Inhalation exposure by cigarette smoke: Effects on the progression of bleomycin- and lipopolysaccharide-induced lung injuries in rat models.

The toxic substances of cigarette smoke (CS) induce inflammatory responses in the lung by recruiting inflammatory cells. In this study, we investigated the effects of CS on the progression of lung disease in bleomycin (BLM) and lipopolysaccharide (LPS)-induced lung injury rat models. Briefly, rats were exposed to CS via inhalation (nose-only) for 28 consecutive days, for 4 h per day. Using an automatic video instillator, rats were administered a single dose of 2.5 mg/kg BLM (day 1) or 0.5 mg/kg LPS (day 26), prepared in 50 µL phosphate-buffered saline (PBS) solution. Examination of the bronchoalveolar lavage fluid (BALF) revealed that the number of neutrophils increased in a concentration-dependent manner of CS. Exposure to CS also enhanced the expression of cytokines, i.e., CCL2 (MCP-1), CCL3 (MIP-1α), CXCL2 (CINC3), CXCL10 (IP-10), TNF-α, IFN-γ, IL-2, IL-4 in the BALF of the vehicle (VC) and BLM groups in a concentration-dependent manner. In particular, the expressions of CCL2, CXCL10 and TNF-α were remarkably upregulated in the BLM + CS 300 treatment as compared to VC, while there were no differences in these cytokine levels in the serum following CS exposure. Exposure to CS resulted in compacted alveolar spaces and macrophage aggregation in the lung tissues following BLM and LPS treatments. Compared to VC, pulmonary fibrosis and chronic inflammation of bronchioloalveoli were observed in the BLM + CS treatment and inflammatory cell infiltration of bronchioloalveoli was observed in the LPS + CS treatment in a concentration-dependent manner by CS. The expression levels of CCL2 and IFN-γ in the lung tissues were increased similar to the levels obtained in BALF, in a concentration-dependent manner by CS. Taken together, these results indicate that repeated exposure to CS may exacerbate the lung injury initially caused by BLM and LPS.

Retinal capillary hemangioma treated with verteporfin photodynamic therapy and intravitreal triamcinolone acetonide.

PURPOSE: To report a case of retinal capillary hemangioma treated with verteporfin photodynamic therapy combined with intravitreal triamcinolone acetonide. METHODS: A 15-year-old female presented with metamorphopsia in the left eye for 7 days. Examination showed peripheral endophytic retinal capillary hemangioma, macular edema, and a best-corrected visual acuity of 20/50. The hemangioma and macular edema were treated with verteporfin photodynamic therapy and intravitreal triamcinolone acetonide. RESULTS: After 5 months of follow-up, involution of the hemangioma, reduction of macular edema, decrease of the feeder and draining vessel diameter, and improvement of best-corrected visual acuity to 20/25 was seen. CONCLUSIONS: This verteporfin photodynamic therapy combined with intravitreal triamcinolone acetonide appeared to cause involution of the hemangioma with reduction in macular edema and improvement in visual acuity.

Anterior lens capsule abnormalities in Alport syndrome.

Alport syndrome is a hereditary, progressive disease characterized by progressive nephritis, sensorineural deafness, and ocular abnormalities, including anterior lenticonus. The ultrastructure of the lens capsule abnormalities in Alport syndrome is reported. Four anterior lens capsules from 31-year-old patient and 26-year-old patient with lenticonus who were affected by the Alport syndrome were obtained at capsulectomy. And all four anterior lens capsules were examined by transmission electron microscopy. The histopathologic findings showed that the thickness of the anterior lens capsules was decreased (4-13 microm) and that there were many vascular dehiscences localized at the inner part of the lens capsule. There were large numbers of capsular dehiscences containing fibrillar materials and vacuoles. The anterior capsules were clearly fragile in this disease, forming the basis for the progressive lenticonus and anterior polar cataract.

Platelet activation in patients with diabetic retinopathy.

To clarify the diabetic complications mediated by increased platelet activity, we undertook a study of the mean platelet component (MPC), as determined by an automated hematologic analyzer (ADVIA 120, Bayer). Prothrombin time (PT), activated partial thromboplastin time (aPTT), and fibrinogen were also measured to investigate blood viscosity abnormalities. MPC was determined in 100 healthy controls and in 100 diabetic patients, the latter of which were subdivided into no diabetic retinopathy (DR) (n = 25), nonproliferative DR (n = 30), and proliferative DR (n = 45) groups. The mean MPC level was 26.9 g/dl in the control group and 22.5 g/dl in the diabetic patients (p < 0.05). PT and aPTT were similar for the diabetic patients and the controls; however, their corresponding fibrinogen levels were significantly different between the two groups(3.26 +/- 1.14 g/L vs. 4.21 +/- 2.35 g/L, p < 0.05). Our results suggest that platelet hyperfunction in diabetic patients may be implicated in the pathogenesis of diabetic retinopathy.