Intraventricular alloxan eliminates feeding elicited by 2-deoxyglucose.

Evidence suggests that alloxan reacts with membrane-bound glucoreceptors and that it competes with glucose molecules for these sites. We therefore administered small quantities of alloxan into the cerebrospinal fluid of rats to determine what effect this might have on their ability to react to changes of glucose concentration. Rats treated in this manner did not eat as much as controls in response to the intraperitoneal administration of 2-deoxyglucose or to a 24-hour fast, and they became hypoglycemic significantly sooner than controls when fasted. The data suggest that the function of brain glucoreceptors is to protect the body from sudden decreases of glucose and that these glucoreceptors play little if any role in the normal regulation or maintenance of feeding, body weight, or blood glucose concentrations.

Transport of Sr2+ and SrEDTA2- in partially-saturated and heterogeneous sediments.

Strontium-90 has migrated deep into the unsaturated subsurface beneath leaking storage tanks in the Waste Management Areas (WMA) at the U.S. Department of Energy's (DOE) Hanford Reservation. Faster than expected transport of contaminants in the vadose zone is typically attributed to either physical hydrologic processes such as development of preferential flow pathways, or to geochemical processes such as the formation of stable, anionic complexes with organic chelates, e.g., ethylenediaminetetraacetic acid (EDTA). The goal of this paper is to determine whether hydrological processes in the Hanford sediments can influence the geochemistry of the system and hence control transport of Sr(2+) and SrEDTA(2-). The study used batch isotherms, saturated packed column experiments, and an unsaturated transport experiment in an undisturbed core. Isotherms and repacked column experiments suggested that the SrEDTA(2-) complex was unstable in the presence of Hanford sediments, resulting in dissociation and transport of Sr(2+) as a divalent cation. A decrease in sorption with increasing solid:solution ratio for Sr(2+) and SrEDTA(2-) suggested mineral dissolution resulted in competition for sorption sites and the formation of stable aqueous complexes. This was confirmed by detection of MgEDTA(2-), MnEDTA(2-), PbEDTA(2-), and unidentified Sr and Ca complexes. Displacement of Sr(2+) through a partially-saturated undisturbed core resulted in less retardation and more irreversible sorption than was observed in the saturated repacked columns, and model results suggested a significant reservoir (49%) of immobile water was present during transport through the heterogeneous layered sediments. The undisturbed core was subsequently disassembled along distinct bedding planes and subjected to sequential extractions. Strontium was unequally distributed between carbonates (49%), ion exchange sites (37%), and the oxide (14%) fraction. An inverse relationship between mass wetness and Sr suggested that sandy sediments of low water content constituted the immobile flow regime. Our results suggested that the sequestration of Sr(2+) in partially-saturated, heterogeneous sediments was most likely due to the formation of immobile water in drier regions having low hydraulic conductivities.

Peptides and the control of meal size.

There are now a large number of experiments demonstrating that peripheral administration of exogenous cholecystokinin or its synthetic analogue, CCK-8, reduces meal size in a number of species. The peptide interacts with other factors which influence satiety, and treatments thought to be effective in eliciting secretion of cholecystokinin have predictable effects on meal size. Cholecystokinin is effective in the genetically obese Zucker rat, obese rats with lesions of the ventromedial hypothalamus, and subdiaphragmatically vagotomized rats. Somatostatin and bombesin are also reasonable candidates for satiety factors. Intraperitoneal naloxone reduces meal size in rats, and beta-endorphin injected intraventricularly causes an increase in meal size of 50% over 30 minutes. We conclude that cholecystokinin and bombesin may interact in weight regulation and control of meal time food intake.

Subarachnoid molecular hemoglobin after subarachnoid hemorrhage in rats: effect on the area of hypoperfusion.

A previous study indicated that diaspirin-crosslinked hemoglobin (DCLHb) decreases cerebral ischemia after subarachnoid hemorrhage. However, the study was limited in that DCLHb was given to animals with an intact vasculature. As extravasated hemoglobin has been implicated in the pathogenesis of cerebral vasospasm, DCLHb in the subarachnoid space might in theory have a detrimental effect on cerebral perfusion after subarachnoid hemorrhage. In the current study, autologous blood was administered into the cistema magna of isoflurane-anesthetized rats. After 30 minutes, the animals received one of the following in the cistema magna (n=8 for each group): The control group received mock cerebral spinal fluid, the "blood" group received autologous blood, the "DCLHb" group received DCLHb, and the "Alb" group received human serum albumin. After 20 minutes, areas of reduced cerebral blood flow (CBF, 0-20 and 21-40 ml/100 g/min) were assessed in five coronal brain sections with 14C-iodoantipyrine. The data were evaluated by analysis of variance. The areas of 0-20 ml/100 g/min CBF were greater in all five brain sections in the Blood group than in the other three groups; were greater in four brain sections in the DCLHb group than in the Control group; and were greater in three brain sections in the Alb group than in the Control group (p < 0.05). The areas of 21-40 ml/100 g/min CBF were greater in three sections in the Blood group than in the other three groups; and were greater in two brain sections in the DCLHb group than in the Alb group (p < 0.05). These data support a hypothesis that subarachnoid blood induces cerebral hypoperfusion, and that although molecular hemoglobin decreases CBF, the potential adverse effects are less than those produced by blood.

Influence of flow rate on transport of bacteriophage in shale saprolite.

The objective of this study was to investigate the influence of flow rate on transport and retention of bacteriophage tracers in a fractured shale saprolite, which is a highly weathered, fine-grained subsoil that retains much of the fabric of the parent bedrock. Synthetic ground water containing PRD-1, MS-2, and bromide was passed through a saturated column of undisturbed shale saprolite at rates ranging from 0.0075 to 0.96 m d '. First arrival of the bacteriophage tracers in effluent samples in each of the experiments occurred within 0.01 to 0.04 pore volumes (PV) of the start of injection, indicating that bacteriophage were advectively transported mainly through fractures or macropores. Bacteriophage transport velocities, based on first arrival in the effluent, were very similar to fracture flow velocities calculated using the cubic law for flow in a fractured material. For MS-2, maximum concentration and mass of tracer recovered both increased steadily as flow rate increased. For PRD-1, these values initially increased, but were nearly constant at flow rates above 0.039 m d(-1), indicating that approximately 50% of the observed losses were independent of flow rate. Evaluation of the data indicates that physical straining and electrostatic or hydrophobic attachment to fracture or macropore walls were the dominant retention processes. Inactivation and gravitational settling playing secondary roles, except at the slowest flow rates. The study suggests that microbial contamination from sources such as septic fields and sewage ponds may pose a threat to the quality of ground water and surface water in areas with saprolitic subsoils.

Influence of soil geochemical and physical properties on the sorption and bioaccessibility of chromium(III).

There are numerous Cr(III)-contaminated sites on Department of Defense (DoD) and Department of Energy (DOE) lands that are awaiting possible clean up and closure. Ingestion of contaminated soil by children is the risk driver that generally motivates the likelihood of site remediation. The purpose of this study was to develop a simple statistical model based on common soil properties to estimate the hioaccessibility of Cr(III)-contaminated soil upon ingestion. Thirty-five uncontaminated soils from seven major soil orders, whose properties were similar to numerous U.S. DoD contaminated sites, were treated with Cr(III) and aged. Statistical analysis revealed that Cr(III) sorption (e.g., adsorption and surface precipitation) by the soils was strongly correlated with the clay content, total inorganic C, pH, and the cation exchange capacity of the soils. Soils with higher quantities of clay, inorganic C (i.e., carbonates), higher pH, and higher cation exchange capacity generally sequestered more Cr(III). The amount of Cr(III) bioaccessible from the treated soils was determined with a physiologically based extraction test (PBET) that was designed to simulate the digestive process of the stomach. The bioaccessibility of Cr(III) varied widely as a function of soil type with most soils limiting bioaccessibility to <45 and <30% after I and 100 d soil-Cr aging, respectively. Statistical analysis showed the bioaccessibility of Cr(III) on soil was again related to the clay and total inorganic carbon (TIC) content of the soil. Bioaccessibility decreased as the soil TIC content increased and as the clay content decreased. The model yielded an equation based on common soil properties that could be used to predict the Cr(III) bioaccessibility in soils with a reasonable level of confidence.

Functional and structural similarities between protease nexin I and C1 inhibitor.

Protease nexin I is a proteinase inhibitor that is secreted by human fibroblasts and forms stable complexes with certain serine proteinases; the complexes then bind to the fibroblasts and are rapidly internalized and degraded. In this report, we show that this inhibitor, which is present in very low concentrations in plasma, has functional and structural similarities to C1 inhibitor, an abundant proteinase inhibitor in plasma. Both inhibitors complex and inactivate certain proteinases that previously were known to rapidly react only with C1 inhibitor. Kinetic inhibition studies show that protease nexin I inhibits Factor XIIa and plasma kallikrein with second-order rate constants of 2.3 x 10(3) and 2.5 x 10(5) M-1 s-1, respectively, which are similar to the rate constants for inhibition of these proteinases by C1 inhibitor. Protease nexin I inhibits C1s about one-tenth as rapidly as does C1 inhibitor. Alignment of the amino acid sequences of protease nexin I and C1 inhibitor shows that these proteins have similarity at their reactive centers (from sites P7 to P1). The remaining regions of the two proteins share much less similarity. In contrast to protease nexin I, C1 inhibitor is not secreted by human fibroblasts. Although 125I-C1s-protease nexin I complexes readily bind to human fibroblasts, binding of 125I-C1s-C1 inhibitor complexes or other 125I-proteinase-C1-inhibitor complexes to these cells is not detectable. Thus, protease nexin I and C1 inhibitor may control some common regulatory proteinases in the extravascular and vascular compartments, respectively.

Suppression of food intake by intravenous nutrients and insulin in the baboon.

Intravenous nutrients were infused at 25 and 50% of total base-line daily caloric intake to determine the role of circulating factors on spontaneous food ingestion in young adult male baboons (Papio cynocephalus). Glucose infusion suppressed food intake (15.1%) when 25% of total calories was infused (P less than 0.05) and 41.8% when 50% of total calories was infused (P less than 0.05) for 14-21 days. Both infusions produced basal hyperglycemia (82-172 mg/dl during 25% glucose and 120-239 mg/dl during 50% glucose). Both infusions also caused an increase in circulating insulin (48.1-63.1 microU/ml during 25% glucose and 68.5-77.2 microU/ml during 50% glucose). The simultaneous infusion of exogenous insulin (0.33 mU X kg-1 X min-1) prevented hyperglycemia (85.8-87.9 mg/dl during 25% glucose) but maintained raised basal peripheral insulin levels (52.4-84.4 microU/ml). The 13% suppression of food intake (P less than 0.05) was similar to glucose infusion alone. Comparable infusions of Intralipid as 25 and 50% of total daily calories also suppressed spontaneous food intake but did not produce hyperglycemia or elevated insulin levels. The magnitude of suppression was similar to that of glucose: 16% when 25% of basal calories was infused (P less than 0.05) and 31.3% when 50% of basal calories was infused (P less than 0.05). However, the pattern was different with a more rapid effect, which tended to diminish in time, rather than the slow effect found with glucose, which was maintained for 14 days. We conclude that circulating nutrients can regulate food intake independent of gastrointestinal absorption in primates.(ABSTRACT TRUNCATED AT 250 WORDS)

Peptides and the control of meal size.

There are now a large number of experiments demonstrating that peripheral administration of exogenous cholecystokinin or its synthetic analogue, CCK-8, reduces meal size in a number of species. The peptide interacts with other factors which influence satiety, and treatments thought to be effective in eliciting secretion of cholecystokinin have predictable effects on meal size. Cholecystokinin is effective in the genetically obese Zucker rat, obese rats with lesions of the ventromedial hypothalamus, and subdiaphragmatically vagotomized rats. Somatostatin and bombesin are also reasonable candidates for satiety factors. Intraperitoneal naloxone reduces meal size in rats, and beta-endorphin injected intraventricularly causes an increase in meal size of 50% over 30 minutes. We conclude that cholecystokinin and bombesin may interact in weight regulation and control of meal time food intake.