Toxoplasmosis and cytomegalovirus infection and their role in Egyptian autistic children.

Autism is a neurodevelopmental disorder with a significantly increased incidence rate across the world over the past few years. Toxoplasmosis and cytomegalovirus (CMV) infection are globally prevalent and have been associated with diverse neurological and psychiatric disorders. A few studies have demonstrated the role of toxoplasmosis and CMV as potential etiological factors for autism. Accordingly, this study was performed to estimate the relationship between toxoplasmosis and CMV infection in children with autism as well as to assess their impact on the Childhood Autism Rating Scale (CARS) score. A total of 45 autistic children (6 girls, 39 boys) and 45 (21 girls, 24 boys) healthy control children were enrolled in our study. Their blood samples were collected and tested for the presence of Toxoplasma and CMV (IgG and IgM) antibodies and DNA by ELISA and real-time PCR (RT-PCR), respectively. Toxoplasmosis was detected in 11 (24.4%) autistic children through the ELISA [10 (22.2%) IgG + /IgM - and 1 (2.2%) IgG + /IgM +]; however, RT-PCR assay recorded only 1 positive case (2.2%), while it was detected in 10 (22.2%) control children through ELISA [9 (20%) IgG + /IgM - and 1 (2.2%) IgG + /IgM +] and 1 (2.2%) by RT-PCR. On the other hand, CMV infection was detected in all autistic children with 44 (97.8%) testing positive by ELISA [24 (53.3%) IgG + /IgM - , 18 (40%) IgG + /IgM + and 2 (4.4%) IgG - /IgM +] and 25 (55.6%) testing positive by RT-PCR assay. In addition, ELISA assay recorded 43 (95.6%) [19 (42.2%) IgG + /IgM + and 22 (48.9%) IgG + /IgM - and 2 (4.4%) IgG-/IgM +] and RT-PCR recorded 21 (46.7%) positive samples in control children with CMV. No significant difference was noted between autistic and control children for the overall prevalence of Toxoplasma or/and CMV infection. Similarly, the CARS score indicated a non-significant difference with Toxoplasma or/and CMV infection. Our data does not show an association between autism and toxoplasmosis or/and CMV infection. Nevertheless, considering that autistic children are at a high risk of contracting these infections, further studies with a larger sample size are recommended.

UreA and cagA genes of Helicobacter pylori in Egyptian patients with laryngeal squamous cell carcinoma and benign laryngeal polyps: a cohort study.

This work aims to estimate the prevalence of Helicobacter pylori ureA gene and evaluate cagA gene-positive strains in both patients of laryngeal squamous cell carcinoma (LSCC) and those with benign laryngeal polyps. This study included 49 patients confirmed pathologically to have LSCC and 15 patients with benign laryngeal polyps over a period from June 2013 to March 2015. Samples of laryngeal tissue were collected during direct laryngoscope under general anesthesia to be pathologically evaluated followed by analysis for H. pylori detection. Each laryngeal tissue sample was divided into three parts; one for bacteriological examination, the second for pathological examination and the third for PCR to detect both ureA and cagA genes. Out of 49 LSCC samples, 31 (64.6 %) was positive for ureA by PCR. Out of them, 29 samples (93.5 %) were cagA positive. Only three cases (20 %) of the benign laryngeal polyp were ureA positive by PCR and one of them was cagA positive by PCR. By the bacteriological culture, only eight samples (25.8 %) gave growth. All of them were ureA positive and only seven of them were cagA positive. There was a significant association between presence of H. pylori and LSCC as compared to benign laryngeal polyp which may contribute in the pathogenesis of laryngeal carcinoma. These results should be confirmed by further studies over larger number of cases.

Association of the CagA gene positive Helicobacter pylori and tissue levels of interleukin-17 and interleukin-8 in gastric ulcer patients.

It has been reported that CagA gene positive Helicobacter pylori (CagA+ H. pylon) induces severe gastric mucosal inflammation. On the other hand, Interleukin (IL)-17 is known to stimulate IL-8 release by the gastric epithelial cells which facilitates chemotaxis of neutrophils through an IL-8-dependent mechanism. The aim of the study is to determine the role of IL-17 and IL-8 in the development of gastritis and gastric ulcer in H. pylori infected patients. Mucosal biopsy samples were obtained from the ulcer site of gastric mucosa of 28 patients with gastric ulcer (GU), 27 with gastritis and 8 controls subjects without gastritis or ulcers. Infection with H. pylori of patients and controls was assessed by a rapid urease test, histological examination and culture. Measurement of the tissue levels of IL-17 and IL-8 were assayed by ELISA. H. pylori cagA gene was assessed by polymerase chain reaction (PCR). Out of the 28 patients with GU, 18 (64.2%) patients were positive for H. pylori infection, while 13 (48.1%) patients with gastritis and none of the controls were positive for H. pylori infection The CagA gene was detected in 12 (66.6%) in H. pylori GU patients, and 7 (53.8%) H. pylori positive gastritis. IL-17 was significantly higher in GU-CagA+ve H. pylori compared to GU-CagA- H. pylori (P <0.05), while IL-8 showed no significant difference between groups. The mean levels of IL-8 in gastritis-CagA+ H. pylori) was significantly higher compared to gastritis--CagA- H. pylori- (P <0.05). IL-17 showed significant association with the number of neutrophils in both GU and gastritis (r = 0.689, P < 0.05 & r = 0.618, P < 0.05). Also, IL-8 showed significant association with the number of neutrophils in both GU and gastritis n (r = 0.468, P < 0.05 & r = 0.727, P < 0.05). It is concluded that the Cag+ve H. pylori is associated with induction of mucosal injury. Also, IL-8 and IL-17 plays a role in the development of GU and gastritis especially in CagA+ H. pylori.

Gene expression in HCV-associated hepatocellular carcinoma--upregulation of a gene encoding a protein related to the ubiquitin-conjugating enzyme.

BACKGROUND/AIMS: To investigate gene expression in HCV-associated human hepatocellular carcinomas (HCC) by identifying up- and down-regulated genes. METHODS: Differential display RT-PCR was used to compare levels of gene expression in tumorous and non-tumorous tissues from the same livers. Differential expression was confirmed using a ribonuclease protection assay (RPA). The relative expression levels of one candidate gene were studied in various normal tissues and malignant cell lines using a multiple tissue expression (MTE) array. Further characterisation of this gene was carried out using nucleotide sequence analysis programmes and Northern hybridisation. RESULTS: Fifty-two differentially expressed cDNA fragments were identified and 29 were cloned, sequenced and compared with the nucleotide sequence database. RPA confirmed reproducibly that one particular cDNA was upregulated in the tumour cells. Analysis using the MTE array revealed that this selected candidate gene is expressed at high levels in various human tumour cell lines. The expression levels in HCV-associated HCC were higher than in other tumours. Investigation revealed that this novel gene lies on chromosome 17. The transcript is approximately 2.5 kb in size and encodes a protein similar to the ubiquitin-conjugating enzyme. CONCLUSIONS: The ubiquitin system may be involved in HCV-related hepatocarcinogenesis and in the development of other cancers.