Full-length sequence of mouse acupuncture-induced 1-L (aig1l) gene including its transcriptional start site.

We have been investigating the molecular efficacy of electroacupuncture (EA), which is one type of acupuncture therapy. In our previous molecular biological study of acupuncture, we found an EA-induced gene, named acupuncture-induced 1-L (Aig1l), in mouse skeletal muscle. The aims of this study consisted of identification of the full-length cDNA sequence of Aig1l including the transcriptional start site, determination of the tissue distribution of Aig1l and analysis of the effect of EA on Aig1l gene expression. We determined the complete cDNA sequence including the transcriptional start site via cDNA cloning with the cap site hunting method. We then analyzed the tissue distribution of Aig1l by means of northern blot analysis and real-time quantitative polymerase chain reaction. We used the semiquantitative reverse transcriptase-polymerase chain reaction to examine the effect of EA on Aig1l gene expression. Our results showed that the complete cDNA sequence of Aig1l was 6073 bp long, and the putative protein consisted of 962 amino acids. All seven tissues that we analyzed expressed the Aig1l gene. In skeletal muscle, EA induced expression of the Aig1l gene, with high expression observed after 3 hours of EA. Our findings thus suggest that the Aig1l gene may play a key role in the molecular mechanisms of EA efficacy.

[A case of complete response treated by S-1 with concurrent radiotherapy for a gefitinib-resistant non-small cell lung cancer patient].

A 35-year-old woman with a clinical diagnosis of stage T2N2M0 lung adenocarcinoma received 3 courses of preoperative chemotherapy with cisplatin and docetaxel. The treatment response was no change. A left inferior lobectomy with mediastinal and hilar lymph-node dissection (ND2a) was performed. The pathological diagnosis was stage T2N2M0 lung cancer. Gefitinib was administered postoperatively. After 2 months of oral treatment, gefitinib was discontinued because of enlarged subcarinal lymph nodes and an elevated level of serum Sialyl LewisX-i antigen (SLX). Starting 4 months after surgery, the mediastinum was irradiated with a total dose of 50 Gy. Chemotherapy with S-1 was started 5 months after surgery. S-1 was administered in a dose of 100 mg/day in two divided doses for 4 weeks, followed by 2 weeks of rest. The patient received 6 courses of chemotherapy with S-1, without increasing the dose. The enlarged mediastinal lymph nodes disappeared, and the serum SLX level returned to normal. The patient had a complete response, and was subsequently followed on an outpatient basis while receiving oral UFT. More than 36 months have elapsed since surgery, with no evidence of recurrence.

Bronchiolar disease associated with gold compounds administration in a patient with rheumatoid arthritis.

We report the case of a female patient with rheumatoid arthritis (RA) treated with gold sodium thiomalate and auranofin who developed bronchopulmonary involvement. Chest X-ray films showed diffuse mottled infiltrates and bronchial wall thickness in both lungs. Computed tomography revealed opacities along the thickening of the bronchovascular bundles. The pathologic findings were indistinguishable from those of diffuse panbronchiolitis. After discontinuation of gold compounds and initiation of steroid administration, her subjective symptoms immediately subsided. We conclude that our patient, who had suffered from chronic sinusitis and had a predisposition to bronchiolar disease, had bronchiolar disease induced by gold compounds.