No abstract available.

Abnormalities in the anatomy of pulmonary arteries may have heritable or environmental causes and involve a reduction or enlargement in transverse diameters of the blood vessels eg, congenital and developmental disorders, acquired intrinsic causes, extrinsic compression, and constriction. Pulmonary hypertension, pulmonary artery aneurysm and pseudoaneurysm, and idiopathic dilatation can also increase the diameter of a pulmonary artery. Multi-detector computed tomography (CT) is useful to evaluate each pulmonary artery and to diagnose the conditions that alter the diameter of the pulmonary artery. It is important to be familiar with the CT features of a variety of disorders to allow for accurate diagnoses and appropriate therapeutic management.

Recent evidence supports a neuroprotective role of Src homology 2-containing protein tyrosine phosphatase 2 (SHP-2) against ischemic brain injury. However, the molecular mechanisms of SHP-2 activation and those governing how SHP-2 exerts its function under oxidative stress conditions are not well understood. Recently we have reported that reactive oxygen species (ROS)-mediated oxidative stress promotes the phosphorylation of endogenous SHP-2 through lipid rafts, and that this phosphorylation strongly occurs in astrocytes, but not in microglia. To investigate the molecules involved in events leading to phosphorylation of SHP-2, raft proteins were analyzed using astrocytes and microglia. Interestingly, caveolin-1 and -2 were detected only in astrocytes but not in microglia, whereas flotillin-1 was expressed in both cell types. To examine whether the H2O2-dependent phosphorylation of SHP-2 is mediated by caveolin-1, we used specific small interfering RNA (siRNA) to downregulate caveolin-1 expression. In the presence of caveolin-1 siRNA, the level of SHP-2 phosphorylation induced by H2O2 was significantly decreased, compared with in the presence of control siRNA. Overexpression of caveolin-1 effectively increased H2O2-induced SHP-2 phosphorylation in microglia. Lastly, H2O2 induced extracellular signal-regulated kinase (ERK) activation in astrocytes through caveolin-1. Our results suggest that caveolin-1 is involved in astrocyte-specific intracellular responses linked to the SHP-2-mediated signaling cascade following ROS-induced oxidative stress.
Animals ; Astrocytes/*metabolism ; Caveolin 1/*genetics/metabolism ; Caveolin 2/genetics ; Cell Line ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression ; Humans ; Microglia/metabolism ; Phosphoric Monoester Hydrolases/*metabolism ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 11/*metabolism ; Rats ; Reactive Oxygen Species/*metabolism

BACKGROUND/AIMS: Cyclophosphamide (CP) is a promising treatment for severe cases of paraquat (PQ) poisoning. We investigated the effective dose of CP for mitigating PQ-induced lung injury. METHODS: Adult male Sprague-Dawley rats were allocated into five groups: control, PQ (35 mg/kg, intraperitoneal injection), and PQ + CP (1.5, 15, or 30 mg/kg). The dimensions of lung lesions were determined using X-ray microtomography (micro-CT), and histological changes and cytokine levels were recorded. RESULTS: The micro-CT results showed that 15 mg/kg CP was more effective than 1.5 mg/kg CP for treating PQ-induced lung injury. At a dose of 1.5 mg/kg, CP alleviated the histological evidence of inflammation and altered superoxide dismutase activity. Using 15 mg/kg CP reduced the elevated catalase activity and serum transforming growth factor (TGF)-beta1 level. CONCLUSIONS: A CP dose of > 15 mg/kg is effective for reducing the severity of PQ-induced lung injury as determined by histological and micro-CT tissue examination, possibly by modulating antioxidant enzyme and TGF-beta1 levels.
Animals ; Catalase/metabolism ; Cyclophosphamide/*pharmacology ; Cytokines/metabolism ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Immunosuppressive Agents/*pharmacology ; Inflammation Mediators/metabolism ; Lung/*drug effects/metabolism/pathology/radiography ; Lung Injury/chemically induced/diagnosis/*drug therapy/metabolism ; Male ; Oxidative Stress/drug effects ; *Paraquat ; Pulmonary Edema/chemically induced/diagnosis/*drug therapy/metabolism ; Rats ; Rats, Sprague-Dawley ; Severity of Illness Index ; Superoxide Dismutase/metabolism ; Transforming Growth Factor beta1/metabolism ; X-Ray Microtomography