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S S Ko

Publications and source records attributed to S S Ko.

23 records · Page 2Linked to original sources
PubMed1991

[Expression of keratin 16 in normal and lesional skin of solitary and multiple Bowen's disease using monoclonal antibody Ks 8.12 staining].

Bowen's disease is an intraepidermal squamous cell carcinoma usually consisting of a solitary lesion. However, multiple Bowen's lesions are one of the characteristics of arsenicalism in endemic areas where people drink deep well water containing high concentrations of arsenic along the southwest coast of Taiwan. This work seeks to clarify the differences between multiple Bowen's disease in the blackfoot disease endemic area, and solitary Bowen's disease in a non-endemic area by means of Ks 8.12 monoclonal cytokeratin antibody staining. Ks 8.12 may be regarded as a specific antibody for Keratin 16 in the skin and is used as a marker for hyperproliferation. Our results show that Ks 8.12 staining of normal skin in patients with a solitary Bowen's lesion is patchy and always restricted to the basal cell layer. By contrast, the normal skin of patients with multiple Bowen's lesions shows diffuse Ks 8.12 staining of the basal cell layer and various degrees of staining of the suprabasal layers. Similar results were observed in both solitary and multiple Bowen's lesions showing diffuse Ks 8.12 staining of the epidermis. Our results revealed clear differences in keratin expression between the clinically normal skin of patients with solitary Bowen's disease and that of patients with chronic arsenicalism. Finally the clinically normal skin of patients with multipole Bowen's disease showed characteristic changes in the expression of Keratin 16 in the suprabasal layers.

Aged↗
PubMed1989

Mechanistic studies of lanosterol 14 alpha-methyl demethylase: substrate requirements for the component reactions catalyzed by a single cytochrome P-450 isozyme.

Lanosterol 14 alpha-methyl demethylation is a cytochrome P-450-dependent process that proceeds through the oxidative sequence of alcohol, aldehyde followed by decarbonylation with formic acid release. Microsomal metabolism studies shown here indicate that only lanostenols and 32-oxy-lanostenols with unsaturation at either the delta 7 or delta 8 position in the sterol can be demethylated. The 14 alpha-methyl group of either lanostan-3 beta-ol or delta 6 lanostenol is not oxidized to the anticipated C-32 alcohol or aldehyde by the enzyme, nor are the corresponding 32-oxy-lanostanols demethylated when incubated with microsomal preparations. Despite the lack of metabolism, the saturated and delta 6 sterol analogues are effective competitive inhibitors of demethylase activity. Utilizing preferred substrates, comparison of the component reactions of the demethylation sequence shows that both the oxidative function and lyase function are sensitive to common inhibitors and that both activities require NADPH. These findings strongly support the premise that a P-450 isozyme does catalyze each phase of the lanosterol 14 alpha-methyl demethylation sequence. Collectively these results demonstrate the double-bond requirement for both components of the demethylation sequence and suggest that the olefinic electrons at delta 7 or delta 8 but not delta 6 may participate directly during demethylation. This participation may involve stabilizing a transition state intermediate or directing activated oxygen insertion as part of the P-450 monoxygenase mechanism.

Animals↗
PubMed1984

The increase in intracellular free calcium associated with IgG gamma 2b/gamma 1 Fc receptor-ligand interactions: role in phagocytosis.

The concentration of cytosolic free calcium, [Ca2+]i, was measured in J774 mouse macrophages by use of the fluorescent indicator quin-2. Resting [Ca2+]i was 87 nM. Addition of a number of specific ligands to the immunoglobulin gamma 2b/gamma 1 Fc receptor resulted in a transient increase in [Ca2+]i, the magnitude of which depended on the extent of receptor aggregation. Monovalent ligands gave only a small Ca2+ signal but blocked cell response to subsequent addition of multivalent ligands. Incubation with antibody-coated erythrocytes raised macrophage [Ca2+]i to micromolar levels. [Ca2+]i changes were only partially inhibited by the absence of external Ca2+, suggesting the release of Ca2+ from internal stores in addition to an influx of external Ca2+. These internal stores were not limited to mitochondria. An optimal range of [Ca2+]i was required for phagocytosis. Buffering [Ca2+]i with quin-2 and treating cells with quinine in the absence of external Ca2+ resulted in inhibition of phagocytosis. Increasing [Ca2+]i to micromolar levels with the calcium ionophore A23187 also resulted in similar inhibitory effects. We suggest the involvement of localized cytosolic Ca2+ gradients in generating the signals necessary for phagocytosis.

Aminoquinolines↗