Department of neurology in Toyama university hospital was founded on June 16, 2005 by Prof. Kortaro Tanaka, M.D., Ph.D. as the first chairperson. At the beginning, the faculty consisted of only 3 neurologists and 1 student of graduate medical school. Today, the department has grown to include over 10 full-time and associated doctors with a full range of clinical activities, research and education of medical students, residents, and fellows. Our neurologists are experts in the wide range of neurologic disorders, treating the most common ones such as stroke, Parkinson's disease, dementia, migraine and so on as well as those that are rare. Our department has become the major neurological center in Hokuriku area for various disorders affecting the brain, spinal cord, peripheral nerves and muscles. I hope that many young doctors will become part of our department family to get the excellent training and pursue various careers in clinical neurology and research.

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　Background/Aims: Platelet-derived growth factor (PDGF) is implicated in the activation of hepatic stellate cells (HSCs), the key cell population in liver fibrogenesis. We depleted the expression of PDGF receptor-ß (PDGFR-ß) and assessed the role in the activation of HSCs. Methods: We used the wildtype and mutant mice whose PDGFR-ß gene was flanked by two loxP sequences, and isolated/cultured HSCs from these two mice, respectively. These cells were infected with Cre recombinase-expressing adenovirus. Results: After Cre-adenovirus infection, PDGFR-ß expression was depleted in HSCs from mutant mice (PDGFR-ß^Δ/Δ), but was preserved in those from wild-type. We detected the expression of PDGFR-α and PDGF-A, -B, -C, and -D at similar levels between WT and PDGFR-ß^Δ/Δ. BrdU-incorporation in PDGFR-ß^Δ/Δ was suppressed in serum-starved/non-stimulated and PDGF-BB stimulated conditions, respectively. PDGF-BB-induced wound closure was apparently delayed in PDGFR-ß^Δ/Δ. α1 (I) collagen mRNA was low in PDGFR-ß^Δ/Δ, sparing α-smooth muscle actin mRNA at WT levels. Conclusions: The HSCs expressed two types of PDGFR; however, PDGFR-ß was distinctively relevant in the activation of HSCs by mediating both endogenous and exogenous PDGF signals.

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　The association of contextual fear memory (CS-US association) occurs when a conditioned stimulus (CS) is paired with an unconditioned stimulus (US). When the association occurs, many brain regions are thought to be inter-connected each other and form a complex network. Thus, CS-US association may occur in many brain regions that receive convergent CS and US inputs. In this study, we employed a behavioral paradigm, context-pre-exposure facilitation effect (CPFE) paradigm, in which mice received paired or unpaired presentations of the CS and US during conditioning. Using this behavioral paradigm, we performed Arc catFISH analysis to detect brain regions required for the CS-US association and found that basolateral amygdala, hippocampal CA1, prefrontal cortex, piriform cortex, entorhinal cortex, anterior cingulate cortex, ectorhinal cortex, sensory cortex, visual cortex, and retrosplenial cortex that responded to CS-US signals. Furthermore, we found that the number of CSUS responsive neurons significantly increased in basolateral amygdala, CA1, prefrontal cortex, piriform cortex, and entorhinal cortex of paired group. These results suggest that these brain regions regulate the CS-US association of contextual fear memory.

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　Nonequilibrium atmospheric pressure plasma (NEAPP) has been focused as a cancer therapy, recently. We applied NEAPP on the cultured human osteosarcoma MG-63 cells. The cell growth was inhibited by direct effects of NEAPP compared with control group assessed by CCK-8 (p<0.05). The viable cells decreased time-dependently, and showed cell death phenomenon until 8 hours. On the other hand, the growth-inhibition was not observed in the indirect-NEAPP group, which was exposed medium-only.

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　A 67-year-old male was admitted to our hospital due to shaking chills and high fever on a summer day after having eaten raw fish on the previous day to admission. Promptly after antibiotics were administered to the patient, he recovered in a few days without symptoms of shock or necrotizing fasciitis. Classically, Vibrio vulnificus infections are considered life-threatening as they are associated with high mortality and thought to often affect immunosuppressed patients such those with liver cirrhosis. However, ours is a rare case having no signs of liver cirrhosis or immunosuppressive trouble. A precise picture of the course of Vibrio vulnificus infections should be developed through collecting and analyzing more cases including mild ones such as the one discussed here. Additionally, this is the first Vibrio vulnificus infection case ever reported in Toyama Prefecture.

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　The patient was a 9-year-old boy. He was injured during a catheterization procedure performed in infancy that was treated with surgical repair. Angiography performed at the age of 1 year revealed occlusion of the left external ileac artery, the progress of which was observed. At the age of 5 years, intermittent claudication appeared, which worsened at the age of 9 years. At the same time, the patient was found to have lower left and right limb length discrepancy (LLD). A revascularization procedure was performed using an autologous vein. The claudication disappeared post-surgery. By 4 years post-surgery, the lower left and right limb length discrepancy had diminished. Proactive revascularization was useful in the development of the child in the present case.

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　A 78-year-old man underwent surgery for acute type B dissection 25 years ago. However, the false lumen became patent postoperatively and was left unrepaired. The false lumen subsequently dilated, and thoracic endovascular aortic stent grafting was performed to stop blood flow. An aortic closure device was then used to successfully occlude the false lumen. This method may be effective when repeat surgery or thoracotomy would be difficult.

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