The value of prenatal ultrasonography in the diagnosis of congenital anal atresia / 中国基层医药

Objective To evaluate the clinical value of prenatal ultrasound in the diagnosis of congenital anal atresia.Methods A retrospective analysis was studied from January 2013 to December 2015 which analyzed abnormal sonographic features by prenatal ultrasound screening in 13 cases of anal atresia.Results 13 cases of anal atresia were confirmed after abortion,miscarriage or birth which were not probed target ring signby prenatal ultrasound screening.That included 2 simple atresia cases and 11 cases associated with other malformations and abnormalities including 8 cases with bowel dilatation and 3 cases with intestine visible echogenic meconium. Conclusion Prenatal ultrasound screening for fetal congenital anal atresia can be detected.But for lacking of specific diagnostic standard,the detection rate of anal atresia remains very low.

Role of andrographolide in protection of CCl4-induced acute liver injury in mice / 实用医学杂志

Objective To investigate the role of andrographolide (AP) in protection of carbon tetrachloride (CCl4)-induced acute liver injury in mice and the possible mechanisms. Methods The mice were randomly divided into five groups, including two groups with different doses of AP (50 mg/kg and100 mg/kg), a control group, a CCl4 model group, and a silymarin group. Serum levels of alanine aminotransferase (ALT), aspartateminotransferase (AST), hepatic malondialdehyde (MDA), and glutathione (GSH) were examined. Pathological changes in the liver were observed. RT-PCR was used to detect the expressions of tumor necrosis factor-a (TNF-α) and heme oxygenase-1 (HO-1) mRNA. Results As compared with CCl4 model group, serum levels of ALT and AST and hepatic MDA activity were significantly decreased in AP group (100 mg·kg-1), along with a remarkable increase in hepatic GSH content. Pretreatment with AP at a high dose alleviated histopathological changes induced by CCl4. A markedly increased level of TNF-a induced by CCl4 was reduced by AP, while HO-1at transcriptional level was dramatically elevated following AP pretreatment. Conclusions AP plays a role in protection of CCl4-induced acute liver injury by inhibiting lipid peroxidation and reducing formation of free radicals, the mechanism may be involved in inhibition of TNF-αand activation of HO-1.

Establishment of a murine model of hepatic steatosis induced by chronic viral hepatitis / 南方医科大学学报

<p><b>OBJECTIVE</b>To establish a animal model of hepatic steatosis induced by chronic viral hepatitis in C(57)BL/6 mice.</p><p><b>METHODS</b>C(57)BL/6 mice were randomly assigned to control group, high-fat diet group, mouse hepatitis virus strain A59 (MHV-A59) virus infection group, and high-fat diet plus virus infection group. At 13 weeks of the experiment, serum samples were collected to detect MHV antibodies and transaminase and lipid levels. The hepatic pathologies of the mice were examined with Oil red O staining of the frozen sections the and HE staining of paraffin-embedded sections.</p><p><b>RESULTS</b>The mice in the two virus infection groups showed strong positivity of MHV antibodies in the serum. Compared with the control group, the mice in high-fat diet group and the two virus infection groups had significantly increased AST and ALT levels with also elevated TC and LDL-C levels. The two virus infection groups both exhibited obvious pathologies in the liver characteristic of chronic viral hepatitis with increased lipid accumulation in the hepatocytes.</p><p><b>CONCLUSION</b>We have successfully established a mouse model of hepatic steatosis induced by chronic viral hepatitis, which provides the basis for further study of the disease mechanism.</p>

Study on the pathological changes of the lung and brain in mice during heat stress / 中华急诊医学杂志

Objective To prepare mouse model with heat stress and determine its pathological changes of the lung and brain during heat stress. Methods BALB/c mouse were randomly (random number) divided into two groups, control group and heat stress group. The animals in the control group were sham- heated at a temperature of ( 25 ± 0.5) ℃ and humidity of (35 ± 5 ) %. The animals of heat stress group were placed in a prewarmed incubator maintained at (35.5 ± 0.5) ℃ and relative humidity of (60 ± 5) %. Rectal temperature (Tc) was monitored, and when Tc respectively reached 39 ℃, 40 ℃ , 41 ℃ and 42 ℃, those study animals were killed. The other animals were removed from the incubator and allowed to cool at an ambient temperature of (25 ±0. 5)℃ and humidity of (35 ±5)% , respectirvely for 12 and 24 hrs when Tc reached 41 ℃ , and for 6 hrs when Tc reached 42 ℃. The lung and brain of all the animals were isolated. Hematoxylin and eosin stain and light microscope were used to detect their pathological changes. Results All the animals displayed uniform response to the heat stress. Low degree of heat stress could induced obviously pathological changes of the lung, progressively greater damage to lung with further congestion of lung matrix, asystematic hemorrhage of alveolar space, abscission of alveolar epithelial cell and disappear of pulmonary alveolus tissue structure were detected with the rise of Tc to 42 ℃. However, absorption of congestion and hemorrhage and recovery of pulmonary alveolus tissue structure could also be seen with cooling at ambient temperature. With low degree of heat stress, the brain only showed moderate edema. Neuronal denaturation and necrosis were detected when Tc reached to 42 ℃. Interestingly, the lesions of brain further aggravated even through cooling treatment after Tc reached to 42 ℃ , but recovery could been observed after cooling treatment followed with Tc of 41 ℃. Conclusions The pathological changes of the lung and brain showed distinctive lesions to heat stress and cooling treatment, and these changes were correlated with the timing and time of cooling treatment, which provide the experimental basis to further study the mechanisms between the heatstroke and multiple organ dysfunction syndrome (MODS).