No abstract available.
Infarction*

BACKGROUND AND PURPOSE: Negative findings on diffusion-weighted imaging (DWI) does not exclude the possibility of brainstem infarction, particularly in the acute stage of medullary lesion. Our aim was to investigate the false-negative rate of DWI in patients with acute lateral medullary infarction. METHODS: We applied DWI to 26 patients with a clinical diagnosis of lateral medullary infarction within 72 h of the onset. We assessed relationships between initial DWI findings and time-to-MRI (the time between onset of symptoms and initial DWI), number of clinical symptoms and signs, and final lesion volume. RESULTS: There were 8 cases (31%) of false negatives in the initial DWI results. The occurrence of false-negative DWI findings decreased significantly as the time-to-MRI increased (P=0.014). However, the false-negative rate was not significantly correlated with the number of clinical symptoms and signs or the final lesion volume. CONCLUSIONS: The diagnosis of lateral medullary infarction should not be ruled out on the basis of early negative DWI. To confirm the lesion, follow-up DWI or further MRI should be performed in cases with early negative DWI results
Brain Stem Infarctions ; Diagnosis ; Diffusion* ; Follow-Up Studies ; Humans ; Infarction* ; Magnetic Resonance Imaging

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology

BACKGROUND/AIMS: Oxidative stress may contribute to gastric epithelial damage and mutagenesis caused by Helicobacter pylori (H. pylori). H. pylori induces recruitment and activation of inflammatory cells, which produces reactive oxygen species. H. pylori extract directly induces the synthesis of reactive oxygen species in gastric epithelial cells and causes DNA damage. The aim of this study was to investigate the association between the levels of glutathione (GSH) and H. pylori density, histological findings, endoscopic findings, clinical variables, and virulence factors. METHODS: Gastric biopsy specimens were obtained from 73 consecutive patients. The 5,5'-dithiobis-(2-nitrobenzoic acid) reaction was used to determine GSH levels. RESULTS: The infection rate of H. pylori was 68.5%. The GSH level was not related to age, sex, alcohol intake, and endoscopic findings. The GSH level was lower in patients infected with H. pylori. GSH levels were not correlated significantly with the grades of neutrophil, intestinal metaplasia, and atrophy. However, the GSH levels were significantly correlated with H. pylori density (r=-0.296, p=0.01) and monocyte grade (r=-0.257, p=0.02). The GSH levels were not related to CagA, VacA, and UreA. CONCLUSIONS: This study suggests that H. pylori causes oxidative stresses which deplete GSH in gastric mucosa of patients infected with H. pylori.
Adolescent ; Adult ; Aged ; Female ; Gastric Mucosa/*metabolism/pathology ; Glutathione/*metabolism ; Helicobacter Infections/*metabolism/pathology ; *Helicobacter pylori ; Humans ; Male ; Middle Aged ; Oxidative Stress ; Stomach Diseases/*metabolism/microbiology/pathology