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Background: Gastric cancer is one of the most common types of cancer worldwide. Helicobacter pylori infection is clearly correlated with gastric carcinogenesis. Therefore, the use of a new non-invasive test, known as the GastroPanel test, can be very helpful to identify patients at a high risk, including those with atrophic gastritis, intestinal metaplasia, and dysplasia. This study aimed to compare the results of GastroPanel test with the pathological findings of patients with gastric atrophy to find a safe and simple alternative for endoscopy and biopsy as invasive methods.Methods: This cross-sectional study was performed on patients with indigestion, who were referred to Motahari Clinic and Shahid Faghihi Hospital of Shiraz, Iran, since April 2017 until August 2017 for endoscopy of the upper gastrointestinal tract. The serum levels of gastrin-17 (G17), pepsinogen I (PGI), and pepsinogen II (PGII), as well as H. pylori antibody IgG, were determined by ELISA assays. Two biopsy specimens from the antrum and gastric body were taken for standard histological analyses and rapid urease test. A pathologist examined the biopsy specimens of patients blindly. Results: A total of 153 patients with indigestion (62.7% female; mean age, 63.7 years; 37.3% male; mean age, 64.9 years) were included in this study. The G17 levels significantly increased in patients with chronic atrophic gastritis (CAG) of the body (9.7 vs. 32.8 pmol/L; P = 0.04) and reduced in patients with antral CAG (1.8 vs. 29.1 pmol/L; P = 0.01). The results were acceptable for all three types of CAG, including the antral, body, and multifocal CAG (AUCs of 97%, 91%, and 88% for body, antral, and multifocal CAG, respectively). The difference in PGII level was not significant. Also, the PGI and PGI/PGII ratio did not show a significant difference (unacceptably low AUCs for all). The H. pylori antibody levels were higher in patients infected with H. pylori (251 EIU vs. 109 EIU, AUC = 70, P = 0.01). There was a significant relationship between antibody tests and histopathology.Conclusion: Contrary to Biohit’s claims, the GastroPanel kit is not accurate enough to detect CAG; therefore, it cannot be used for establishing a clinical diagnosis.

Background: The leading cause of mutations in the hepatitis B virus (HBV) genome is the high rate of nucleotide misincorporation during reverse transcription. Most mutations were found within the “a” determinant of the S gene’s major hydrophilic region (MHR). They resulted in escape mutants due to amino acid changes in the MHR. However, mutations outside the MHR can also trigger escape mutants. Objectives: This study focused on further molecular studies on the MHR of genotype D of HBV DNA isolated from patients with chronic HBV infection, together with the coexistence of hepatitis B surface antigen (HBsAg) and hepatitis B surface antibodies (anti-HBs) in their serum samples. Methods: In this study, serum samples from 83 patients with chronic HBV infection were analyzed by serological and immunological tests for the concurrence of HBsAg and anti-HBs. In addition, the mutation in the HBV DNA was assessed by nucleotide sequencing of S genes within, upstream, and downstream of the MHR. Results: Among 83 patients with chronic HBV infection, the coexistence of HBsAg and anti-HBs were detected in 11 (13.25%) individuals. Mutations in eight amino acids of seven samples analyzed for nucleotide sequencing were observed at 27 different sites in three locations, namely upstream, within, and downstream of the MHR. The mutations affected the structure of the epitope and the appearance of an escape mutant. Conclusions: The results indicated that mutations downstream and upstream of the MHR play a role in the coexistence of HBsAg and anti-HBs in patients with chronic HBV infection.

Aim: Human respiratory syncytial virus (HRSV) is a common cause of respiratory infections, particularly in infants and the elderly. Ribavirin is the only US FDA-approved antiviral drug for HRSV infection, but it has unwanted side effects. Methods: We engineered an shRNA targeting the HRSV- M gene to antagonize HRSV replication. Results: The results showed that shRNA had a similarly significant reduction in viral load (99.8%) as ribavirin. In addition, combined treatment with ribavirin and M-shRNA resulted in a significant reduction in viral load compared with ribavirin or M-shRNA alone. Conclusion: These results suggest that M-shRNA could be a potential new inhibitor of HRSV replication and could offer a safer and more effective treatment option for HRSV infection in the future.