S-(β-Aminoethyl)-l-cysteine (SAEC), a sulfur analog of l-lysine, significantly inhibited the growth of wild-type strains of Candida species. The growth inhibition of C. pelliculosa depended on SAEC concentrations, but l-Iysine and l-α-aminoadipate restored growth effectively. SAEC-resistant mutants were induced from the wild-type strain of C. pelliculosa by ultraviolet irradiation and N-methyl-N′-nitro-N-nitrosoguanidine treatment. Almost all resistant mutants excreted some l-lysine into the medium. Lysine excretion increased after repeated mutations. The mutant strain SR-V–1263 extracellularly produced about 2 mg/ml of l-lysine after shaking culture for 96 hr. The effect of various factors on lysine accumulation was investigated with strain SR-V–1263. The concentration of extracellular lysine reached a maximum (3.2 mg/ml) in medium containing 2% polypeptone under the experimental conditions.
Nociceptin is a 17-amino acid peptide and acts as a potent endogenous agonist of the opioid receptor-like1 receptor. Nociceptin is reported to depress glutamatergic transmission and to block the spinal facilitation that is thought to be mediated by the N-methyl-D-aspartate (NMDA) receptor. In the present study, the authors investigated the effect of intrathecally administered nociceptin and NMDA antagonists on the level of thermal hyperalgesia after partial sciatic nerve injury in the rat.Partial sciatic nerve injury was created by tight ligation of one third to one half of the right sciatic nerve. The level of thermal hyperalgesia was evaluated by the difference score, which was calculated by subtracting the paw withdrawal latency against thermal nociceptive stimulation in the uninjured paw from that in the injured paw. Drugs were administered intrathecally 7 or 11 days after the nerve injury, and the level of thermal hyperalgesia was measured 5, 15, 30, 60, and 90 min after the drug injection.Intrathecal injection of nociceptin, but not of NMDA antagonists, attenuated the level of thermal hyperalgesia in a dose-dependent manner at a dose of 0.17-17 nM (post-drug difference score: saline-treated rats, -4.9 +/- 2.2 s; 17 nM nociceptin-treated rats, -1.3 +/- 0.9 s).Intrathecal injection of nociceptin attenuated the level of thermal hyperalgesia induced by partial sciatic nerve injury, and NMDA receptor-dependent spinal facilitation does not play an important role in maintaining thermal hyperalgesia in rats with partial sciatic nerve injury.
Since the first report of pediatric deaths in 1997-1999 in the United States, community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) has become an increasingly important public health problem worldwide.
The ST5 lineage of methicillin-resistant Staphylococcus aureus (MRSA) is one of the most globally disseminated hospital-associated MRSA (HA-MRSA) lineages. We isolated a new local variant (designated ST764) over at least 5 years that causes invasive infections, including necrotizing fasciitis, and is carried by medical students, as well as household members. Analysis of the genome sequence of one isolate compared to that of the reference ST5 strain revealed that ST764 had acquired virulence traits similar to those of community-associated MRSA (CA-MRSA) through the acquisition of two new mobile genetic elements, ACMEII and SaPInn54, which carried ACME arcA and the staphylococcal enterotoxin B gene (seb), respectively, and through enhanced expression of cytolytic peptide genes, although ST764 was negative for Panton-Valentine leukocidin. Other differences between ST764 and ST5 included the acquisition of an ACMEII-related cassette (cJR1), prophage φ2NN54, and streptococcal Tn5251 and decreased numbers of copies of Tn554. As for superantigen genes, although the two possessed seg, sei, sem, sen, and seo, ST764 lacked tst, sec, sel, and sep. The data suggest that ST764 MRSA is a novel hybrid variant of ST5 HA-MRSA with the characteristics of CA-MRSA and that the evolution of ST764 includes multiple steps, e.g., acquisition of novel or nonstaphylococcal mobile elements.
