[Effect of Chai-ling-tang (Sairei-to) for methotrexate concentration degradation delay by methotrexate high-dose therapy].

When methotrexate (MTX) salvage chemotherapy is performed for primary brain malignant lymphoma, use of leucovonrin rescue must often be extended due to delays in the degradation of blood concentration. We examined whether delay in MTX blood concentration degradation could be prevented by chai-ling-tang (Sairei-to) which has diuretic action. In the five cases examined were MTX blood concentration 72 hours after MTX administration was more than 1 x 10(-7) M. A single dose of 3 g of chai-ling-tang was administered three times on the day the MTX salvage chemotherapy was subsequently performed. MTX blood concentration at 72 hours post MTX administration and subsequent chai-ling-tang administration was less than 1 x 10(-7) M in all five cases. In addition, urea nitrogen and creatinine levels in serum increased and creatinine clearance decreased following MTX administration, however these changes induced by MTX administration were reduced by chai-ling-tang administration. Chai-ling-tang was effective in preventing an MTX deferent delay in MTX high-dose therapy by improving renal blood flow.

Dopaminergic hypofunctions and prepulse inhibition deficits in mice lacking midkine.

Midkine is a 13-kDa retinoic acid-induced heparin-binding growth factor involved in various biological phenomena such as cell migration, neurogenesis, and tissue repair. We previously demonstrated that midkine-deficient (Mdk(-/-)) mice exhibited a delayed hippocampal development with impaired working memory and increased anxiety only at the age of 4 weeks. To assess whether midkine gene could play important roles in development and maintenance of central nervous system, we investigated biochemical and behavioral parameters in dopamine and glutamate neurotransmission of Mdk(-/-) mice. The Mdk(-/-) mice exhibited a hypodopaminergic state (i.e., decreased levels of dopamine and its receptors in the striatum) with no alterations of glutamatergic system (i.e., normal level of glutamate, glutamine, glycine, d-serine, l-serine, and NMDA receptors in the frontal cortex and hippocampus). We also found prepulse inhibition deficits reversed by clozapine and haloperidol in the Mdk(-/-) mice. Our results suggested that midkine deficiency may be related to neurochemical and behavioral dysfunctions in dopaminergic system.

Neurophysiological mechanisms of conduction impairment of the auditory nerve during cerebellopontine angle surgery.

OBJECTIVE: Intraoperative auditory brainstem response (ABR)-monitoring is useful for hearing preservation in patients undergoing cerebellopontine angle surgery. Prolongation of the latency of wave V, for example, is observed under surgical stress such as cerebellar retraction. We analyzed intraoperative ABR findings to study the neurophysiological mechanism(s) underlying latency prolongation. METHODS: The ABR recorded during microvascular decompression surgery was studied in 18 patients with hemifacial spasm. We measured each trace of the ABR records, both the latency of each wave and some interpeak latencies. We also analyzed their waveforms especially in the early component, to assess changes during surgery. RESULTS: The latency of wave V varied with cerebellar retraction. The delayed latency of wave V was correlated with the prolonged interpeak latency of waves I-III. An additional wave (designated wave I') between waves I and II was appeared; it was accompanied by a prolongation in the latency of wave V. Wave I' contributed to prolongation of the interpeak latency of waves I-III, resulting in a delay in the latency of wave V. Chronological analysis revealed that the minimum latency of wave I' was the same as wave IN, suggesting that wave I' arose near the porus acusticus internus (PAI). CONCLUSION: Our study showed that cerebellar retraction may result in conduction impairment of the auditory nerve near the PAI, suggesting that the Obersteiner-Redlich zone is an electrophysiologically vulnerable site and wave I' is derived from the change in the vector of wave IN. SIGNIFICANCE: Our findings may provide neurophysiological evidence to support the theoretical model of ABR generators by Scherg and von Cramon.