Kinetics of degradation of sulphur mustard on impregnated carbons.

Kinetics of degradation of sulphur mustard (HD) on the surface of NaOH/CrO3/C, NaOH/CrO3/EDA/C and RuCl3/C systems has been examined by using gas chromatography technique by extracting and analyzing the residual HD periodically. The carbons were prepared by impregnating activated carbon with 4% sodium hydroxide plus 3% Cr(VI) as CrO3 with and without 5% ethylene diamine (EDA) and 5% ruthenium chloride by using their aqueous solutions. Obtained carbons were characterized for surface area analysis by BET conventional method. Kinetic plots reveal that the observed reactions are fast at the initial stages, slow at the later stages and progress to a steady state indicating the first order behavior. Effect of moisture on kinetic rate is also observed. In the case of NaOH/CrO3/C system the rate constant is decreased from 13.36 to 5.53 x 10(-2) h(-1) and half life is increased from 5.2 to 12.54 h while moisture content is increased from 1.9% to 11.2%. Whereas, the rate constant of HD degradation reaction is decreased from 10.4 to 4.14 x 10(-2) h(-1) and half life is increased from 6.7 to 16.72 h while moisture content is increased from 2.1% to 10.8% on NaOH/CrO3/EDA/C. Reaction on RuCl3/C system also behaves in the similar manner. Extracted reaction products were characterized by GC/MS and it is found that on NaOH/CrO3/C, HD degrades to hemisulphur mustard, thiodiglycol and 1,4-oxathiane. Whereas, on NaOH/CrO3/EDA/C, HD is degraded to 1,4-thiazane and it is degraded to divinyl sulphone on RuCl3/C. All these investigations reveal that above mentioned carbons can be used in nuclear, biological and chemical (NBC) filtration systems for protection against sulphur mustard.

Symptomatic congenital syphilis presenting at birth.

We report here a case of congenital syphilis presenting in a newborn infant at birth. A negative infant VDRL test, pseudoparesis and more notably, joint swellings (arthritis) were features seen uncommonly. Florid skeletal involvement, which is rarely seen in the early neonatal period, prompted us to draw attention to the varied presentation of this disease, rightly referred to as the "master masquerader".

Actions and interactions of cholinolytics and cholinesterase reactivators in the treatment of acute organophosphorus toxicity.

Different drug combinations consisting of cholinolytic and a cholinesterase (ChE) reactivator provide greater therapeutic efficacy in acute organophosphorus (OP) poisoning in mice than when used alone. Maximum protection, as determined by a shift of the LD50 for the two OP agents, was observed with the cholinolytic benactyzine. A protection index (P.I.) of 42 was obtained when benactyzine was given along with obidoxime in diisopropylphosphorofluoridate (DFP) intoxication. With the more toxic OP agent soman (o-pinacolylmethylphosphonofluoridate), the same cholinolytic only offered a maximum P.I. of 3.2 when administered with HS-6, another bispyridinium ChE reactivator. This beneficial effect of benactyzine is possibly due to its greater antimuscarinic effect in the central nervous system than atropine or dexetimide.

Role of liver and brain lysosomal and mitochondrial enzymes in development of delayed neuropathy in hens by 0,0-diisopropyl phosphorofluoridate.

Subacute dose of 0,0-diisopropyl phosphorofluoridate (DFP), a potent organophosphorus ester capable of producing delayed neurotoxicity (OPIDN), did not produce any significant change in the levels of lysosomal and mitochondrial marker enzymes of brain, liver and serum at any time after treatment in hens protected with atropine. The results suggest the absence of any involvement of mitochondrial and lysosomal enzymes at any stage in the development of OPIDN in susceptible species by treating with DFP.

Studies on the efficacy of diethyxime as an antidote against organophosphorus intoxication in rats.

Diethyxime, a non-quaternary cholinesterase reactivator was evaluated for its antidotal efficacy against organophosphorus intoxication in rats using the protection index, cholinesterase reactivation and neuromuscular function as the experimental protocol. Diethyxime along with atropine produced a marked antidotal effect against dimethyl dichlorovinyl phosphate (DDVP) poisoning on all the parameters studied. The action of diethyxime was mainly peripheral. The protective efficacy against diisopropyl fluorophosphate (DFP) poisoning was not observed with this reactivator.

The lymphokine "inhibitor of DNA synthesis" (IDS) suppresses human T lymphocyte proliferation by an interleukin-2-independent mechanism.

IDS is a soluble glycoprotein product of activated T cells that inhibits lymphocyte proliferation induced by antigens and by lectin mitogens. This immunosuppressive lymphokine has been distinguished from lymphotoxin, Proliferation Inhibitory Factor, Colony Inhibitory Factor, Macrophage Inhibitory Factor, and interferon. Using IDS partially purified by isoelectric focusing from culture supernatants of concanavalin A-stimulated human peripheral blood mononuclear cells (PBMC), we investigated IDS inhibition of T cell proliferation with respect to the interleukin pathway. At concentrations that produced 75-90% suppression of proliferation in PHA-stimulated PBMC cultures, IDS caused no decrease in interleukin 2 (IL2) production (determined by bioassay) or in IL2 receptor expression (determined with anti-Tac antibody). Moreover, adding exogenous IL2 to IDS-inhibited cultures failed to restore proliferation. IDS inhibited growth of several IL2-dependent and IL2-independent cell lines, and suppressed proliferation of PBMC induced by the phorbol ester TPA (12-0-tetradecanoyl-13-phorbol acetate) or by the calcium ionophore A23187, thus distinguishing its mechanism of action from that of cyclosporin A, dexamethasone, OKT11A antibody, and other inhibitors. These data extend earlier findings that IDS acts late in G1 phase of the cell cycle, and provide evidence that IDS inhibits T cell proliferation through an IL2-independent mechanism.

Responses of pre-implantation mouse embryos to thalidomide exposure in utero.

PIP: On Day 1 of pregnancy, a thalidomide suspension (.05 ml) in saline at concentrations of 5 and 10 mcg/ml was infused into the uterine horns via the cervical route of 2 1/2-3 month old Swiss albino mice. Another group was infused on Day 0 at the doses mentioned. Parallel experiments were conducted after intrauterine infusions of saline. Following infusion, the mice were sacrificed on Days 2, 3, and 4 of gestation. Zygote and 4- and 8-cell stages of embryogenesis were most sensitive to the teratogen in terms of the induction of morphological anomalies and cell death. Drug effect was also observed in the postmorula embryos as abnormalities of varying degrees. There was an overall increase in the incidence of mitotic cells.^ieng