Background:Toxoplasma gondii (T. gondii) is an opportunistic parasite that causes serious diseases in humans, particularly immunocompromised individuals and pregnant women. To date, there are limited numbers of therapeutics for chronic toxoplasmosis which necessitate the discovery of effective and safe therapeutics. In the present study, we aimed to evaluate the antitoxoplasmosis potential of ginger extract in mice with experimentally induced chronic toxoplasmosis. Results: Treatment with ginger extract significantly reduced cysts count in the brains of T. gondii-infected mice with a marked alleviation of edema and inflammation, and a reversal of neuronal injury. Moreover, ginger extract treatment reduced inflammation in liver and lungs and protected hepatocytes from infection-induced degeneration. Consistently, apoptosis was significantly mitigated in the brains of ginger extract-treated mice compared to infected untreated animals or spiramycin-treated animals. Methods: Four groups of Swiss albino mice (10 mice each) were used. The first group was not infected, whereas 3 groups were infected with Me49 T. gondii strains. One infected group remained untreated (infected untreated), whereas the other two infected groups were treated with either ginger extract (250 mg/kg) or spiramycin (positive control; 100 mg/kg), respectively. The therapeutic potential of ginger extract was evaluated by calculation of the parasite burden in infected animals, and examination of the infected tissues for reduced pathologic changes. Conclusions: Our results showed for the first time that ginger extract exhibited marked therapeutic effects in mice with chronic T. gondii infection which indicates that it can be used as a safe and effective treatment for chronic toxoplasmosis.

Background: Previous studies have reported involvement of Toxoplasma gondii (T. gondii) infections in the pathogenesis of some autoimmune diseases, such as polymyositis, rheumatoid arthritis, autoimmune thyroiditis, and Crohn’s disease. However, data on the association between T. gondii infections and Type 1 diabetes mellitus (T1DM) are still controversial. Therefore, in the present study, we aimed to investigate the pancreatic pathological changes in mouse models with acute and chronic toxoplasmosis and their association with T1DM. Materials and Methods: Three groups (10 mice each) of male Swiss Albino mice were used. One group of mice was left uninfected, whereas the second and third groups were infected with the acute virulent T. gondii RH strain and the chronic less virulent Me49 T. gondii strain, respectively. T. gondii-induced pancreatic pathological changes were evaluated by histopathological examination of pancreatic tissues. Moreover, the expression of insulin, levels of caspase-3, and the pancreatic infiltration of CD8⁺ T cells were evaluated using immunohistochemical staining. Results: Pancreatic tissues of T. gondii-infected animals showed significant pathological alterations and variable degrees of insulitis. Mice with acute toxoplasmosis exhibited marked enlargement and reduced numbers of islets of Langerhans. However, mice with chronic toxoplasmosis showed considerable reduction in size and number of islets of Langerhans. Moreover, insulin staining revealed significant reduction in β cell numbers, whereas caspase-3 staining showed induced apoptosis in islets of Langerhans of acute toxoplasmosis and chronic toxoplasmosis mice compared to uninfected mice. We detected infiltration of CD8⁺ T cells only in islets of Langerhans of mice with chronic toxoplasmosis. Conclusions: Acute and chronic toxoplasmosis mice displayed marked pancreatic pathological changes with reduced numbers of islets of Langerhans and insulin-producing-β cells. Since damage of β cells of islets of Langerhans is associated with the development of T1DM, our findings may support a link between T. gondii infections and the development of T1DM.

Non-small cell lung cancer (NSCLC) is a pervasive and challenging global health concern. This research delves into the intricate relationship between NSCLC and ACE2 expression, exploring the potential impact of COVID-19 history on this interaction. Tissue samples were meticulously gathered from a cohort of 32 NSCLC patients, 18 of whom had a documented history of COVID-19 infection. The methodology included extensive investigations, such as cell dissociation, histopathological analysis, immunohistochemistry, cell culture, adhesion assays, immunocytochemistry, RNA isolation, and RT-PCR analysis. The results of this comprehensive study unearthed intriguing findings regarding ACE2 expression patterns within NSCLC tissues. Notably, variations were observed in ACE2 profiles between individuals with and without a prior record of COVID-19 infection, hinting at a dynamic interplay. These discoveries carry profound implications for both the understanding of NSCLC progression and the response to COVID-19 in patients with pre-existing NSCLC. The interrelationship between ACE2 expression, NSCLC, and COVID-19, as revealed in this study, may significantly influence patient outcomes and, potentially, therapeutic strategies. In summary, this research serves as an essential contribution to the growing body of knowledge on NSCLC, offering unique insights into the intricate connections between ACE2, COVID-19, and NSCLC. This information may open new avenues for tailored treatment approaches and clinical management strategies, ultimately benefiting patients grappling with NSCLC in the background of the current COVID-19 pandemic.

Background: Gnathiids are considered excellent ectoparasites widely distributed along the fish body with a biphasic life cycle including parasitic larval stages and free-living adults. This study focused on gnathiids infecting the brown-spotted grouper fish and confirming the identity of the host species. Methods: Twenty Epinephelus chlorostigma (Serranidae) were collected from the Red Sea Coast (especially off Jeddah, Saudi Arabia) and examined for gnathiid fish parasites. Species identification of the larvae was based on morphological criteria of Smit and Basson (2002). In contrast, the taxonomy of fish species was supported by amplification and sequencing of host DNA via the mitochondrial DNA genes (COI and 16S rRNA) using gnathiids’ blood meals. Result: Praniza larvae of a gnathiid isopod were collected from the gill chambers of the examined fish. The prevalence rate was 60% and mean intensity of the pranzia larvae was 16. The pranzia larva is described microscopically and distinguished by large body size (3.51-5.90 mm), the presence of 8th teeth in the mandible, maxilliped with 5-7th teeth on the first palp and the endite hooked, pleotelson with concave anterolateral margins and rami of uropods extend its apex. The recovered larvae could be identified as pranzia larvae of Gnathia pantherina Smit and Basson, 2002 due to the morphological resemblance. The host species identity was confirmed molecularly with COI and 16S rRNA genes and showed highly stringent criteria with the previously E. chlorostigma sequence data. The obtained host DNA sequences were deposited in NCBI database under accession numbers ON384530.1 for COI and ON384544.1 for 16S rRNA.