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Suzuki H.,Mie University | Kanamaru K.,Suzuka Kaisei Hospital | Suzuki Y.,Red Cross | Aimi Y.,Red Cross | And 7 more authors.
Neurological Research | Year: 2010

Objective: Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) has been hypothesized to occur because of both inflammation-mediated sustained contraction of smooth muscle cells and vascular remodeling. As our recent study showed that tenascin-C (TN-C), an extracellular matrix glycoprotein which is up-regulated in inflammatory states and is associated with tissue remodeling, causes vasospasm-like changes in arterial walls, we examined whether TN-C might be induced in relation to the occurrence of cerebral vasospasm experimentally and clinically. Methods: First, rat models were produced by means of a single cisternal injection of either autologous arterial blood or saline. Immunostaining for TN-C was performed with basilar arteries obtained from nonoperated rats (n=3) and on days 1-4 in SAH (n=18) or saline-injected (n=12) rats. Second, levels of TN-C were prospectively measured in serum in 31 consecutive patients diagnosed with aneurysmal SAH on days 1-12 and compared between those with and without subsequent cerebral vasospasm. Results: In SAH rats, marked induction of TN-C immunoreactivity was shown throughout the vasospastic arterial wall, especially in the smooth muscle cell layers, in comparison with control rats. In a clinical study, serum TN-C levels increased transiently, the extent being significantly greater in patients with subsequent vasospasm; the peak occurred 2.4 days before an increase in the mean transcranial Doppler velocity to >120 cm/s and 3.6 days before the onset of symptomatic vasospasm (n=14). Discussion: This is the first study suggesting TN-C increases with close linkage to the occurrence of vasospasm after SAH. © W.S. Maney & Son Ltd 2010. Source


Machida T.,Gunma University | Miyashita K.,Immuno Biological Laboratories | Sone T.,Fujikura Ltd | Tanaka S.,Fujikura Ltd | And 6 more authors.
Clinica Chimica Acta | Year: 2015

Lipoprotein lipase (LPL) plays a central role in triglyceride-rich lipoprotein metabolism by catalyzing the hydrolysis of triglycerides. Quantification of serum LPL is useful for diagnosing lipid disorders, but there is no rapid method of measuring LPL for clinical use. Methods: We developed a rapid and sensitive latex particle-enhanced turbidimetric immunoassay (LTIA) serum LPL using latex bead-immobilized anti-LPL monoclonal antibodies. The assay was performed on a Hitachi 7700 P analyzer and evaluated for its validity as a method of quantitating the serum LPL concentration in parallel with ELISA. Results: Dilution tests using LTIA produced a calibration curve from 0.5 to 800. ng/ml. Within-run CV was obtained in the range of 2.2-5.5%. No interference was observed in the testing of specimens containing potentially interfering substances such as bilirubin-F and C, hemoglobin, triglycerides and rheumatoid factor. A strong correlation between LTIA and ELISA was confirmed (n. = 40, r. = 0.967, y=0.99x-1.86). The normal range of LPL in pre-heparin serum was 50-77. ng/ml and in post-heparin plasma 354-410. ng/ml, respectively. Conclusion: The LTIA assay is applicable in quantitating the concentration of LPL in both pre-heparin serum and post-heparin plasma. This assay is more convenient and faster than ELISA and highly suitable for clinical routine analysis. © 2015 Elsevier B.V. Source


Fukamachi K.,Nagoya City University | Iigo M.,Nagoya City University | Hagiwara Y.,Immuno Biological Laboratories | Shibata K.,Nagoya City University | And 6 more authors.
PLoS ONE | Year: 2014

Pancreatic ductal adenocarcinoma (PDA) is a highly lethal disease, which is usually diagnosed in an advanced stage. We have established transgenic rats carrying a mutated K-ras gene controlled by Cre/loxP activation. The animals develop PDA which is histopathologically similar to that in humans. Previously, we reported that serum levels of N-ERC/mesothelin were significantly higher in rats bearing PDA than in controls. In the present study, to determine whether serum levels of N-ERC/mesothelin correlated with tumor size, we measured N-ERC/mesothelin levels in rats bearing PDA. Increased serum levels of N-ERC/mesothelin correlated with increased tumor size. This result indicates an interrelationship between the serum level of N-ERC/mesothelin and tumor size. We next investigated the effect of chemotherapy on serum N-ERC/mesothelin levels. Rat pancreatic cancer cells were implanted subcutaneously into the flank of NOD-SCID mice. In the mice treated with 200 mg/kg gemcitabine, tumor weight and the serum level of N-ERC/mesothelin were significantly decreased compared to controls. These results suggest that serum N-ERC/mesothelin measurements might be useful for monitoring response to therapy. © 2014 Fukamachi et al. Source


Utsunomiya A.,Imamura Bun in Hospital | Choi I.,National Kyushu Cancer Center | Chihara D.,Aichi Cancer Center Research Institute | Seto M.,Kurume University | Seto M.,Immuno Biological Laboratories
Cancer Science | Year: 2015

Recent advances in treatment for adult T-cell leukemia-lymphoma (ATL) are reviewed herein. It is currently possible to select a therapeutic strategy for ATL and predict prognosis by classification of patients by clinical subtypes and clinicopathological factors. Although the overall survival (OS) of patients with ATL has increased marginally because of advances in chemotherapy, further prolongation of survival might be difficult with conventional chemotherapy alone. Promising results have been reported for antiviral therapy using zidovudine and interferon-α, and, indeed, antiviral therapy is currently the standard treatment for patients with ATL in western countries. Remarkably, the 5-year OS rates are 100% for both the smoldering-type and chronic-type ATL. Recently, treatments for ATL have included allogeneic hematopoietic stem cell transplantation and molecular targeted therapies. Furthermore, the anti-CCR4 monoclonal antibody mogamulizumab has been shown to have marked cytotoxic effects on ATL cells, especially in the leukemic type of ATL. In the lymphoma type of ATL, the response rate may be improved by combining mogamulizumab with chemotherapy. It should be recognized that prevention of infection from carriers of human T-cell leukemia virus type-I and transfer of the virus from mother to infant are crucial issues for the eradication of ATL. © 2015 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association. Source


Torii T.,National Health Research Institute | Miyamoto Y.,National Health Research Institute | Nakamura K.,Immuno Biological Laboratories | Maeda M.,Immuno Biological Laboratories | And 2 more authors.
Cellular Signalling | Year: 2012

Proper regulation of morphological changes in neuronal cells is essential for their differentiation. Complex signaling mechanisms mediate a variety of morphological changes such as formation of neurites. It is well established that a number of small GTPases control neurite behavior before the connection with the target tissue. However, their regulatory mechanisms remain to be fully understood. Here, we show that the Arf6 guanine-nucleotide exchange factor (GEF), cytohesin-2 (CYTH2), interacts with the cytoskeletal protein actinin-1 (ACTN1) and regulates neurite extension in N1E-115 cells used as the model. Knockdown of ACTN1, as well as that of CYTH2, in cells inhibits cellular Arf6 activity and neurite extension. The C-terminal polybasic region of CYTH2 participates in interacting directly with the EFh2 domain of ACTN1. Expression of CYTH2 mutant deficient of the EFh2 domain in cells also inhibits Arf6 activation and neurite extension. Furthermore, FRET analysis detects that the respective interactive region peptides, tagged with cell-permeable short peptides, greatly decrease Arf6 activation at growth cones in a time-dependent manner. Collectively, the signaling through CYTH2 and ACTN1 properly regulates neurite extension in N1E-115 cells, demonstrating the unexpected interaction of CYTH2 and ACTN1 in the regulation of cellular Arf6 activity involved in neurite extension. © 2012 Elsevier Inc. Source

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