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Background: Hepatocellular carcinoma (HCC) is a common malignancy that occurs secondary to viral hepatitis B and C cirrhosis under the influence of environmental factors. In early stages, clinical diagnosis is often difficult and distinguishing HCC from cirrhosis and other hepatic masses by conventional tests is frequently not feasible. Physicians usually depend on measuring serum alpha-fetoprotein (AFP), but this marker has low sensitivity and specificity. The aim of this research was to determine any role of serum cytokeratin-18(Ck-18) as a marker for diagnosis of HCC in patients with liver cirrhosis. Patients and methods: We used ELISA to measure the serum levels of AFP and CK 18 in 60 Egyptian patients (30 cirrhotic and 30 with HCC) and 30 controls. Results: The Ck-18 level was significantly elevated in the HCC group (1247.8± 105.3U/L) when compared to the liver cirrhosis (834.1± 38.8 U/L) and control groups (265.2±83.1U/L). Ck-18 as a marker showed 95.6% sensitivity, 93.3% specificity and 98.8% accuracy. The mean serum AFP was 4901.4±2185.8ng/ml in the HCC group, 100.7±71.7 ng/ml in the cirrhotic group, and 4.0±1.2ng/ ml in controls. AFP showed 55. 7% sensitivity, 97. 7% specificity and 84.4% accuracy. Combined use of both Ck-18 and AFP improved the sensitivity to 98%. Conclusion: Serum cytokeratin-18 level can be used as a diagnostic biomarker for HCC with a higher sensitivity than AFP.

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AIM: To investigate the role of p53 antibodies (p53Abs), metallothioneins (MTs) and oxidative stress markers in the early detection of dysplasia in chronic ulcerative colitis (UC). METHODS: The study included 30 UC patients, 15 without dysplasia (group II) and 15 with dysplasia (group III), in addition to 15 healthy volunteers (group I, control subjects). The enzyme-linked immunosorbent assay technique was used to measure serum p53Abs and MTs, while advanced oxidation protein products (AOPPs), and reduced glutathione (GSH) levels were measured by spectrophotometric method in all subjects. RESULTS: In group II and group III compared to group I, there were significant increases in serum levels of AOPPs (145.94 ± 29.86 µmol/L and 192.21 ± 46.71 µmol/L vs 128.95 ± 3.06 µmol/L, P < 0.002 and P < 0.001, respectively), MTs (8.18 ± 0.35 µg/mL and 9.20 ± 0.58 µg/mL vs 6.12 ± 0.25 µg/mL, P < 0.05 and P < 0.05, respectively), and p53Abs (20.19 ± 3.20 U/mL and 34.66 ± 1.34 U/mL vs 9.42 ± 1.64 U/mL, P < 0.001 and P < 0.001, respectively). There were significantly higher levels of AOPPs (P < 0.05) and p53Abs (P < 0.001) in UC patients with dysplasia compared to those without dysplasia, while MTs showed no significant difference between the 2 groups (P > 0.096). In contrast, GSH levels showed a significant decrease in both patients' groups (1.87 ± 0.02 µmol/mL and 1.37 ± 0.09 µmol/mL vs 2.49 ± 0.10 µmol/mL, P < 0.05 and P < 0.05 in groups II and III, respectively) compared with group I, and the levels were significantly lower in group III than group II (P < 0.05). There was a positive correlation between AOPPs and both MTs (r = 0.678, P < 0.001) and p53Abs (r = 0.547, P < 0.001), and also between p53Abs and MTs (r = 0.739, P < 0.001). There was a negative correlation between AOPPs and GSH (r = -0.385, P < 0.001), and also between GSH and both MTs (r = -0.662, P < 0.001) and p53Abs (r = -0.923, P < 0.001). CONCLUSION: Oxidative stress and oxidative cellular damage play an important role in the pathogenesis of chronic UC and the associated carcinogenetic process. p53Abs levels could help in early detection of dysplasia in these conditions.

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Toxocariasis is a widespread soil-transmitted parasitic disease. Toxocara canis larvae migrate through the tissues with a special predilection for the central nervous system. Recently, neurotoxocariasis is being diagnosed in humans with increasing frequency due to improved diagnostic tools. The present study aimed at exploring the biochemical and immunopathological alterations in the brain in experimental T. canis infection. For this purpose, 75 Toxocara-infected mice were sacrificed at 2, 5, and 16 weeks post-infection. The brains were removed and assayed for total larval count, pro-inflammatory cytokines (TNF-alpha, IL-6), and central neurotransmitters (gamma-aminobutyric acid, glutamate, dopamine, norepinephrine, and serotonin). Brain sections were also stained for histopathological study, and for assessment of the expression of inducible nitric oxide synthase (iNOS), and glial fibrillary acidic protein (GFAP) by immunohistochemical methods. We found that larval recovery showed progressive increase over the course of infection. Furthermore, the infected mice displayed increased expression of pro-inflammatory cytokines and iNOS, as well as significant disturbances in neurotransmitter profile. Astrocytic activation, evidenced by enhanced expression of GFAP, was also manifest in infected animals. These changes were maximal in the chronic stage of infection or intensified over time. In conclusion, experimental neurotoxocariasis is associated with significant biochemical, immunological, and pathological changes.

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