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PubMedDate not supplied

Beneficial effect of macrophage activating agent NK-4 on Thai HIV-infected patients.

BACKGROUND: We examined the effect of NK-4 (4,4'-[3-[2-(1-ethyl-4(1H)-quinolinylidene) ethylidene] propenylene] bis(-ethylquinolinium iodide)) on the clinical course of Thai HIV-infected patients receiving antiretroviral drugs. PATIENTS AND METHODS: Twelve subjects with CD4 count < 500/mm3 were enrolled to receive 0.5 mg of NK-4 orally once daily for 8 weeks and then twice daily during the follow-up. RESULTS: Most patients showed vitality, increased appetite, stable body-weight, increased CD4 counts and no serious adverse effects due to viral load. We suggest that the increased CD4 counts are due to the macrophage activating effect of NK-4. The patients with increased CD4 counts showed lower alpha-N-acetylgalactosaminidase (alpha-NaGalase) activity than those with decreased CD4 counts. CONCLUSION: These results suggest that the macrophage activating agent NK-4, as an inexpensive and safe drug for HIV-infected patients, may play a beneficial role in the clinical treatment of HIV-infected patients.

Adult↗
PubMed1992

Trypanosomal antigen and antibody levels in field camels following treatment with two trypanocidal drugs.

The efficacy of treatment in 61 naturally trypanosome-infected camels was evaluated by antigen and antibody detection. Following treatment of 14 infected field camels with an arsenical drug (RM110) no trypanosomal antigens could be detected in the animals which were treated with 0.6 mg/kg body weight and 1.2 mg/kg body weight, 90 days thereafter. In two out of three camels treated with 0.4 mg/kg body weight no trypanosomal antigens could be detected by day 90 post-treatment. However, there was evidence of trypanosomal antigens in camels treated with 0.2 mg/kg body weight and untreated positive controls. Antibody levels were still high in all the 14 camels, 90 days post-treatment. In another group of 55 field camels, of which 47 camels were parasite-positive and eight parasite-negative, trypanosomal antigens could not be detected in 42 camels, 28 and 48 days post-treatment with Quinapyramine Prosalt. However, antigen levels were still high in five parasite-positive camels, 48 days post-treatment. In all the parasite-positive camels, antibody levels were still high 48 days after treatment. In the eight parasite-negative camels, antigens were detected in four camels before treatment. By day 48 post-treatment, all the four camels were antigen-negative. However, four of the eight parasite-negative camels were still antibody-positive by day 48 post-treatment. These observations indicated that antigen-detection could be used to evaluate the success of therapeutic trials where trypanosome detection tests may fail to pick low patent infections.

Animals↗
PubMed1991

Lipid mediators of tumor necrosis factor-alpha-induced uveitis.

The authors tested the hypothesis that platelet-activating factor (PAF) and cyclooxygenase metabolites of arachidonic acid mediate the ocular inflammatory response to intravitreally injected tumor necrosis factor-alpha (TNF alpha). Rabbits were treated with the PAF receptor antagonist SRI 63-441, the cyclooxygenase inhibitors indomethacin and naproxen, or SRI 63-441 and indomethacin. At 24 hr after intravitreal injection of TNF (20,000 U), the severity of inflammation was assessed based on iridal hypermia, aqueous humor leukocyte number and aqueous humor protein, immunoreactive-prostaglandin E (I-PGE), and leukotriene B4 (LTB4) concentrations. Although all of the treatments significantly reduced the severity of anterior uveitis, SRI 63-441 plus indomethacin was the most effective, indomethacin and naproxen were intermediately effective, and SRI 63-441 was the least effective. The results of this study are consistent with an important role for cyclooxygenase metabolites of arachidonic acid in the inflammatory response to TNF alpha, particularly with respect to dilation of iridal blood vessels. Although naproxen was nearly as effective as indomethacin in reducing aqueous humor I-PGE levels, indomethacin conferred significantly more protection to the blood-aqueous barrier as shown by lower protein levels in the aqueous humor. Thus, although cyclooxygenase inhibition may partially explain the protection afforded the blood-aqueous barrier by these nonsteroidal anti-inflammatory agents, the data suggest that indomethacin may also exert anti-inflammatory effects that are independent of cyclooxygenase inhibition. Furthermore, the data are consistent with TNF alpha releasing PAF in the eye and PAF acting both directly, by increasing vascular permeability, and indirectly, by promoting release of cyclooxygenase and lipoxygenase metabolites of arachidonic acid.

Animals↗
PubMed1991

Effects of platelet-activating factor antagonist SRI 63-441 on endotoxin-induced changes in rat mesenteric microcirculation.

Intravenous injection of E. coli endotoxin 30 mg/kg to rats resulted in a systemic hypotension and rapid decrease in mesenteric arteriolar blood flow velocity (MABFV). The mesenteric arterioles constricted within 3 min followed by a short period of vasodilation after endotoxin administration. Pretreatment with the platelet-activating factor receptor antagonist SRI 63-441 attenuated the endotoxin-induced systemic hypotension and the decrease in MABFV, and abolished the mesenteric vasodilation effect of endotoxin infusion. The results suggest that PAF may be a mediator of endotoxic shock.

Animals↗
PubMed1990

Torpedo acetylcholinesterase is inactivated by thiol reagents.

A number of sulphydryl reagents inhibit AChE of Torpedo california with pseudo-first-order kinetics, and inhibition can be retarded by quaternary ligands which bind at either the catalytic or peripheral anionic binding sites. Colorimetric determination with one of the inhibitory sulphydryl agents, 5,5'-dithiobis (2-nitrobenzoic acid), reveals the presence of a single thiol group per catalytic subunit; our data thus suggest that inhibition is achieved by reaction with the single free sulphydryl group of Cys231.

4-Chloromercuribenzenesulfonate↗