The binding-sites of rabbit muscle aldolase.
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Animals↗
Biomedical subjects
R Barker
Publications and source records attributed to R Barker.
An exploration of the active site of aldolase using structural analogs of fructose diphosphate.
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Catalysis↗
The in vivo survival of human red cells with low oxygen affinity prepared by the osmotic pulse method of inositol hexaphosphate incorporation.
The purpose of this study was to determine the posttransfusion survival of low-affinity red cells (RBCs) containing the hemoglobin modifier, inositol hexaphosphate (IHP). An osmotic pulse technique was used to incorporate IHP, a compound that normally does not cross the RBC membrane. Two groups of six volunteers were studied. RBCs were treated under conditions that resulted in a relatively large increase in mean corpuscular volume (delta MCV = 11.8 +/- 4.0, 1 SD) in Group I, but a relatively small increase (delta MCV = 5.5 +/- 1.9) in Group II. The groups had a similar decrease in mean corpuscular hemoglobin (delta MCH = -3.8 +/- 0.9 for Group I and -3.1 +/- 1.1 for Group II). The 24-hour posttransfusion RBC survival, measured with 3 mL of 51Cr-labeled autologous RBCs, correlated with the induced change in oxygen affinity, and larger shifts were associated with poorer survival. An acceptable 75-percent 24-hour posttransfusion survival was achieved for p50 increases up to approximately 15 torr. Cells that survived 24 hours appeared to have a normal lifespan. This study is the first demonstration of adequate survival for human RBCs with a potentially long-lasting decrease in oxygen affinity.
Blood Transfusion↗
The biology and behaviour of intracerebral adrenal transplants in animals and man.
The catecholamine containing chromaffin cells of the adrenal medulla have recently been employed as intracerebral grafts in man and animals with lesions of the nigrostriatal dopaminergic system. This review outlines the basic biology of the chromaffin cell with reference to its efficacy as a source of dopamine in the grafted state. This is followed by an evaluation of the use of these grafts in experimentally lesioned animals and in patients with Parkinson's disease.
Adrenal Medulla↗
Tachykinins, neurotrophism and neurodegenerative diseases: a critical review on the possible role of tachykinins in the aetiology of CNS diseases.
The tachykinins are a family of undecapeptides that are widely distributed throughout the body, including the central nervous system (CNS). They have several well defined roles in non-CNS sites as well as in the dorsal horn, where they are involved in the transmission of nociceptive information. However their function(s) in other CNS sites is unclear, but there is some evidence that they function as neuromodulators rather than neurotransmitters. This neuromodulation includes a possible role in maintaining the integrity of neuronal populations, analogous to the functions of neurotrophic factors. This review critically evaluates the role of tachykinins as neurotrophic factors, with particular reference to the common neurodegenerative diseases of the CNS.
Alzheimer Disease↗
Raging against fate.
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Adjustment Disorders↗
Interspecies comparison of the pharmacokinetics of aldose reductase inhibitors.
The pharmacokinetics of three aldose reductase inhibitors (ARIs) were evaluated in various species, including rat, dog, cynomolgus monkey, rhesus monkey, chimpanzee, and man. The three ARIs (AL01567, AL01576, and AL01750) were administered intravenously as a single dose to all species except rat, which was dosed orally with AL01750, and man, who was dosed orally with AL01567 and AL01576. Plasma drug concentrations were measured by HPLC or liquid scintillation spectrometry and various pharmacokinetic parameters (clearance, CL; Vd, volume of distribution; and t1/2) were calculated from the data. Overall the pharmacokinetics of the three compounds were quite similar, each being characterized by low CL, intermediate Vd, and long t1/2. For AL01576, mean CL ranged from 0.21 ml/min/kg in cynomolgus monkey to 0.91 ml/min/kg in dog, mean Vd from 0.66 liter/kg in cynomolgus monkey to 2.4 liters/kg in dog and man and mean t1/2 from 29 hr in dog to 72 hr in man. Mean CL of AL01567 ranged from 0.14 ml/min/kg in man to 1.4 ml/min/kg in dog, mean Vd from 0.45 liter/kg in rat to 3.5 liters/kg in dog and mean t1/2 from 22 hr in rhesus monkey to 63 hr in man. Mean CL of AL01750 ranged from 0.13 ml/min/kg in chimpanzee to 1.3 ml/min/kg in dog, mean Vd from 0.40 liter/kg in rat to 1.8 liters/kg in dog and mean t1/2 from 12 hr in rhesus monkey to 62 hr in chimpanzee. For all three drugs, CL and Vd corrected for body weight were quite similar in all species except dog, whose CL and Vd were two- to fourfold greater than the other animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Aldehyde Reductase↗
Quantitative variation of free amino acids in the central nervous system of MoMuLV-ts1-infected mice.
A temperature-sensitive mutant of Moloney murine leukemia virus (MoMuLV-ts1) induces polioencephalomyelopathy and hind limb paralysis in highly susceptible FVB/N strains of neonatal mice. This disease is characterized by progressive motor neurons loss and severe gliosis within specific target areas of the central nervous system (CNS). The mechanism(s) of this neurodegeneration is unknown. In the neonatal infection of the CNS, the MoMuLV-ts1 virus was reported to replicate within the endothelial, ependymal, astrocytes and microglial cells. Since no virus or viral products were recognized in the degenerating neurons, it is postulated that an indirect mechanism(s) caused the loss of neurons in the neonatally infected mice. This study was undertaken to investigate the possible pathogenic role of excitatory amino acids (EAAs) such as glutamate and other nonneurotransmitters amino acids (NAAs) in this animal model. The free amino acids concentration was analysed by a fluorometric HPLC method. The temporal measurements of the free amino acids concentration, glutamate, glutamine and arginine from the brain stem and spinal cord of MoMuLV-ts1-infected mice was significantly decreased when compared with the control non-infected mice. The concentration of EAAs during the course of this infection indicated a sharp decline in glutamate and its precursor, glutamine with early infection (10 days post infection-dpi). This deficiency persisted (20 and 30 dpi) in the spinal cord, where the neuronal loss was most severe, but not in the brain stem. A similar pattern occurs with the amino acid arginine. These observations suggest that an astrocyte-induced metabolic disturbance of glutamate and arginine in the CNS of developing mice, could be, in part responsible for the loss of motor neurons observed in this model.
Amino Acids↗