In this study, comparative supervised machine learning approaches were applied to the rat liver TG-GATEs dataset to develop feature selection and predictive testing. We identified ten gene biomarkers using three different feature selection methods that predicted liver necrosis with high specificity and selectivity in an independent validation dataset from the Microarray Quality Control (MAQC)-II study. Nine of the ten genes that were selected with the supervised methods are involved in metabolism and detoxification (Car3, Crat, Cyp39a1, Dcd, Lbp, Scly, Slc23a1, and Tkfc) and transcriptional regulation (Ablim3). Several of these genes are also implicated in liver carcinogenesis, including Crat, Car3 and Slc23a1. Our biomarker gene signature provides high statistical accuracy and a manageable number of genes to study as indicators to potentially accelerate toxicity testing based on their ability to induce liver necrosis and, eventually, liver cancer.