Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a consecutive series of 60 right lobe adult-to-adult live donor liver transplantations (ALDLTs), safety and efficacy of the University of Wisconsin (UW) and histidine-tryptophan-ketoglutarate (HTK) solution were evaluated. The first 30 liver grafts were perfused with UW solution and the subsequent 30 by HTK solution. Donor and recipient characteristics of both groups were comparable. All liver graft implantations were performed with cross-clamping of the inferior vena cava (IVC) and without veno-venous bypass. Main outcome measures were posttransplantation liver biochemistry, prothrombin time, and recipient morbidity, as well as graft and recipient survival. There were no significant differences of the outcome measures between the 2 groups. The low potassium content of the HTK solution nonetheless offered logistic advantages. In 25 of the 30 recipients of the HTK group, portal vein anastomosis was performed with a clamp on the donor portal vein while the clamps on the IVC were already released. This shortened the period during which the IVC was being cross-clamped. HTK solution was as safe and effective as a cold storage solution as UW solution in ALDLT. Its low potassium content has advantage of earlier restoration of patency of the IVC and thus hemodynamic stability. The cost of using HTK solution was also lower.
 ...
PMID:Applicability of histidine-tryptophan-ketoglutarate solution in right lobe adult-to-adult live donor liver transplantation. 1549 50

The ATPases (+/-Ca2+) of myofibrils from rabbit soleus (a slow muscle) and psoas (a fast muscle) have different Ea: -Ca2+, 78 and 60 kJ/mol and +Ca2+, 155 and 71 kJ/mol, respectively. At physiological temperatures, the two types of myofibrillar ATPase are very similar and yet the mechanical properties of the muscles are different (Candau et al. (2003) Biophys J 85: 3132-3141). Muscle contraction relies on specific interactions of the different chemical states on the myosin head ATPase pathway with the thin filament. An explanation for the Ea data is that different states populate the pathways of the two types of myofibril because the rate limiting steps are different. Here, we put this to the test by a comparison of the transient kinetics of the initial steps of the ATPases of the two types of myofibril at 4 degrees C. We used two methods: rapid flow quench ('cold ATP chase': titration of active sites, ATP binding kinetics, k(cat); 'Pi burst': ATP cleavage kinetics) and fluorescence stopped-flow (MDCC-phosphate binding protein for free Pi; myofibrillar tryptophan fluorescence for myosin head-thin filament detachment and ATP cleavage kinetics). We find that, as with psoas myofibrils, the most populated state on the cross-bridge cycle of soleus myofibrils, whether relaxed or activated, is (A)M.ADP.Pi. We propose a reaction pathway that includes several (A)M.ADP.Pi sub-states that are either 'weak' or 'strong', depending on the mechanical condition.
 ...
PMID:Does phosphate release limit the ATPases of soleus myofibrils? Evidence that (A)M. ADP.Pi states predominate on the cross-bridge cycle. 1554 66

Celsior solution (CS), a new preservation solution in thoracic organ transplantation, was evaluated for its efficacy in cold preservation of human liver endothelial cells (HLEC) and was compared to University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK, Custodiol). HLEC cultures were preserved at 4 degrees C in CS, UW, and HTK, for 2, 6, 12, 24, and 48 hours, with 6 hours of reperfusion. Levels of lactate dehydrogenase (LDH), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and adenosine 5'-triphosphate (ATP) were measured after each interval of ischemia and the respective phase of reperfusion. Preservation injury of HLEC as measured by LDH release, intracellular ATP level, and MTT reduction were overall significantly (P <or= .01, P <or= .01, P < .05, respectively) lower in UW than in CS and HTK. CS demonstrates a modest superiority to HTK in HLEC preservation. Furthermore, cold preservation remains the main cause of preservation injury of HLEC regardless of the preservation solution used. Additionally, the maintenance of a high intracellular ATP level of HLEC after ischemia and reperfusion, as shown by UW, could be taken as a beneficial effect, particularly in long-term ischemia. In conclusion, our cell culture model reveals the order of efficacy to protect HLEC against preservation injury as: UW >> CS > HTK.
 ...
PMID:UW is superior to Celsior and HTK in the protection of human liver endothelial cells against preservation injury. 1555 36

Hypothermia is an important preservation method for tissues and solid organs. The aim of the present study was to assess in rat cremaster muscle the effect of hypothermia, without or with pre-ischaemic HTK (histidine-tryptophan-ketoglutarate-Bretschneider solution) perfusion, on microvascular consequences of 4 or 6 h ischaemia and 2 h of reperfusion. Intravital microscopy was applied to examine capillary perfusion and leucocyte-endothelium interactions. The cremaster muscle was subjected to 4 or 6 h of cold (4 degrees C) or warm (33-34 degrees C) ischaemia and 2 h of reperfusion. Measurements were performed at baseline, prior to HTK perfusion and ischaemia, and at 0, 1 and 2 h after blood flow restoration. Hypothermia completely prevented the 50% reduction in capillary perfusion that was observed previously at start of reperfusion after 4 h warm ischaemia. After 6 h of warm ischaemia, perfusion resumed in only 45% of capillaries and remained at this low level during reperfusion. In contrast, only a slight decrease (< 10%) in capillary perfusion was observed after 6 h of cold ischaemia. Pre-ischaemic HTK perfusion had no beneficial effect on tissue perfusion. Both hypothermia and HTK attenuated the significant increase in venular leucocyte-vessel wall interactions, which was observed after 4 h of warm ischaemia in a previous study. Combined application of both interventions had no additional effects. After 6 h of warm ischaemia, no increase in leucocyte-vessel wall interactions was observed, possibly due to venular flow reduction. In conclusion, hypothermia preserves capillary perfusion and prevents an increase in leucocyte-vessel wall interactions during reperfusion after muscle tissue ischaemia. Preischaemic perfusion of the vasculature with HTK does not improve the effects of cold storage on tissue perfusion, but attenuates the inflammatory response independently of temperature effect.
 ...
PMID:Effect of hypothermia and HTK on the microcirculation in the rat cremaster muscle after ischaemia. 1561 71

Histidine-tryptophan-ketoglutarate (HTK) preserves rat muscle function during cold storage. We examined the effect of HTK perfusion on preservation of microvascular function during 4 h of warm ischemia and subsequent reperfusion (I/R) in the rat cremaster muscle. Leukocyte-endothelium interactions, capillary perfusion, and arteriole diameters were quantified prior to HTK-perfusion and/or ischemia, and at 0, 1, and 2 h after restoration of blood flow. In all groups, the number of rolling leukocytes increased with time, whereas I/R induced a slight increase in leukocyte adhesion. After ischemia, capillary perfusion rapidly recovered to about 50% and returned to near normal (90%) after 2 h. HTK at 22 degrees C did not affect the assessed microcirculation variables, whereas HTK at 4 degrees C reduced leukocyte rolling, but not adhesion. Therefore, microvascular function of HTK-perfused muscles was not better preserved during warm I/R than that of nonperfused muscles. Contrary to other preservation solutions, HTK perfusion in itself was not detrimental to the microcirculation.
 ...
PMID:Effect of HTK on the microcirculation in the rat cremaster muscle during warm ischemia and reperfusion. 1570 26

The aim of this study was to determine the potential benefit of aerobic machine preservation (MP) with non-colloidal histidine-tryptophan-ketoglutarate (HTK) solution compared with MP with Belzer machine perfusion solution (MPS) and standard cold storage, after marginal kidneys had been obtained from non-heart-beating donors. Cardiac arrest was electrically induced in anaesthetized German landrace pigs (20-25 kg bw). Their kidneys were harvested 40 min thereafter, flushed with HTK by gravity of 100 cm H2O via the renal artery and then stored in HTK for 18 h at 4 degrees C. Other organs were subjected to oxygenated (pO2>500 mmHg) hypothermic pulsatile low-flow machine perfusion with HTK or MP with Belzer MPS at P(max)=40 mmHg, yielding transrenal flow values of 0.2-0.3 ml/min per g with HTK and approximately twice that amount with Belzer MPS. A well-preserved vascular endothelium and intact tubular epithelium were documented by electron microscopy at the end of perfusion preservation in both solutions as well as after cold storage. Concentrations of ATP (in micromoles per gramme) in tissue homogenates at the end of perfusion preservation with HTK were 1.18+/-0.12 vs 0.16+/-0.02 (P<0.05) after simple cold storage and 2.43+/-0.23 after perfusion with Belzer MPS, thus documenting a relevant effect of low-flow perfusion on tissue oxygenation. Viability of the grafts was followed for 1 week after heterotopic transplantation and bilateral nephrectomy in the recipient pigs. Machine perfusion with HTK significantly improved cortical microcirculation upon early reperfusion in vivo, as well as maximal serum levels of urea and creatinine, compared to recipients receiving cold-stored grafts. No differences could be found between MP with HTK or Belzer MPS. In conclusion, provision of oxygen during storage is possible by low-flow perfusion with HTK as with Belzer MPS and apparently improves graft viability after transplantation.
 ...
PMID:Kidney transplantation from non-heart-beating donors after oxygenated low-flow machine perfusion preservation with histidine-tryptophan-ketoglutarate solution. 1571 15

In an earlier investigation, homologous mutant lines resistant to growth inhibition by 5-methyltryptophan (5MT) were selected from a callus that had been irradiated with a 50-Gy gamma ray during embryo culture. In order to identify the 5MT-resistant mechanism, we have continued our investigations of these mutant lines and studied the anthranilate synthase activity of the M5) advanced lines by direct fluorometric detection of the anthranilate formed in both control plants and mutant lines grown on 500 microM 5MT. The anthranilate synthase activity of the mutant plants was 2.2- to 3-fold higher than that of the control. In a kinetic analysis with tryptophan, an anthranilate synthase of the mutant lines was insensitive to feedback inhibition. These lines showed an enhanced accumulation of storage proteins and amino acids. The increased rates of protein synthesis in the mutant lines, relative to that of the control seeds, were 17-28.5%. The amino acid contents were 2.4-fold (MRI-40-2) to 2.6-fold (MRI-110-6) higher in the MRI lines than in the control seeds, and 2.4-fold (MRII-12-5) to 3.5-fold (MRII-8-1) higher in the MRII lines than in the control seeds. Significant increases among the amino acids of the MR lines were observed for tryptophan, phenylalanine, and tyrosine, which had been biosynthesized through the shikimate pathway. The transcript levels of putative OASA2, which is one of the key-regulating enzyme subunits in the tryptophan biosynthesis pathway, were studied in the control and 5MT-resistant mutant lines subjected to inhibition by two tryptophan analogs (5MT and alphaMT) and to other abiotic stresses (ABA, NaCl, and cold). The putative OASA2 gene in the 5MT-resistant mutant lines was highly expressed in at a low 5MT concentration and at an early stage of the 5MT and alphaMT treatments. However, mRNA accumulation of the putative OASA2 gene in the mutant plants gradually decreased when the plants were subjected to abiotic stresses such as NaCl and cold. These results indicated that the 5MT resistance in the mutant lines is due to altered anthranilate synthase forms.
 ...
PMID:Characterization of the altered anthranilate synthase in 5-methyltryptophan-resistant rice mutants. 1577 37

The effect of histidine-tryptophan-ketoglutarate (HTK) solution for myocardial protection has been shown in experimental and clinical studies using long ischemic times and high dosages. In our study we compared myocardial protection in isolated coronary bypass with a short period of ischemia using low dosage HTK and cold crystalloid cardioplegia. Each group contained 21 coronary artery disease patients. Cardioplegic solutions were administered antegrade in 10 to 15 mL/kg in one shot. This dosage of HTK was lower than that mentioned in the literature. We measured malondialdehyde, lactate, creatine kinase, creatine kinase-MB, and troponin-I levels. Aortic clamping time in the HTK group 33.9 +/- 8.2 minutes, versus 36.2 +/- 11.3 minutes in the crystalloid cardioplegia group (P > .05). Levels of creatine kinase and malondialdehyde were lower in HTK group at 24 hours and 2 minutes, respectively. Lactate levels were lower in the crystalloid cardioplegia group at 2 minutes in the coronary sinus serum sample, but there were no statistically differences among ischemic serum markers in both groups. Only intervals between aortic clamping and cardiac arrest were statistically meaningful (HTK 63.3 +/- 14.7 seconds versus crystalloid cardioplegia 53.6 +/- 15.6 seconds, P = .044). Our study shows that use of low-dose HTK for short clamping time operations is as successful for myocardial protection as crystalloid cardioplegia. Longer times for fibrillation can be explained with the low levels of potassium in HTK solution, but this length did not cause a biochemical or clinical difference.
 ...
PMID:Low-dose histidine-tryptophan-ketoglutarate solution for myocardial protection. 1621 52

In May 2003, at Indiana University, the standard cold preservation solution University of Wisconsin (UW) solution was replaced by histidine-tryptophan ketogluatarate (HTK) solution. Earlier, we presented our initial experience with HTK in pancreas preservation with an analysis of the first 10 pancreas transplants. Here we report updated results with HTK in pancreas transplantation over the past 18 months. Between May 2003 and March 2005, a total of 87 pancreas transplants were performed with 78 of these organs utilizing HTK. Seventy five patients received 78 organ transplants. Surgical procedures performed were: simultaneous kidney pancreas transplantation (n = 50, 64%), pancreas after kidney transplantation (n = 19, 24%), solitary pancreas transplantation (n = 9, 12%). Donor and recipient data were collected with primary outcomes as primary nonfunction and 30-day graft and patient survivals, and compared to the UW cohort from our original report. Donor and recipient demographics were similar. Mean follow-up time is 12 +/- 6 months. The mean cold ischemia time was 9 +/- 3 hours. There were no cases of primary graft nonfunction. Thirty-day and 1-year patient survivals were 99% and 93%. The 30-day and 1-year graft survivals were 96% and 93%. There were five grafts lost, including three within the first month (two venous and one arterial thrombosis). There was one case of chronic rejection and one noncompliance. All other patients were insulin-independent by discharge. Serum fasting blood glucose and serial amylase remained comparable at all intervals posttransplantation. Within this range of cold ischemia time, HTK appears to provide effective pancreas preservation.
 ...
PMID:Follow-up experience using histidine-tryptophan ketoglutarate solution in clinical pancreas transplantation. 1629 49

In eukaryotic cells many cell surface proteins are attached to the membrane via the glycosylphosphatidylinositol (GPI) moiety. In yeast, GPI also plays important roles in the production of mannoprotein in the cell wall. We previously isolated gwt1 mutants and found that GWT1 is required for inositol acylation in the GPI biosynthetic pathway. In this study we isolated a new gwt1 mutant allele, gwt1-10, that shows not only high temperature sensitivity but also low temperature sensitivity. The gwt1-10 cells show impaired acyltransferase activity and attachment of GPI to proteins even at the permissive temperature. We identified TAT2, which encodes a high affinity tryptophan permease, as a multicopy suppressor of cold sensitivity in gwt1-10 cells. The gwt1-10 cells were also defective in the import of tryptophan, and a lack of tryptophan caused low temperature sensitivity. Microscopic observation revealed that Tat2p is not transported to the plasma membrane but is retained in the endoplasmic reticulum in gwt1-10 cells grown under tryptophan-poor conditions. We found that Tat2p was not associated with detergent-resistant membranes (DRMs), which are required for the recruitment of Tat2p to the plasma membrane. A similar result was obtained for Fur4p, a uracil permease localized in the DRMs of the plasma membrane. These results indicate that GPI-anchored proteins are required for the recruitment of membrane proteins Tat2p and Fur4p to the plasma membrane via DRMs, suggesting that some membrane proteins are redistributed in the cell in response to environmental and nutritional conditions due to an association with DRMs that is dependent on GPI-anchored proteins.
 ...
PMID:Glycosylphosphatidylinositol-anchored proteins are required for the transport of detergent-resistant microdomain-associated membrane proteins Tat2p and Fur4p. 1636 Dec 52


<< Previous 1 2 3 4 5 6 7 8 9 10