No abstract available.

No abstract available.

No abstract available.

No abstract available.
Hypertension, Renovascular*

No abstract available.
Heart Ventricles*

No abstract available.
Glomerulonephritis*

The pathogenetic role of intrauterine infection to the neonatal pulmonary injury and bronchopulmonary dysplasia was assessed by studying the interleukin-6 (IL-6) level in the umbilical cord blood and the early morphologic changes of the neonatal lung. Patients were grouped into bronchopulmonary dysplasia (4 cases), chorioamnionitis without chronic lung injury (4 cases), and 6 cases without morphologic evidence of chronic lung injury or placental inflammation. IL-6 level of umbilical cord blood was higher in babies with bronchopulmonary dysplasia (17.7 pg/ml) compared to those with chorioamnionitis (4.7 pg/ml) or those with morphologically normal lung and placenta (6.2 pg/ml). Morphologic parameters of neonatal pulmonary injury were hyaline membrane, terminal bronchiole inflammation, terminal bronchiole regeneration, alveolar collapse and fibroblastic proliferation. Bronchiolar regeneration was the most peculiar feature seen in the lung with bronchopulmonary dysplasia. Alveolar collapse and interstitial fibroblastic reaction were commonly seen in bronchopulmonary dysplasia. The postnatal age at death was higher in those with bronchopulmonary dysplasia, although the occurrence of the morphologic changes was related with the chronicity of those lesions. These findings suggest that intrauterine infection is an aggravating factor for the neonatal pulmonary injury and bronchopulmonary dysplasia, although the early stage of the lung injury is not a definitive indicator for the progressive pulmonary damage leading to the bronchopulmonary dysplasia.
Bronchioles ; Bronchopulmonary Dysplasia* ; Chorioamnionitis ; Cytokines ; Female ; Fetal Blood ; Fibroblasts ; Humans ; Hyalin ; Hyaline Membrane Disease ; Infant, Newborn ; Inflammation ; Interleukin-6 ; Lung ; Lung Injury* ; Membranes ; Placenta ; Pregnancy ; Regeneration

No abstract available.
Humans ; Patient Education as Topic* ; Spondylitis, Ankylosing*

Acute posterior multifocal placoid pigment epitheliopathy(APMPPE), first described in 1968 by Gass, is chracterized by rapid loss of central vision secondary to multifocal, yellow-white placoid lesions at the level of the pigment epithelium and choroid and significant visual improvement after spontaneous resolution of the active lesions within several weeks or months. Fluorescein angiography shows chracteristically that the chtoidal fluorescence is not visible at the site of acute lesion in the early arterial and arteriovenous phases and become hyperfluorescent due to staining of the lesions in the late venous phases. We experienced a case of acute multifocal placoid pigment epitheliopathy in 26 years old female patient occurring in both eyes.
Adult ; Choroid ; Epithelium ; Female ; Fluorescein Angiography ; Fluorescence ; Humans