Since June, 2018, the Gravity Recovery and Climate Experiment Follow-On (GRACE-FO) is extending the 15-year monthly mass change record of the GRACE mission, which ended in June 2017. The GRACE-FO instrument and flight system performance has improved over GRACE. Better attitude solutions and enhanced pointing performance result in reduced fuel consumption and gravity range rate post-fit residuals. One accelerometer requires additional calibrations due to unexpected measurement noise. The GRACE-FO gravity and mass change fields from June 2018 through December 2019 continue the GRACE record at an equivalent precision and spatiotemporal sampling. During this period, GRACE-FO observed large interannual terrestrial water variations associated with excess rainfall (Central US, Middle East), drought (Europe, Australia), and ice melt (Greenland). These observations are consistent with independent mass change estimates, providing high confidence that no intermission biases exist from GRACE to GRACE-FO, despite the 11-month gap. GRACE-FO has also successfully demonstrated satellite-to-satellite laser ranging interferometry. Plain Language Summary Mass change is a fundamental climate system indicator and provides an integrated global view of how Earth's water cycle and energy balance are evolving. The Gravity Recovery and Climate Experiment (GRACE) mission monitored mass changes every month from 2002 through 2017. Since June 2018, GRACE Follow-On (GRACE-FO) continues this data record, tracking and monitoring changes in ice sheets and glaciers, near-surface and underground water storage, as well as changes in sea level and ocean currents. GRACE-FO instruments have been successfully calibrated and are providing new monthly mass change observations at a consistent spatial resolution and data quality with GRACE. Since its launch, GRACE-FO has measured record land water storage changes in 2018 and 2019 in response to extreme heat waves and droughts over Europe and Australia, as well as to extreme rainfall events over the United States and Middle East. In the summer of 2019, GRACE-FO measured record-level Greenland mass loss rates. A novel laser ranging interferometer was successfully demonstrated on GRACE-FO, laying the groundwork for improved future satellite gravity observations.

Passive immunization with hepatitis B surface antibody (anti-HBs) is important to prevent hepatitis B virus (HBV) recurrence after orthotopic liver transplantation for chronic HBV cirrhosis. Hepatitis B immune globulin (HBIG) dosing regimens have been poorly defined, utilize numerous routes of administration, and result in a high rate of HBV relapse and mortality. Twenty-five of 27 (93%) patients transplanted (four retransplants) for chronic HBV cirrhosis show no evidence of recurrent HBV (range, 2-55 months). Anti-HBs titers necessary to minimize the risk of hepatitis B surface antigen detectability were >500 IU/L for days 0 to 7, >250 IU/L for days 8 to 90, and >100 IU/L thereafter. Pretransplant HBV E antigen (HBeAG)-positive patients required more HBIG to achieve these goals than HBeAG-negative individuals. The elimination of anti-HBs changed continually for the initial 3 posttransplant months. The anti-HBs half-life increased from 0.7 days to 14.1 days. Anti-HBs elimination was significantly different in HBeAG+ and HBeAG- patients for the first week, but was subsequently indistinguishable after week 1. After 3 months, the half-life was statistically less for HBeAG+ patients, but the difference did not influence the clinical treatment regimens. Quantitative hepatitis B DNA levels did not predict the amount of HBIG required. HBV recurrence after orthotopic liver transplantation can be reduced by aggressive passive immunization. Pharmacokinetic analysis of anti-Hbs elimination can improve immunoglobulin therapy and prevent recurrence of clinical hepatitis.

Therefore, in nonemergency situations attention to these factors in donor allocation may minimize the possibility of HAT.

Hepatitis C viral recurrence after orthotopic liver transplantation is almost universal. Hepatitis C induced graft failure may occur, but the clinical and histologic profiles are not well defined. The aim of this study was to describe the pattern of early graft failure in patients with recurrent hepatitis C after liver transplantation. Thirty patients with hepatitis C underwent liver transplantation from October 1989 through September 1994. Four patients were excluded because of death (2 patients), graft failure unrelated to hepatitis C (1 patient), and lost to follow-up (1 patient). Hepatitis C recurred in 24 of the 26 remaining patients. In 4 patients with hepatitis C virus recurrence and cholestasis, graft failure developed at 5.25, 11.0, 11.0, and 18.5 months. The medical records and liver biopsies were reviewed. In all 4 patients, a histologic pattern characterized by centrilobular ballooning degeneration developed and progressed to involve more than two-thirds of the lobules. Moderate to severe cholestasis and bridging fibrosis were present in all grafts at explant. Two patients had portal inflammation on 3-month biopsies consistent with viral hepatitis. All patients had mild macrovesicular steatosis, but only 1 patient had significant lymphoid aggregates. No patient had evidence of hepatic artery thrombosis. One patient had potential drug-induced cholestasis. One patient had 3 episodes of rejection that were not believed to contribute to graft loss. All 4 patients developed clinical features of hepatic failure and were retransplanted. Two patients had early recurrence of graft failure. We conclude that a pattern of progressive centrilobular ballooning degeneration, bridging fibrosis, and cholestasis occurs in some patients with hepatitis with early graft failure, similar to fibrosing cholestatic hepatitis seen in some transplant patients with recurrent hepatitis B.

Effective clinical trials of islet transplantation have been limited by the inability to transplant enough viable human islets into patients with type I (insulin-dependent) diabetes mellitus to eliminate their exogenous insulin requirement. We report the first type I diabetic patient with an established kidney transplant on basal cyclosporin immunosuppression who was able to eliminate the insulin requirement after human islet transplantation into the portal vein. We successfully isolated ∼800,000 islets that were 95% pure from 1.4 cadaver pancreases containing 121 U of insulin. Islets were proven viable by in vitro insulin response to glucose challenge. After 7 days of 24°C culture, the islets were transplanted into the portal vein under local anesthesia. Seven days of Minnesota antilymphoblast globulin (20 mg/kg) administration followed the islet transplantation, with maintenance of the cyclosporin. Blood glucose was kept under strict control via intravenous insulin for 10 days posttransplantation, when all insulin therapy was stopped. Off insulin, the average 24-h blood glucose level remained <150 mg/dl, with the fasting glucose level at 115 ± 6 mg/dl and the 2-h postprandial level at 141 ± 8 mg/dl for 22 days posttransplantation (the time of this study). The C-peptide values post-Sustacal testing, although initially rising slower, exceeded the normal range, with peak values of 1.0-1.8 pmol/ml. This preliminary result represents the first essential step required to determine the feasibility of islet transplantation by future clinical trials