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Hokkaido, Japan

Niino M.,Hokkaido Medical Center
Nihon rinsho. Japanese journal of clinical medicine | Year: 2013

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. MS is characterized by axonal degeneration and glial scarring, and the formation of MS lesions is complex, involving cytokines, chemokines, and immunoglobulins. Environmental and genetic risk factors are clearly involved in the occurrence of MS although its etiology and pathophysiology are incompletely understood. In recent genetic studies on MS, approaches of genome-wide association study have been applied, and the several susceptibility genes of MS have been reported. Recent immunological studies have revealed the importance of IL-17 and Th17 cells in the pathogenesis of MS. This review discusses recent findings on etiology and pathophysiolosy of MS. Source


Niino M.,Hokkaido Medical Center
Clinical and Experimental Neuroimmunology | Year: 2013

The genetic contribution to multiple sclerosis susceptibility is undeniable, and genetic background could influence clinical characteristics including magnetic resonance imaging findings. Huang et al. (Clin Exp Neuroimmunol, 4, 2013, 173-180) showed that genetic profiles differ between Japanese multiple sclerosis patients with and without Barkhof brain lesions seen on magnetic resonance imaging. © 2013 Japanese Society for Neuroimmunology. Source


Okamoto H.,Hokkaido Medical Center | Imanaka-Yoshida K.,Mie University
Cardiovascular Therapeutics | Year: 2012

Matricellular proteins are highly expressed in reparative responses to pressure and volume overload, ischemia, oxidative stress after myocardial injury, and modulate the inflammatory and fibrotic process in ventricular remodeling, which leads to cardiac dysfunction and eventually overt heart failure. Generally, matricellular proteins loosen strong adhesion of cardiomyocytes to extracellular matrix, which would help cells to move for rearrangement and allow inflammatory cells and capillary vessels to spread during tissue remodeling. Among matricellular proteins, osteopontin (OPN) and tenascin-C (TN-C) are de-adhesion proteins and upregulate the expression and activity of matrix metalloproteinases. These matricellular proteins could be key molecules to diagnose cardiac remodeling and also might be targets for the prevention of adverse ventricular remodeling. This review provides an overview of the role of matricellular proteins such as OPN and TN-C in cardiac function and remodeling, as determined by both in basic and in clinical studies. © 2011 Blackwell Publishing Ltd. Source


Niino M.,Hokkaido Medical Center
Clinical Neurology | Year: 2014

The various lesions affecting the central nervous system in multiple sclerosis (MS) lead to a wide range of symptoms. Until now, physical disabilities have been the main focus of studies on the symptoms of MS; however, cognitive impairment that prominently affects sustained attention and information processing speed has been found by neuropsychological studies to affect over half of all MS patients. Because this cognitive impairment typically involves domain-specific deficits rather than global cognitive decline, it is usually difficult to detect. Cognitive dysfunction in MS patients could influence social activities, such as employment status. Therefore, we must pay greater attention to cognitive function in the milieu of clinical neurology. Source


Niino M.,Hokkaido Medical Center
Clinical and Experimental Neuroimmunology | Year: 2014

The non-glycosylated protein, leptin, plays a key role in regulating energy intake and energy expenditure. It was also recently shown to be involved in regulating innate and adaptive immune responses. Ehsan et al. reported significantly higher serum leptin levels in patients with multiple sclerosis and neuromyelitis optica, and these levels were correlated with disability in those with progressive multiple sclerosis. Leptin's role as a mediator in the link between the immune responses and metabolic function is clearly important to consider in developing immune therapeutic targets for reducing inflammation and autoimmunity. © 2014 Japanese Society for Neuroimmunology. Source

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