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R L Anderson

Publications and source records attributed to R L Anderson.

At least 505 records · Page 28Linked to original sources
PubMed1975

Phosphocellobiase.

Explore the source record for details and available documents.

Ammonium Sulfate↗
PubMed1975

Glucogenic and ketogenic capacities of lard, safflower oil, and triumdecanoin in fasting rats.

The glucogenic and ketogenic capicities of lard, safflower oil, and triundecanoin were compared. Rats were fed diets containing 30 percent of either lard (a ketogenic fat), triundercanoin (a glucogenic fat), or safflower oil (a fat high in linoleic acid). After 61 days, the rats were fasted for 72 hours. Plasma glucose and ketone body concentrations and carcass fatty acid loss were measured during fasting. The lard-fed animals, which lost mostly saturated even-chain length fatty acids during fasting, did not maintain their prefasting plasma glucose levels and became ketotic. The animals that had been fed triundecanoin (which mobilized considerable odd-chain fatty acid) maintained their prefasting plasma glucose levels and did not become ketotic. The animals fed safflower oil (which mobilized massive amounts of linoleic acid) showed even lower levels of plasma glucose and higher levels of ketone bodies than did the animals fed lard. This failure of safflower oil to avert fasting hypoglycemia suggests that linoleic acid is oxidized in a manner more like the saturated fatty acid of lard than like the glucogenic odd-chain fatty acid (undecanoic).

Animal Nutritional Physiological Phenomena↗
PubMed1975

Nationwide epidemic of septicemia caused by contaminated intravenous products: mechanisms of intrinsic contamination.

Between 1 July 1970 and April 1971, in many hospitals in this country, there were outbreaks of nosocomial septicemia caused by Enterobacter cloacae of E. agglomerans (formerly Erwinia, herbicola-lathyri). All of these hospitals used infusion products manufactured by one company, Abbott Laboratories, and all affected patients had onset of septicemia while receiving the company's infusion products. Septicemia was epidemiologically and microbiologically traced to intrinsic contamination of the company's screw-cap closure for infusion bottles which was sealed with a newly introduced elastomer liner. Epidemic organisms were isolated from these closures. Investigations both in the laboratory and in the manufacturing plant into the mechanism of contamination of these products revealed the following. (i) Epidemic strains were present in numerous areas throughout the manufacturing plants. (ii) Viable microorganisms gained access to the interior of screw-cap closures after the autoclave step of production. (iii) Cooling closures actively drew moisture through the thread interstices into the inner-most depths of the closure. (iv) Transfer of contaminants from closures to fluid was easily effected by simple manipulations duplicating normal in-hospital use. (v) The red-rubber liner used in the company's screw-cap closures before the introduction of elastomer contained a broad-spectrum antimicrobial inhibitor. The findings from this epidemic and the associated studies show that the screw-cap closure as it is now designed cannot be considered secure for products that must remain sterile.

Cross Infection↗
PubMed1974

In-use contamination of intravenous infusion fluid.

During the 1970 to 1971 nationwide epidemic of septicemias caused by Enterobacter cloacae and Enterobacter agglomerans traced to intrinsic contamination of Abbott intravenous infusion products, 94 infusion systems manufactured by Baxter Laboratories were studied microbiologically and epidemiologically during hospital use. Intravenous fluid from 10 systems (11%) contained microorganisms, usually Staphylococcus or Bacillus species; one infusion was heavily contaminated with Klebsiella pneumoniae. No national epidemic organisms, E. cloacae or E. agglomerans (formerly Erwinia), were recovered, suggesting that during this period frequent contamination with these organisms was unique to Abbott's infusion products. Contamination in this study appeared to be extrinsic in origin (introduced during clinical use) and related to the duration of continuous intravenous therapy. Nine of 61 systems (15%) that had been used longer than 48 h were contaminated, whereas only 1 of 33 used less than 48 h (3%) contained microorganisms. This study and the recent national outbreak indicate that contamination of infusion fluid, both from intrinsic and extrinsic sources, must be recognized as an additional risk of intravenous therapy; however, a once-daily replacement of the delivery apparatus can significantly diminish this hazard.

Bacillus↗
PubMed1974

Trehalose metabolism by Bacillus popilliae.

Trehalose was found to be utilized more readily than glucose for the growth of Bacillus popilliae NRRL B-2309MC. The pathway of degradation of trehalose was elucidated and found to differ from that reported for other organisms. Trehalase and trehalose phosphorylase activities could not be detected. Rather, trehalose was found to undergo phosphoenolpyruvate (PEP)-dependent phosphorylation, and the resulting trehalose 6-phosphate was cleaved by a phosphotrehalase to equimolar amounts of glucose and glucose 6-phosphate. The phosphotrehalase was purified 34-fold and shown to have a pH optimum of 6.5 to 7.0 and a K(m) for trehalose 6-phosphate of 1.8 mM. A mutant missing the phosphotrehalase failed to grow on trehalose but grew normally on other sugars. The mutant accumulated [(14)C]trehalose as [(14)C]trehalose 6-phosphate. Phosphorylation of trehalose by dialyzed extracts was at least 25 times faster with PEP than with adenosine 5'-triphosphate, and the phosphorylation activity was associated primarily with the particulate fraction. These data and the results of studies of [(14)C]trehalose uptake suggest that trehalose is transported into the cell as trehalose 6-phosphate by a PEP:sugar phosphotransferase system. Cell extracts of other strains of B. popilliae were also found to produce [(14)C]sugar phosphate from [(14)C]trehalose and to have phosphotrehalase activity.

Bacillus↗
PubMed1974

Genetic evidence for the physiological significance of the D-tagatose 6-phosphate pathway of lactose and D-galactose degradation in staphylococcus aureus.

Mutants of Staphylococcus aureus were isolated which were unable to utilize d-galactose or lactose, but which were able to utilize all other carbohydrates tested. Growth of the mutants on a peptone-containing medium was inhibited by d-galactose. Of those mutants selected for further study, one (tagI2) was missing d-galactose 6-phosphate isomerase, one (tagK3) was missing d-tagatose 6-phosphate kinase, and one (tagA4) was missing d-tagatose 1, 6-diphosphate aldolase. Each of these mutants accumulated the substrate of the missing enzyme intracellularly. Spontaneous revertants of each of the mutants simultaneously regained their ability to utilize d-galactose and lactose, lost their sensitivity to d-galactose, regained the missing enzymatic activities, and no longer accumulated intermediates of the d-tagatose 6-phosphate pathway. These data support our previous contention that the physiologically significant route for the metabolism of d-galactose and the d-galactosyl moiety of lactose in S. aureus is the d-tagatose 6-phosphate pathway. Furthermore, a mutant constitutive for all three enzymes of this pathway was isolated, indicating that the products of the tagI, tagK, and tagA genes are under common genetic control. This conclusion was supported by the demonstration that d-galactose 6-phosphate isomerase, d-tagatose 6-phosphate kinase, and d-tagatose 1, 6-diphosphate aldolase are coordinately induced in the parental strain.

Aldehyde-Lyases↗