PubMed Health⌕ Search

Biomedical subjects

Yoshihiko Koga

Publications and source records attributed to Yoshihiko Koga.

8 recordsLinked to original sources
PubMed2005

Clinical application of single-pulse transcranial magnetic stimulation for the treatment of depression.

Transcranial magnetic stimulation (TMS) has been recently suggested for the treatment of patients with major depression. Based on the results of the authors' pilot study showing a possible antidepressive effect of single-pulse TMS, a clinical trial was conducted involving patients with major depression. For the present study single-photon emission computed tomography (SPECT) was recorded for six of the target patients to study the effects of TMS on the local blood flow volume. Twenty-three inpatients meeting the Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM-IV) criteria for major depression were invited to participate in the study. Depressive symptoms were rated using the Hamilton Rating Scale for Depression (HAM-D). Patients were given 10 stimuli over the frontal area of both sides for a total of 20 stimuli in a session. The subjects had daily TMS session for 5 days as an add-on therapy. In addition, six patients had their quantitative (99m)Tc-ethyl cysteinate dimer SPECT images measured before and after TMS treatment. Compared with the value 2 days prior to the start of TMS therapy (24.2 +/- 4.9), the average HAM-D scale dropped significantly to 15.3 +/- 6.6 on the day after completion of such therapy. The results of SPECT showed that the regional cerebral blood flow (rCBF) of the bilateral frontal region had increased in four out of six patients when comparing before and after treatment. The present study shows that single-pulse TMS, which is widely used as a neurological test method, possesses a wide range of antidepressive effects without inducing adverse reactions. The results suggest that although repetitive TMS is steadily becoming the mainstay technique today, single-pulse TMS also possesses sufficient antidepressive effects.

Aged↗
PubMed2004

Structural organization of the mouse neurochondrin gene.

Neurochondrin is a brain and bone specific leucine-rich protein. We previously cloned the two types of mRNAs (neurochondrin-1; 729 amino acids and neurochondrin-2; 712 amino acids) from mouse and human species. As a first step, to better understand the mechanism of the bone and brain specific and developmentally regulated expression of the neruochondrin gene, the genomic organization of murine neurochondrin was determined. It consists of 7 exons and spans about 10 kb; all splice junctions conform to the GT/AG rule. It codes for two alternatively spliced messenger RNAs, neurochondrin-1 containing all 7 exons and neurochondrin-2 lacking exon 1b but containing the other exons. Cap site analysis showed that the major transcription initiation occurs at 765 bp upstream of the ATG start codon of neurochondrin-1. The promoter region has no TATA and CAAT box-like sequence but contains potential AP-1 and SP-1 binding sites. The neurochondrin gene is localized to mouse chromosome 4D1 and rat chromosome 5q36.11.

5' Flanking Region↗
PubMed2003

Targeted disruption of the neurochondrin/norbin gene results in embryonic lethality.

Neurochondrin/norbin is a cytoplasmic protein involved in dendrite outgrowth. The expression of the gene has been restricted to neural, bone, and chondral tissues. To identify the functions of the gene in vivo, we have generated mice with a disrupted mutation in the neurochondrin/norbin gene. Histological analysis of heterozygous mutant mice indicates the possibility of specific functions of neurochondrin/norbin in chondrocyte differentiation. We defined the expression patterns of neurochondrin/norbin-lacZ fusion protein in the central nervous system. In the developing olfactory bulb, beta-galactosidase activity was detected in the mantle layer at 12.5 dpc and the strongest activity was detected in the presumptive mitral or tufted cell layer at 15.5 dpc. beta-Galactosidase activity was also detected in the lateral choroid plexus. In homozygous (-/-) mutant mice, the disruption of the neurochondrin/norbin gene leads to early embryonic death between 3.5 and 6.5 dpc. This result indicates that neurochondrin/norbin gene function is essential for the early embryogenesis.

Animals↗