ABSTRACT
This study investigated the expression of lung surfactant proteins (SP-B and SP-C), and regulatory factors [forkhead box A2 (FOXA2) and nitrolyogenic FOXA2 (N-FOXA2)] in the fetal lung of rats with gestational diabetes mellitus (GDM) in order to study the mechanism of pulmonary dysplasia. The rat GDM model was established by using streptozotocin intraperitoneally in the first stage of pregnancy. There were 10 rats in the GDM group, and 10 healthy rats in normal control group without any treatment. Fetal lungs of two groups were taken at day 21 of pregnancy. Blood glucose levels of maternal rats and fetal rats were measured by Roche blood glucose meter. The histological changes in the fetal lung were observed under the light microscope in both groups. The SP-B, SP-C and FOXA2 were determined in the fetal lung of two groups immunohistochemically. The expression levels of SP-B, SP-C, total FOXA2, FOXA2 in nucleus (n-FOXA2), N-FOXA2 proteins were detected by Western blotting, and the relative expression levels of SP-B, SP-C, FOXA2 mRNA in the fetal lung of two groups were detected by RTPCR. The results showed that blood glucose levels of maternal rats and fetal rats in GDM group were higher than those in control group. The light microscope revealed fetal lung development retardation in GDM group. The expression of SP-B and SP-C in GDM group was significantly reduced as compared with control group (P<0.05). As compared with control group, the n-FOXA2 expression was significantly decreased in the fetal lung tissue, and N-FOXA2 was significantly increased in control group (P<0.05), but there was no significant changes in the total FOXA2 (P>0.05). It was concluded that GDM can cause fetal lung development and maturation disorders, and FOXA2 in fetal lung tissue decreases while nitrocellulose FOXA2 increases.
Subject(s)
Diabetes, Gestational/genetics , Hepatocyte Nuclear Factor 3-beta/genetics , Peptides/genetics , Pulmonary Surfactant-Associated Protein B/genetics , Animals , Blood Glucose , Diabetes Mellitus, Experimental/blood , Diabetes Mellitus, Experimental/genetics , Diabetes Mellitus, Experimental/pathology , Diabetes, Gestational/blood , Diabetes, Gestational/pathology , Disease Models, Animal , Female , Gene Expression Regulation, Developmental/genetics , Humans , Lung/growth & development , Lung/metabolism , Lung/pathology , Pregnancy , Pulmonary Surfactant-Associated Proteins/blood , Pulmonary Surfactant-Associated Proteins/genetics , RatsABSTRACT
This study investigated the expression of lung surfactant proteins SP-B and SP-C, and their modulating factors TTF-1 and PLAGL2 in the fetal lung of rats with fetal growth restriction (FGR). The rat FGR model was established by prenatal hypoxia in the first stage of pregnancy, 180 rats for experiment served as hypoxia group, and 197 healthy rats served as normal control group. The FGR incidence in hypoxia was compared with that in normal control group. The histological changes in the fetal lung were observed under the light microscope and electronic microscope in two groups. The SP-B, SP-C, TTF-1 and PLAGL2 proteins were determined in the fetal lung of two groups immunohistochemically. The expression levels of SP-B, SP-C, TTF-1 and PLAGL2 protein and mRNA in the fetal lung of two groups were detected by using Western blotting and RT-PCR respectively. The FGR rat model was successfully established by using hypoxia. Pathologically the fetal lung developed slowly, and the expression levels of SP-B, SP-C, TTF-1 and PLAGL2 protein and mRNA in the fetal lung were significantly reduced in hypoxia group as compared with those in normal control group. It was suggested that maternal hypoxia in the first stage of pregnancy could induce FGR, and reduce the expression of SP-B and SP-C, resulting in the disorder of fetal lung development and maturation.
Subject(s)
Fetal Growth Retardation , Lung/metabolism , Peptides/metabolism , Pulmonary Surfactant-Associated Protein B/metabolism , Animals , Base Sequence , DNA Primers , Female , Lung/embryology , Pregnancy , Rats , Real-Time Polymerase Chain ReactionABSTRACT
BACKGROUND: Inflammatory pseudotumor of the biliary tract is a benign disease, and is extremely rare. Its diagnosis often depends on pathological examination after operation. The histopathological examination shows inflammatory lesions with a polymorphous infiltration and variable amounts of fibrous tissue. This study was undertaken to elucidate that an inflammatory pseudotumor in the right hepatic duct is especially difficult to distinguish from hilar cholangiocarcinoma. METHOD: The clinical data of one patient with inflammatory pseudotumor of the right hepatic duct were analyzed. RESULTS: An occupying lesion of the right hepatic duct was revealed by abdominal ultrasound and magnetic resonance cholangiopancreatography. The right hepatic duct inflammatory pseudotumor was not identified during the operation but was confirmed by postoperative histopathological analysis. The patient recovered well without any serious complication. CONCLUSIONS: The preoperative evaluation for optimizing surgical management is important to the diagnosis of hepatobiliary occupying lesions. The evaluation involves clinical manifestations, imaging appearance and tumor markers. Malignant tumors and possible benign lesions should be considered to avoid aggressive surgical treatment.
