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In this study, we examined the relationship between the effect of a zinc coating on protecting carbon steel against biofilm formation in both air and water environments. SS400 carbon steel coupons were covered with a zinc thermal spray coating or copper thermal spray coating. Coated coupons were exposed to either air or water conditions. Following exposure, the surface conditions of each coupon were observed using optical microscopy, and quantitatively analyzed using an x-ray fluorescence analyzer. Debris on the surface of the coupons was used for biofilm analysis including crystal violet staining for quantification, Raman spectroscopic analysis for qualification, and microbiome analysis. The results showed that the zinc thermal spray coating significantly inhibited iron corrosion as well as biofilm formation in both air and water environments. The copper thermal spray coating, however, accelerated iron corrosion in both air and water environments, but accelerated biofilm formation only in a water environment. microbially-influenced-corrosion-related bacteria were barely detected on any coupons, whereas biofilms were detected on all coupons. To summarize these results, electrochemical corrosion is dominant in an air environment and microbially influenced corrosion is strongly involved in water corrosion. Additionally, biofilm formation plays a crucial rule in carbon steel corrosion in both air and water, even though microbially-influenced-corrosion-related bacteria are barely involved in this corrosion.

Drug-coated balloon angioplasty (DCBA) has been recognized for its utility in preventing in-stent re-restenosis (ISR); however, imaging of the neointima immediately after treatment and during follow-up has only been described in a few case reports. This study aimed to determine the efficacy and mechanism of the DCBA using imaging studies both immediately after the DCBA and during the follow-up period. We enrolled 15 consecutive patients who underwent DCBA for in-stent restenosis (ISR). The in-stent neointimal volume was evaluated using optical coherence tomography (OCT), and the in-stent yellow grade was assessed using coronary angioscopy (CAS) immediately after DCBA and during the median follow-up period of 9 (8-15) months. The neointimal volume was significantly reduced from 77.1 ± 36.2 mm 3 at baseline to 60.2 ± 23.9 mm 3 immediately after DCBA (p = 0.0012 vs. baseline) and to 46.7 ± 21.9 mm 3 during the follow-up (p = 0.0002 vs. post DCBA). The yellow grade of the residual plaques at the ISR lesion, which indicated plaque vulnerability, was significantly decreased in the follow-up CAG (from baseline: 1.79 ± 1.03, during the follow-up: 0.76 ± 0.82; p < 0.0001). These data suggest that DCBA may inhibit neointimal formation and provide angioscopic intimal stabilization for ISR lesions.

Saphenous vein graft aneurysm (SVGA) is one of the chronic complications after coronary aorta bypass grafting (CABG) and may be caused by atherosclerosis-like phenomena of the vein graft, weakness around the vein valve, rupturing of the suture of the graft anastomosis, or perioperative graft injury. We describe a case of a large, growing saphenous vein graft aneurysm that was followed serially by chest radiography and computed tomography. Eighteen years after CABG, an SVGA (23 × 24 mm) was incidentally detected. The patient was asymptomatic and was followed conservatively. Four years later, coronary computed tomographic angiography showed that the giant aneurysm had grown to 52.1 by 63.8 mm and revealed a second, smaller aneurysm. Finally, the SVG was ultimately resected without bypass via off-pump surgery. Therefore, this case suggested that aggressive treatment that includes surgical intervention should be considered before the aneurysm becomes larger, even if it is asymptomatic.

Serum KL-6 reflects alveolar damage and regeneration of type II pneumocytes, indicating disease activity in various interstitial lung diseases. We conducted a descriptive and observational multiple case-control study to determine the distribution of serum KL-6 levels in pediatric patients with or without respiratory diseases. Subjects were recruited from the patients of a teaching hospital in the suburb of Tokyo. A consecutive series of 401 children (0-16 years old) underwent blood sampling for many clinical reasons. They comprised the following four groups: pneumonia (n = 96), bronchial asthma (n = 101), measles (n = 102), and nonrespiratory diseases (n = 102) as a control group. Standard upper limits of serum KL-6 in a group of children with nonrespiratory disease were 250 U/mL, or half the adult level. No gender or age differences were observed. Elevated serum KL-6 concentrations were observed in severe pneumonia, acute exacerbations of asthma, and measles pneumonia. In the measles group, KL-6 values reflected the presence and severity of complicating pneumonia. We conclude that serum KL-6 levels exceeding 250 U/mL were rarely observed in children without respiratory diseases. In contrast, a substantial proportion of children with common respiratory diseases showed mild to moderate increases in serum KL-6 levels. Elevated serum KL-6 in these children may reflect the presence of alveolar damage, followed by regeneration of type II pneumocytes. However, in order to use serum KL-6 as a marker of interstitial lung diseases in children, a cutoff level should be determined separately., (Copyright 2002 Wiley-Liss, Inc.)

Endothelial cells (EC) produce cytokines, such as interleukin (IL)-1, IL-6, IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF). These cytokines have an important role in the proliferation and differentiation of hematopoietic progenitor cells. On the other hand, anticancer agents generally cause hematopoietic disorders. However, little is known about the effects of chemotherapeutic agents on the secretion of cytokines from EC. Therefore, we investigated if treatment with platinum compounds may stimulate EC to secrete cytokines. EC newly isolated from a human umbilical vein were exposed to cisplatin, carboplatin, or TRK-710 for 80 min, then the cells were washed and placed in fresh medium. The levels of cytokines in the fresh medium were measured by the ELISA method, the levels of intracellular hydrogen peroxide (H2O2) were measured by flow cytometry, and the rhodamine 123-stained live mitochondria of the EC were observed under a confocal laser microscope. Platinum compounds induced cytokine production in human EC: cisplatin most prominently induced the release of IL-1 and IL-6, and TRK-710 had the greatest ability to induce the release of GM-CSF. Intracellular H2O2 production and IL-8 release were transiently induced immediately after treatment with platinum compounds, leading to IL-1 release when H2O2 production was eliminated. These results may provide new insights into the hematological toxicity induced by anticancer agents and the role of IL-1 and IL-6 secreted from EC in this toxicity.