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Biomedical subjects

S Nagy

Publications and source records attributed to S Nagy.

168 records · Page 10Linked to original sources

Journal reading practices of RNs in NSW public hospitals.

Eight hundred and ninety-seven registered nurses working in NSW public hospitals were surveyed on their use of professional journals. Fifty per cent of participants were found to be regular readers, 30% occasional and 20% infrequent readers. Journals were most likely to be read when they were available at ward or departmental level. Ten per cent of participants reported that they frequently incorporated research findings into their practice and 44% that they never did so. The implications of these findings for the development of nursing as a profession are discussed.

Adult↗

The genetic tree.

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Audiovisual Aids↗

Effect of silymarin on experimental liver lesions.

The effect of Silymarin (Legalon) upon liver lesions was investigated using four experimental models: In acute galactosamine-hepatitis, Silymarin administration achieved protection of the liver structure (electron-microscopy included), liver cell glycogen, RNA and enzymatic activity, Galactosamine-depressed gluconeogenesis in the isolated perfused rat liver was significantly preserved by Silymarin treatment. In lead and cadmium poisoning the structural damage and histochemical and histoenzymatic changes were partly but significantly prevented. The complex noxious effects of Imuran overdoses were favourably influenced by Silymarin, without diminishing the cytostatic-immunosuppressive action of Imuran.

Animals↗

Effects of two benzo[a]phenothiazines on multi-drug resistance (mdr) and tumor antigen expression.

Two benzo[a]phenothiazines 5H-benzo[a]phenothiazin-5-one (1), and its derivative 6-methyl-5H-benzo[a]phenothiazin-5-one (2) inhibited the proliferation of human and mouse tumor cell lines. The multi-drug resistant (mdr) subline was more sensitive than its parent cell line to 5H-benzo[a]phenothiazin-5-one (1), 6-methyl-5H-benzo[a]phenothiazin-5-one (2) was equally antiproliferative against the three cell lines tested. Rhodamine 123 efflux of mdr cells was more efficiently inhibited by 5H-benzo[a]phenothiazin-5-one (1) than by 6-methyl-5H-benzo[a]phenothiazin-5-one (2). The exposure of adenovirus infected cells to 5H-benzo[a]phenothiazin-5-one (1) resulted in a reduction of tumor-antigen expression, whereas 6-methyl-5H-benzo[a]phenothiazin-5-one (2) enhanced the T-antigen expression.

Animals↗

Antitumor activity of phenothiazine-related compounds.

One of the biggest challenges in health care is the fight against tumors. Some phenothiazines have antitumor activity on HEp-2 tumor cells. In this study, we tested the antitumor effects of three series such as 10-nonsubstituted phenothiazines, 10-[n-(phthalimido)alkyl]-2-substituted-10H-phenothiazines and 1-(chloroethyl)-3-(2-substituted-10H-phenothiazines-10-yl)alkyl-1-ureas with H, Cl and CF3 substitution at position C2. The TCID50 of phenothiazines was affected by the H, Cl and CF3 at C2. Trifluoromethyl derivative of phenothiazine showed potent (R = CF3, TCID50 = 4.7 micrograms) activity, whereas the chlorine derivative of phenothiazine (R = Cl, TCID50 = 62.5 micrograms) had a relatively weak effect. In the group of 10-[n-(phthalimido)alkyl]-2-substituted-10H-phenothiazines, 10-[3-(phthalimido)propyl]-10H-phenothiazine (R = H, n = 3, TCID50 = 11.5 micrograms), 10-[4-(phthalimido)butyl]-10H-phenothiazine (R = H, n = 4, TCID50 = 7.8 micrograms) and 10-[3-(phthalimido)propyl]-2-trifluoromethyl-10H- phenothiazine (R = CF3, n = 3, TCID50 = 11.5 micrograms) was very effective. On the other hand, TCID50 of 10-[3-(phthalimido)propyl]-2-chloro-10H-phenothiazine (R = Cl, n = 3, TCID50 = 75.0 micrograms), 10-[4-(phthalimido)butyl]-2-chloro-10H-phenothiazine (R = Cl, n = 4, TCID50 = 31.3 micrograms) and 10-[4-(phthalimido)butyl]-2-trifluoromethyl-10H-phenothiazine (R = CF3, n = 4, TCID50 = 50.0 micrograms) were about 4-8 times less effective than 10-[4-(phthalimido)butyl]-10H-phenothiazine (R = H, n = 4, TCID50 = 7.8 micrograms). Among six 1-(chloroethyl)-3- (2-substituted-10H-phenothiazin-10-yl)alkyl-1-ureas, two chlorine compounds such as 1-(2-chloroethyl)-3-(2-chloro-10H-phenothiazin-10-yl)propyl-1-urea (R = Cl, n = 3, TCID50 = 6.3 micrograms), 1-(2-chloroethyl)-3-(2-chloro-10H-phenothiazin-10-yl) butyl-1-urea (R = Cl, n = 4, TCID50 = 7.8 micrograms), and 1-(2-chloroethyl)-3-(2-trifluoromethyl-10H-phenothiazin-10-yl)buty l-1-ur ea (R = CF3, n = 4, TCID50 = 7.8 micrograms) were significantly active. Tests showed that the substitution at 2C position apparently affected the anti-HEp-2 tumor cell activity; that the length of the aliphatic side chain at 10N contributes to the anti-tumor activity; and that the TCID50 values of the derivatives with butylene group (-C4H8-) were lower than those with propylene group (-C3H6-) except 10-[4-(phthalimido) butyl]-2-trifuoromethyl-10H-phenothiazine and 1-(2-chloroethyl)-3-(2-chloro-10H-pheno-thiazin-10-yl) butyl-1-urea.

Antineoplastic Agents↗

Synthesis and antitumor activity of 1-[2-(chloroethyl)-3-(2-substituted-10H-phenothiazin-10-yl)alkyl- 1-urea s as potent anticancer agents.

10-[N-(Phthalimido)alkyl]-2-substituted-10H-phenothiazines and 1-(2-chloroethyl)-3-(2-substituted-10H-phenothiazin-10-yl)alkyl-1- ureas were synthesized and found to have antiproliferative effects on human HEp-2 and L5178Y cell cultures. The multi-drug resistant subline of mouse lymphoma was sensitive to the reversal effects of some 10-[N-(phthalimido)alkyl]-2-substituted-10H-phenothiazines, while 1-(2-chloro-ethyl)-3-(2-substituted-10H-phenothiazin-10-yl)alkyl-1 -ureas were less effective but had a similar degree of antiproliferative effect on both cell lines.

Animals↗