Thermal Resistance of Vibrio parahaemolyticus in Clam Homogenate.

Nine strains of Vibrio parahaemolyticus from widely varied sources were exposed to heat in sterile clam homogenates. D-values were determined at temperatures ranging from 49 to 55 C for four strains, and at 51 C for the remaining five strains. The D-values in minutes, corrected for thermal lag and lethality during thermal lag, were 0.

Lack of protection by pyridoxine or hydrazine pretreatment against monosodium L-glutamate-induced seizures.

Pretreatment of rats with hydrazine (100 mg/kg), a compound which raises brain gamma-aminobutyric acid (GAGA) 175 percent in 12 hr was not able to prevent the occurrence of seizures induced by monosodium L-glutamate (MSG). Pyridoxine (50 mg/kg) the cofactor essential in the conversion of glutamate to GABA, also failed to prevent convulsions induced by parenteral MSG administration. It is concluded that the mechanism of action of MSG-induced seizures is neither by decreasing brain GABA levels or interfering with the pyridoxine cofactor.

Isolation and characterization of Vibrio parahaemolyticus from Cape Cod soft-shell clams (Mya arenaria).

Vibrio parahaemolyticus was isolated from soft-shell clams (Mya arenaria) taken from 10 different clamming areas on Cape Cod, Mass., during July and August 1972. Direct plating on thiosulfate-citrate-bile salts-sucrose agar was found to be superior to either direct plating on Vanderzant modified salt starch agar or enrichment with Trypticase soy broth containing 7% salt for isolation from clam samples.

Monosodium L-glutamate-induced convulsions: temporary alteration in blood-brain barrier permeability to plasma proteins.

Monosodium L-glutamate (MSG), a commonly used food additive, induces convulsive disorders in rats. A reversible change in the cerebrovascular permeability of plasma proteins occurs during convulsions induced by the intraperitoneal administration of 4.0 g/kg of MSG to the neonatal rat.