Abstract. Objective: To investigate the effect of ischemic postconditioning on protein aggregation caused by transient ischemia and reperfusion and to clarify its underlying mechanism.. Methods: Two-vessel-occluded transient global ischemia rat model was used. The rats in ischemic postconditioning group were subjected to three cycles of 30-s/30-s reperfusion/clamping after 15min of ischemia. Neuronal death in the CA1 region was observed by hematoxylin-eosin staining, and number of live neurons was assessed by cell counting under a light microscope. Succinyl-LLVY-AMC was used as substrate to assay proteasome activity in vitro. Protein carbonyl content was spectrophotometrically measured to analyze protein oxidization. Immunochemistry and laser scanning confocal microscopy were used to observe the distribution of ubiquitin in the CA1 neurons. Western blotting was used to analyze the quantitative alterations of protein aggregates, proteasome, hsp70 and hsp40 in cellular fractions under different ...

Objectives. Pharmacological treatment of reperfusion injury using insulin and GSK3β inhibition has been shown to be cardioprotective, however, their interaction with the endogenous cardioprotective strategy, ischemic postconditioning, is not known. Design. Langendorff perfused ex vivo rat hearts were subjected to 30 min of regional ischemia and 120 min of reperfusion. For the first 15 min of reperfusion hearts received either vehicle (Ctr), insulin (Ins) or a GSK3β inhibitor (SB415286; SB41), with or without interruption of ischemic postconditioning (IPost; 3 × 30 s of global ischemia). In addition, the combination of insulin and SB41 for 15 min was assessed. Results. Insulin, SB41 or IPost significantly reduced infarct size versus vehicle treated controls (IPost 33.5 ± 3.3%, Ins 33.5 ± 3.4%, SB41 30.5 ± 3.0% vs. Ctr 54.7 ± 6.8%, p , 0.01). Combining insulin and SB415286 did not confer additional cardioprotection compared to the treatments given alone (SB41 + Ins 26.7 ± 3.5%, ns). ...

Background-Ischemic postconditioning has been reported to reduce infarct size in patients with ST-segment elevation myocardial infarction (STEMI). However, cardioprotective effects of postconditioning have not been demonstrated in a large-scale trial. Methods and Results-We performed a multicenter, prospective, randomized, open-label, blinded endpoint trial. A total of 700 patients undergoing primary percutaneous coronary intervention (PCI) for STEMI within 12 hours after symptom onset were randomly assigned to the postconditioning group or the conventional primary PCI group in a 1:1 ratio. Postconditioning was performed immediately after restoration of coronary flow as follows: the angioplasty balloon was positioned at the culprit lesion, and inflated 4 times for 1 minute with low-pressure (, 6 atm) inflations, each separated by 1 minute of deflation. The primary endpoint was complete ST-segment resolution (the percentage resolution of ST-segment elevation ,70%) measured at 30 minutes after ...

Acute myocardial infarction (AMI) is one of the leading causes of death in the world, demands early and complete reperfusion in therapy strategy. Reperfusion is the definitive treatment to salvage ischaemic myocardium from infarction. A primary determinant of infarct size is the duration of ischaemia. In myocardium that has not been irreversibly injured by ischaemia, reperfusion induces additional injury in the area at risk. Ischaemic postconditioning (IPO), brief intermittent ischaemia during the onset of reperfusion, both are known as endogenous protective mechanism, which could markedly limit myocardial infarction and render the myocardium more resistant to the subsequent I/R injury. Endoplasmic reticulum (ER) is the most important organelle in eukaryocyte, serving for macromolecules biosynthesis, stress action and calcium homeostasis adjusting. Recently study show that ischaemia/reperfusion injury (I/R) can affect ER function, namely ER stress (ERs). ERs induces ER molecular chaperones such ...

The expression of Hes1 is increased following myocardial infarct and other ischemic cardiomyopathies, but the role of Hes1 in cardioprotection provided by ischemic postconditioning (IPost) remains unclear. In this study, we used gain and loss of func

Hyperglycemia-Induced Inhibition of DJ-1 Expression Compromised the Effectiveness of Ischemic Postconditioning Cardioprotection in Rats. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

A large randomized controlled trial of ischemic postconditioning in patients who had experienced the deadliest form of heart attack -- ST-segment elevation myocardial infarction (STEMI) -- failed to show that this procedure significantly reduces death from any cause or hospitalization for heart failure, according to research presented at the American College of Cardiologys 65th Annual Scientific Session.

Ischemic postconditioning refers to several transient reperfusion and ischemia cycles after an ischemic event and before a long duration of reperfusion. The procedure produces neuroprotective effects. The mechanisms underlying these neuroprotective effects are poorly understood. In this study, we found that most neurons in the CA1 region died after 10 minutes of ischemia and is followed by 72 hours of reperfusion. However, brain ischemic postconditioning (six cycles of 10 s/10 s reperfusion/re-occlusion) significantly reduced neuronal death. Significant up-regulation of Glutamate transporter-1 was found after 3, 6, 24, 72 hours of reperfusion. The present study showed that ischemic postconditioning decreases cell death and that upregulation of GLT-1 expression may play an important role on this effect.

Sigma-Aldrich offers abstracts and full-text articles by [Hongzhu Li, Chao Zhang, Weiming Sun, Lina Li, Bo Wu, Shuzhi Bai, Hongxia Li, Xin Zhong, Rui Wang, Lingyun Wu, Changqing Xu].

This study explored the neuroprotective effects of post-positioning on ischemic stroke patients with randomized, double-blinded and controlled method. Patients are divided into experimental and placebo groups to receive remote ischemic post-conditioning for 30 days. Remote ischemic post-conditioning is performed by the inflating tourniquets to certain extents on bilateral arms with 5 cycles of 5min inflation and 5min relax alternation for the total of 30 consecutive days. It is 200mmHg for RIPC group and 60mmHg for control group. Evaluation parameters include CRP, TNF-α, ICAM-1 and GFAP in blood at 0, 3, 7, 15 and 30 days after treatment; and MRI at 0 and 30 days after treatment ...

Methods Between Oct. 2006 and Jan. 2009 at affiliated hospital of Beihua University, 64 patients diagnosed with STEMI undergoing emergency percutaneous transluminal coronary angioplasty (PTCA) and stenting within 12 h from onset of symptoms to open the infarct-related coronary artery, were randomly divided in two groups: the control group (n=34) which were treated by implantation stent after PTCA, and the experimental group (n=30) which were treated by ischaemic postconditioning within first minutes of reflow by 3 episodes of 30-seconds inflation and 30-seconds deflation of the angioplasty balloon. All patients were first onset of STEMI, and did not have the inverse perfusion from collateral circulation. Two groups were observed and compared with reperfusion arrhythmias within 5 min after beginning put into practice reperfusion.. ...

Cardiovascular diseases remain the main cause of death and disability in the world. In patients su??ering myocardial infarction, the infarct size is a..

UCL Discovery is UCLs open access repository, showcasing and providing access to UCL research outputs from all UCL disciplines.

Purpose: Sevoflurane postconditioning (SpostC) provides been shown to safeguard the center from ischemia-reperfusion (We/R) damage. anesthetic gas monitor (Datex Capnomac Ultima Department of Instrumentarium Corp Helsinki Finland). The respiratory rate was adjusted to maintain partial pressure of carbon dioxide within physiologic limits (end-tidal carbon dioxide 35 mmHg). After exposure of the heart a 6.0 silk ligation suture was looped round the LAD for subsequent occlusion. The ligature success of the LAD was judged by a color switch at the area at risk (AAR) which was further confirmed by a QRS wave switch during electrocardiography (ECG). Ultrastructure examination Thirty minutes after reperfusion the rat hearts were removed. Two samples of new myocardial tissue (approximately 1 mm3 in size) were obtained 3 mm above the apex from your AAR of the left ventricle (LV). The tissues were fixed with 5% glutaraldehyde overnight at 4 °C washed 3 times with phosphate-buffered saline and fixed again ...

The protective aftereffect of ischaemic postconditioning (short cycles of reperfusion and reocclusion of the previously occluded vessel) was identified over ten years ago commanding intense interest as a strategy for changing reperfusion injury which plays a part in infarct size in acute myocardial infarction. understand enhance the signalling pathways recruited in postconditioning. Cohort size and power, affected person selection, and zero scientific infarct size estimation may all represent main obstacles to evaluating the therapeutic efficiency of postconditioning. Furthermore, chronic treatment of the sufferers with medications 1206801-37-7 IC50 like ACE inhibitors, statins and nitrates may enhance signalling, inhibiting the defensive aftereffect of postconditioning mimetics, or conversely induce a maximally guarded state wherein no more benefit could be exhibited. Arguably, effective translation of postconditioning cannot happen until of the issues are resolved, thats, experimental ...

Our group demonstrated previously that postconditioning by angioplasty reduces infarct size, as assessed by early CK release, in the human heart.16 This was the first study demonstrating that postconditioning can reduce lethal reperfusion injury in the human heart. In a retrospective study, Darling et al23 similarly reported a reduced release of CK in ST-segment-elevation MI patients who underwent ,4 inflations of the angioplasty balloon at the time of reperfusion compared with those who received ,3 inflations. The present study is in agreement with the initial results of the Staat study, further reporting a mean reduction of 47% of the area under the curve of TnI in postconditioned versus control groups. This infarct size reduction was observed with the control and postconditioned groups having similar duration of ischemia and size of the area at risk, ie, 2 major determinants of infarct size. Area at risk was assessed by measurement of the percentage of abnormally contracting segments on ...

6Uludag University, Faculty of Medicine, Department of Pathology, Bursa, Turkey AIM: Apoptosis after cerebral ischemia/reperfusion (I/R) injury leads to the process of cell death. The deal therapeutic approach would target the apoptosis after I/R. Ischemic postconditioning is a recently discovered neuroprotective strategy that involves the application of brief mechanical reperfusion with a specific algorithm at the onset of reperfusion following an ischemic period.. MATERIAL and METHODS: Transient MCAo was performed on male SD (275 25g) rats with intraluminal thread insertion for 2hrs. Rats (n:36) were treated with postconditioning after 60 minutes of occlusion. The postconditioning algorithm was 30 secs of brief reperfusion followed by 30 secs of MCAo and this cycle was repeated 3 times at the onset of reperfusion.. RESULTS: After I/R injury, % change of the malonyldialdehyde (MDA) levels in the cortex, which is an index of lipid peroxidation, was found significantly higher in the I/R group. On ...

In this thesis different factors that promote or inhibit heart remodelling induced by angiotensin II were studied. The following conclusions can be drawn: 1. The presence of elevated levels of Ang II in the perfusion buffer did not increase myocardial injury during ischemia-reperfusion. However, the ability to protect the heart by ischemic postconditioning was lost. This seemed to be due to blockade of ERK1/2 signalling and GSK3-β inhibition induced by postconditioning. Elevated levels of Ang II, which is seen in untreated cardiovascular disease and in kidney disease, could therefore contribute to limit the outcome of the potential clinical use of postconditioning. 2. Non-compensatory (non-hypertrophic) heart remodelling was triggered by high-dose Ang II. This leads to changes in the contractile apparatus and reduced tolerance to ischemia in the absence of cellular hypertrophy. Increased expression of key genes involved in fibrosis was followed by an increase in interstitial fibrosis in heart ...

TY - JOUR. T1 - Az ischaemiás posztkondicionálás hatása az oxidatív stresszre és a szöveti struktúrára vékonybél meleg ischaemiás és autotranszplantációs modellekben.. AU - Nedvig, Klára. AU - Völgyi, Edina. AU - Wéber, G.. AU - Rőth, E.. AU - Ferencz, A.. PY - 2011/12. Y1 - 2011/12. N2 - Our study investigated the effect of ischemic postconditioning (IPO) in intestinal warm ischemia/reperfusion (I/R) and autotransplantation models. Warm ischemia was performed by occlusion of superior mesenteric artery for 1, 3 and 6 hours in white domestic pigs (n = 15). Prior to 3 hours reperfusion the intestine was postconditioned by 3 cycles of 30-seconds ischemia and 30-seconds reperfusion (IPO protocol). In the cold ischemia group (n = 15) the bowel was preserved in University of Wisconsin solution for 1, 3, and 6 hours. Prior to 3 hours reperfusion IPO protocol was applied, too. Tissue samples were collected after laparotomy (control) and at the end of the reperfusion periods. As far as ...

Ischaemic preconditioning is the most powerful endogenous mechanism for limiting myocardial infarct size in the experimental setting. Its clinical application is limited to scenarios in which the index episode of ischaemia and reperfusion can be anticipated such as in the setting of cardiac surgery • Ischaemic postconditioning represents an endogenous cardioprotective strategy which is applied at the onset of myocardial reperfusion, thereby allowing its use as an adjunct to reperfusion in patients presenting with an acute myocardial infarction • Both ischaemic preconditioning and postconditioning recruit a common signal transduction pathway at the time of myocardial reperfusion, which can be targeted by pharmacological agents administered as adjuncts to reperfusion. ...

Article: Hyperglycemia-induced inhibition of DJ-1 expression compromised the effectiveness of ischemic postconditioning cardioprotection in ...

Intérêt de lAssociation Bupivacaïne-Fentanyl-Morphine Intrathécale pour lAnalgésie Post-Césarienne au Centre Hospitalier Universitaire de Libreville

Abstract Introduction: This article aims to provide a narrative review of the most recent primary literature on the pathways associated with the neuroprotective effects of remote ischaemic post-conditioning (RIPC) in …. ...

Somers SJ. The role of signal transducer and activator of transcription-3 (STAT-3) in ischaemic and pharmacological postconditioning. [Thesis]. University of Cape Town ,Faculty of Health Sciences ,Department of Medicine, 2011 [cited yyyy month dd]. Available from: http://hdl.handle.net/11427/ ...

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After having shown that postconditioning allowed a significant 36% reduction of infarct size as assessed by blood levels of myocardial enzymes in acute myocardial patients, the investigators objective is to assess the effect of postconditioning in acute myocardial infarction (AMI) patients on microvascular obstruction lesions defined by cardiac MRI images ...

SELECT UCS.mcr_ucrs UcasCode,srs_ipo.ipo_seqn,srs_ipp.ipp_code,srs_ipp.ipp_iref,srs_ipp.ipp_titl,srs_ippn.*,ins_dpt.dpt_name,ins_dpt.dpt_snam,men_xon.xon_newv,UCS.mcr_olbc,UCS.mcr_olb3,srs_ipo.ipo_begd,ins_lca.lca_name,srs_crs.crs_leng crs_leng,UCS.mcr_cgpc ApplyRoute,ins_moa.moa_name , ins_moa.moa_code,srs_ipp.ipp_iuse IPPUSE, UCS.mcr_iuse MCRUSE,UCS.mcr_schc, ins_cmp.cmp_name, ins_dpt.dpt_code, Case WHEN srs_ipo.ipo_iuse is null then Y else srs_ipo.ipo_iuse end AS ipo_iuse, srs_crs.crs_uomc, srs_ipo.ipo_end2,srs_ipo.ipo_ayrc,UCS.MCR_RECR, srs_ipo.ipo_udf9, srs_ipp.ipp_prgc, CRS_UDFI, srs_ipp.ipp_subj, CASE WHEN (SELECT TOP 1 mcr_uvst FROM srs_mcr WHERE mcr_code LIKE Substring(srs_ipp.ipp_code, 1, 6) + % AND mcr_uvst = Y AND mcr_iuse = Y AND mcr_aesc = U) = Y THEN True ELSE False END AS Clearing, CASE WHEN (SELECT TOP 1 crs_udf4 FROM srs_crs WHERE crs_code LIKE Substring(srs_ipp.ipp_code, 1, 6) + % AND crs_udf4 IS NOT NULL AND crs_iuse = Y AND crs_schc = PWLV) IS NOT NULL ...

SELECT UCS.mcr_ucrs UcasCode,srs_ipo.ipo_seqn,srs_ipp.ipp_code,srs_ipp.ipp_iref,srs_ipp.ipp_titl,srs_ippn.*,ins_dpt.dpt_name,ins_dpt.dpt_snam,men_xon.xon_newv,UCS.mcr_olbc,UCS.mcr_olb3,srs_ipo.ipo_begd,ins_lca.lca_name,srs_crs.crs_leng crs_leng,UCS.mcr_cgpc ApplyRoute,ins_moa.moa_name , ins_moa.moa_code,srs_ipp.ipp_iuse IPPUSE, UCS.mcr_iuse MCRUSE,UCS.mcr_schc, ins_cmp.cmp_name, ins_dpt.dpt_code, Case WHEN srs_ipo.ipo_iuse is null then Y else srs_ipo.ipo_iuse end AS ipo_iuse, srs_crs.crs_uomc, srs_ipo.ipo_end2,srs_ipo.ipo_ayrc,UCS.MCR_RECR, srs_ipo.ipo_udf9, srs_ipp.ipp_prgc, CRS_UDFI, srs_ipp.ipp_subj, CASE WHEN (SELECT TOP 1 mcr_uvst FROM srs_mcr WHERE mcr_code LIKE Substring(srs_ipp.ipp_code, 1, 6) + % AND mcr_uvst = Y AND mcr_iuse = Y AND mcr_aesc = U) = Y THEN True ELSE False END AS Clearing, CASE WHEN (SELECT TOP 1 crs_udf4 FROM srs_crs WHERE crs_code LIKE Substring(srs_ipp.ipp_code, 1, 6) + % AND crs_udf4 IS NOT NULL AND crs_iuse = Y AND crs_schc = PWLV) IS NOT NULL ...

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[Preventive effects of ischemic postconditioning and penehyclidine hydrochloride on gastric against ischemia-reperfusion injury in rats]. - Tao Wang, Yu-fang Leng, Yue Zhang, Yu-qing Kang, Xing Xue, Yan Zhang

Background Ischemic postconditioning (PostC) protects the liver against ischemia-reperfusion (IR) injury. Milrinone, a phosphodiesterase 3 inhibitor, has been reported to exhibit preconditioning properties against hepatic IR injury; however, its PostC properties remain unknown. This study investigated whether milrinone has PostC properties against hepatic IR injury and the roles of phosphatidylinositol 3-kinase (PI3K) and nitric oxide synthase (NOS). Materials and methods Male Wistar rats were separated into six groups: (1) group S: animals that underwent sham operation without ischemia, (2) group C: ischemia followed by reperfusion with no other intervention, (3) group M: milrinone administered immediately after reperfusion, (4) group MW: wortmannin, a PI3K inhibitor, injected before milrinone administration, (5) group MN: l-NAME, a NOS inhibitor, injected before milrinone administration, and (6) group MD, milrinone administered 30 min after reperfusion. Except for group S, all groups underwent ...

The anti-inflammatory actions of sevoflurane postconditioning are suggested as an important mechanism of sevoflurane postconditioning-induced neuroprotection against cerebral ischemia. Here, we determined whether the anti-inflammatory effects of sevoflurane postconditioning were mediated via inhibition of the toll-like receptor (TLR)-4/nuclear factor kappa B (NF-κB) pathway after global transient cerebral ischemia in rats. Forty-five rats were randomly assigned to five groups as follows: (1) control (10 min of ischemia, n = 10); (2) sevoflurane postconditioning (two periods of sevoflurane inhalation after ischemia for 10 min with a wash period of 10 min, n = 10); (3) resatorvid (intraperitoneal injection of a selective TLR-4 antagonist (3 mg/kg) 30 min before ischemia, n = 10); (4) sevoflurane postconditioning plus resatorvid (n = 10), and sham (n = 5). The numbers of necrotic and apoptotic cells in the hippocampal CA1 region, the expression levels of TLR-4, NF-κB, cleaved caspase-3, and tumor

The anti-inflammatory actions of sevoflurane postconditioning are suggested as an important mechanism of sevoflurane postconditioning-induced neuroprotection against cerebral ischemia. Here, we determined whether the anti-inflammatory effects of sevoflurane postconditioning were mediated via inhibition of the toll-like receptor (TLR)-4/nuclear factor kappa B (NF-κB) pathway after global transient cerebral ischemia in rats. Forty-five rats were randomly assigned to five groups as follows: (1) control (10 min of ischemia, n = 10); (2) sevoflurane postconditioning (two periods of sevoflurane inhalation after ischemia for 10 min with a wash period of 10 min, n = 10); (3) resatorvid (intraperitoneal injection of a selective TLR-4 antagonist (3 mg/kg) 30 min before ischemia, n = 10); (4) sevoflurane postconditioning plus resatorvid (n = 10), and sham (n = 5 ...

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BACKGROUND The aim of this study was to evaluate the role of remote ischemic postconditioning (RIPC) of the upper arm on protection from cardiac ischemia-reperfusion injury following primary percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI). MATERIAL AND METHODS Eighty patients with STEMI were randomized into two groups: primary PCI (N=44) and primary PCI+RIPC (N=36). RIPC consisted of four cycles of 5 minutes of occlusion and five minutes of reperfusion by cuff inflation and deflation of the upper arm, commencing within one minute of the first PCI balloon dilatation ...

Lacerda L. Role of Tumour Necrosis Factor Alpha (TNFa) in ischaemic and pharmacological postconditioning. [Thesis]. University of Cape Town ,Faculty of Health Sciences ,Department of Medicine, 2010 [cited yyyy month dd]. Available from: http://hdl.handle.net/11427/ ...

Cardioprotection encompasses several regimens that have shown to preserve function and viability of cardiac muscle cell tissue subjected to ischemic insult or reoxygenation. Cardioprotection includes strategies that are implemented before an ischemic event (preconditioning, PC), during an ischemic event (perconditioning, PerC) and after the event and during reperfusion (postconditioning, PostC). These strategies can be further stratified by performing the intervention locally or remotely, creating classes of conditioning known as remote ischemic PC (RIPC), remote ischemic PostC and remost ischemic PerC. Classical (local) preconditioning has an early phase with an immediate onset lasting 2-3 hours that protects against myocardial infarction. The early phase involves post-translational modification of preexisting proteins, brought about by the activation of G protein-coupled receptors as well as downstream MAPKs and PI3/Akt. These signaling events act on the ROS-generating mitochondria, activate ...

During early reperfusion (in the first minutes), occurs a rapid correction of acidosis (low intracellular pH) through the Na+/H+ exchanger, and through the entry of the ion HCO3 by the Na/HCO3 symporter (Figure 2). Additionally, the lactate, previously accumulated, is washed out with the restored blood flow diminishing the acidosis. However, all these events cause accumulation of Na+. This additional augment in intracellular sodium induces a secondary activation of the Na+/Ca2+ exchanger in the reverse mode to move out Na+ ions; however, this aggravates cytosolic Ca2+ accumulation. On the other hand, the abrupt re exposure of the ischemia inhibited mitochondrial respiratory chain to oxygen generates a membrane potential to drive ATP synthesis, which leads to a rapid overload of Ca2+ in the matrix and massive production of reactive oxygen species (ROS), which by themselves are capable of damaging cellular membranes and to induce oxidative stress. These two factors (cytosolic Ca accumulation and ...

Reperfusion injury is a complex process involving several cell types (endothelial cells, neutrophils, and cardiomyocytes), soluble proinflammatory mediators, oxidants, ionic and metabolic dyshomeostas

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Abstract 17556: Inserte J, Hernando V, Vilardosa U, Poncelas M, Agullo L, Garcia-Dorado D. Delayed Phospholamban Phosphorylation During Reperfusion in Postconditioned Myocardium Favours Ca2+ Normalization Through Na+/Ca+-exchanger and Contributes to Protection. Circulation. 2013;128:A17556. Look at the presentation using this Link.. ...

Abstract 17556: Inserte J, Hernando V, Vilardosa U, Poncelas M, Agullo L, Garcia-Dorado D. Delayed Phospholamban Phosphorylation During Reperfusion in Postconditioned Myocardium Favours Ca2+ Normalization Through Na+/Ca+-exchanger and Contributes to Protection. Circulation. 2013;128:A17556. Look at the presentation using this Link.. ...

Yanrong Zheng is the author of this article in the Journal of Visualized Experiments: Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

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For example, to animate a spinning top or a flying saucer: a spinning can easily be created with rotate on axis Z local (shortcut R, Z, Z), but if I further add some global animations to the object , the IPO merges both local and global rotations and the result for the other frames is a mess ...

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The reason why bones have their own Ipo datablocks, is that each bone has several animatable parameters, such as rotation, scale and movement. Since each RVK only has one parameter, influence, it would be pretty silly IMO to have an IPO datablock per RVK. I agree that the ability to mix IPOs is crucial, but this could just as well be achieved if you could key all the RVKs together in IPO chunks. These chunks could then, as with all other IPOs, be blended and modified in the NLA, and with driven keys, each curve could independently be assigned to other parameters ...

Please note: This action will also remove this member from your connections and send a report to the site admin. Please allow a few minutes for this process to complete. ...

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