Background: Human obstructive airway diseases are histopathologically characterized by inflammatory cell infiltration, goblet cell hyperplasia, and mucus hypersecretion in airways. We prepared a rat model of airway injury by exposure of sulfur dioxide (SO₂) and then evaluated the effects of S-carboxymethylcysteine (S-CMC), a mucoregulant. Methods: Rats were exposed to SO₂ gas for 44 days and orally given S-CMC at 250 mg/kg, twice daily, from 21 to 44 days of exposure for histopathological and immunohistochemical evaluation. Results: SO₂ exposure induced inflammatory cell infiltration and mucus cell increase in rat airways. S-CMC treatment significantly decreased this inflammatory cell infiltration in proximal and peripheral airways. Morphometrically, SO₂ exposure significantly increased the number of Alcian blue (pH 2.5)- and periodic acid-Schiff (AB/PAS)-positive cells in rat airways (11.8 × 10^–2 cell/nuclear profiles per micrometer basement membrane) compared to normal rat airways (1.6 × 10^–2 cell/nuclear profiles per micrometer basement membrane). S-CMC treatment significantly decreased the number of AB/PAS-positive cells (4.4 × 10^–2 cell/nuclear profiles per micrometer basement membrane, p < 0.01 vs. SO₂-exposed rats). Immunohistochemically, SO₂ exposure increased the expression of mucin 5AC (MUC5AC) protein in the airway epithelium of rats, but S-CMC treatment inhibited the increase. Conclusions: The increased mucus cells and MUC5AC protein expression seem associated with SO₂-induced airway inflammation in rats. The fact that S-CMC suppresses airway inflammation and the increase in mucus cells and MUC5AC protein expression suggests that this mucoregulant may be advantageous in the treatment of inflammatory airway diseases with goblet cell hyperplasia.

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Abstract:We encountered with a case of spontaneously occurring malignant cystic schwannoma on the intracranial trigeminal nerve in a rat (32-week-old male Crj:Wistar). The tumor was intermixtures of the solid and cystic areas. The solid area was densely cellular, and pleomorphic spindle-shaped cells with elongated bizarre nuclei, and mitoses were present. The cystic area was less cellular, and cells with less cytoplasm were sporadically present in the area. Morphologically and immunohistochemically (staining with S-100), the solid and cystic areas were considered typical Antoni type A and B, respectively. Taken together, the results indicate that the tumor is a spontaneous malignant cystic schwannoma. In this connection, most cells lining the cysts were positive for S-100 and negative for Factor VIII, while HE staining showed that degenerative vessels were absent in the tumor. Therefore, in this case, we assumed that the origin of the cysts was not from the vessel but from the tumor per se. ( Spontaneously occurring peripheral nerve tumors of rats are infrequent and especially malignant schwannoma in the intracranial trigeminal nerve is rare [1][2][3][4] . Experimentallyinduced tumors of cranial, spinal, and peripheral nerves have been reported in rats treated with direct-acting alkylating agents (for example, N-nitrosoethylurea, methylmethane sulfonate) 5 , and such tumors sporadically with cysts are found in the central and peripheral nerve in rats. However, spontaneous occurrence of intracranial schwannoma with cysts is extremely rare and uncertain. Recently, we encountered with a case of spontaneously occurring malignant cystic schwannoma on the intracranial trigeminal nerve in rats, and will report here on its gross, histological and immunocytochemical characteristics.A 32-week-old male Crj:Wistar rat (SPF, Charles River, Japan) found in the extreme state of rapid body weight loss, emaciation, unkempt fur, and dyspnea, was euthanized under deep ether anesthesia to death in line with the standard operational procedures for the institutional animal care management. At necropsy, edema-like infiltrative mass was found at the bottom of the cranial cavity (Fig. 1). The pituitary gland and the trigeminal nerve were involved in this mass. The mass compressed the ventral brain. Other findings included small-in-size spleen and liver, involution of thymus, discoloration of prostate, and dilatation of brain ventricle.The cranium including the tumor was fixed in 10% buffered formalin. A protrusion (probably pituitary gland) from the brain base was removed and used for tissue specimen without decalcification. The entire rest (the cranium, tumor, and brain base) was decalcified with 5% formic acid in formalin, and then the center and portion near to the nasal cavity of the tumor was sectioned in a coronary form and paraffin-embedded. For light-microscopic observation, the protrusion, the cranium, and the nasal cavity were stained with hematoxylin-eosin (HE), Klüver-Barreta's stain. For immuno-histochemical observation, ea...

To clarify the involvement of peroxisome proliferator‐activated receptors (PPARs) in atherosclerotic plaque formation, we investigated the expression patterns of mRNA and protein of PPARα and PPARγ in human aorta. Atheromatous plaque, fatty streak, and diffuse intimal thickening (DIT) were separated macroscopically, and each sample was divided into halves. Half of them were used for analysis of mRNA expression with reverse transcription‐polymerase chain reaction and the others were used for histologic analysis. Both PPARα and PPARγ mRNA were detected in all atheromatous plaques, all fatty streaks, and in some DIT. However, expressions of PPARα and PPARγ were obviously less frequently found in DIT than in atheromatous plaques, and the intensity of these expressions was stronger in the atheromatous plaques than in the DIT. Compared with PPARα, PPARγ mRNA was expressed more frequently in atheromatous plaques. In atheromatous plaques, PPARγ mRNA was expressed independently, whereas PPARα mRNA was coexpressed with PPARγ. PPARγ protein was obviously found in the nuclei of endothelial cells, macrophages, mononuclear cells, and smooth muscle cells in the aortic intima. These results suggest that expressions of PPARα and PPARγ in human aortic wall are involved in atherogenesis from the early stages.