ABSTRACT
<p><b>OBJECTIVE</b>To explore the characters of lung injury induced by tin dusts and to provide the diagnosis evidence of tin pneumoconiosis.</p><p><b>METHODS</b>Forty SD rats were randomly divided into four groups: the group exposed to tin dusts from smelting workshop, the group exposed to tin dusts from tin refining workshop, the positive control group exposed to standard quartz dusts and the negative control group exposed to saline. The pathological changes of rat lungs were observed dynamically.</p><p><b>RESULTS</b>In rats exposed to tin dusts, on the 30th day after exposure to tin dusts, the scattered hoar tip size of the spots in surface and section of the lungs were observed, the scattered focal granulomatous inflammation around the small bronchi and dust particles in lung tissue were observed under microscope; on the 90th day after exposure to tin dusts, the granulomatous inflammation increase, the fibroblasts proliferation, collagen fibers formation and positive VG staining were found. There were significant differences, as compared with positive or negative controls (P < 0.05). These pathological changes were basically the characters of specific pathological changes in early tin pneumoconiosis.</p><p><b>CONCLUSION</b>Non-ferrous metal tin dusts can induce the specific lung injury (granuloma formation) in lung tissue of rats exposed to tin dusts, which fulfilled the diagnostic criteria of specific pathological changes in early tin pneumoconiosis.</p>
Subject(s)
Animals , Rats , Dust , Lung , Pathology , Lung Injury , Diagnosis , Pathology , Rats, Sprague-Dawley , TinABSTRACT
<p><b>OBJECTIVE</b>To investigate the diagnostic value of histopathological changes in the liver of patients with neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD).</p><p><b>METHODS</b>Liver specimens from 10 cases of NICCD were evaluated by hematoxylin-eosin stain, histochemistry and immunohistochemistry (EnVision method). SLC25A13 mutation analysis was performed to correlate with histopathology.</p><p><b>RESULTS</b>Most specimens showed varying degrees of fat deposition in hepatocytes, necrotic inflammation, cholestasis and fibrosis (so-called tetralogy). The combination of the above four histological changes was highly characteristic for NICCD. With the progression of the disease, hepatic fibrosis deteriorated and ultimately led to cirrhosis.</p><p><b>CONCLUSIONS</b>NICCD should be suspected in the presence of cholestasis during infancy. A liver biopsy must be performed to rule out other liver diseases. The tetralogy of the hepatic histopathological changes has a highly diagnostic value for NICCD, which is also practical for accurately assessing the degree of inflammation and fibrosis, and similarly the progression of hepatic cirrhosis.</p>
Subject(s)
Female , Humans , Infant , Male , Biopsy , Calcium-Binding Proteins , Genetics , Metabolism , Cholestasis, Intrahepatic , Genetics , Pathology , Disease Progression , Hepatocytes , Pathology , Liver , Pathology , Liver Cirrhosis , Pathology , Mitochondrial Membrane Transport Proteins , Genetics , Mutation , Organic Anion Transporters , Genetics , MetabolismABSTRACT
Nerve growth factor (NGF) is mainly secreted by the neuroglia cells, which can exert biological effect through its receptors on the specific target cell surface. NGF is closely related to neurocyte growth, differentiation and apoptosis. As a neurotropic virus, HSV-1 an easily lead to neurocyte, neuroglia cells death or apoptosis. In this study, the U251 human glioma cells were chosen as target cells to study the change of NGF and its receptors in the apoptosis process of HSV-1 infection. Our results showed that U251 cells were permissive to HSV-1 replication. In the apoptosis process of HSV-1 infected U251 cells, the expression of both NGF and P75NTR increased and then decreased, while the expression of TrkA decreased gradually. These result indicated that HSV-1 was able to induce the abnormal expression of NGF and its receptors in U251 cells.