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Biomedical subjects

G A Robinson

Publications and source records attributed to G A Robinson.

At least 55 records · Page 3Linked to original sources

A comparison of diethylstilbestrol- and estradiol-17 beta-induced vitellogenesis in quail.

Japanese quail were injected intramuscularly with .125 to 32 mumole/100 g body weight of estradiol-17 beta (E2) or diethylstilbestrol (DES). During the following 8 days, vitellogenesis was assessed in these birds by measuring plasma concentrations of protein-bound phosphorus (PBP; vitellogenin is a phosphoprotein), calcium, and total protein. Blood packed cell volumes were recorded also. Plasma PBP concentrations of E2-injected male and female quail increased to .83 and .96 mg/ml from control values of .004 and .12 mg/ml, respectively. Doses of 8 to 32 (males) or 4 to 32 (females) mumole E2/100 g body weight induced similar initial rates of vitellogenesis, but the duration of vitellogenesis increased with increasing doses of hormone. In male quail, low doses of DES (.5 to 4.0 mumole/100 g body weight) were more effective than equal doses of E2 in inducing increases in plasma PBP levels. However, the maximum PBP concentrations attained with high doses of DES were less than those attained with equal doses of E2 (.53 and .83 mg/ml, respectively).

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Distribution of 153Gd in F1 quail.

Eggs laid by 153 Gd-labeled Japanese quail were collected each day for 24 days. Maximum transference of the lanthanide to an oocyte approximated 27% of the dose given the quail and occurred usually for the egg collected on the third day. The 24 largest oocytes from each of 2 quail were removed 18 hr after labeling the quail. The curve for a plot of percent 153Gd vs. gram of oocyte for these 24 oocytes approximated a log-log function. Eggs double-labeled with 153 Gd and Sudan black B showed no label in the latebra. Quail hatched from labeled eggs were dissected at various times up to 67 days of age. The percent of egg 153 Gd that was found in the F1 quail decreased from 100% to approximately 55% during the first 14 days. The percentage recovery for mature quail was 55.8%. The major portion of the 153Gd present in each F1 quail was found in the yolk sac and ranged from 96.0% for hatchlings a few hours old to 73.3% for mature quail. The weight of the yolk sac decreased from .7 g for hatchlings to .04 g for mature quail. The first 5 eggs laid by producing F1 quail contained a total of .643% of the 153 Gd in these quail. The graph curve for these eggs for percent 153Gd vs. day of collection approximated an exponential function, in contrast to the marked maximum seen for 153Gd levels in eggs laid by the parent quail.

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153Gadolinium as a useful radiolanthanide for long-term labeling of tissues in Japanese quail.

153Gadolinium (153Gd), with gamma energies of 97 keV (30%) and 103 keV (20%), and a nuclear-life of 242 days and with no primary charged particles, was selected as the radiolanthanide for labeling proteins and tissues in Japanese quail. Ranges of dose-responses 18 hr after giving Gd (153Gd labeled) were: males, livers 24.4% for .00015 mumol/100 g to 63.8% for .15 mumol/100 g; laying females, livers 6.5% for .00015 mumol/100 g to 72.7% for 15 mumol/100 g and growing oocytes 83.2% for .00015 mumol/100 g to 6.4% for 15 mumol/100 g. Accumulation of .015 mumol/100 g doses of 153Gd in tissues common to both sexes were greater in males than in females at 1, 6, and 18 hr. The exception was the pancreas, where for all three sampling times the percentages for females were twice those for males. Comparison of 153Gd with 140lanthanum (140La) showed 18-hr levels of 27%/g liver in males and 1.6%/g liver and 11.8%/g growing oocyte in females for both nuclides. Double-labeling with 153Gd and 144cerium (144Ce) showed that a near-toxic dose of La (15 mumol/100 g) caused a marked decrease in labeling of growing oocytes (e.g., largest oocyte, La-treated females, Gd 14.6%, Ce 6.1%; controls Gd 42.2%, Ce 35.5%) and a marked increase in labeling of livers (La-treated, Gd 51.2%, Ce 43.3%; controls; Gd 7.62%, Ce 4.75%).

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Comparison of the accumulation of 125I and 144Ce in the growing oocytes of the Japanese quail.

Japanese quail were doubly-labeled with 125I (carrier free, as sodium iodide) and 144Ce (.015 micromol/100 g, as trichloride). by 1 hr after administration, the growing oocytes and the ova had accumulated 29% of the 125I and 21% of the 144Ce. By 18 hr, the accumulations were 30% of the 125I and 79% of the 144Ce. Lanthanum (15 micromol/100 g, as trichloride), given iv 5 min before the radionuclides, resulted in 1-hr accumulations of 4% for 125I and 23% for 144Ce. On fractionation of the oocyte yolk, 86% of the 125I present in the yolk was found in the low density fraction and 69% of the 144Ce remained with the phosvitin fraction. These results were consistent with the suggestion of Schjeide and Prahlad (1977) that, in plasma, iodide becomes associated with the calcium-containing vitellogenin complex.

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Copper-induced skeletal myopathy in rabbits.

Doses of 1.66 mg Cu/kg/day, as cupric acetate in aqueous solution, were injected intramuscularly into the lateral thigh muscles of rabbits. The rate of loss of Cu from the injection site was estimated from in vivo measurements of 64Cu injected on the 15th day. Biological half-life values were 1.0 h for the first component (accounting for 65.2% of the 64 Cu) and 14.6 h for the second component (34.8% of the 64Cu). For the control group, values were 0.8 h and 62.2%, 14.6 h and 37.8%. Grossly visible lesions of dermatitis were noted on the paws, i.e. at sites removed from the site of injection, in some rabbits injected with Cu acetate two days post injectionem (p.i.). Histologically detectable lesions of acute inflammation were seen as early as 24 hours p.i. at the injection site of rabbits which had been exposed to the Cu once. Multiple injections and longer time periods resulted in lesions of acute and chronic inflammation. Cu was detected by the use of rubeanic acid stain. Signs of muscle degeneration and regeneration were seen as early as three days p.i. in rabbits which had received two injections of Cu. Rabbits which had been killed six days p.i. after a single injection showed chronic inflammatory changes and newly formed myofibres. Rabbits which had been killed 37 days p.i. after 17 injections showed lesions of acute and chronic inflammation of muscle and surrounding connective tissue, as well as signs of muscle regeneration. The gangrene visible grossly was attributed to the ischaemia caused by conglomerations of Cu.

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Radiolanthanides as markers for vitellogenin-derived proteins in the growing oocytes of the Japanese quail.

Producing Japanese quail were given intravenous injections of radiolanthanides as trichlorides in .03N HCl solution. In quail given 15 mumol lanthanide pr 100 g body weight, the liver accumulated 46 to 82% of the dose by 18 hr after the injection. The growing oocytes accumulated 6 to 24% of the dose. The spleen had the greatest concentration of radiolanthanide (14 to 38%/g), the liver 9 to 19%/g, and the most heavily labeled oocytes 3 to 9%/g. The atomic number of the lanthanide for the 9 lanthanides used was not a factor in these accumulations. Levels of 140La were maximal in the membranes of the growing oocytes by 6 hr (4%) and in the contents by 2 days (19%). The smaller the number of mumol the greater was the percent accumulation in the oocytes. Thus, for .015 mumol 140La/100 g, 75% was present in the oocytes by 18 hr. The most heavily labeled oocytes contained 21%/g vs. 2.9%/g for the liver and 1.3%/g for the spleen. The sum of 140La depositions in eggs laid over 8 days (11 quail, 87 eggs) was, per quail, 89.6 +/- .6% (mean +/- SE) of the injected dose. The half-time value for deposition of 140La in the growing oocytes was 1.8 hr. This value represented the rate of loss of labeled vitellogenin from the plasma as vitellogenin-derived proteins were transferred into the oocytes.

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Accumulation of 125I in the oocytes, thyroids, and plasma of laying Japanese quail treated with cyclic AMP, theophylline, or prostaglandins E1 or E2.

Dibutyryl cyclic AMP, theophyline, or prostaglandins E1 or E2 were injected intraperitoneally into laying Japanese quail in an attempt to stimulate increased transference of iodide by the ovarian membranes. Theophyline induced increased 18-hr 125I accumulations (by 7 to 18% of the injected dose) of borderline significance in the growing oocytes of some test groups. Theophyline plus DBcAMP treatment lead to a slight increase in 125I accumulation in the thyroid. Other treatments had no apparent effect on 125I transference. The prostaglandins induced oviposition within minutes of injection, as has been reported for uterine application of prostaglandins by other investigators. Means for plasma 125I levels for treated quail were 1.7 to 12.5 times greater than control levels. Values for oocyte to plasma and thyroid to plasma 125I ratios, it appeared that DBcAMP, theophyline, and the prostaglandins inhibited rather than stimulated the accumulation of 125I by the ovary and thyroid of the quail.

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The role of free fatty acids in the regulation of lipolysis by human adipose tissue cells.

The effect of added fatty acid on lipolysis and cyclic AMP concentration of human adipose tissue cells was studied. The addition of sodium oleate decreased the lipolytic response of adipocytes to 10(-7) M isoproterenol. Inhibition was detectable with the lowest quantity of oleate added, 0.2 mM, and was progressively greater with increasing quantities of added fatty acid. Palmitic and linoleic acids were as effective as oleic acid in suppressing isoproterenol-stimulated lipolysis. Suppression of cyclic AMP formation was detectable within one minute after the addition of oleate. Cyclic AMP formation, suppressed by accumulated fatty acids, could not be stimulated by the addition of fresh isoproterenol. However, after the accumulated fatty acids were removed by buffer change, cyclic AMP formation was stimulated by fresh isoproterenol. These findings are consistent with the view that fatty acids are physiologically significant regulators of lipolysis.

Adipose Tissue↗

The pathogenesis of Trypanosoma congolense infection in calves. I. Clinical observations and gross pathological changes.

Holstein calves infected with Trypanosoma congolense TREU 112 had intermittent fever, debility and a poor hair coat. At postmortem examination the most significant findings were enlargement of the liver, kidneys and spleen and increased volume of hematopoietic marrow. A group of 13 calves infected for 18 weeks had marked enlargement of lymph nodes throughout the body and hemal nodes were prominent in the sublumbar area caudal to the kidneys. Another group infected for 7 weeks had no increase in the weight of lymph nodes. Studies with 51Cr labelled autologous red cells given shortly before postmortem examination showed that the liver was the most active organ with respect to sequestration of labelled red cells.

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Distribution of 140La and 47Ca in female Japanese quail and in the eggs laid.

140La accumulations in 20 tissues and tissue products of laying Japanese quail 1, 6 and 18 hr. after an intravenous dose of 15 mumol. La/100 g. body weight were greatest in the liver (43.1% at 18 hr.) and the growing oocytes (8.19% at 18 hr.). 47Ca accumulations 6 hr. after intravenous injection as compared with 140La levels were: shell 87.7% Ca, 0.0028% La; liver 0.110% Ca, 38.5% La; oocytes 0.852% Ca, 6.50% La. La3+ administered with the 47Ca did not alter the 47Ca levels. Deposition in eggs laid over an 8-day period was: 47Ca, shells 95.7%, maximum 77.6% on day 1; 140La, yolks 25.3%, maximum 8.35% on day 4.

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Comparison of the transfer of 125I, 82Br, and 26Cl into the growing oocytes of the Japanese quail.

Laying Japanese quail were doubly-labeled with either 125I and 36Cl or 82Br and 36Cl. Eighteen-hour accumulations, expressed as percent of tracer doses, were: growing oocytes, 125I 48.2 vs. 36Cl 2.07, 82Br 4.01 vs. 36Cl 1.99; thyroids, 125I 10.6 vs. 36Cl .030, 82Br .027 vs. 36Cl .020. Concentrations (expressed as percent per gram) of the radionuclides in the growing oocytes and the thyroids as compared with concentrations in the plasma were: for oocytes, the mean 125I concentration was 199 times the mean plasma concentration, 82Br was .34 x and 36Cl was .13 x; for thyroids, 125I was 13,500 x, 82Br was .48 x, and 36Cl was .41 x the mean plasma concentration. Eight day totals for yolks of eggs laid were 125I 29% vs. 36Cl 3.7%.

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Excess iodide and the accumulation of 125I by the thyroid, plasma and developing oocytes of the Japanese quail.

1. Developing oocytes of the Japanese quail accumulated 0-44 microgram of each 1 microgram of 125I-labelled iodide after intra-muscular injection of doses up to 500 microgram iodide as NaI but only 0-007 microgram after injection of more than this: the abrupt change in the rate of accumulation was attributed to saturation of the iodide transport mechanism. 2. The proportion of available iodide transferred into the oocytes appeared to be more dependent on the amount of iodide injected and the total weight of growing oocytes than on a requirement for either a store of iodide for the embryo or an iodide excretory pathway for the hen. 3. The thyroid was about four times more active in accumulating iodide than the oocyte. 4. The percentage of iodide accumulated by the plasma was the same at all dose rates.

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Lithium induction of premature oviposition by the Japanese quail.

1. The intramuscular injection of LiCl into laying Japanese quail 6 or 12 h subsequent to an oviposition induced early oviposition of the next egg. 2. The shells of eggs from Li-treated birds were without speckling and weighed half or less as much as shells from Na-treated birds. Many eggs were also deficient in albumen.

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Suppression of radioiodide accumulation by the thyroids and oocytes of Japanese quail with perrhenate.

Japanese quail, 50% inhibition of the 3-h accumulation of 131I occurred with 2.0 micromol KReO4, 2.2 micromol KClO4 and 13 micromol KSCN for the growing oocytes, 1.7, 1.9 and 4.2 micromol for the thyroids of females and 0.20, 0.47 and 5.6 micromol for the thyroids of males. 2. KReO4 inhibition failed after 24 h in males and 36 h in females. 3. Maxima at 6 h in the 131I curves for the plasma, the livers and the testes of KReO4-treated birds were attributed to retention of 131I in the plasma.

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Accidental suppression of the accumulation of radioiodide by the thyroids of Japanese quail exposed to an iodinated disinfectant.

The walls and floor of a room housing a Japanese quail colony were treated with a commercial disinfectant containing iodine complexed to organic molecules. The room was washed vigorously with hot water using a pressure hose, a procedure discouraged by instructions on the shipping container. A condensate, tinged yellow-brown presumably by elemental iodine, settled on the walls, ceiling and quail pens. Accumulations of tracer doses of iodide-125 or iodide-131 by the thyroid glands of these birds were approximately one-seventh (6-hour uptake) to one-thirtieth (18-hour uptake) as great as for control birds from non-disinfected areas.

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Lithium-induced inhibition of 125I accumulation by thyroids and growing oocytes of Japanese quail.

A single dose of 975 mumol. Li Cl suppressed thyroidal accumulation of iodide in laying Japanese quail as measured at 1, 6, and 18 hr. after injecting 125 I and in mature male quail at 1 hr. Thyroidal accumulation was above control values in males by 18 hr. Levels of 125 I were unchanged in growing oocytes but in testes were 3 to 60 times the control levels. When accumulations were expressed relative to the concentration of 125I in the plasma, in lithium-treated quail levels in thyroids were 0.02 to 0.5 times, in oocytes 0.2 to 0.9 and in testes 0.7 to 0.8 times control values. Results indicate that a single large dose of LiCl caused retention of 125I in the extracellular fluid of Japanese quail and thereby in the testes but inhibited transport of the tracer into the thyroid and growing oocytes.

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