Biography:

In the past Shin-ichiro Nakamura has collaborated on articles with Hideyuki Yamawaki and Fumio Imamura. One of their most recent publications is Research reportMyelinated afferents sprout into lamina II of L3–5 dorsal horn following chronic constriction nerve injury in rats. Which was published in journal Brain Research.

More information about Shin-ichiro Nakamura research including statistics on their citations can be found on their Copernicus Academic profile page.

Shin-ichiro Nakamura's Articles: (5)

Research reportMyelinated afferents sprout into lamina II of L3–5 dorsal horn following chronic constriction nerve injury in rats

AbstractIn order to investigate the consequences of chronic constriction injury (CCI) to nerve, we explored the relationship between the development of mechanical allodynia and the reorganization of primary afferent terminals in the sensory lamina of the rat spinal cord dorsal horn. Following sciatic CCI neuropathy, mechanical allodynia developed in the corresponding footpad within two weeks and persisted throughout the experimental period which extended for an additional two weeks. The neuropathy of the sciatic injury includes extensive Wallerian-like degeneration of myelinated fibers but relative sparing of unmyelinated fibers. We observed that there was no significant change in the dorsal horn termination of unmyelinated C fibers in lamina II of the dorsal horn, using nerve injections of wheat germ agglutin-horseradish peroxidase for transganglionic axonal tracing of these fibers from the nerve injury site, and no evidence of sprouting into adjacent lamina. In contrast, myelinated afferent fibers were observed to be sprouting into lamina II of the dorsal horn, as indicated by cholera toxin β-subunit-horseradish peroxidase retrograde axonal tracings. This region of the dorsal horn is associated with nociceptive-specific neurons that are not generally associated with myelinated fiber input from mechanical and proprioceptive receptors. As previously suggested in nerve transection and crush injuries, and now demonstrated in CCI neuropathy, these morphological changes may have significance in the pathogenesis of chronic mechanical allodynia.

Pharmacology lettersMorphological and functional changes of rabbit mesenteric artery cultured with fetal bovine serum

AbstractThe aim of this study was to examine the morphological and functional changes in rabbit mesenteric arterial tissue cultured with fetal bovine serum. In the endothelium-denuded arteries cultured under a serum-free condition for one week (serum-free arteries), morphology of the smooth muscle layer was intact. In the serum-free arteries, high K+-induced contraction did not change but norepinephrine-induced contraction slightly decreased compared with that in the freshly isolated arteries, whereas the sensitivity to these stimulants was significantly augmented. In the medial layer of the arteries cultured with 10% fetal bovine serum for one week (serum-treated arteries), proliferation, disorientation and death of smooth muscle cells were observed. In the serum-treated arteries, both the amplitude of contractions induced by high K+ and norepinephrine and the sensitivity to these stimulants were significantly reduced compared with those of the serum-free arteries. The reduced norepinephrine-induced contraction in the serum-treated arteries was partially recovered by adding NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthase inhibitor, to the assay medium. In α-toxin permeabilized arteries, the amplitude of Ca2+-induced contraction and the sensitivity of the contractile apparatus to Ca2+ were significantly reduced after serum-treatment. These results suggest that chronic serum-treatment of rabbit mesenteric arteries impairs muscle contractility by the morphological and phenotypic changes in smooth muscle cells. NO production in smooth muscle cells is also responsible for the decreased contractility after the serum-treatment.

Percutaneous brachytherapy for small-sized non-small cell lung cancer

AbstractA patient with a small-sized pulmonary adenocarcinoma was successfully treated by percutaneous high dose rate interstitial brachytherapy alone. The patient, who had an adenocarcinoma with 12-mm diameter in the lingular lobe of left lung, was judged to be inoperable because of poor pulmonary function due to emphysema and extensive pleural adhesion. The tumor was punctured with a 21-gauge fine applicator needle followed by the introduction of an iridium 192 (192Ir) radioactive source through the applicator needle using a remote afterloader. The tumor was irradiated for 225.1 s in one fraction. The tumor was in the inside of the iso-dose line of 40 Gy. The delivered doses calculated at nine reference points, which were 12.5 mm distant from the center of the tumor, distributed between 19.225 and 32.169 Gy, with a mean of 24.8 Gy. No apparent side effect including pneumothorax and hemoptysis was observed. The tumor shrank and showed no increment of the size for about 2 years.

Original ArticleTransduction Properties of Adenovirus Serotype 35 Vectors After Intravenous Administration Into Nonhuman Primates

Adenovirus serotype 35 (Ad35) vectors have shown promise as effective gene delivery vehicles. However, the transduction profiles of Ad35 vectors in conventional mice allow only a limited estimation of transduction properties of these vectors, because the mouse analog of the subgroup B Ad receptor, CD46, is restricted to the testis. In order to assess the transduction properties of Ad35 vectors more completely, we performed transduction experiments using cynomolgus monkeys, which ubiquitously express CD46 in a pattern similar to that in humans. In vitro transduction experiments demonstrated that cultured cells from the cynomolgus monkey were efficiently transduced with Ad35 vectors. In contrast, after intravenous administration into live monkeys hardly any evidence of Ad35 vector–mediated transduction was found in any of the organs, although Ad35 vector genomes were detected in various organs. Less severe histopathological abnormalities were found in the Ad35 vector–infused monkeys than in the conventional Ad5 vector–injected monkeys. In the latter, serious tissue damage and inflammatory responses, such as hepatocyte necrosis and lymphatic hyperplasia in the colon, were induced. Both Ad35 and Ad5 vectors caused similar hematological changes (increase in CD3+ cells, and decrease in CD16+ cells and CD20+ cells) in peripheral blood cells. These results should provide valuable information for the clinical application of Ad35 vectors.

Original ArticlemiR-122a-Regulated Expression of a Suicide Gene Prevents Hepatotoxicity Without Altering Antitumor Effects in Suicide Gene Therapy

The combined use of adenovirus (Ad) vectors expressing herpes simplex virus thymidine kinase (HSVtk) and ganciclovir (GCV) offers a potential therapeutic strategy against cancer. However, intratumorally injected Ad vectors are disseminated into the systemic circulation and efficiently transduce the liver, resulting in severe hepatotoxicity. In order to overcome this problem, an Ad vector carrying a microRNA (miRNA)-regulated expression system was developed by inserting into the 3′-untranslated region (3′-UTR) of the expression cassette four tandem copies of sequences with perfect complementarity to miR-122a, which exhibits liver-specific expression. Transgene expression from the Ad vector carrying the miR-122a target sequences was 7- to 70-fold lower in cells with high miR-122a expression as compared to expression from a conventional Ad vector. Intratumoral injection of the Ad vector containing the miR-122a target sequences resulted in a 130- to 1,500-fold reduction in hepatic transgene products (without affecting the transgene expression in the tumor) when compared with those from a conventional Ad vector. In suicide gene therapy, the inclusion of the miR-122a target sequences in the HSVtk expression cassette achieved not only significant antitumor effects, but also a dramatic reduction in HSVtk/GCV-induced hepatotoxicity. These results indicate that Ad vectors that mediate miR-122a-regulated HSVtk expression provide a safe and efficient suicide gene therapy strategy.

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