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Myint, Aye Mu,Steinbusch, Harry W.M.,Goeghegan, Liam,Luchtman, Dirk,Kim, Yong Ku,Leonard, Brian E. Karger 2007 NEUROIMMUNOMODULATION -BASEL- Vol.14 No.2
<P><I>Background:</I> The olfactory bulbectomised (OBX) rat model is a chronic model of depression in which behavioural and neuroimmunoendocrine changes are reversed only after chronic antidepressant treatment. The cyclooxygenase 2 (COX-2) inhibitor celecoxib has been shown to improve the depressive symptoms in patients with major depression. <I>Methods:</I> The association between blood and brain immunological and behavioural changes in chronic treatment with COX-2 inhibitor was explored in the OBX rats and their sham-operated controls. <I>Results:</I> The OBX group showed significantly higher locomotor activity than the other groups in the first 5 min in the open field. In the home cage emergence test, the OBX group showed a significantly shorter latency period compared to the sham group (z = -3.192, p = 0.001) but there was no difference between the other three groups. In the hypothalamus, the OBX group had a significantly higher interleukin 1β (IL-1β) concentration than the OBX + celecoxib group (z = -1.89, p = 0.05) as well as a significantly higher IL-10 concentration (z = -1.995, p = 0.046). In the prefrontal cortex, the OBX group showed significantly higher concentrations of tumour necrosis factor α (z = -2.205, p = 0.028) and IL-1β (z = -3.361, p = 0.001) than the OBX + celecoxib group, but a significantly lower concentration of IL-10 (p = -3.361, p = 0.001) than the OBX + celecoxib group. <I>Conclusions:</I> The results of this study supported the potential therapeutic role of the COX-2 inhibitor celecoxib. It is possible that the behavioural changes following the chronic administration of celecoxib to the OBX rats are associated with an attenuation of the increase in the pro-inflammatory cytokines in the brain.</P><P>Copyright © 2007 S. Karger AG, Basel</P>
Knabben Ingo,Lars Regestein,Julia Schauf,Sven Steinbusch,Jochen Buchs 한국미생물 · 생명공학회 2011 Journal of microbiology and biotechnology Vol.21 No.2
To yield high concentrations of protein expressed by genetically modified Escherichia coli, it is important that the bacterial strains are cultivated to high cell density in industrial bioprocesses. Since the expressed target protein is mostly accumulated inside the E. coli cells, the cellular product formation can be directly correlated to the bacterial biomass concentration. The typical way to determine this concentration is to sample offline. Such manual sampling, however, wastes time and is not efficient for acquiring direct feedback to control a fedbatch fermentation. An E. coli K12-derived strain was cultivated to high cell density in a pressurized stirred bioreactor on a pilot scale, by detecting biomass concentration online using a capacitance probe. This E. coli strain was grown in pure minimal medium using two carbon sources (glucose and glycerol). By applying exponential feeding profiles corresponding to a constant specific growth rate, the E. coli culture grew under carbon-limited conditions to minimize overflow metabolites. A high linearity was found between capacitance and biomass concentration, whereby up to 85 g/L dry cell weight was measured. To validate the viability of the culture, the oxygen transfer rate (OTR) was determined online, yielding maximum values of 0.69 mol/l/h and 0.98mol/l/h by using glucose and glycerol as carbon sources, respectively. Consequently, online monitoring of biomass using a capacitance probe provides direct and fast information about the viable E. coli biomass generated under aerobic fermentation conditions at elevated headspace pressures.
Olfactory neuropathology in Alzheimer’s disease: a sign of ongoing neurodegeneration
( Gowoon Son ),( Ali Jahanshahi ),( Seung-jun Yoo ),( Jackson T. Boonstra ),( David A. Hopkins ),( Harry W. M. Steinbusch ),( Cheil Moon ) 생화학분자생물학회(구 한국생화학분자생물학회) 2021 BMB Reports Vol.54 No.6
Olfactory neuropathology is a cause of olfactory loss in Alzheimer’s disease (AD). Olfactory dysfunction is also associated with memory and cognitive dysfunction and is an incidental finding of AD dementia. Here we review neuropathological research on the olfactory system in AD, considering both structural and functional evidence. Experimental and clinical findings identify olfactory dysfunction as an early indicator of AD. In keeping with this, amyloid-β production and neuro-inflammation are related to underlying causes of impaired olfaction. Notably, physiological features of the spatial map in the olfactory system suggest the evidence of ongoing neurodegeneration. Our aim in this review is to examine olfactory pathology findings essential to identifying mechanisms of olfactory dysfunction in the development of AD in hopes of supporting investigations leading towards revealing potential diagnostic methods and causes of early pathogenesis in the olfactory system. [BMB Reports 2021; 54(6): 295-304]