Involvement of protein kinase C in the nitric oxide-mediated peripheral nerve disturbance in endotoxemic rats.

The role of protein kinase C (PKC) in nitric oxide (NO)-mediated peripheral nerve disturbance in lipopolysaccharide (endotoxin, LPS)-treated rat was studied. The impaired Na+,K+ -ATPase activities in sciatic nerves from LPS-treated rats were prevented by aminoguanidine (NO synthase inhibitor) and corrected by PKC agonist in vitro. Using Western blot to determine PKC isoforms alpha and beta polypeptide levels in LPS-treated rat sciatic nerves, we found that alpha isoform was markedly reduced in the particulate fraction, but the beta isoform was unaffected. The alpha and beta isoforms in the cytosolic fractions were not significantly different as compared with control. This diminished particulate PKC alpha isoform was prevented by the treatment of aminoguanidine. Moreover, the motor nerve conduction velocity was significantly reduced in endotoxemic rats and corrected by aminoguanidine. These results indicate that the alteration of PKC alpha isoform in Na+,K+ -ATPase-enriched fraction of sciatic nerve may be related to the NO-mediated peripheral nerve disturbance in endotoxemic rats.

In vitro cytotoxicity of IgG antibodies on vascular endothelial cells from patients with endemic peripheral vascular disease in Taiwan.

A unique peripheral vascular disorder called 'blackfoot disease' is endemic in a limited area on the south-west coast of Taiwan. Clinically, the signs and symptoms of blackfoot disease (BFD) are similar to those of arteriosclerosis and Buerger's disease. A destruction of vascular endothelial cells (ECs) takes place at an early stage in the affected limbs. Currently, the cause of BFD is believed to be artesian drinking water containing a high concentration of arsenic and/or humic substances, although the mechanism of EC destruction is not entirely understood. The purpose of the present study was to examine the factors related to EC damage in BFD. Thus, we investigated the effects of purified IgG collected from patients with BFD (BFD-IgG) and from normal controls (N-IgG) on cultured EC. We found that: (1) EC binding activity of BFD-IgG was significantly higher than that of N-IgG; (2) BFD-IgG, at a concentration higher than 100 microg/ml but not N-IgG, induced concentration-dependent EC cytotoxicity; (3) BFD-IgG at a concentration of 100 microg/ml stimulated neither the release of von Willebrand factor nor the expression of intercellular adhesion molecule-1 by EC. Fluorescent video microscopic examination revealed an increase in transcapillary and interstitial diffusion of nailfold capillary loops in clinically normal fingers of BFD patients. These findings strongly suggested that immunological mechanisms played a significant role in the pathogenesis of BFD. We propose that only persons who produce the IgG anti-endothelial cell antibody are potential victims of BFD.

[Study on cutaneous physio-immuno-pathological status in tinea versicolor].

This study examined 20 cases of tinea versicolor to assess the dermato-physiological, immunological and pathological status of lesion sites as compared to 20 normal control subjects. Lesion sites showed a significant decrease in sebaceous gland secretions and water content and an increase in pH value compared to normal skin. There was no significant change in involucrin, filaggrin, or number of stratum corneum cell layers. However, lesions showed weak positive staining of IL-1 alpha. A possible mechanism for these changes is that profuse sweat gland secretions predispose to fungal growth and acid mantle destruction, with the pathogens consuming amino acids and sebum as nutrients. Slight increases in IL-1 alpha levels seen in infected areas could be due to a fungus-stimulated immune reaction in the stratum corneum.

[Mycosis fungoides--report of a case].

A 61-year-old female suffered from scaly, violaceous, reddish patches and plaques on the face, trunk and upper arms for two years. Histopathology showed that atypical lymphocytes had infiltrated the epidermis and dermis. Epidermotropism was noted but Pautrier microabscesses was not identified. The electron microscopy revealed the atypical lymphocytes had convoluted contour and peripheral hyperchromatic nuclei. By immunohistochemical study, the labelling of OKT4, OKT8 and OKT11 was positive for the cells, which appeared in the majority of helper T-cells, infiltrating the dermis. The diagnosis was mycosis fungoides, plaque stage. The patient received UVA therapy for 3 months but discontinued due to a worsening of her physical condition.