Delayed presentation of transdermal cyanide poisoning.

A 45-year-old man attended to a warehouse fire involving burning plastic, without wearing full protective equipment. He subsequently presented to hospital with shortness of breath and his trachea was intubated for airway protection due to initial concerns of inhalational injury. However, a post-intubation bronchoscopy was normal. The patient's serum lactate level was normal on admission but was increased when measured 14 h after the initial event and accompanied by a metabolic acidosis. Transdermal cyanide poisoning was suspected given this delayed biochemical presentation and the absence of another apparent cause. A handheld chemical detector detected a high level of toxins on the patient's skin. Clinical improvement was not observed after the first dose of intravenous hydroxocobalamin, which was administered before full body decontamination. After decontamination and the administration of a second dose of hydroxocobalamin, the patient's acid-base status rapidly improved and serum lactate level returned to normal. Clinicians should have a high index of suspicion for transdermal cyanide poisoning in patients presenting after exposure to a fire.

The death of Sir Thomas Stamford Raffles (1781-1826).

The authors reviewed a rare autopsy report of Sir Thomas Stamford Raffles and offer a fresh interpretation of the cause of his death, with illustrations on the implied findings.

Regulation of methyl beta-galactoside permease activity in pts and crr mutants of Salmonella typhimurium.

We have studied the regulation of the synthesis and activity of a major galactose transport system, that of methyl beta-galactoside (MglP), in mutants of Salmonella typhimurium. Two classes of mutation that result in a (partially) defective phosphoenolpyruvate: sugar phosphotransferase system (PTS) interfere with MglP synthesis. pts mutations, which eliminate the general proteins of the PTS Enzyme I and/or HPr and crr mutations, which result in a defective glucose-specific factor IIIGlc of the PTS, lead to a low MglP activity, as measured by methyl beta-galactoside transport. In both ptsH,I, and crr mutants the amount of galactose binding protein, one of the components of MglP, is only 5%-20% of that in wild-type cells, as measured with a specific antibody. We conclude that synthesis of MGlP is inhibited in pts and crr mutants. Once the transport system is synthesized, its transport activity is not sensitive to PTS sugars (i.e., no inducer exclusion occurs). The defect in pts and crr mutants with respect to MGlP synthesis can be relieved in two ways: by externally added cyclic adenosine 3',5-monophosphate (cAMP) or by a mutation in the cAMP binding protein. The conclusion that MglP synthesis is dependent on cAMP is supported by the finding that its synthesis is also defective in mutants that lack adenylate cyclase. pts and crr mutations do not affect growth of S. typhimurium on galactose, however, since the synthesis and activity of the other major galactose transport system, the galactose permease (GalP), is not sensitive to these mutations. If the galactose permease is eliminated by mutation, growth of pts and crr mutants on low concentrations of galactose becomes very slow due to inhibited MglP synthesis. Residual growth observed at high galactose concentrations is the result of yet another transport system with low affinity for galactose.