RESUMO
Acute fetal hypoxia (AFH) can elicit postnatal motor deficits and cognitive impairments. To test whether lifelong acclimatization to middle altitude (MA) hypoxia has protective effects on the impairments caused by AFH, ICR mice bred at 1 900 m altitude for 6-7 generations were evaluated under AFH. On gestation day 9 (GD 9), 13 (GD 13) or 17 (GD 17), pregnant mice received a single exposure to acute hypoxia (7% O, 6 h). Physiological and neurodevelopmental behaviors, motor function (open field), spatial learning and memory (Morris water maze), and anxiety level (elevated plus maze) were examined in the offspring from neonate to adulthood. In the neonatal age, among all the physiological and behavioral landmarks, almost no differences were found in the hypoxia groups. In the juvenile period, no obvious impairments of motor function and anxiety level were found in the hypoxia groups. In the adult period, no obvious impairment of motor function was found in hypoxia groups; Interestingly, AFH groups' offspring showed normal or enhanced long-term spatial memory ability after AFH. These data suggest that AFH cause little abnormalities in the offspring of MA-adapted mice. To further investigate the underlying mechanisms, the neuronal numbers in behavior-related brain areas (accumbens nucleus, basal amygdala and hippocampus) were counted, and the physiological parameters of the blood were measured. The morphological data showed that no obvious neuronal necrosis was found in all hypoxia groups. In addition, blood tests showed that red blood corpuscle count, hemoglobin concentration and hematocrit levels in mice raised at MA were markedly higher in both males and females, compared with controls raised at the sea level. These data suggest that lifelong acclimatization to MA hypoxia has protective effects against development delay, motor deficits and spatial learning and memory impairments induced by AFH, and the protective effects may be due to higher hemoglobin concentration and hematocrit levels in the blood. The findings may provide a better understanding of fetal hypoxia and potential intervention treatments.
RESUMO
To investigate the effects of the iron chelatordeferoxamine [DFA] on inhibition formicroglia activation and protection of secondary nerve injury after intracerebral hemorrhage [ICH] in rats. The rats were randomly divided into sham operation group, ICH group and DFA treatment group. The collagenase was used to prepare ICH model of basal gangliain rats and Ih after the beginning of the operation, the intraperitoneal injection with DFA was arranged every 12 h and for a total of 7d. The changes of Iron ion concentration were measured at perihematomaat different time points after the medicine was given. OX42 immunohistochemical staining observed microglia change at perihematoma. ELISA method determined the changes of IL-13 and TNF-a content of brain tissue. Neurological deficit scores and Nissl staining were used to observe the situation of neurological function and neuronal loss of rats after DFA treatment. 1 d After the start of ICH, the concentration of iron in perihematoma was significantly higher than that of animalsin sham-operated group and could sustain for28 d. At the same time, the quantities of local microglial cells were significantly increased. After applying DFA, the concentration of iron ions in the brain tissue around the hematoma was significantly reduced, so did the number of microglial cells and activation of neurotoxic cytokines [IL-10 and TNF-a content] secreted by microglial cells was significantly reduced. At the same time, the loss of neurons in the tissue around of the hematoma was significantly reduced and neurological deficit scores were significantly reduced, iron ions which were sustainedly released by hematoma after ICH can activate the local microglia and cause secondary brain injury. DFA curb excessive activation of microglia and reduce neuronal death of ICH by means of clearinf away iron ions of brain tissue surrounding the hematoma, thus improve secondary neurological dysfunction
RESUMO
Objective To study the expression of p53,p16,PCNA protein in esophageal carcinoma and its relationship to sexual distinction,the location of disease,the biological level,the depth of invasion and lymph node metastasis.Methods 118 patients with esophageal carcinoma were included in the study,all of them were treated for the first time.p53,p16 and PCNA protein in the 118 cases of esophageal carcinoma were detected by immunohistochemical assay(SP technique). Results The positive expression of p53, p16, PCNA protein in 118 patients was 80 %(92/118),42%(50/118)and 97%(115/118),respectively.The positive expression of p53,PCNA protein were irrelated to the sexual distinction,the location of disease,the biological level,the depth of invasion and the lymph node metastasis.The loss of p16 was significantly related to the depth of invasion and the lymph node metastasis(P