Oxidative stress is involved in many neurodegenerative diseases. Chronic ozone exposure causes a secondary increase of reactive oxygen species, which cause an oxidative stress state in the organism. Ozone is one of the main components of photochemical pollution. Our purpose was to test that oxidative stress caused by chronic low doses of ozone, by itself, alters adult neurogenesis and causes progressive neurodegeneration in the hippocampus, which actions lead to the loss of brain plasticity in the mature central nervous system of rats. Animals were exposed to an ozone-free air stream and for 15, 30, 60, and 90 days to low doses of ozone to cause oxidative stress. Each group was then tested by (1) a spectrophotometer test to quantify lipid peroxidation (LPO) levels; (2) immunohistochemistry testing against doublecortin, Neu-N, p53, microglia, and glial fibrillary acidic protein; (3) Western blot tests for doublecortin and Neu-N; and (4) a one-trial passive avoidance test. Our results indicated that ozone causes an increase of LPO levels, morphological changes in the nucleus and the cytoplasm, and cell swelling in neurons. The Western blot shows a decrease for Neu-N and doublecortin. Activated and later phagocytic microglia and an increased number of astrocytes were found. There was a memory deficiency positively related to the amount of ozone exposure. These alterations suggest that oxidative stress caused by low doses of ozone causes dysregulation of inflammatory processes, progressive neurodegeneration, chronic loss of brain repair in the hippocampus, and brain plasticity changes in the rat analogous to those seen in Alzheimer’s disease.

Gastric cancer (GC) incidence has not declined in Mexico. We assessed whether the intake of capsaicin (CAP), the pungent compound of chili peppers, increases the risk of GC independently of H. pylori positivity (Hp). From 1994 to 1996, a hospital‐based case‐control study was performed in 3 areas of Mexico; 234 cases of GC and 468 matched controls were enrolled and their diet and other characteristics were inquired. Chili pepper intake was queried by interview and CAP content of chilies was determined in a separate analysis by gas chromatography to estimate CAP intake; IGg Hp serum antibodies were determined by ELISA. The risk of GC was increased (OR = 1.71; 95% CI = 0.76–3.88) among high‐level consumers of CAP (90–250 mg of capsaicin per day, approximately 9–25 jalapeño peppers per day) as compared to low‐level consumers (0–29.9 mg of capsaicin per day, approximately 0 to less than 3 jalapeño peppers per day; p for trend p = 0.026); this effect was independent of Hp status and other potential GC determinants and was higher among diffuse GC cases (OR = 3.64; 95% CI = 1.09–12.2; p for trend = 0.002) compared to intestinal GC cases (OR = 1.36; 95% CI = 0.31–5.89; p for trend = 0.493). No significant interaction was found between CAP intake and Hp on GC risk. Chili pepper consumption might be an independent determinant of GC in Mexico.

Objective. To identify bacterial DNA in synovial fluid cells of patients with active juvenile onset spondyloarthropathy (SpA). Methods. The main group of study constituted 22 patients with juvenile onset SpA. In addition, five patients with adult onset SpA and nine with rheumatoid arthritis (RA) were studied. Polymerase chain reaction (PCR) with either genus‐ or species‐specific primers was performed on synovial fluid cells to detect DNA sequences of Chlamydia trachomatis, Yersinia enterocolitica, Salmonella sp., Shigella sp., Campylobacter sp. and Mycobacterium tuberculosis. The presence of antibacterial antibodies in sera and synovial fluid was also determined by enzyme‐linked immunoassay. Results. The synovial fluid of nine patients with juvenile onset SpA, three with adult onset SpA and one with RA contained bacterial DNA. Five juvenile onset SpA samples had DNA of one single bacterium; two juvenile onset SpA and three adult onset SpA had DNA of two bacteria and two juvenile onset SpA had DNA of three bacteria. Overall, Salmonella sp. DNA was detected in seven synovial fluid samples, Shigella sp., Campylobacter sp. and M. tuberculosis were found in four samples each, and C. trachomatis was found in two. The bacterial DNA findings correlated with neither diagnosis nor disease duration. One RA synovial fluid had DNA of Campylobacter sp. Neither serum nor synovial fluid antibacterial antibodies correlated with DNA findings or clinical diagnosis. Conclusion. In this study, single and several combinations of bacterial DNA were identified in the synovial fluid of patients with long‐term undifferentiated and definite juvenile onset SpA and adult onset SpA. Of relevance is that bacterial DNA corresponds to bacteria producing endemic disease in our population.