[Study of the causes of death in fires].
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Biomedical subjects
Publications and source records attributed to R A Anderson.
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Recycled mesodermal growth factor (R-MGF) is a pool of proteins of 26,000 molecular weight obtained by recycling gel chromatography of male murine submaxillary gland extracts. R-MGF strikingly accelerates corneal stromal wound healing in vivo, fibroblast growth and migration in cultured corneal buttons and is showing here to stimulate stromal fibroblast growth and division in tissue culture. Chromatographic fractionation of R-MGF has yielded several components, none of which has a greater biological potency than the parent R-MGF. In contrast, two components, MGF-I and -II, when recombined synergistically stimulate fibroblast response in tissue culture and organ culture in excess of those obtained with the parent R-MGF. Three MGF components (I, III, and IV) have been purified and are inactive at 10-15 micrograms/ml in organ culture but potently stimulate fibroblast responses when combined in pairs containing 7.5 micrograms of each component. The striking synergism in organ culture suggests that the stimulation of wound healing by R-MGF in vivo may also reflect synergistic action of more than one R-MGF component. Procedures for isolating gram quantities of R-MGF and for the purification of different R-MGF components by ion exchange chromatography are detailed.
Ltk- aprt- mouse L cells were transformed to the tk+ phenotype with 10 ng of the herpes simplex virus-1 thymidine kinase (tk) gene and 20 micrograms of pBR322 or simian virus 40 (SV40) DNA. DNAs from five cloned cell lines show restriction endonuclease fragments that hybridize to both tk and pBR322 or SV40 DNA. In all of the cell lines some of these fragments also contain cellular DNA sequences. The use of carrier DNAs with defined sequences has enabled us to demonstrate that the joining of carrier and selectable gene sequences occurs in mouse cells. In one case we have been able to use the ampicillin resistance marker of pBR322 to "rescue" a recombinant plasmid. An analysis of the junction between pBR322 and tk in this plasmid suggests that a small area of homology (16 of 19 base pairs) might be involved in the recombination process.
The utilization of inorganic chromium by free-living human subjects was studied in 76 volunteers (male, 48; female, 28) who were supplemented with 200 micrograms of inorganic chromium as chromic chloride or a placebo tablet for 3 months in a double-blind, cross-over experiment. For all subjects, initial mean +/- SEM urinary chromium (Cr) level was 0.20 +/- 0.01 (range, 0.05 to 0.58) ng/ml and did not differ by sex. Initial chromium/creatinine ratio (Cr/Ct) was 0.15 +/- 0.01 (range 0.03 to 0.36) ng Cr/mg creatinine for females and was significantly lower, 0.10 +/- 0.01 (range 0.03 to 0.36) for males. Mean urinary Cr level increased to 1.0 +/- 0.12 after 2 and to 1.13 +/- 0.08 ng/ml after 3 months' supplementation. The Cr/Ct ratio increased to 0.69 +/- 0.10 for females and to 0.50 +/- 0.04 for males after 2 months' supplementation; values were similar after 3 months. An increase in urinary Cr excretion in response to a glucose load was demonstrated for nonsupplemented normal free-living subjects but not for subjects supplemented daily with trivalent chromium. Urinary Cr excretion after a glucose challenge was not predictable and did not depend on Cr status.
Ethanol reduced the in vitro fertilizing capacity of mouse spermatozoa in a dose-dependent manner, at concentrations commonly observed after ethanol ingestion by man and experimental animals (100-400 mg%). At these ethanol levels, sperm motility and the integrity and fertilizing capacity of the oocyte were not affected, nor was parthenogenic cleavage induced. Data indicated that ethanol prevents the capacitation of the spermatozoa. Its inhibitory effect could be reversed by incubation of the alcohol-treated spermatozoa in alcohol-free capacitation medium. At similar concentrations, t-butanol had no effect on fertilization, suggesting that inhibition by ethanol is mediated by a mechanism other than a "solvent" effect. Although the alcohol dehydrogenase inhibitor, pyrazole, prevented the inhibition of fertilization by ethanol, acetaldehyde (the product of ethanol oxidation) was without effect. These data indicate that the inhibition of capacitation by ethanol is mediated via its metabolism by spermatozoa but not by the immediate product of ethanol oxidation.
Acute sporadic non-A, non-B hepatitis is reported for the first time in New Zealand. Examination of sera from 94 patients with biochemical evidence of hepatitis showed that 26 (27%) had acute hepatitis B (HB), 22 (23%) had acute hepatitis A (HA) and 25 (26%) had acute non-A, non-B hepatitis (NANBH). Nine (10%) patients had Epstein-Barr virus (EBV) associated hepatitis and one (1%) had cytomegalovirus (CMV) hepatitis. There were 11 (13%) patients with mixed infections; eight with HA plus HB, one with HB plus EBV, one with HA plus EBV and one with HB plus CMV. Thus NANBH and EBV associated hepatitis must be considered in the differential diagnosis of patients presenting with clinical hepatitis with no history of possible percutaneous infection.
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Chromium is involved in normal glucose metabolism. To test whether chromium is also associated with the exercise-induced increases in glucose utilization, urinary chromium excretion, serum glucose, insulin, and glucagon of nine male runners (23-46 yr) were evaluated. Blood samples were taken prior to, immediately following, and 2 h after a strenuous 6-mile run. Urine samples were also taken at these times, and total daily urine collections were made the day of the run and the following day. Mean serum glucose for all runners immediately after running was 185 +/- 19 mg/dl compared with 90 +/- 1 mg/dl (mean +/- SE) prior to running. Mean serum glucagon immediately after running was significantly elevated compared with that observed prior to or 2 h after running; serum insulin levels were not altered significantly. Mean urinary chromium concentration was increased nearly five-fold 2 h after running; similar results were obtained when chromium concentration was expressed per mg of creatinine. Total daily urinary Cr excretion was approximately two times higher the day of running compared with the following nonrun day. Daily urinary excretion of sodium, potassium, and calcium were measured to determine if exercise had a general nonspecific effect on renal function; daily urinary excretion of these was not changed by exercise. These data demonstrate that accompanying the exercise-induced changes associated with increased glucose utilization, there is a significant increase in chromium excretion.
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This paper draws attention to the widespread problems associated with an epidemic of influenza at all levels--personal, family and society. In the absence of effective policies of prevention and cure, there is a need for a system which will constantly survey the scene on a clinical basis and give an early warning of an impending epidemic. The means hitherto available have been crude and rather slow to react. A system is described which is based on weekly telephoned reports from a geographically widely spread network of general practitioners, mainly in Tayside. The co-ordinated system operates during the influenza 'season', and provides information to the contributors, health planners, epidemiologists and to WHO. Examples of the work of the 'spotter practices' are drawn from the season 1980-81. The material is validated by virological sampling studies, by the internal consistency of the figures, and by reference to what is happening in other geographical areas. The feasibility of the system has been demonstrated (even under epidemic conditions), and it is suggested that a national co-ordinating system be established.
A high-molecular-weight form of acrosin (alpha-acrosin, EC 3.4.21.10) was extracted from spermatozoa obtained from frozen semen and purified over 300-fold. Purification was effected by sequential use of Sephadex G-150, CM-cellulose and DEAE-cellulose chromatography. Properties of human acrosin were compared with those of human pancreatic trypsin. The molecular weight (Mr) of acrosin (70000) was greater than that of trypsin (Mr 21000). Isoelectric points for acrosin (pI = 9.0) and trypsin (pI = 8.2) were also different. alpha-N-Benzoyl-L-arginine ethyl ester was hydrolysed 50% more rapidly by acrosin than by trypsin. Acrosin had similar kcat. values for the hydrolysis of esters with different acylating groups (i.e. benzoyl-L-arginine and p-tosyl-L-arginine esters). In contrast, trypsin had dissimilar kcat. values for the hydrolysis of esters with different acylating groups. Kinetic data argue against deacylation as the rate-limiting step in ester hydrolysis by acrosin. Acrosin was less sensitive than trypsin to inhibition by 7-amino-1-chloro-3-L-tosylamidoheptan-2-one ('TLCK'), di-isopropyl fluorophosphate and soya-bean trypsin inhibitor. D-Fructose and D-arabinose inhibited acrosin, but had no effect on trypsin. The data indicate that definite differences exist between human acrosin and trypsin.
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Chromium is an essential trace element required for normal carbohydrate metabolism. The biological function of chromium is closely associated with that of insulin and most chromium-stimulated reactions are also insulin dependent. Proper chromium nutrition leads to a decreased requirement for insulin and also an improved blood lipid profile. Most fresh foods and minimally processed foods are good sources of dietary chromium. Inorganic chromium does not potentiate insulin action and must be converted to an organic biologically active form. An organic form of chromium capable of potentiating insulin has been isolated from brewer's yeast and was shown to contain: Cr, nicotinic acid and a combination of amino acids. Synthetic insulin potentiating organic chromium complexes containing chromium, nicotinic acid, glycine, cysteine, and glutamic acid or chromium, nicotinic acid and glutathione have been prepared. These complexes have not been purified to homogeneity since they dissociate during purification. Suitable analytical bioassays are available to measure total chromium and the organic biologically-active forms of chromium, respectively.
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It is well documented that children with the fetal alcohol syndrome are a direct consequence of heavy maternal ethanol consumption during pregnancy. The mechanism by which ethanol exerts its teratogenic effect is however, far from understood. Recent experimental evidence has shown alcohol to have a direct inhibitory effect on embryogenesis. Little information, however, is available concerning other factors associated with maternal drinking which may contribute to abnormal fetal development. Proper materno-fetal hormonal balance is essential to insure successful pregnancy outcome. Of particular importance with respect to normal fetal development, are the levels of placental tropic hormones; pituitary hormones such as prolactin and oxytocin; adrenal cortical hormones; both maternal and fetal thyroid hormones; maternal and fetal sex hormones; and maternal insulin. Ethanol alters the levels of a variety of hormones associated with the hypothalamic/pituitary-gonadal, -adrenal and -thyroid axes. Many of these alterations have been observed in the male, however, with little data available on the female. In spite of the known adverse effect of ethanol on certain aspects of female reproductive function, few if any studies have examined the effects of alcohol ingestion during pregnancy on maternal endocrine balance. It is hoped that the present review will provide a rationale for the examination of alcohol effects on maternal endocrine hormones, as well as to provide possible target areas with respect to fetal development subsequent to ethanol-induced endocrine imbalance.