High Prevalence of Bovine Cardiac Cysticercosis in Upper Egypt: An Epidemiological and Histopathological Study.

Bovine cysticercosis is categorized as a serious parasitic zoonotic infestation. The infection is mainly caused by the tapeworm Taenia saginata, which infects cattle and humans. The larval stage, Cysticercus bovis (C. bovis), is found in the skeletal and cardiac muscles of infected cattle. Despite its potential public health concern, few studies have been conducted on cardiac cysticercosis in Upper Egypt. This study investigates the prevalence, epidemiology, and impact of cardiac cysticercosis in Upper Egypt, emphasizing how histopathological changes in cardiac muscle and physiological parameters might be associated with the infection. From December 2022 to October 2023, a total of 941 animals from Assiut province, Upper Egypt, were slaughtered and their cardiac muscles were examined for the presence of C. bovis. Cysts were classified as viable or degenerated through macroscopic inspection. The overall prevalence of C. bovis infected hearts made up 10.8% of the total examined. The highest prevalence rate was in the summer season followed by spring; winter had the lowest infections. The histopathological examination of infected tissues revealed immune cell infiltration around Cysticercus-infected areas. Additionally, Bax immunostaining demonstrated the apoptotic effect of cysticercosis. Regarding the measured physiological parameters, there were non-significant changes in plasma levels of total protein and albumin in cattle infected with cysticercosis compared with control animals. Moreover, there was a significant decrease in total antioxidant capacity (TAC) combined with a significant increase in lipid peroxide (Malondialdehyde) (MDA), troponin T, and lactate dehydrogenase (LDH) activity in infected animals. The present work documented a set of epidemiological and pathological findings, revealing that C. bovis is a potentially harmful parasite and can cause significant health problems in both cattle and humans.

Gallic acid rescues uranyl acetate induced-hepatic dysfunction in rats by its antioxidant and cytoprotective potentials.

BACKGROUND: The liver was identified as a primary target organ for the chemo-radiological effects of uranyl acetate (UA). Although the anti-oxidant and anti-apoptotic properties of gallic acid (GA) make it a promising phytochemical to resist its hazards, there is no available data in this area of research. METHODS: To address this issue, eighteen rats were randomly and equally divided into three groups. One group was received carboxymethyl cellulose (vehicle of GA) and kept as a control. The UA group was injected intraperitoneally with UA at a single dose of 5 mg/kg body weight. The third group (GA + UA group) was treated with GA orally at a dose of 100 mg/kg body weight for 14 days before UA exposure. UA was injected on the 15th day of the experiment in either the UA group or the GA + UA group. The biochemical, histological, and immunohistochemical findings in the GA + UA group were compared to both control and UA groups. RESULTS: The results showed that UA exposure led to a range of adverse effects. These included elevated plasma levels of aspartate aminotransferase, lactate dehydrogenase, total protein, globulin, glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol, and very-low-density lipoprotein and decreased plasma levels of high-density lipoprotein cholesterol. The exposure also disrupted the redox balance, evident through decreased plasma total antioxidant capacity and hepatic nitric oxide, superoxide dismutase, reduced glutathione, glutathione-S-transferase, glutathione reductase, and glutathione peroxidase and increased hepatic oxidized glutathione and malondialdehyde. Plasma levels of albumin and alanine aminotransferase did not significantly change in all groups. Histopathological analysis revealed damage to liver tissue, characterized by deteriorations in tissue structure, excessive collagen accumulation, and depletion of glycogen. Furthermore, UA exposure up-regulated the immuno-expression of cleaved caspase-3 and down-regulated the immuno-expression of nuclear factor-erythroid-2-related factor 2 in hepatic tissues, indicating an induction of apoptosis and oxidative stress response. However, the pre-treatment with GA proved to be effective in mitigating these negative effects induced by UA exposure, except for the disturbances in the lipid profile. CONCLUSIONS: The study suggests that GA has the potential to act as a protective agent against the adverse effects of UA exposure on the liver. Its ability to restore redox balance and inhibit apoptosis makes it a promising candidate for countering the harmful effects of chemo-radiological agents such as UA.

Risperidone impedes glutamate excitotoxicity in a valproic acid rat model of autism: Role of ADAR2 in AMPA GluA2 RNA editing.

Several reports indicate a plausible role of calcium (Ca2+) permeable AMPA glutamate receptors (with RNA hypo-editing at the GluA2 Q/R site) and the subsequent excitotoxicity-mediated neuronal death in the pathogenesis of a wide array of neurological disorders including autism spectrum disorder (ASD). This study was designed to examine the effects of chronic risperidone treatment on the expression of adenosine deaminase acting on RNA 2 (Adar2), the status of AMPA glutamate receptor GluA2 editing, and its effects on oxidative/nitrosative stress and excitotoxicity-mediated neuronal death in the prenatal valproic acid (VPA) rat model of ASD. Prenatal VPA exposure was associated with autistic-like behaviors accompanied by an increase in the apoptotic marker "caspase-3" and a decrease in the antiapoptotic marker "BCL2" alongside a reduction in the Adar2 relative gene expression and an increase in GluA2 Q:R ratio in the hippocampus and the prefrontal cortex. Risperidone, at doses of 1 and 3 mg, improved the VPA-induced behavioral deficits and enhanced the Adar2 relative gene expression and the subsequent GluA2 subunit editing. This was reflected on the cellular level where risperidone impeded VPA-induced oxidative/nitrosative stress and neurodegenerative changes. In conclusion, the present study confirms a possible role for Adar2 downregulation and the subsequent hypo-editing of the GluA2 subunit in the pathophysiology of the prenatal VPA rat model of autism and highlights the favorable effect of risperidone on reversing the RNA editing machinery deficits, giving insights into a new possible mechanism of risperidone in autism.

Sonic hedgehog pathway as a new target of atypical antipsychotics: Revisiting of amisulpride and aripiprazole effects in a rat model of schizophrenia.

OBJECTIVES: Schizophrenia is a chronic mental illness presented by cognitive deficits that precede its positive and negative symptoms. Sonic hedgehog (Shh)-pathway contributes to its pathophysiology. Shh has a role in neurogenesis as it regulates proliferation and survival of neural cells. In this study, effects of the anti-psychotics Amisulpride and/or Aripiprazole on the Shh-pathway and its relation to cognitive functions and neurogenesis in a rat model of schizophrenia were tested. METHODS: 60 male Wistar rats were allocated into the following groups: control, socially isolated, amisulpride and/or aripiprazole-treated groups. Rats were then subjected to behavioral, biochemical, and histopathological tests to assess the impact of these drugs on Shh-pathway. KEY FINDINGS: Cognitive-dysfunction was evidenced in socially isolated group in novel object, three-chamber, and Morris water maze tests, associated by disorganised Shh-pathway proteins levels concentrations, increased glial fibrillary acidic protein (GFAP)-stained astrocytes. Treated groups favorably reversed these changes evidenced by increased Shh, transmembrane patched-1 and smoothened, glioma-associated-oncogene (GLI)-1 levels, dopamine-1 receptors and brain derived neurotrophic factor, and decreased GLI-3 protein, GFAP immune reaction in astrocytes and inflammatory markers compared to socially isolated group. CONCLUSION: Amisulpride and/or aripiprazole have a favorable role in turning on Shh-pathway with subsequent beneficial cognitive and neurogenesis effects.

Garlic antagonizes skeletal muscle ischemia reperfusion injury through regulating inflammation, apoptosis and desmin expression in adult male rats.

BACKGROUND: Skeletal muscle injuries with subsequent bleeding is common cause of death on both sports and battle grounds. Application and removal of tourniquet is fast intervention to control hemorrhage resulting ischemia reperfusion (IR) injury. The effect of IR in skeletal muscle is far more severe compared to other body tissues because of the devastating systemic complication. Garlic has beneficial effects in IR of various organs. However, using garlic in IR of skeletal muscle is deficient Goals: To investigate the possible protective effect of garlic in rat model of hind limb IR and its possible mechanisms of action. METHODS: Fifty adult male rats divided into five groups; C: control, IR: ischemia/reperfusion group subjected to 2 hours ischemia followed by 2 hours reperfusion (2/2 hr IR) and three garlic treated groups; G1+IR: 24 hr before I/R, G2+IR: 30 min before IR and G3+IR: immediately before reperfusion. We measured wet to dry weight ratio (W/D) of gastrocnemius muscle, serum creatine kinase (CK), Interleukin 1ß (IL-1ß), Interleukin-10 (IL-10), gastrocnemius caspase-3 and desmin expression and histopathological damage score. RESULTS: Garlic treatment caused significant decrease in W/D, serum CK, IL-1ß, caspase-3 expression and significant increase in IL-10 as well as desmin expression when compared to IR group. Garlic ameliorated IR-induced histopathological damage and significantly reduced the apoptosis score. Better results obtained with earlier administration before IR. CONCLUSION: Garlic protected against IR-induced skeletal muscle damage through reducing inflammation, apoptosis score and elevating desmin expression. We recommend the earlier use of garlic as prophylactic natural medicine in skeletal muscle IR.