BACKGROUND: Organic chemicals have been known to cause allergic diseases such as bronchial asthma and hypersensitivity pneumonitis; however, the possibility that they do not cause irreversible pulmonary fibrosis has not been considered. Polyacrylic acid (PAA), an organic chemical, has caused irreversible progressive pulmonary fibrosis in exposed workers, indicating its potential to induce pulmonary inflammation and fibrosis. Although intratracheal instillation studies are commonly used for evaluating lung pathology, traditional methods face challenges with chemical substances, particularly nanoparticles, which tend to aggregate in suspension and prevent uniform pulmonary distribution. Such aggregation alters the qualitative and quantitative responses to lung injury, limiting accurate assessment of lung pathology. To overcome this limitation, we developed a 'molecular dispersion method' that uses pH modification to negative charges to PAA particles, maintaining their dispersion. Using this method, we investigated the effects of PAA on pulmonary inflammation and fibrosis in a rat model. METHODS: F344 rats were intratracheally instilled with PAA using molecular dispersion (0.1 mg/rat, 1.0 mg/rat), PAA without molecular dispersion (1.0 mg/rat), and normal saline (control group). Rats were sacrificed at 3 days, 1 week, 1 month, 3 months, and 6 months after exposure to examine inflammatory and fibrotic responses. RESULTS: PAA caused persistent increases in neutrophil influx in the bronchoalveolar lavage fluid (BALF) from 3 days to 1 month following instillation. In histopathological findings, the group with molecular dispersion had almost no inflammatory masses in the lung tissue compared to the group without molecular dispersion, and exhibited relatively uniform dispersion. CONCLUSION Intratracheal instillation of dispersed PAA induced neutrophil inflammation and fibrosis in the rat lung, suggesting that PAA might have pulmonary inflammogenicity and fibrogenicity. Intrapulmonary dispersion of PAA particles following intratracheal instillation studies using the molecular dispersion method was similar to that following inhalation studies.
Animals ; Rats, Inbred F344 ; Acrylic Resins/adverse effects* ; Rats ; Inhalation Exposure/adverse effects* ; Male ; Pulmonary Fibrosis/pathology* ; Pneumonia/pathology* ; Lung/pathology* ; Bronchoalveolar Lavage Fluid/cytology*

We report a case of 76 year-old woman who had previously undergone coronary artery bypass grafting (CABG) with the right internal thoracic artery (RITA) bypassed to the left anterior descending artery. Six years after CABG, she developed acute type A aortic dissection, and she was medically treated because the false lumen was thrombosed and it was considered that surgical intervention would be high risk for the patent RITA graft crossing between the sternum and the ascending aorta. During follow-up, her aortic aneurysm enlarged to 57 mm in diameter, and finally she was referred to our hospital for surgical intervention. In this case, preservation of the patent RITA graft was thought to be critical because the RITA graft was the only blood source for the left anterior descending artery. Prior to re-median sternotomy, we performed a right anterior minithoracotomy to make sufficient space between the sternum and the RITA graft, and then instituted peripheral cardiopulmonary bypass to decompress the heart. After re-sternotomy, we ensured minimum dissection of the RITA graft, and we successfully accomplished graft replacement of the ascending aorta to the aortic arch without injuring the patent RITA graft. In cases with a patent RITA graft and an ascending aortic aneurysm close to the sternum, our strategy is considered to be efficient for re-median sternotomy.

Cestode zoonosis cases confirmed by PCR-based mitochondrial DNA analysis were investigated. The cestodiosis included taeniasis, cysticercosis, alveolar echinococcosis, cystic echinococcosis, sparganosis mansoni, diphyllobothriasis and diplogonoporiasis. DNA samples were extracted from the ethanol-fixed, formalin-fixed, paraffin-embedded sections, HE-stained, and the PAS- or acetocarmine-stained samples submitted for histopathology. For PCR-based analysis, cytochrome c oxidase subunit 1 and⁄or cytochrome b genes were amplified by multiplex PCR or conventional PCR coupled with DNA sequencing. Although DNA molecules were degraded in most formalin-fixed samples, smaller gene fragments were successfully amplified and the species causing cestodiosis could be identified by DNA sequence analysis of the amplicons. This review describes cestode zoonosis cases in which mitochondrial DNA analysis was useful not only for routine and retrospective diagnosis, but also for genetic polymorphism analysis and molecular identification of the species associated with pathogenicity. The significance of molecular diagnosis using histopathological specimens for cestode zoonoses is also discussed.