Serum Concentrations of 15 Elements Among Helicobacter Pylori-Infected Residents from Lujiang County with High Gastric Cancer Risk in Eastern China.

Helicobacter pylori (H. pylori) infection can interfere with the absorption of most elements, and the variations of some element levels are related to the incidence of gastric cancer. However, there have been conflicting results concerning the influence of H. pylori infection on serum element levels. The present study aimed to compare the serum element concentrations of H. pylori-infected local residents with uninfected residents from Lujiang County with high gastric cancer risk in Eastern China. We used data and serum samples from the H. pylori screening-survey program which was a cross-sectional study. We took 155 samples randomly from the screening survey, identified 74 H. pylori-positive residents and 81 H. pylori-negative residents by a serological test. The serum concentrations of 15 elements (calcium, magnesium, iron, zinc, selenium, copper, molybdenum, chromium, cobalt, nickel, lead, cadmium, mercury, arsenic, and aluminum) were determined using inductively coupled plasma mass spectrometry. Serum cobalt was found at higher levels in the H. pylori-infected residents than the H. pylori-uninfected residents (0.246 vs 0.205 µg/L, P = 0.022), but no statistically significant differences in the serum levels of other elements were found. This is the first study to report the serum concentrations of 15 elements and their relationships with the infection status of H. pylori among local residents from Lujiang County with high gastric cancer risk. Although the International Agency for Research on Cancer has classified cobalt and other soluble cobalt salts as possibly carcinogenic to human beings, our results may provide a clue to the relationships between cobalt, H. pylori, and gastric cancer.

Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation.

Peroxisome proliferator-activated receptor (PPAR)-γ is highly expressed in human and rodent placentas. Nevertheless, its function remains obscure. The present study investigated the effects of rosiglitazone, a PPAR-γ agonist, on LPS-induced fetal death. All pregnant mice except controls were intraperitoneally injected with LPS (150 µg/kg) daily from gestational day (GD)15 to GD17. As expected, maternal LPS injection caused placental inflammation and resulted in 63.6% fetal death in dams that completed the pregnancy. Interestingly, LPS-induced fetal mortality was reduced to 16.0% when pregnant mice were pretreated with RSG. Additional experiment showed that rosiglitazone pretreatment inhibited LPS-induced expressions of tumor necrosis factor (Tnf)-α, interleukin (Il)-1ß, Il-6, macrophage inflammatory protein (Mip)-2 and keratinocyte-derived chemokine (Kc) in mouse placenta. Although rosiglitazone had little effect on LPS-evoked elevation of IL-10 in amniotic fluid, it alleviated LPS-evoked release of TNF-α and MIP-2 in amniotic fluid. Further analysis showed that pretreatment with rosiglitazone, which activated placental PPAR-γ signaling, simultaneously suppressed LPS-evoked nuclear factor kappa B (NF-κB) activation and blocked nuclear translocation of NF-κB p65 and p50 subunits in trophoblast giant cells of the labyrinth layer. These results provide a mechanistic explanation for PPAR-γ-mediated anti-inflammatory activity in the placentas. Overall, the present study provides additional evidence for roles of PPAR-γ as an important regulator of placental inflammation.

[Impact of oral vitamin D supplementation in early life on diabetic mice induced by streptozotocin].

OBJECTIVE: To evaluate the effect of oral vitamin D supplementation in early life on blood glucose, insulin content, diabetes incidence, and histomorphology in pancreatic islet induced by streptozotocin. METHODS: Three-week-old C57BL/6 mice were given either control diet (American Institute of Nutrition [AIN]-93G), or three different dose of vitamin D-supplemented diet. Nine weeks after dietary intervention, C57BL/6 mice were treated with streptozotocin i.p. for 5 consecutive days. After injection of STZ, The fasting blood glucose and diabetes incidence was tested once a week. The insulin content, histomorphology in pancreatic islets was conducted at the end of experiments. RESULTS: (1) Vitamin D supplementation in early life can decrease the fasting blood glucose values induced by STZ, and the decreases effect of high dose vitamin D-supplemented group is the most significant (P<0.01). (2) Vitamin D supplementation in early life can prevent diabetes incidence, and the decreases effect of high dose vitamin D-supplemented group is the most significant, fully suppress the onset of diabetes about four weeks later after injected by STZ (P<0.01). (3) As compared to the control group, insulin content in medium and high dose vitamin D-supplemented groups were significantly up-regulated after injection of STZ (P<0.05), and the effect of high dose vitamin D-supplemented group is the most significant. (4) The damage of pancreatic islets induced by STZ was clearly restored in medium and high dose vitamin D-supplemented groups, and effect of high dose vitamin D-supplemented group is the most significant. CONCLUSION: Oral vitamin D supplementation in early life can decrease the fasting blood glucose values, prevent diabetes incidence, up-regulate insulin content, restored the damage of pancreatic islets induced by STZ, and effects of high dose vitamin D-supplementde group are all the most significant.