Creatine kinase BB: A response marker in liver and other organs
Stephen D. H. Malnick, Daniel D. Bass, Alvin M. Kaye, Michel Vaubourdolle, Jacqueline Giboudeau, Olivier Chazouillères, Raoul Poupon – 1 January 1994
Stephen D. H. Malnick, Daniel D. Bass, Alvin M. Kaye, Michel Vaubourdolle, Jacqueline Giboudeau, Olivier Chazouillères, Raoul Poupon – 1 January 1994
Laurie N. Fishman, Joel E. Lavine – 1 January 1994 – A recessive mutation was identified in a family of transgenic mice that resulted in a reversal of left‐right polarity (situs inversus) in 100 percent of the homozygous transgenic mice tested. Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci. During early embryonic development, the direction of postimplantation turning, one of the earliest manifestations of left‐right asymmetry, was reversed in homozygous transgenic embryos.
Soonho Um, Osamu Nishida, Masaki Tokubayashi, Fumiko Kimura, Yukinobu Takimoto, Hideyuki Yoshioka, Ryoichi Inque, Toru Kita – 1 January 1994 – In chronic portal‐hypertensive rat models, such as portal vein constriction or cirrhosis, the portal blood flow that effectively perfuses the hepatocytes is substantially reduced because of anatomical or functional shunts. It is possible therefore that a feedback mechanism from the liver to the splanchnic bed is responsible for the splanchnic hyperemia observed in chronic portal hypertension.
Mario Strazzabosco, Carlo Poci, Carlo Spirlí, Leonardo Sartori, Alexander Knuth, Gaetano Crepaldi – 1 January 1994 – Recent studies in perfused livers and isolated hepatocytes indicate that ursodeoxycholic acid‐induced HCO3‐rich hypercholeresis originates at the ductule/duct level. The bile duct epithelium may be involved in bile alkalinization by passively reabsorbing the protonated unconjugated ursodeoxycholic acid, by directly secreting in response to an ursodeoxycholic acid‐induced increase in acid/base transporter activity or by taking up UDCA− in exchange for a base equivalent.
Hiroko Oka, Akihiro Tamori, Tetsuo Kuroki, Kenzo Kobayashi, Sukeo Yamamoto – 1 January 1994 – The usefulness of measurements of serum α‐fetoprotein elevation for diagnosis of the development of hepatocellular carcinoma was evaluated by a prospective study of 260 patients with cirrhosis. Hepatocellular carcinoma was found in 55 patients during the 5‐yr follow‐up, excluding 7 found to have hepatocellular carcinoma in the first 6 mo.
Paolo Angeli, Manuela Dalla Pria, Erica de Bei, Grazia Albino, Lorenza Caregaro, Carlo Merkel, Giulio Ceolotto, Angelo Gatta – 1 January 1994 – Although some clinical studies seem to prove the efficacy of nonantialdosteronic potassium‐sparing diuretics in the treatment of ascites, no controlled study has compared the efficacy of these drugs with that of antialdosteronic diuretics. Forty nonazotemic cirrhotic patients were randomized to receive amiloride (group A, n = 20) or potassium canrenoate (group B, n = 20).
Antonio Francavilla, Qihua Zeng, Lorenzo Polimeno, Brian I. Carr, Dantong Sun, Kendrick A. Porter, David H. van Thiel, Thomas E. Starzl – 1 January 1994 – Orthotopic liver transplantation was performed in 60 recipient rats weighing 200 to 250 gm. Sixty rats of the same strain were used as liver donors, 30 weighing 100 to 140 gm (small for size) and the other 30 weighing 200 to 250 gm (same size).
Nan Ni, James D. Yager – 1 January 1994 – Ethinyl estradiol is a weak complete carcinogen and potent tumor promoter. In vivo, ethinyl estradiol causes a rapid but transient increase in liver growth, whereas in cultured female hepatocytes it enhances DNA synthesis induced by epidermal growth factor and is thus classified as a comitogen.
Shushma Aggarwal, David Kramer, Howard Yonas, Walter Obrist, Yoogoo Kang, Maureen Martin, Raymond Policare – 1 January 1994 – The purpose of this retrospective study was to determine cerebral hemodynamic and metabolic changes in comatose patients with fulminant hepatic failure. Computerized tomography of the brain and cerebral blood flow measurements by the xenoncomputerized tomography scan or intravenous xenon‐133 methods were obtained in 33 patients with fulminant hepatic failure.