Deep glance on the antiparasitic anticancer activities of wheat germ oil in chronically infected immunosuppressed mice with cryptosporidiosis.

Cryptosporidium species are the major cause of water-borne epidemics of diarrhea in both developing and developed countries that vary from self-limited in immunocompetent patients to severe life-threatening in the immunocompromised hosts. There was a proven correlation between cryptosporidiosis and colorectal cancers, although, studies in this field are still limited. Wheat germ oil (WGO) is a natural product with a known antiparasitic effect and potential antiproliferative activities. This study aimed to evaluate the antiparasitic and anticancer activities of WGO in chronically infected immunosuppressed mice compared to Nitazoxanide (NTZ). This experimental case-control study was performed in the period from January till September 2021. Eighty immunosuppressed bred laboratory mice were divided into 4 groups, 20 mice each; GI non-infected; negative control (NC), GII infected non treated; positive control (PC), GII infected, and treated with NTZ, GIV infected, and treated with WGO. Parasitological, histopathological, and immunohistochemical examinations were performed with estimating the rate of maximal survival for the study groups. Parasitological examination revealed a marked reduction in the mean Cryptosporidium spp. oocyst counts in the stool of GIV compared to PC, and GIII (P-value < 0.001). Histopathological and immunohistochemical examinations showed the best results with GIV which revealed restoration of normal villous pattern, with no dysplasia or malignancy could be detected. GIV showed the best survival rate compared to PC and GIII. WGO is an extremely promising agent that has an excellent therapeutic effect against cryptosporidiosis with the ability to control the tumorigenesis process in the chronically infected immunosuppressed hosts.

Evaluation of Osteopontin as a Biomarker in Hepatocellular Carcinomas in Egyptian Patients with Chronic HCV Cirrhosis

Background: Hepatocellular carcinoma (HCC) is a high incidence disease in Egypt with a poor prognosis and survival. Biomarkers are important for diagnosis of HCC at an early stage. Osteopontin (OPN), a glycoprotein secreted by macrophages, osteoblasts, and T cells, is also highly expressed in a variety of tumors, such as examples in the breast, colon, and stomach. The present study aimed to correlate the serum level of OPN in HCV-positive hepatocellular carcinoma patients, with OPN expression in tumor and non-tumor liver tissues in order to identify its efficacy as a biomarker for diagnosis. Material and Methods: Out of total of 146 patients, 80 were selected for inclusion in the study. Blood samples as well as specimens of tumor and non-tumor liver tissue were collected. In addition, blood samples from 20 healthy volunteers were obtained as controls. Serum OPN and alpha-fetoprotein (AFP) were evaluated by ELISA for HCC and control groups. OPN and AFP gene expression were examined by real-time PCR, after homogenization and DNA extraction from serum samples and liver tissues. Results: It was found that serum OPN levels were significantly higher in the HCC group compared to normal group (P=0.009), with a strong positive correlation with AFP expression. However, there was no significant difference between OPN expression in tumor and non-tumor liver tissue. Conclusion: Serum OPN is highly suggested to be a professional candidate for HCC early diagnosis, with a diagnostic ability and accuracy equal or higher than for AFP.

Differential Expression of Glypican-3 and Insulin­Like Growth Factor-II mRNAs and Alpha-Fetoprotein and Ki-67 Markers in HCV Related Hepatocellular Carcinomas In Egyptian Patients

Background: Increasing evidence indicates that in hepatocellular carcinomas (HCCs) abnormal gene expression, for example of glypican-3 (GPC-3) and insulin-like growth factor-II (IGF-II), are associated with the occurrence and progression of HCC. The objective of this study was to evaluate the differential expression of GPC-3 and IGF-II mRNAs in HCC tissues with a background of chronic hepatitis C virus (HCV) genotype 4 cirrhosis, in relation to Ki-67 and alpha-feto protein (AFP) tissue markers. Methods: One hundred and five patients with HCCs who had undergone hepatectomy, were included, after obtaining informed consent. Total RNA was extracted from malignant and corresponding peri-malignant liver tissues, and GPC-3 and IGF-II mRNAs in addition to beta-actin mRNA as an internal control, were evaluated in all samples by reverse transcriptase-polymerase chain reactions (RT-PCR). Routine histopathological diagnosis as well as immunohistochemical (IHC) staining using monoclonal antibodies for Ki-67 and AFP were also performed. Result: Expression of GPC-3 mRNA was positive in all HCC malignant tissue, with overexpression in 86/105 (81.9%); in respect to the grade of the tumor (1-3 grades), while in peri-malignant tissue it was over expressed only in 20/105 (19%). The IGF-II mRNA was over expressed in only 10/105 (9.5%) malignant and peri-malignant samples. AFP was expressed in 33.3% of malignant samples but absent in peri-malignant tissues. Ki-67 expression was significantly increased in malignant compared to peri-malignant tissue. Conclusion: GPC-3 and IGF II mRNAs may be good molecular markers for HCC, especially with a background of cirrhosis due to chronic HCV infection. Significant correlations were noted with the pattern of AFP and Ki-67 expression.

Effect of schistosoma mansoni egg deposition on multiple low doses streptozotocin induced insulin dependent diabetes.

To explore the role of Schistosoma mansoni infection in the prevention of autoimmune mediated insulin dependant diabetes mellitus, we examined the effects of multiple low doses of the pancreatic islets beta cell toxin, streptozotocin (STZ) 40mg/kg body weight i.p., given 8 weeks post infection, period of S. mansoni egg deposition, on S. mansoni infected C57BL/6J mice, in comparison to non-infected STZ given group. Mice treated with STZ (G III) became gradually hyperglycemic reaching highest level on days 17 post STZ with mean blood glucose level of 334.9 +/- 14.9 vs 130.3 +/- 9.2 mg/dl in control group (G IV). S. mansoni infection (G II) significantly reduced the elevation in blood glucose levels from days 7 post STZ onwards reaching 224mg/dl +/- 12.7 on days 17 (P < .0.001). Morphologic examination of pancreas on day 21 post STZ, revealed that the non-infected STZ (G III) given mice had significantly smaller mean islets area (5,060.51 mu2 +/- 1,567.28) and significantly fewer mean number of beta cells/islets (76.23 +/- 19.18) than the infected STZ given group (G II) which had mean islets area (9,305. 3l mu2 +/- 3,277.59) and 116.75 +/- 27.27 beta-cells/islets. Pancreatic tissue revealed also focal degeneration in the cells of islets of Langrhans in the non-infected STZ given mice (G III), in comparison, to the infected STZ given group (G II). which had much less evident cells degeneration. These findings revealed that S. mansoni egg deposition which leads to a shift from Th1 (IFN-gamma mainly) to Th2 (IL4, IL5, IL10 and TGF-beta cytokine profiles causes down-regulation of the Th1 cell mediated autoimmune insulin dependant diabetes mellitus (IDDM). On the other hand, S. mansoni eggs excretions were significantly lower in the infected STZ given group (G II) than the infected group (G I). This finding may be the result of impaired maturation of egg in diabetic mice. It is concluded that the modulation of immune response in S. mansoni infected mice with S. mansoni egg deposition, can suppress the autoimmune type 1 insulin dependant diabetes mellitus induced by multiple low doses streptozotocin.