Exposure of limulus hemocytes to bacterial endotoxins (lipopolysaccharide, LPS) results in the activation of the intracellular clotting system, consisting of several protein components. During the separation of these components, a potent anticoagulant, named anti-LPS factor, which inhibits the endotoxin-mediated activation of the coagulation cascade, was found in hemocytes from both Tachypleus tridentatus and Limulus polyphemus (Tanaka, S., et al. (1982) Biochem. Biophys. Res. Commun. 105, 717-723). The principle isolated from the Tachypleus hemocyte lysate by column chromatographies on dextran sulfate-Sepharose CL-6B and Sephadex G-50 under sterile conditions was a simple basic protein with an apparent molecular weight of 15,000. It consisted of a single chain polypeptide containing a total of 128 amino acids. The COOH-terminal end was presumed to be histidine, but no NH2-terminal end reactive to phenylisothiocyanate was detected. The isolated anti-LPS factor specifically inhibited the endotoxin-mediated activation of factor C, which has recently been identified as an LPS-sensitive serine protease zymogen in the hemocytes. This inhibition appeared to be due to the binding of anti-LPS factor with LPS. Moreover, anti-LPS factor had an antibacterial effect on the growth of Gram-negative bacteria (Salmonella minnesota R595 and 1114W) but not on that of Gram-positive bacteria (Staphylococcus aureus 209P). These biological activities of the isolated anti-LPS factor suggest an important role in cellular defence of limulus against microbial invasion.

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Antiepileptics used for treating neuropathic pain have various actions including voltage-gated Na+ and Ca2+ channels, glutamate-receptor inhibition, and GABAA-receptor activation, while local anesthetics are also used to alleviate the pain. It has not been fully examined yet how nerve conduction inhibitions by local anesthetics differ in extent from those by antiepileptics. Fast-conducting compound action potentials (CAPs) were recorded from frog sciatic nerve fibers by using the air-gap method. Antiepileptics (lamotrigine and carbamazepine) concentration dependently reduced the peak amplitude of the CAP (IC50 = 0.44 and 0.50 mM, resp.). Carbamazepine analog oxcarbazepine exhibited an inhibition smaller than that of carbamazepine. Antiepileptic phenytoin (0.1 mM) reduced CAP amplitude by 15%. On the other hand, other antiepileptics (gabapentin, sodium valproate, and topiramate) at 10 mM had no effect on CAPs. The CAPs were inhibited by local anesthetic levobupivacaine (IC50 = 0.23 mM). These results indicate that there is a difference in the extent of nerve conduction inhibition among antiepileptics and that some antiepileptics inhibit nerve conduction with an efficacy similar to that of levobupivacaine or to those of other local anesthetics (lidocaine, ropivacaine, and cocaine) as reported previously. This may serve to know a contribution of nerve conduction inhibition in the antinociception by antiepileptics.

It was possible to detect the ARM in all patients and to obtain information about the origin by IA-CTA. This method is considered useful for preoperative assessment of a descending thoracic or a thoracoabdominal aorta for aortic aneurysm or dissection.