S Issaragrisil, D Kaufman, A Thongput, K Chansung, T Thamprasit, A Piankijagum, T Anderson, S Shapiro, P Leaverton, N S Young – 30 December 2003 – Aplastic anemia is more common in the Orient than in western countries, with an incidence in Thailand that is 2‐ to 3‐fold higher than in Europe. Aplastic anemia after hepatitis is a well characterized clinical entity, and clinical hepatitis is also prevalent in the Far East. We performed a prospective case‐control study to determine risk factors for aplastic anemia in Bangkok and two rural regions during 1989 to 1994.

S J Samuel, S P Tzung, S A Cohen – 30 December 2003 – Previous studies from this laboratory identified a 28‐kd nonreducible protein, liver‐derived immunoinhibitory factor (LDIF) from the mouse liver. Isolation of this protein resulted in the co‐purification of another unique protein called heat responsive protein 12 kd (Hrp12). In contrast to LDIF, Hrp12 was totally reducible to a protein of 12 kd suggesting a dimer.

C A Bradham, R F Stachlewitz, W Gao, T Qian, S Jayadev, G Jenkins, Y Hannun, J J Lemasters, R G Thurman, D A Brenner – 30 December 2003 – The injury resulting from cold ischemia and warm reperfusion during liver transplantation is a major clinical problem that limits graft success. Kupffer cell activation plays a pivotal role in reperfusion injury, and Kupffer cell products, including free radicals and tumor necrosis factor α (TNF‐α), are implicated as damaging agents.

G Y Minuk, B T Kren, R Xu, X Zhang, F Burczynski, N P Mulrooney, G Fan, Y Gong, C J Steer – 30 December 2003 – The stimulus responsible for inducing hepatocytes to enter the cell cycle following partial hepatectomy (PHx) remains to be identified. One suggested candidate is the change in hepatocyte membrane potential (PD) that occurs immediately following PHx.

Carlos Moreno, Antoni Sabaté – 30 December 2003

Kaichiro Yahagi, Yoshiyuki Ueno, Yutaka Mano, Tooru Shimosegawa – 30 December 2003

Gregory T. Everson – 30 December 2003 – 1Approximately 10% to 25% of hepatitis C virus–infected recipients of liver allografts will develop cirrhosis within 5 years of transplantation; this acceleration of the natural history of hepatitis C is caused in part by immunosuppression.2Risk factors for aggressive recurrence, graft loss, and death are treated acute cellular rejection, methylprednisolone pulse therapy, and use of OKT3.

Santiago J. Muñoz – 30 December 2003 – 1Livers from donors previously exposed to hepatitis B virus (HBV) can fail after transplantation as a result of severe HBV reactivation in the transplant recipient.2Antibody against hepatitis B core antigen (HBcAb) in the donor is a marker for risk for transmission of HBV and reactivation after liver transplantation.3Recipient HBcAb positivity and antibody to hepatitis B surface antigen (HBsAb) positivity are associated with less risk for HBV reactivation.

Junichi Kaneko, Yasuhiko Sugawara, Masatoshi Makuuchi – 30 December 2003 – A 57‐year‐old woman underwent liver transplantation and developed osteomyelitis in the femur attributable to Aspergillus fumigatus. The patient was treated successfully with amphotericin B and 5‐fluorocytosine for 30 days, and then switched to itraconazole for 12 months. Plasma (1‐>3)‐beta‐D‐glucan levels decreased significantly after the chemotherapy. Early diagnosis by (1‐>3)‐beta‐D‐glucan measurement and extended treatment with itraconazole can improve the prognosis of invasive Aspergillus infection.

Cynthia L. Cotton, Sanjay Gandhi, Paul T. Vaitkus, Malek G. Massad, Enrico Benedetti, Robert G. Mrtek, Thelma E. Wiley – 30 December 2003 – Portopulmonary hypertension (PPHTN) is a recognized complication of end‐stage liver disease that adversely affects the outcome of orthotopic liver transplantation (OLT). There are limited data on the role of Doppler echocardiography in assessing pulmonary artery systolic pressure (PASP) in this population.