|1.||Abraham, Nader G: 3 articles (01/2015 - 02/2004)|
|2.||Morita, Kiyoshi: 3 articles (07/2010 - 09/2003)|
|3.||Takahashi, Toru: 3 articles (07/2010 - 09/2003)|
|4.||Drummond, G S: 3 articles (12/2001 - 07/2001)|
|5.||Kappas, A: 3 articles (12/2001 - 07/2001)|
|6.||Cao, Jian: 2 articles (01/2015 - 01/2013)|
|7.||Shimizu, Hiroko: 2 articles (07/2010 - 09/2003)|
|8.||Morimatsu, Hiroshi: 2 articles (07/2010 - 02/2008)|
|9.||Inoue, Kazuyoshi: 2 articles (07/2010 - 02/2008)|
|10.||Omori, Emiko: 2 articles (07/2010 - 02/2008)|
11/01/2012 - "Tin-mesoporphyrin in the treatment of refractory hyperbilirubinemia due to Rh incompatibility."
01/01/2006 - "The use of tin mesoporphyrin (SnMP) has been proposed for interdicting the development of severe hyperbilirubinemia in a variety of conditions. "
07/01/2005 - "The possible strategies for implementing an approach to the management of hyperbilirubinemia (especially the haemolytic kind) in the presence of BBS may include an exchange transfusion carried out at lower TSB concentration than previously recommended or an early administration of Sn-mesoporphyrin."
09/01/2003 - "Tin-mesoporphyrin in the treatment of severe hyperbilirubinemia in a very-low-birth-weight infant."
10/01/2002 - "In a near future enzymatic inhibitors such as Sn-mesoporphyrin will be probably available for the treatment of severe hyperbilirubinemia."
06/01/1995 - "Congenital nonobstructive, nonhemolytic jaundice: effect of tin-mesoporphyrin."
01/01/1994 - "Control of jaundice in preterm newborns by an inhibitor of bilirubin production: studies with tin-mesoporphyrin."
11/01/1993 - "Long-term treatment with the heme oxygenase inhibitor tin-mesoporphyrin produces an iron deficiency anemia in rats analogous to that we reported in patients with the Crigler-Najjar type I syndrome receiving prolonged treatment with the inhibitor to ameliorate severe jaundice [Pediatrics 1992; 89: 175-182]. "
07/01/2001 - "We assessed in healthy, direct Coombs test-negative Greek newborns of >/=38 weeks' gestational age 1) the current burden of G-6-PD deficiency-associated severe jaundice, and 2) the efficacy of preventive use of Sn-mesoporphyrin (SnMP), a potent inhibitor of heme oxygenase activity and thus of bilirubin production, in ameliorating jaundice in G-6-PD-deficient neonates. "
|3.||Body Weight (Weight, Body)
06/01/1989 - "Tin-mesoporphyrin is cleared from the plasma of normal subjects with dose-dependent pharmacokinetics (T1/2 = 3.8 hr following i.v. administration of 1 mumole per kg body weight), and small amounts (less than 1% of administered dose) are excreted into the urine and feces. "
02/01/1992 - "They were treated with intermittent plasmapheresis and two periods of tin-mesoporphyrin therapy comprising, in the first study period, 40 doses of 0.5 mumol/kg body weight and in the second study period, 70 doses of 1.0 mumol/kg body weight. "
06/01/1989 - "High doses (1 mumole per kg body weight) of tin-mesoporphyrin resulted in significant decreases in plasma bilirubin concentrations at 24 and 48 h after treatment of normal subjects. "
05/01/2006 - "Adult HO-1-luc reporter mice were administered 30 micromol/kg body weight of tin mesoporphyrin (SnMP), zinc bis glycol deuteroporphyrin (ZnBG), or zinc protoporphyrin (ZnPP), or vehicle by oral gavage. "
11/01/2010 - "Inhibiting HO activity in ANG II-treated rats by tin mesoporphyrin further increased renal vascular resistances, decreased renal blood flow, and blunted the rise in arterial pressure without inducing oxidative stress or altering expression of selected vasoactive/injury/inflammation-related genes; tin mesoporphyrin did not alter vasorelaxation of mesenteric resistor vessels. "
02/01/2008 - "Of note, inhibition of HO activity by tin-mesoporphyrin resulted in an aggravation of HS-induced tissue inflammation and apoptotic cell death. "
07/01/2010 - "Pretreatment of HSR animals with tin-mesoporphyrin (0.5 micromol/kg), a specific competitive inhibitor of HO activity, resulted in a significant decrease in HO activity and exacerbated tissue inflammation and apoptotic cell death as judged by the marked increase in expression of TNF-alpha and iNOS, and in activated caspase-3-positive cells, and the significant reduction in Bcl-2 expression, respectively. "
|2.||Heme Oxygenase (Decyclizing) (Heme Oxygenase)
|3.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|5.||tin protoporphyrin IX
|9.||cobaltous chloride (cobalt(II)chloride)
|1.||Phototherapy (Light Therapy)
|2.||Transplantation (Transplant Recipients)