E. Edward Evans

Effect of temperature on antibody synthesis in the reptile, Dipsosaurus dorsalis.

Summary Antibody synthesis at 25°C was compared with that at 35°C in the lizard, Dipsosaurus dorsalis. After 2 weeks immunization against S. typhosa, H-agglutinin titers of 1:80 to 1:640 were demonstrable in animals maintained at 35°C. At 25°C, on the other hand antibody level did not exceed 1:10 if detectable. Increasing temperature of 25°C group to 35°C for one week caused a relative increase in antibody synthesis. Thus, antibody synthesis in this species appears dependent on environmental temperature.

Lack of a bactericidal response in the earthworm Lumbricus terrestris after immunization with bacterial antigens

Abstract To determine whether the earthworm Lumbricus terrestris could show a bactericidal response, 775 worms were injected with various bacterial antigens: (a) five bacterial strains isolated from the slime and gut cavity of earthworms, (b) a gram-negative bacillus (EMB-1) from a representative crustacean and (c) Salmonella typhosa H antigen. Controls consisted of worms injected with 0.85% saline, formalized saline at 0.3%, and shams which were only punctured with a needle without injection of any antigen. Responses were looked for after 12 hr and 7 days at antigenic concentrations of 106 and 108 cells. In addition, one antigen (L-1) was injected at concentrations of 104 and 106 cells. Worms challenged initially with the highest doses were injected again for secondary responses and tested 33–42 days later. Bactericidal responses assayed by means of the Schwab and Reeves technique were not observed in any of the experimental groups. Although earthworms are capable of specific apparently cellular responses to allogeneic and xenogeneic tissue antigens, they seem to be incapable of synthesizing detectable humoral substances to certain bacterial antigens.

Induced bactericidal response in the California spiny lobster Panulirus interruptus.

Summary When killed gram-negative bacilli (EMB-1) were injected into California spiny lobsters (Panulirus interruptus) an induced bactericidin appeared in the hemo-lymph. This reached a maximum level within 7 days after the primary injection and persisted without further stimulation for at least 60 days. Some elevation of bactericidal titers followed secondary injections of the same bacteria after 60 days. This rise was reminiscent of the anamestic response in antibody synthesis of higher vertebrates. Specificity of the response was not absolute, but the degree of induced reactivity decreased in the order: homologous inoculum (EMB-1) > Salmonella typhosa > bovine serum albumin. The response to bovine serum albumin was no greater than a sham control or those controls inoculated with sodium chloride-formalin solution.

Hypoxic-ischemic brain injury exacerbates neuronal apoptosis and precipitates spontaneous seizures in glucose transporter isoform 3 heterozygous null mice

We examined the effects of 45‐min hypoxia (FiO2 0.08; Hx) vs. normoxia (FiO2 0.21; Nx) on the ipsilateral (Ipsi) and contralateral (Ctrl) sides of the brain in neuronal glucose transporter isoform 3 (Glut3) heterozygous null mice (glut3+/−) and their wild‐type littermates (WT), undergoing unilateral carotid artery ligation. Glut3+/− mice, under Nx, demonstrated a compensatory increase in blood–brain barrier/glial Glut1 protein concentration and a concomitant increase in neuronal nitric oxide synthase (nNOS) enzyme activity and Bax protein, with a decrease in procaspase 3 protein (P < 0.05 each). After Hx, reoxygenation in FiO2 of 0.21 led to no comparable adaptive up‐regulation of the ipsilateral brain Glut3 or Glut1 protein at 4 hr and Glut1 at 24 hr in glut3+/− vs. WT. These brain Glut changes in glut3+/− but not WT mice were associated with an increase in proapoptotic Bax protein and caspase‐3 enzyme activity (P < 0.01 each) and a decline in the antiapoptotic Bcl‐2 and procaspase‐3 proteins (P < 0.05 each). Glut3+/− mice after Hx demonstrated TUNEL‐positive neurons with nuclear pyknosis in most ipsilateral (hypoxic‐ischemia) brain regions. A subset (∼55%) of glut3+/− mice developed spontaneous seizures after hypoxic‐ischemia, confirmed by electroencephalography, but the WT mice remained seizure‐free. Pentylenetetrazole testing demonstrated an increased occurrence of longer lasting clinical seizures at a lower threshold in glut3+/− vs. WT mice, with no detectable differences in monamine neurotransmitters. We conclude that hypoxic‐ischemic brain injury in glut3+/− mice exacerbates cellular apoptosis and necrosis and precipitates spontaneous seizures.