Hepatic regeneration and growth factors

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Further steps of hepatic stimulatory substance purification

The hepatic stimulatory substance (HSS) extracted from weanling rat livers was purified 381,000-fold using chromatographic techniques including nondissociating polyacrylamide gel electrophoresis (nondenaturing PAGE). The activity of this highly purified HSS, named Acr-F4, was assessed in two in vivo models. In 40% hepatectomized rats, it produced a fivefold increase in the proliferative rate normally seen following this partial hepatectomy. In Eck fistula dogs, the level of base increase in hepatocyte renewal was amplified threefold by an infusion of Acr-F4 (50 ng/kg/day). Acr-F4 had no influence on the regenerative response of the kidney following a unilateral nephrectomy or of the bowel following a 40% resection of the small bowel. On the basis of these findings, it can be concluded that HSS (Acr-F4) has a high biological activity and is organ specific. © 1991 Plenum Publishing Corporation

Studies on mechanisms of augmentation of liver regeneration by cyclosporine and FK 506

Evidence could not be found of immune modulation of liver regeneration. The powerful immunosuppressive drug FK 506, which augments the response after partial hepatectomy in normal rats, had the same effect in T cell—deficient nude rats. The cytotoxicity of natural killer cells in treated nude rats was not significantly changed by FK 506 therapy. However, the serum of FK 506—treated nude rats increased hepatocyte proliferation when added to third‐party hepatocyte cultures, suggesting that FK 506 had induced a serum growth factor in the nude rats or had suppressed an inhibitory factor. A hypothesis was advanced that FK 506 (and cyclosporine) affects hepatic growth by nonimmunological pathways. (HEPATOLOGY 1991;14:140–143.) Copyright © 1991 American Association for the Study of Liver Disease

Effects of glucagon on the growth of Neurospora

Effects of glucagon on the growth of Neurospora

Processing and initial comparison of PSR data from CAMEX-3 to SSM/I and TMI data

A multiband Polarimetric Scanning Radiometer (PSR) was integrated on a NASA DC-8 aircraft and flown from August through September of 1998 during the third Convection and Moisture Experiment (CAMEX-3). The PSR is a new conically-scanning imaging radiometer with channels at 10.7, 18.7, 21.5, 37.0 and 89.0 GHz, including both vertical and horizontal polarizations at each of these frequencies. These channels correspond to several key sensing bands of the DMSP (Defense Meteorological Satellite Program) SSM/I (Special Sensor Microwave Imager) and the NASA TRMM (Tropical Rainfall Measuring Mission) TMI (TRMM Microwave Imager). The PSR was developed by Georgia Institute of Technology and the NOAA Environmental Technology Laboratory and is the first airborne imaging radiometer to provide a research quality dataset of high spatial resolution multiband polarimetric microwave imagery within and around a hurricane. The authors describe the processing and calibration of the PSR CAMEX-3 dataset. They also provide a qualitative analysis and comparison of the PSR imagery to the SSM/I and TMI with specific regard to the spatial structure of a hurricane eyewall and surrounding rainbands.Peer ReviewedPostprint (published version

A dog model for acetaminophen-induced fulminant hepatic failure.

The development of a large animal model of fulminant hepatic failure produced with acetaminophen that should be useful in the development and evaluation of potential medical therapies for the important clinical problem of fulminant hepatic failure is described. Acetaminophen in dimethyl sulfoxide (600 mg/ml) given as three subcutaneous injections, with the first dose (750 mg/kg body wt) being given at noon, the second dose (200 mg/kg body wt) being given 9 h later, and the third dose (200 mg/kg body wt) being given 24 h after the initial dose consistently produces fulminant hepatic failure in dogs. The dimethyl sulfoxide vehicle, injected intramuscularly, does not influence either animal survival or hepatic function in control-treated dogs. No deaths occur within the first 36 h. By 72 h after initial drug administration, the mortality is 90%. Histopathological and biochemical investigations demonstrate a high degree of hepatocellular necrosis in nonsurviving animals without appreciable damage to the kidneys, lungs, or heart. The drug schedule and preparation outlined avoids the administration of large volumes of vehicle and results in prolonged high levels of acetaminophen in the blood sufficient to induce severe hepatic injury. Ranitidine (120 mg/kg body wt i.m.) given 30 min before each acetaminophen dose significantly reduces the mortality and hepatic necrosis produced using this model. This model satisfies all criteria established by Miller et al. for the production of a suitable large animal model of fulminant acute hepatic failure

A dog model for acetaminophen-induced fulminant hepatic failure.

The development of a large animal model of fulminant hepatic failure produced with acetaminophen that should be useful in the development and evaluation of potential medical therapies for the important clinical problem of fulminant hepatic failure is described. Acetaminophen in dimethyl sulfoxide (600 mg/ml) given as three subcutaneous injections, with the first dose (750 mg/kg body wt) being given at noon, the second dose (200 mg/kg body wt) being given 9 h later, and the third dose (200 mg/kg body wt) being given 24 h after the initial dose consistently produces fulminant hepatic failure in dogs. The dimethyl sulfoxide vehicle, injected intramuscularly, does not influence either animal survival or hepatic function in control-treated dogs. No deaths occur within the first 36 h. By 72 h after initial drug administration, the mortality is 90%. Histopathological and biochemical investigations demonstrate a high degree of hepatocellular necrosis in nonsurviving animals without appreciable damage to the kidneys, lungs, or heart. The drug schedule and preparation outlined avoids the administration of large volumes of vehicle and results in prolonged high levels of acetaminophen in the blood sufficient to induce severe hepatic injury. Ranitidine (120 mg/kg body wt i.m.) given 30 min before each acetaminophen dose significantly reduces the mortality and hepatic necrosis produced using this model. This model satisfies all criteria established by Miller et al. for the production of a suitable large animal model of fulminant acute hepatic failure

Scaling of resistivities and guided vortex motion in MgB2 thin films

Longitudinal and transverse voltages have been measured on thin films of MgB2 with different superconducting transition widths. The study has been performed in zero and non-zero external magnetic fields. The non-zero transverse voltage has been observed in close vicinity of the critical temperature in zero external magnetic field, while further away from Tc this voltage becomes zero. In magnetic field it becomes a transverse voltage which is an even function with respect to the direction of the field. The usual Hall voltage starts to appear with increasing magnetic field and in large fields the even voltage disappears and only the Hall voltage is measurable (i.e. the transverse even voltage is suppressed with increasing magnetic field and increasing transport current). New scaling between transverse and longitudinal resistivities has been observed. This correlation is valid not only in the zero magnetic field but also in nonzero magnetic field where transverse even voltage is detected. Several models trying to explain observed results are discussed. The most promising one seems to be guided motion of the vortices, though further theoretical work will be required to confirm this