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Intelligent Shimming for Deep Drawing Processes
Søren Tommerup,Benny Endelt,Joachim Danckert,Karl Brian Nielsen 한국소성가공학회 2011 기타자료 Vol.2011 No.8
This paper demonstrates the use of an intelligent shimming system to compensate for changes in process output due to tool wear. A new tool concept with integrated hydraulic cavities used as actuators in feedback control system is presented. By prescribing a hydraulic pressure in the individual cavities the blank-holder force distribution can be controlled during the punch stroke. By means of a sequence of numerical simulations abrasive wear is imposed to the deep drawing of a rectangular cup. The abrasive wear is modelled by changing the tool surface geometry using an algorithm based on the sliding energy density. As the tool surfaces are changed the material draw-in is significantly altered when using conventional open-loop control of the blank-holder force. A feed-back controller is presented which is capable of reducing the draw-in difference to a certain degree. Further a learning algorithm is introduced to the system, which is able to improve the response of the feed-back system significantly.
International Repercussions of Source-based Capital Income Taxation
Christensen, Thomas Alslev,Nielsen, Søren Bo 세종대학교 국제경제연구소 1995 Journal of Economic Integration Vol.10 No.1
The paper is concerned with international effects of source-based capital income taxation in a large economy. We derive, within the context of a twocountry overlapping generations model in continuous time, the implications of such taxation for the world interest rate and for investment, consumption, saving and external balances at home and abroad. Furthermore, we argue that higher source-based taxes will hurt foreigners alive at the time of the policy change, whereas future citizens abroad stand to benefit. Finally, the effects of source-and residence-based taxed are compared.
( Martin Skott ),( Rikke Nørregaard ),( Hanne Birke Sørensen ),( Johan Palmfeldt ),( Tae Hwan Kwon ),( Thomas Jonassen ),( Jørgen Frøkiær ),( Søren Nielsen ) 대한신장학회 2014 Kidney Research and Clinical Practice Vol.33 No.2
Background: The primary aim of the study was to investigate the cytokine/chemokine response in the kidney, lung, and liver following acute kidney injury(AKI). The secondary aim was to test whether α-melanocyte-stimulating hormone(α-MSH) could prevent a reduction in organ function, and attenuate the inflammatorycytokine/chemokine response within the kidney, lung, and liver following AKIin rats with or without preexisting chronic kidney disease (CKD). Methods: A two-stage animal model, in which AKI was induced in rats withpreexisting CKD, induced by 5/6 nephrectomy (Nx), was used. Six weeks later, AKIwas induced by intestinal ischemia and reperfusion (IIR). Sham procedures [S(Nx)and S(IIR)] were also performed. Results: Increasing levels of serum creatinine (sCr) demonstrated progressive developmentof CKD in response to Nx, and following IIR sCr levels increased furthersignificantly, except in the S(Nx) group treated with α-MSH. However, no significantdifferences in the fractional increase in sCr were observed between any of the groupsexposed to IIR. In kidney, lung, and liver tissue the levels of interleukin (IL)-1β weresignificantly higher in rats undergoing IIR when compared to the S(IIR) and control rats. The same pattern was observed for the chemokine monocyte chemoattractant protein(MCP)-1 in lung and liver tissue. Furthermore, kidney IL-1β and RANTES levels weresignificantly increased after IIR in the Nx rats compared to the S(Nx) rats. Conclusion: Both the functional parameters and the cytokine/chemokine response areas dramatic when AKI is superimposed onto CKD as onto non-CKD. No convincingprotective effect of α-MSH was detected.
Jung, Hyun Jun,Kim, Sang-Yeob,Choi, Hyo-Jung,Park, Eui-Jung,Lim, Jung-Suk,Frøkiaer, Jørgen,Nielsen, Søren,Kwon, Tae-Hwan American Physiological Society 2015 American journal of physiology. Renal physiology Vol.308 No.5
<P>Aquaporin-2 (AQP2) mediates arginine vasopressin (AVP)-induced water reabsorption in the kidney collecting duct. AVP regulates AQP2 expression primarily via G(s)alpha/cAMP/PKA signaling. Tankyrase, a member of the poly(ADP-ribose) polymerase family, is known to mediate Wnt/beta-catenin signaling-induced gene expression. We examined whether tankyrase plays a role in AVP-induced AQP2 regulation via ADP-ribosylation of G protein-alpha (G alpha) and/or beta-catenin-mediated transcription of AQP2. RT-PCR and immunoblotting analysis revealed the mRNA and protein expression of tankyrase in mouse kidney and mouse collecting duct mpkCCDc14 cells. dDAVP-induced AQP2 upregulation was attenuated in mpkCCDc14 cells under the tankyrase inhibition by XAV939 treatment or small interfering (si) RNA knockdown. Fluorescence resonance energy transfer image analysis, however, revealed that XAV939 treatment did not affect dDAVP-or forskolin-induced PKA activation. Inhibition of tankyrase decreased dDAVP-induced phosphorylation of beta-catenin (S552) and nuclear translocation of phospho-beta-catenin. siRNA-mediated knockdown of beta-catenin decreased forskolin-induced AQP2 transcription and dDAVP-induced AQP2 expression. Moreover, inhibition of phosphoinositide 3-kinase/Akt, which was associated with decreased nuclear translocation of beta-catenin, diminished dDAVP-induced AQP2 upregulation, further indicating that beta-catenin mediates AQP2 expression. Taken together, tankyrase plays a role in AVP-induced AQP2 regulation, which is likely via beta-catenin-mediated transcription of AQP2, but not ADP-ribosylation of G alpha. The results provide novel insights into vasopressin-mediated urine concentration and homeostasis of body water metabolism.</P>
Targeted disruption of the Cl-/HCO3- exchanger Ae2 results in osteopetrosis in mice.
Josephsen, Kaj,Praetorius, Jeppe,Frische, Sebastian,Gawenis, Lara R,Kwon, Tae-Hwan,Agre, Peter,Nielsen, Søren,Fejerskov, Ole National Academy of Sciences 2009 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.106 No.5
<P>Osteoclasts are multinucleated bone-resorbing cells responsible for constant remodeling of bone tissue and for maintaining calcium homeostasis. The osteoclast creates an enclosed space, a lacuna, between their ruffled border membrane and the mineralized bone. They extrude H(+) and Cl(-) into these lacunae by the combined action of vesicular H(+)-ATPases and ClC-7 exchangers to dissolve the hydroxyapatite of bone matrix. Along with intracellular production of H(+) and HCO(3)(-) by carbonic anhydrase II, the H(+)-ATPases and ClC-7 exchangers seems prerequisite for bone resorption, because genetic disruption of either of these proteins leads to osteopetrosis. We aimed to complete the molecular model for lacunar acidification, hypothesizing that a HCO(3)(-) extruding and Cl(-) loading anion exchange protein (Ae) would be necessary to sustain bone resorption. The Ae proteins can provide both intracellular pH neutrality and serve as cellular entry mechanism for Cl(-) during bone resorption. Immunohistochemistry revealed that Ae2 is exclusively expressed at the contra-lacunar plasma membrane domain of mouse osteoclast. Severe osteopetrosis was encountered in Ae2 knockout (Ae2-/-) mice where the skeletal development was impaired with a higher diffuse radio-density on x-ray examination and the bone marrow cavity was occupied by irregular bone speculae. Furthermore, osteoclasts in Ae2-/- mice were dramatically enlarged and fail to form the normal ruffled border facing the lacunae. Thus, Ae2 is likely to be an essential component of the bone resorption mechanism in osteoclasts.</P>
O'Neill, Heidi,Lebeck, Janne,Collins, Patrick B,Kwon, Tae-Hwan,Frøkiaer, Jørgen,Nielsen, Søren Springer International ; Oxford University Press 2008 Nephrology, dialysis, transplantation Vol.23 No.5
<P>BACKGROUND: Diabetes mellitus (DM) is associated with a significant polyuria and natriuesis as well as increased plasma aldosterone and anti-diuretic hormone arginine vasopressin (AVP). This study aimed to determine whether diabetic kidneys compensate for the urinary sodium and water losses by increasing apical targeting of epithelial sodium channel (ENaC) subunits and aquaporin-2 (AQP2) in the collecting duct, in addition to the previously observed changes in ENaC subunit protein expression in different kidney zones. METHODS: Female rats were investigated 2 weeks after induction of DM by streptozotocin administration. Kidneys were examined by immunohistochemisty and semiquantitative immunoblotting. RESULTS: We demonstrated that the protein expression of renal AQP2, Ser-256 phosphorylated AQP2, AQP3, beta- and gamma-ENaC (but not alpha-ENaC) increased consistently with an increased AVP response. In contrast, there were no significant changes in the relative apical targeting of beta-, gamma- and alpha-ENaC, and the shift in the molecular weight of gamma-ENaC from 85 kDa to 70 kDa was not observed despite increased plasma aldosterone levels. These results were supported by changes in the functional data showing increased solute-free water reabsorption, increased fractional excretion of sodium and an unchanged ratio of potassium to sodium in the urine. CONCLUSIONS: The data demonstrate that diabetic kidneys have a reduced sensitivity to the anti-natriuretic action of elevated plasma aldosterone levels with no relative increase in ENaC subunit apical targeting, whereas there is increased expression of beta- and gamma-ENaC, which alone may play a role in the increased sodium reabsorption in the kidney in DM.</P>
Oklinski, Michal K.,Skowronski, Mariusz T.,Skowronska, Agnieszka,Rü,tzler, Michael,Nørgaard, Kirsten,Nieland, John D.,Kwon, Tae-Hwan,Nielsen, Søren MDPI 2016 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.17 No.12
<P>Aquaporins (AQPs) are water channel proteins robustly expressed in the central nervous system (CNS). A number of previous studies described the cellular expression sites and investigated their major roles and function in the brain and spinal cord. Among thirteen different mammalian AQPs, AQP1 and AQP4 have been mainly studied in the CNS and evidence has been presented that they play important roles in the pathogenesis of CNS injury, edema and multiple diseases such as multiple sclerosis, neuromyelitis optica spectrum disorders, amyotrophic lateral sclerosis, glioblastoma multiforme, Alzheimer’s disease and Parkinson’s disease. The objective of this review is to highlight the current knowledge about AQPs in the spinal cord and their proposed roles in pathophysiology and pathogenesis related to spinal cord lesions and injury.</P>