The Experts below are selected from a list of 231 Experts worldwide ranked by ideXlab platform
Dibyajyoti Banerjee - One of the best experts on this subject based on the ideXlab platform.
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Reduction of urinary thiols in nephrotic syndrome--a possible effect of free iron.
Clinica chimica acta; international journal of clinical chemistry, 2020Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti BanerjeeAbstract:Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33+/-4.2 micromol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45+/-10.6 micromol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7+/-0.05 micromol/l), a parameter undetectable in the healthy controls. We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.
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Reduction of urinary thiols in nephrotic syndrome--a possible effect of free iron.
Clinica Chimica Acta, 2005Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti BanerjeeAbstract:Abstract Background Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. Methods We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. Result We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33±4.2 μmol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45±10.6 μmol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7±0.05 μmol/l), a parameter undetectable in the healthy controls. Conclusion We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.
Hisao Hayashi - One of the best experts on this subject based on the ideXlab platform.
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Preliminary study of spontaneous hepatitis in Long-Evans Cinnamon rats: a blood exchange may improve fetal hepatitis.
Nagoya journal of medical science, 2020Co-Authors: Jun Ueyama, Shinya Wakusawa, Yasuyuki Tatsumi, Ai Hattori, Motoyoshi Yano, Hisao HayashiAbstract:Long-Evans Cinnamon rats are a Wilson disease model highly susceptible to fulminant hepatitis around the age of 20 weeks, and hepatoma over the age of one year. Although prophylaxis has been established for the otherwise fatal hepatitis, effective treatment remains unknown. A blood exchange was tested to determine whether the prognosis of spontaneous hepatitis could be modified in icteric female rats. When Bilirubinuria appeared, the rats immediately underwent surgery. Rats under anesthesia were first cannulated into the right atrium via the carotid vein, followed by 2.5 mL of blood exchange with heparinized fresh blood from Long-Evans agouti rats. Treated rats and controls were then observed for 2 months. Compared to the 50% mortality of untreated rats, all icteric rats that received a blood exchange survived the acute episode. We confirmed that Wilson disease animals are highly susceptible to acute hepatitis and show a poor prognosis. However, a single blood exchange improved spontaneous hepatitis in this animal model. This would serve as a first step for establishing a treatment for fatal hepatitis in animals. A blood exchange may improve fulminant hepatitis of Wilson disease model rats.
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Preliminary Study on Spontaneous Hepatitis in Long-Evans Cinnamon Rats: A Blood Exchange May Improve the Fetal Hepatitis
Nagoya Journal of Medical Science, 2010Co-Authors: Jun Ueyama, Shinya Wakusawa, Yasuyuki Tatsumi, Ai Hattori, Motoyoshi Yano, Hisao HayashiAbstract:: Long-Evans Cinnamon rats are a Wilson disease model highly susceptible to fulminant hepatitis around the age of 20 weeks, and hepatoma over the age of one year. Although prophylaxis has been established for the otherwise fatal hepatitis, effective treatment remains unknown. A blood exchange was tested to determine whether the prognosis of spontaneous hepatitis could be modified in icteric female rats. When Bilirubinuria appeared, the rats immediately underwent surgery. Rats under anesthesia were first cannulated into the right atrium via the carotid vein, followed by 2.5 mL of blood exchange with heparinized fresh blood from Long-Evans agouti rats. Treated rats and controls were then observed for 2 months. Compared to the 50% mortality of untreated rats, all icteric rats that received a blood exchange survived the acute episode. We confirmed that Wilson disease animals are highly susceptible to acute hepatitis and show a poor prognosis. However, a single blood exchange improved spontaneous hepatitis in this animal model. This would serve as a first step for establishing a treatment for fatal hepatitis in animals. A blood exchange may improve fulminant hepatitis of Wilson disease model rats.
Indrajit Sinha - One of the best experts on this subject based on the ideXlab platform.
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Reduction of urinary thiols in nephrotic syndrome--a possible effect of free iron.
Clinica chimica acta; international journal of clinical chemistry, 2020Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti BanerjeeAbstract:Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33+/-4.2 micromol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45+/-10.6 micromol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7+/-0.05 micromol/l), a parameter undetectable in the healthy controls. We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.
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Reduction of urinary thiols in nephrotic syndrome--a possible effect of free iron.
Clinica Chimica Acta, 2005Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti BanerjeeAbstract:Abstract Background Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. Methods We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. Result We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33±4.2 μmol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45±10.6 μmol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7±0.05 μmol/l), a parameter undetectable in the healthy controls. Conclusion We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.
Kohji Fujisawa - One of the best experts on this subject based on the ideXlab platform.
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Hemoglobin Hammersmith [β 42(CD1) Phe Ser] causing severe hemolytic anemia in a Japanese girl
Pediatric Blood & Cancer, 2006Co-Authors: Masaharu Akiyama, Shizuko Murayama, Kentaro Yokoi, Takaki Yanagisawa, Yukio Hattori, Yasuhiro Yamashiro, Kohji FujisawaAbstract:Hemoglobin Hammersmith, a rare, unstable hemoglobin variant, was diagnosed in a 9-year-old Japanese girl. She presented with the typical manifestations of this disorder, including neonatal hyperbilirubinemia, followed by progressive hepatosplenomegaly, jaundice, and Bilirubinuria. Because of severe hemolytic anemia, she received transfusions of red blood cells every 3 to 4 weeks. However, she underwent splenectomy at the age of 4 years and has continued to be in partial remission without requiring further transfusions. DNA sequence analysis of the polymerase chain reaction-amplified β-globin gene revealed a point mutation (T C) in the second nucleotide of the 42nd codon of the β-globin chain (β 42(CD1) Phe Ser). Pediatric Blood Cancer 2006;47:839–841. © 2005 Wiley-Liss, Inc.
Frank Murphy - One of the best experts on this subject based on the ideXlab platform.
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Bilirubinuria conjugated hyperbilirubinaemia and delta bilirubinaemia following acute haemolysis
Annals of Clinical Biochemistry, 1997Co-Authors: David Cummins, Andrew Ferrier, Frank MurphyAbstract:A 73-year-old woman became jaundiced after receiving 8 units of red cells during cardiac surgery. Her past medical history included a blood transfusion during a hysterectomy 30 years previously but no reports of liver disease or cholecystitis. Her only medications were aspirin and isosorbide dinitrate. Preoperatively her haemoglobin concentration was 11·6 g/d (reference range, 1l'5-16'5), total serum bilirubin \3Jlmol/L (reference range, 2-17), conjugated bilirubin 3 Jlmol/L (normal, < 9), aspartate transaminase (AST) 19 U/L (reference range, 0--31) and alkaline phosphatase 134 U/L (reference range, 100--280); the red-cell antibody screen was negative. Jaundice was first noted on the fifth postoperative day, when the haemoglobin concentration was 11·1 g/dL, total bilirubin 192 Jlmol/ L (conjugated fraction 92 Jlmol/L), AST 33 U/L and alkaline phosphatase \31 U/L. Her urine tested positive for bilirubin (+ + +) and urobilinogen (+ + +). Ultrasonography of the heart, liver and biliary system was normal. On day 9 the haemoglobin had fallen to 6·2 g/ dL and the serum bilirubin was 530 Jlmol/L (Fig. I). The direct antiglobulin test was positive, anti-Jk" antibody was eluted from the circulating red cells, and 5 of the transfused units were identified as Jk'
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Bilirubinuria, conjugated hyperbilirubinaemia and delta bilirubinaemia following acute haemolysis
Annals of Clinical Biochemistry, 1997Co-Authors: David Cummins, Andrew Ferrier, Frank MurphyAbstract:A 73-year-old woman became jaundiced after receiving 8 units of red cells during cardiac surgery. Her past medical history included a blood transfusion during a hysterectomy 30 years previously but no reports of liver disease or cholecystitis. Her only medications were aspirin and isosorbide dinitrate. Preoperatively her haemoglobin concentration was 11·6 g/d (reference range, 1l'5-16'5), total serum bilirubin \3Jlmol/L (reference range, 2-17), conjugated bilirubin 3 Jlmol/L (normal, < 9), aspartate transaminase (AST) 19 U/L (reference range, 0--31) and alkaline phosphatase 134 U/L (reference range, 100--280); the red-cell antibody screen was negative. Jaundice was first noted on the fifth postoperative day, when the haemoglobin concentration was 11·1 g/dL, total bilirubin 192 Jlmol/ L (conjugated fraction 92 Jlmol/L), AST 33 U/L and alkaline phosphatase \31 U/L. Her urine tested positive for bilirubin (+ + +) and urobilinogen (+ + +). Ultrasonography of the heart, liver and biliary system was normal. On day 9 the haemoglobin had fallen to 6·2 g/ dL and the serum bilirubin was 530 Jlmol/L (Fig. I). The direct antiglobulin test was positive, anti-Jk" antibody was eluted from the circulating red cells, and 5 of the transfused units were identified as Jk'
