Objective To study the value of postmortem imaging on the diagnosis of intestinal perforation.Method Postmortem imaging(PMCT and PMCTA)data of 2 intestinal perforation deaths(and 4 controlled cases)were reviewed retrospectively.Diagnosing capacities of intestinal perforation by postmortem imaging method were further investigated.Results PMCT is sensitive in detecting the free air and liquid induced by intestinal perforation.PMCT can sometimes detect the gravity-dependent purulent secretions in the abdominopelvic cavity.PMCTA can visualize the extravasation of contrast agent from the perforation,which can be used to locate the accurate perforation region.Conclusion Postmortem imaging method(PMCT and PMCTA)is an important tool for the diagnosis of intestinal perforation,which can not only be used as a forensic diagnosis method,but is also useful to locate the perforation site before an forensic autopsy.

Objective:To explore the relationship between hypoxia and fertility in female mice.Methods:Twenty-one clean-grade 14-week Kunming female mice were selected and divided into hypoxia groups ( n=11) and normoxia groups ( n=10), and raised under low oxygen concentration (10%-20.5%) and normal oxygen concentration (20.5%) respectively. Four weeks later, hypoxic mice were returned to normoxia environment. Two groups of 21 females were mated with males, the quantity of the litters and body mass at birth were recorded. These females were maintained until 43 weeks to repeat the hypoxic and mating experiments described above. Two weeks after the secondary hypoxia, mating and delivery, these female mice were sampled under anesthesia for inner canthus blood, and the blood estradiol and progesterone were measured by a Roche biochemical analyzer. The mice were put to death by giving over dosage of anesthesia drug; oocytes, ovaries and uterus tissues were obtained, for detection of reactive oxygen species of the oocytes, and HE staining of the ovaries and uterus. Results:The number of litters produced in the young hypoxia group was 13.64±3.35, which was slightly higher than that in the young normoxia group (13.22±1.92), but the difference was not significant ( P=0.734). The birth body mass of the litters in the young hypoxic group [(1.73±0.20) g] was significantly lower than that in the young normoxic group [(1.82±0.22) g, P<0.001]. The mean number of litters in the old hypoxic group (5.11±3.58) was significantly higher than that in the old normoxic group (1.38±2.56, P=0.022). Compared with 23 weeks female normoxia mice, estradiol levels decreased in both the old hypoxia and old normoxic groups ( P=0.019; P=0.035), but there was no significant difference in estradiol level between old hypoxia and old normoxic groups ( P=0.913). There was no significant difference in reactive oxygen species of the oocytes between old normoxic and old hypoxic mice ( P>0.05). Tissue HE staining showed that the old normoxic mice had obvious uterine hyperemia, and the outlook of the uterus of the old hypoxic mice was normal. The old hypoxia mice had more antral follicles than the normoxic group and the size of the follicles was more even. Conclusion:The hypoxia mice produced more offspring than the normoxia mice, however, the birth body mass of the offspring was significantly lower than that in normoxic mice. The ovaries of the old hypoxic mice contained more follicles than the old normoxic mice.

Objective:To explore the relationship between hypoxia and fertility in female mice.Methods:Twenty-one clean-grade 14-week Kunming female mice were selected and divided into hypoxia groups ( n=11) and normoxia groups ( n=10), and raised under low oxygen concentration (10%-20.5%) and normal oxygen concentration (20.5%) respectively. Four weeks later, hypoxic mice were returned to normoxia environment. Two groups of 21 females were mated with males, the quantity of the litters and body mass at birth were recorded. These females were maintained until 43 weeks to repeat the hypoxic and mating experiments described above. Two weeks after the secondary hypoxia, mating and delivery, these female mice were sampled under anesthesia for inner canthus blood, and the blood estradiol and progesterone were measured by a Roche biochemical analyzer. The mice were put to death by giving over dosage of anesthesia drug; oocytes, ovaries and uterus tissues were obtained, for detection of reactive oxygen species of the oocytes, and HE staining of the ovaries and uterus. Results:The number of litters produced in the young hypoxia group was 13.64±3.35, which was slightly higher than that in the young normoxia group (13.22±1.92), but the difference was not significant ( P=0.734). The birth body mass of the litters in the young hypoxic group [(1.73±0.20) g] was significantly lower than that in the young normoxic group [(1.82±0.22) g, P<0.001]. The mean number of litters in the old hypoxic group (5.11±3.58) was significantly higher than that in the old normoxic group (1.38±2.56, P=0.022). Compared with 23 weeks female normoxia mice, estradiol levels decreased in both the old hypoxia and old normoxic groups ( P=0.019; P=0.035), but there was no significant difference in estradiol level between old hypoxia and old normoxic groups ( P=0.913). There was no significant difference in reactive oxygen species of the oocytes between old normoxic and old hypoxic mice ( P>0.05). Tissue HE staining showed that the old normoxic mice had obvious uterine hyperemia, and the outlook of the uterus of the old hypoxic mice was normal. The old hypoxia mice had more antral follicles than the normoxic group and the size of the follicles was more even. Conclusion:The hypoxia mice produced more offspring than the normoxia mice, however, the birth body mass of the offspring was significantly lower than that in normoxic mice. The ovaries of the old hypoxic mice contained more follicles than the old normoxic mice.

Objective: To establish an animal model of hypoxia-induced bronchopulmonary dysplasia asso-ciated with pulmonary hypertension (BPD-PH). Methods: C57BL/6 male and female specific pathogen free mice mated and female mice with their offspring mice were randomly divided into normoxic group and hypoxia group by way of numerical method.Normoxic group was placed in the indoor environment directly.Hypoxia group was placed in 120 mL/L oxygen concentration environment within 12 hours after birth.Body weight gain and mortality of the neonatal mice were recorded.The mice lungs and hearts were harvested on day 14 for immunofluorescence staining and HE staining, and Western blot was used to observe the morphological changes and vascular endothelial growth factor (VEGF) protein level. Results: The mortality rates of normoxic group and hypoxic group were 11.8% and 47.3%, respectively.Compared with the normoxic group, body weight of hypoxia group increased slowly, as the final body weight of 2 groups were (12.40±2.33) g and (5.50±0.32) g, respectively, and the difference was significant (χ²=13.38, t=20.50, all P<0.01). Hypoxia group showed higher right ventricular hypertrophy index [(96.00±0.15)% vs.(40.40±4.00)%, t=41.67, P<0.01], fusion of alveolar, diminished microvasculature, thickening alveolar septal, decreased alveolar radiation coefficient (RAC)(19.73±2.33 vs.10.90±1.85) and increased mean linear intercept(MLI) (33.2±4.33 vs.58.70±7.27) with statistical significance, respectively (t=16.27, 9.53, all P<0.01). In the lung HE staining, pulmonary arterial thickening, pulmonary smooth muscle cell proliferation and intimal roughness in immunofluorescence, significantly decreased expression of VEGF protein level by Western blot were observed in hypoxic group (0.41±0.04 vs.1.19±0.08, t=15.10, P<0.01). Conclusions Hypoxia-induced mouse BPD-PH model was consistent with the pathophysiological process of pulmonary vascular remodeling of pulmonary hypertension, which increase pulmonary vascular resistance eventually leading to right ventricular hypertrophy.