Yasuda T

References (14)

Title : Endothelial lipase modulates pressure overload-induced heart failure through alternative pathway for fatty acid uptake - Nakajima_2013_Hypertension_61_1002
Author(s) : Nakajima H , Ishida T , Satomi-Kobayashi S , Mori K , Hara T , Sasaki N , Yasuda T , Toh R , Tanaka H , Kawai H , Hirata K
Ref : Hypertension , 61 :1002 , 2013
Abstract : Lipoprotein lipase has been considered as the only enzyme capable of generating lipid-derived fatty acids for cardiac energy. Endothelial lipase is another member of the triglyceride lipase family and hydrolyzes high-density lipoproteins. Although endothelial lipase is expressed in the heart, its function remains unclear. We assessed the role of endothelial lipase in the genesis of heart failure. Pressure overload-induced cardiac hypertrophy was generated in endothelial lipase(-/-) and wild-type mice by ascending aortic banding. Endothelial lipase expression in cardiac tissues was markedly elevated in the early phase of cardiac hypertrophy in wild-type mice, whereas lipoprotein lipase expression was significantly reduced. Endothelial lipase(-/-) mice showed more severe systolic dysfunction with left-ventricular dilatation compared with wild-type mice in response to pressure overload. The expression of mitochondrial fatty acid oxidation-related genes, such as carnitine palmitoyltransferase-1 and medium-chain acyl coenzyme A dehydrogenase, was significantly lower in the heart of endothelial lipase(-/-) mice than in wild-type mice. Also, endothelial lipase(-/-) mice had lower myocardial adenosine triphosphate levels than wild-type mice after aortic banding. In cultured cardiomyocytes, endothelial lipase was upregulated by inflammatory stimuli, whereas lipoprotein lipase was downregulated. Endothelial lipase-overexpression in cardiomyocytes resulted in an upregulation of fatty acid oxidation-related enzymes and intracellular adenosine triphosphate accumulation in the presence of high-density lipoprotein. Endothelial lipase may act as an alternative candidate to provide fatty acids to the heart and regulate cardiac function. This effect seemed relevant particularly in the diseased heart, where lipoprotein lipase action is downregulated.
ESTHER : Nakajima_2013_Hypertension_61_1002
PubMedSearch : Nakajima_2013_Hypertension_61_1002
PubMedID: 23460280

Title : Targeted deletion of endothelial lipase increases HDL particles with anti-inflammatory properties both in vitro and in vivo - Hara_2011_J.Lipid.Res_52_57
Author(s) : Hara T , Ishida T , Kojima Y , Tanaka H , Yasuda T , Shinohara M , Toh R , Hirata K
Ref : J Lipid Res , 52 :57 , 2011
Abstract : Previous studies have shown that targeted deletion of endothelial lipase (EL) markedly increases the plasma high density lipoprotein cholesterol (HDL-C) level in mice. However, little is known about the functional quality of HDL particles after EL inhibition. Therefore, the present study assessed the functional quality of HDL isolated from EL(-/-) and wild-type (WT) mice. Anti-inflammatory functions of HDL from EL(-/-) and WT mice were evaluated by in vitro assays. The HDL functions such as PON-1 or PAF-AH activities, inhibition of cytokine-induced vascular cell adhesion molecule-1 expression, inhibition of LDL oxidation, and the ability of cholesterol efflux were similar in HDL isolated from WT and EL(-/-) mice. In contrast, the lipopolysaccharide-neutralizing capacity of HDL was significantly higher in EL(-/-) mice than that in WT mice. To evaluate the anti-inflammatory actions of HDL in vivo, lipopolysaccharide-induced systemic inflammation was generated in these mice. EL(-/-) mice showed higher survival rate and lower expression of inflammatory markers than WT mice. Intravenous administration of HDL isolated from EL(-/-) mice significantly improved the mortality after lipopolysaccharide injection in WT mice. In conclusion, targeted disruption of EL increased HDL particles with preserved anti-inflammatory and anti-atherosclerotic functions. Thus, EL inhibition would be a useful strategy to raise 'good' cholesterol in the plasma.
ESTHER : Hara_2011_J.Lipid.Res_52_57
PubMedSearch : Hara_2011_J.Lipid.Res_52_57
PubMedID: 20926433

Title : Pitavastatin decreases the expression of endothelial lipase both in vitro and in vivo - Kojima_2010_Cardiovasc.Res_87_385
Author(s) : Kojima Y , Ishida T , Sun L , Yasuda T , Toh R , Rikitake Y , Fukuda A , Kume N , Koshiyama H , Taniguchi A , Hirata K
Ref : Cardiovascular Research , 87 :385 , 2010
Abstract : AIMS: In addition to their cholesterol-lowering effect, statins increase high-density lipoprotein cholesterol (HDL-C) levels. Endothelial lipase (EL) is a regulator of plasma HDL-C levels. In the present study, the effects of statins on EL expression were investigated. METHODS AND RESULTS: The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pitavastatin suppressed basal and cytokine-treated EL expression in endothelial cells. Concomitant treatment with mevalonate or geranylgeranyl pyrophosphate completely reversed the inhibitory effect of pitavastatin, suggesting that geranylgeranylated proteins are involved in the inhibition of EL expression by statins. Inhibition of RhoA activity by overexpression of a dominant-negative mutant of RhoA or a Rho kinase inhibitor decreased EL levels. Pitavastatin reduced phospholipase activities of endothelial cells, and concomitant treatment with mevalonate reversed its inhibitory effect. Pitavastatin reduced RhoA activity and EL expression in mouse tissues. Furthermore, plasma EL concentrations in human subjects were measured by enzyme-linked immunosorbent assays. Plasma EL levels were negatively associated with plasma HDL levels in 237 patients with cardiovascular diseases, and pitavastatin treatment reduced plasma EL levels and increased HDL-C levels in 48 patients with hypercholesterolaemia. CONCLUSION: These findings suggest that statins can reduce EL expression in vitro and in vivo via inhibition of RhoA activity. The inhibition of EL expression in the vessel wall may contribute to the anti-atherogenic effects of statins.
ESTHER : Kojima_2010_Cardiovasc.Res_87_385
PubMedSearch : Kojima_2010_Cardiovasc.Res_87_385
PubMedID: 20045866
Gene_locus related to this paper: human-LIPG

Title : Impact of combined deficiency of hepatic lipase and endothelial lipase on the metabolism of both high-density lipoproteins and apolipoprotein B-containing lipoproteins - Brown_2010_Circ.Res_107_357
Author(s) : Brown RJ , Lagor WR , Sankaranaravanan S , Yasuda T , Quertermous T , Rothblat GH , Rader DJ
Ref : Circulation Research , 107 :357 , 2010
Abstract : RATIONALE: Hepatic lipase (HL) and endothelial lipase (EL) are extracellular lipases that both hydrolyze triglycerides and phospholipids and display potentially overlapping or complementary roles in lipoprotein metabolism. OBJECTIVE: We sought to dissect the overlapping roles of HL and EL by generating mice deficient in both HL and EL (HL/EL-dko) for comparison with single HL-knockout (ko) and EL-ko mice, as well as wild-type mice. METHODS AND RESULTS: Reproduction and viability of the HL/EL-dko mice were impaired compared with the single-knockout mice. The plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, non-HDL cholesterol, and phospholipids in the HL/EL-dko mice were markedly higher than those in the single-knockout mice. Most notably, the HL/EL-dko mice exhibited an unexpected substantial increase in small low-density lipoproteins. Kinetic studies with [(3)H]cholesteryl ether-labeled very-low-density lipoproteins demonstrated that the HL/EL-dko mice accumulated counts in the smallest low-density lipoprotein-sized fractions, as assessed by size exclusion chromatography, suggesting that it arises from lipolysis of very-low-density lipoproteins. HDL from all 3 lipase knockout models had an increased cholesterol efflux capacity but reduced clearance of HDL cholesteryl esters versus control mice. Despite their higher HDL cholesterol levels, neither HL-ko, EL-ko, nor HL/EL-dko mice demonstrated an increased rate of macrophage reverse cholesterol transport in vivo. CONCLUSIONS: These studies reveal an additive effect of HL and EL on HDL metabolism but not macrophage reverse cholesterol transport in mice and an unexpected redundant role of HL and EL in apolipoprotein B lipoprotein metabolism.
ESTHER : Brown_2010_Circ.Res_107_357
PubMedSearch : Brown_2010_Circ.Res_107_357
PubMedID: 20558822
Gene_locus related to this paper: human-LIPC , human-LIPG

Title : Update on the role of endothelial lipase in high-density lipoprotein metabolism, reverse cholesterol transport, and atherosclerosis - Yasuda_2010_Circ.J_74_2263
Author(s) : Yasuda T , Ishida T , Rader DJ
Ref : Circ J , 74 :2263 , 2010
Abstract : Endothelial lipase (EL) is a phospholipase that belongs to the lipoprotein lipase (LPL) family, which includes LPL and hepatic lipase (HL). Similar to LPL and HL, EL regulates lipoprotein metabolism, mainly high-density lipoprotein (HDL) metabolism and HDL cholesterol (HDL-C) levels in humans and mice. Existing data strongly suggest that inhibition of EL in humans would be expected to increase the HDL-C level. However, it has not been definitively established whether the effect of EL activity on HDL-C levels translates into effects on reverse cholesterol transport or atherosclerosis. The available data regarding the impact of EL expression and activity on HDL metabolism, reverse cholesterol transport, and atherosclerosis are reviewed.
ESTHER : Yasuda_2010_Circ.J_74_2263
PubMedSearch : Yasuda_2010_Circ.J_74_2263
PubMedID: 20962428

Title : Role of endothelial lipase in plasma HDL levels in a murine model of hypertriglyceridemia - Tanaka_2009_J.Atheroscler.Thromb_16_327
Author(s) : Tanaka H , Ishida T , Johnston TP , Yasuda T , Ueyama T , Kojima Y , Kundu RK , Quertermous T , Ishikawa Y , Hirata K
Ref : J Atheroscler Thromb , 16 :327 , 2009
Abstract : AIM: Hypertriglyceridemia is the most common cause of low plasma high-density lipoprotein cholesterol (HDL-C) levels; however, the correlation between high triglyceride (TG) and low HDL-C remains unclear. Endothelial lipase (EL) is a determinant of plasma HDL levels. We investigated the role of EL in HDL metabolism in a murine model of acute hypertriglyceridemia. METHODS AND RESULTS: To establish TG-dominant hyperlipidemia, EL-/- and wild-type (WT) mice were injected with Poloxamer-407 (P-407, 0.5 g/kg, i.p.). A single injection of P-407 resulted in a marked increase in plasma TG and cholesterol levels together with a decrease in HDL-C levels. Although plasma TG levels were similar in EL-/- and WT mice after P-407 injection, HDL-C levels were 80% higher and the HDL particle size was significantly larger in EL-/- mice than in WT mice. P-407 treatment inhibited plasma lipoprotein lipase activity and EL phospholipase activity, without decreasing their expressions. Adenovirus-mediated overexpression of EL in the liver reduced plasma HDL-C levels in both normo- and hyperlipidemic mice, while overexpression of catalytically inactive EL reduced HDL-C levels in hyperlipidemic mice. Cell culture experiments revealed that both catalytically active and inactive EL promoted cellular HDL uptake to the same extent. CONCLUSION: EL regulates plasma HDL levels in mice in the normolipidemic as well as the acute hypertriglyceridemic state. EL can modulate plasma HDL-CHOL levels through both its lipolytic and ligand-binding functions in hypertriglyceridemic mice, while lipolytic activity appears to be the main determinant for its effects on HDL metabolism in normolipidemic mice.
ESTHER : Tanaka_2009_J.Atheroscler.Thromb_16_327
PubMedSearch : Tanaka_2009_J.Atheroscler.Thromb_16_327
PubMedID: 19672025
Gene_locus related to this paper: human-LIPG

Title : Targeted inactivation of endothelial lipase attenuates lung allergic inflammation through raising plasma HDL level and inhibiting eosinophil infiltration - Otera_2009_Am.J.Physiol.Lung.Cell.Mol.Physiol_296_L594
Author(s) : Otera H , Ishida T , Nishiuma T , Kobayashi K , Kotani Y , Yasuda T , Kundu RK , Quertermous T , Hirata K , Nishimura Y
Ref : American Journal of Physiology Lung Cell Mol Physiol , 296 :L594 , 2009
Abstract : Endothelial lipase (EL) is a novel phospholipase that determines plasma high-density lipoprotein cholesterol (HDL-C) levels. We have investigated the role of HDL-C in lung allergic inflammation by using EL knockout (EL-KO) mice that are high in HDL-C. EL-KO and wild-type control mice were sensitized and challenged with ovalbumin to evoke eosinophilic inflammation in the lung. EL was expressed in epithelial cells, alveolar type II cells, and endothelial cells in the lung, and its expression was upregulated during inflammation. Concomitant with attenuated hyperresponsiveness of the airway smooth muscles, the number of eosinophils in bronchoalveolar lavage and the expression of VCAM-1 were lower in EL-KO mice than in control mice. HDL reduced cytokine-induced VCAM-1 expression in cultured endothelial cells. When plasma HDL levels were decreased to similar levels in both mouse groups by adenovirus-mediated overexpression of EL, however, eosinophil infiltration was still lower in EL-KO mice. In vitro adhesion assays revealed that EL expression on the cell surface promoted the interaction of eosinophils through the ligand-binding function of EL. In summary, targeted inactivation of EL attenuated allergic inflammation in the lung, and the protective effects in EL-KO mice were associated with high plasma HDL levels, downregulation of VCAM-1, and loss of the direct ligand-binding function of EL. Thus EL is a novel modulator of the progression of allergic asthma.
ESTHER : Otera_2009_Am.J.Physiol.Lung.Cell.Mol.Physiol_296_L594
PubMedSearch : Otera_2009_Am.J.Physiol.Lung.Cell.Mol.Physiol_296_L594
PubMedID: 19168574

Title : Endothelial lipase is increased by inflammation and promotes LDL uptake in macrophages - Yasuda_2007_J.Atheroscler.Thromb_14_192
Author(s) : Yasuda T , Hirata K , Ishida T , Kojima Y , Tanaka H , Okada T , Quertermous T , Yokoyama M
Ref : J Atheroscler Thromb , 14 :192 , 2007
Abstract : AIM: Endothelial lipase (EL) is a member of the lipoprotein lipase family that regulates HDL metabolism. EL is known to act as a bridging molecule for monocytes or lipoproteins in vascular endothelial cells. We investigated the role and regulatory mechanisms of EL expression in macrophages.
METHODS: Macrophages originating from wild-type (EL+/+) and EL-deficient (EL-/-) mice were stimulated with lipopolysaccharide (LPS). The expression of EL mRNA was evaluated by northern blotting. DiI-LDL was used to measure the uptake of native low-density lipoprotein (nLDL).
RESULTS: LPS increased EL mRNA levels by increasing intracellular oxidative stress in the macrophages. LPS did not affect EL expression in macrophages derived from Toll-like receptor 4 (TLR4) gene mutant mice, C3H/HeJ. The uptake of nLDL after LPS-treatment was significantly lower in macrophages from EL-/- mice than those from EL+/+ mice. Simvastatin suppressed the LPS-induced upregulation of EL expression and uptake of nLDL.
CONCLUSIONS: EL expression is upregulated by LPS via TLR4 and promotes the uptake of nLDL by macrophages. Simvastatin inhibits the LPS-induced up-regulation and uptake in macrophages. Thus, our findings provide a novel role for EL in lipoprotein metabolism and would expand the range of anti-atherogenic effects of statins.
ESTHER : Yasuda_2007_J.Atheroscler.Thromb_14_192
PubMedSearch : Yasuda_2007_J.Atheroscler.Thromb_14_192
PubMedID: 17726294

Title : Complete sequencing and characterization of 21,243 full-length human cDNAs - Ota_2004_Nat.Genet_36_40
Author(s) : Ota T , Suzuki Y , Nishikawa T , Otsuki T , Sugiyama T , Irie R , Wakamatsu A , Hayashi K , Sato H , Nagai K , Kimura K , Makita H , Sekine M , Obayashi M , Nishi T , Shibahara T , Tanaka T , Ishii S , Yamamoto J , Saito K , Kawai Y , Isono Y , Nakamura Y , Nagahari K , Murakami K , Yasuda T , Iwayanagi T , Wagatsuma M , Shiratori A , Sudo H , Hosoiri T , Kaku Y , Kodaira H , Kondo H , Sugawara M , Takahashi M , Kanda K , Yokoi T , Furuya T , Kikkawa E , Omura Y , Abe K , Kamihara K , Katsuta N , Sato K , Tanikawa M , Yamazaki M , Ninomiya K , Ishibashi T , Yamashita H , Murakawa K , Fujimori K , Tanai H , Kimata M , Watanabe M , Hiraoka S , Chiba Y , Ishida S , Ono Y , Takiguchi S , Watanabe S , Yosida M , Hotuta T , Kusano J , Kanehori K , Takahashi-Fujii A , Hara H , Tanase TO , Nomura Y , Togiya S , Komai F , Hara R , Takeuchi K , Arita M , Imose N , Musashino K , Yuuki H , Oshima A , Sasaki N , Aotsuka S , Yoshikawa Y , Matsunawa H , Ichihara T , Shiohata N , Sano S , Moriya S , Momiyama H , Satoh N , Takami S , Terashima Y , Suzuki O , Nakagawa S , Senoh A , Mizoguchi H , Goto Y , Shimizu F , Wakebe H , Hishigaki H , Watanabe T , Sugiyama A , Takemoto M , Kawakami B , Watanabe K , Kumagai A , Itakura S , Fukuzumi Y , Fujimori Y , Komiyama M , Tashiro H , Tanigami A , Fujiwara T , Ono T , Yamada K , Fujii Y , Ozaki K , Hirao M , Ohmori Y , Kawabata A , Hikiji T , Kobatake N , Inagaki H , Ikema Y , Okamoto S , Okitani R , Kawakami T , Noguchi S , Itoh T , Shigeta K , Senba T , Matsumura K , Nakajima Y , Mizuno T , Morinaga M , Sasaki M , Togashi T , Oyama M , Hata H , Komatsu T , Mizushima-Sugano J , Satoh T , Shirai Y , Takahashi Y , Nakagawa K , Okumura K , Nagase T , Nomura N , Kikuchi H , Masuho Y , Yamashita R , Nakai K , Yada T , Ohara O , Isogai T , Sugano S
Ref : Nat Genet , 36 :40 , 2004
Abstract : As a base for human transcriptome and functional genomics, we created the "full-length long Japan" (FLJ) collection of sequenced human cDNAs. We determined the entire sequence of 21,243 selected clones and found that 14,490 cDNAs (10,897 clusters) were unique to the FLJ collection. About half of them (5,416) seemed to be protein-coding. Of those, 1,999 clusters had not been predicted by computational methods. The distribution of GC content of nonpredicted cDNAs had a peak at approximately 58% compared with a peak at approximately 42%for predicted cDNAs. Thus, there seems to be a slight bias against GC-rich transcripts in current gene prediction procedures. The rest of the cDNAs unique to the FLJ collection (5,481) contained no obvious open reading frames (ORFs) and thus are candidate noncoding RNAs. About one-fourth of them (1,378) showed a clear pattern of splicing. The distribution of GC content of noncoding cDNAs was narrow and had a peak at approximately 42%, relatively low compared with that of protein-coding cDNAs.
ESTHER : Ota_2004_Nat.Genet_36_40
PubMedSearch : Ota_2004_Nat.Genet_36_40
PubMedID: 14702039
Gene_locus related to this paper: human-ABHD1 , human-ABHD4 , human-ABHD12 , human-ABHD16A , human-ACOT1 , human-LDAH , human-ABHD18 , human-CES1 , human-CES4A , human-CES5A , human-CPVL , human-DAGLB , human-EPHX2 , human-KANSL3 , human-LIPA , human-LPL , human-MEST , human-NDRG1 , human-NLGN1 , human-NLGN4X , human-PRCP , human-PRSS16 , human-SERAC1 , human-TMEM53

Title : nRap GEP: a novel neural GDP\/GTP exchange protein for rap1 small G protein that interacts with synaptic scaffolding molecule (S-SCAM) - Ohtsuka_1999_Biochem.Biophys.Res.Commun_265_38
Author(s) : Ohtsuka T , Hata Y , Ide N , Yasuda T , Inoue E , Inoue T , Mizoguchi A , Takai Y
Ref : Biochemical & Biophysical Research Communications , 265 :38 , 1999
Abstract : Synaptic scaffolding molecule (S-SCAM) has six PDZ domains through which it interacts with N-methyl-d-aspartate receptors and neuroligin at synaptic junctions. We isolated here a novel S-SCAM-binding protein. This protein has one PDZ, one Ras association, one Ras GDP/GTP exchange protein (Ras GEP) domain, and one C-terminal consensus motif for binding to PDZ domains. We named it nRap GEP (neural Rap GEP). nRap GEP moreover has an incomplete cyclic AMP (cAMP)-binding (CAB) domain. The domain organization of nRap GEP is similar to that of Epac/cAMP-guanine nucleotide exchange factor (GEF) I, except that Epac/cAMP-GEFI has complete CAB and Ras GEP domains but lacks the other two domains and the C-terminal motif. nRap GEP showed GEP activity for Rap1 but did not bind cAMP. nRap GEP was specifically expressed in rat brain. Immunohistochemical analysis revealed that nRap GEP and S-SCAM were localized at synaptic areas of the cerebellum. These results suggest that nRap GEP is a novel neural Rap1-specific GEP which is associated with S-SCAM.
ESTHER : Ohtsuka_1999_Biochem.Biophys.Res.Commun_265_38
PubMedSearch : Ohtsuka_1999_Biochem.Biophys.Res.Commun_265_38
PubMedID: 10548487

Title : Dramatic response of postthymomectomy myasthenia gravis with multiple lung nodules to corticosteroids - Kodama_1997_Ann.Thorac.Surg_64_555
Author(s) : Kodama K , Doi O , Higashiyama M , Yokouchi H , Yasuda T , Funai H
Ref : Annals of Thoracic surgery , 64 :555 , 1997
Abstract : A 36-year-old woman underwent thymomectomy and left pneumonectomy with total pleurectomy for stage IVa invasive thymoma without myasthenia gravis. Six years later, a crisis of myasthenia gravis developed associated with multiple lung nodules. Steroid therapy induced remarkable regression of the lung nodules that has persisted for more than 11 months. Concurrently, the clinical severity of her myasthenia gravis markedly decreased and recovered to the extent of permitting her to return to normal life.
ESTHER : Kodama_1997_Ann.Thorac.Surg_64_555
PubMedSearch : Kodama_1997_Ann.Thorac.Surg_64_555
PubMedID: 9262618

Title : Availability of liposomes as drug carriers to the brain - Kobayashi_1996_Acta.Med.Okayama_50_67
Author(s) : Kobayashi K , Han M , Watarai S , Yasuda T
Ref : Acta Med Okayama , 50 :67 , 1996
Abstract : Phospholipid vesicles, also known as liposomes, were examined for their ability to act as a drug carrier to the brain. 9-Amino-1,2,3,4-tetrahydroacridine (THA), a centrally acting acetylcholinesterase inhibitor, was used as a model drug. THA was encapsulated in dehydration-rehydration vesicles (DRV) composed of egg yolk phosphatidylcholine, cholesterol and dipalmitoyl-phosphatidic acid (molar ratio, 10/10/1) and injected into the heart of mice. The toxicity and side effects of THA were reduced by encapsulation in liposomes. The THA concentration in the mouse brain after injection of THA-encapsulated DRV at a dose of 2 mg/kg remained higher than that of free THA at the same dose. Effective concentration of THA in the brain was also prolonged by the use of liposomes, although accumulation of THA in the spleen and kidney was observed. We, therefore, concluded that liposomes are useful as carriers of drugs to the brain.
ESTHER : Kobayashi_1996_Acta.Med.Okayama_50_67
PubMedSearch : Kobayashi_1996_Acta.Med.Okayama_50_67
PubMedID: 8744931

Title : Inverse relationship between serum cholinesterase activity and the administration of cyclophosphamide: an index of cyclophosphamide therapy [see comments] - Imai_1994_Nephrol.Dial.Transplant_9_1240
Author(s) : Imai H , Kodama T , Yasuda T , Nakamoto Y , Miura AB
Ref : Nephrol Dial Transplant , 9 :1240 , 1994
Abstract : To determine whether serum cholinesterase activity can be a monitoring index of cyclophosphamide therapy in patients with steroid-resistant glomerulopathy, we compared the cholinesterase activity of 37 patients who received a combined therapy that included the use of cyclophosphamide, prednisolone, antiplatelet drugs, and anticoagulant drugs, with the cholinesterase activity of 25 patients who received prednisolone therapy that excluded cyclophosphamide from the combined therapy. In the prednisolone and the combined groups, cholinesterase activity declined as shown in the following formula: Y = 371-26.4 x log(X): (r2 = 0.28), Y = 444-147.7 x log(X): (r2 = 0.95), respectively. (Y: cholinesterase activity, X: the day after treatment). In the combined therapy group, the prevalence of adverse reactions following treatment in the subgroup below 200 U/l of cholinesterase activity was significantly greater (P < 0.01) than that in the subgroup above 200 U/l of cholinesterase activity. However, there was no significant difference (P < 0.25) in the prevalence of adverse reactions between the subgroups with more or less than 184 U/l of cholinesterase activity following treatment. These results suggest the importance of not going below 200 U/l of cholinesterase activity after treatment when the normal cholinesterase activity range is between 300 and 760 U/l (e.g. less than 65% of the lowest value of the normal range of other hospitals) in order to eliminate the hazards of cyclophosphamide to the patients with steroid-resistant glomerulopathy.
ESTHER : Imai_1994_Nephrol.Dial.Transplant_9_1240
PubMedSearch : Imai_1994_Nephrol.Dial.Transplant_9_1240
PubMedID: 7816283

Title : Oral zinc therapy normalizes serum uric acid level in Wilson's disease patients - Umeki_1986_Am.J.Med.Sci_292_289
Author(s) : Umeki S , Ohga R , Konishi Y , Yasuda T , Morimoto K , Terao A
Ref : American Journal of Medicine Sci , 292 :289 , 1986
Abstract : The authors investigated changes in the serum uric acid (s-UrA) level seen in a Wilson's disease patient who had to undergo oral zinc therapy because of the occurrence of D-penicillamine-induced acute sensitivity reactions, including neutrophilic agranulocytosis, thrombocytopenia, and skin eruptions. Although s-UrA levels were low before oral zinc therapy (mean +/- SD, 1.60 +/- 0.20), they increased (mean +/- SD, 2.63 +/- 0.32) to within normal range (2.8-8.0 mg/dl) after therapy. There were no significant changes in the renal tubular reabsorption of UrA during oral zinc therapy. This therapy also produced an improvement of the decreased cholinesterase (ChE) values usually seen in Wilson's disease. These results suggest that oral zinc therapy can normalize UrA metabolism in Wilson's disease by improving liver dysfunction and increasing UrA synthesis.
ESTHER : Umeki_1986_Am.J.Med.Sci_292_289
PubMedSearch : Umeki_1986_Am.J.Med.Sci_292_289
PubMedID: 3777013