Search PubMed⌕ Search

Biomedical subjects

K Jones

Publications and source records attributed to K Jones.

At least 379 records · Page 21Linked to original sources
PubMed1988

Brain amino acids and glutathione in progressive supranuclear palsy.

We measured amino acid contents in autopsied brains of seven patients with progressive supranuclear palsy (PSP) and in control subjects dying without brain disease. Glutathione was also quantitated in rapidly frozen brains of PSP patients, Parkinson's disease (PD) patients, and controls. In PSP, we found glutamic acid markedly increased in the nucleus accumbens; taurine significantly increased in nucleus accumbens, substantia nigra, and globus pallidus; and gamma-aminobutyric acid significantly increased in nucleus accumbens and putamen. Glycerophosphoethanolamine contents were significantly increased in most regions. Glutathione, which is significantly decreased in substantia nigra in PD, was increased in this brain region in PSP, suggesting that different mechanisms may be responsible for destruction of dopaminergic nigrostriatal neurons in these two disorders.

Aged↗
PubMed1988

Successful heart-lung transplantation for cystic fibrosis.

Sixteen months after heart-lung transplantation, the FEV1 of a young woman, who had been in the terminal stages of cystic fibrosis, has risen from 16 percent (0.6 L) to 77 percent of her predicted value. Concomitant with the changes in pulmonary function, her ventilatory response to re-breathing carbon dioxide has improved, and so has her exercise tolerance. She has returned to work.

Adult↗
PubMed1988

In vitro activity of azithromycin (CP-62,993), a novel macrolide, against enteric pathogens.

Azithromycin (CP-62,993 [9-deoxy-9A-methyl-9A-aza-9A-homoerythromycin]) is a novel macrolide antimicrobial. In this study the in vitro activity of CP-62,993 has been determined against selected enteropathogens, including Clostridium difficile, and compared with that of erythromycin. MICs were determined using an agar incorporation technique in Mueller-Hinton medium, containing saponin-lysed horse blood at a final concentration of 10% v/v, with an inoculum of 10(4) cfu. CP-62,993 was considerably more active than erythromycin against Salmonella typhi (MIC90 4 and greater than 32 mg/l, respectively), S. enteritidis (MIC90 4 and greater than 32 mg/l), Shigella flexneri (MIC90 2 and 32 mg/l), Sh. dysenteriae (MIC90 2 and 32 mg/l), Sh. sonnei (MIC90 4 and 32 mg/l), Campylobacter jejuni (MIC90 0.12 and 1 mg/l), Vibrio cholerae (MIC90 0.25 and 8 mg/l), V. parahaemolyticus (MIC90 0.5 and 8 mg/l), Yersinia enterocolitica (MIC90 4 and greater than 32 mg/l), Escherichia coli-ETEC (MIC90 4 and 32 mg/l), E. coli-EIEC (MIC90 4 and greater than 32 mg/l), Plesiomonas shigelloides (MIC90 1 and 8 mg/l) and Aeromonas hydrophila (MIC90 4 and 32 mg/l). CP-62,993 (MIC90 2 mg/l) was slightly less active than erythromycin (MIC90 1 mg/l) against isolates of C. difficile. The results suggest a potential clinical role for CP-62,993 in the treatment of enteric infections where antimicrobial therapy is indicated.

Azithromycin↗
PubMed1987

4-phenylpyridine and three other analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine lack dopaminergic nigrostriatal neurotoxicity in mice and marmosets.

C57 black mice were injected repeatedly with maximal tolerated doses of 2 chemical analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP); 4-phenylpyridine and 4-phenyl-1,2,3,6-tetrahydropyridine. Although both compounds were clearly acutely toxic to mice, neither caused any reduction in striatal dopamine content after chronic exposure. Two MPTP analogues which may be formed endogenously during the metabolism of brain monoamines, 2-methyl-1,2,3,4-tetrahydroisoquinoline and 2-methyl-1,2,3,4-tetrahydro-beta-carboline, were injected repeatedly into common marmosets. Again, although both compounds appeared highly toxic, neither caused any reduction in striatal dopamine content. It appears unlikely that any of these 4 MPTP analogues causes idiopathic Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Exposure to cigarette smoke does not decrease the neurotoxicity of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice.

Epidemiological surveys have repeatedly shown that idiopathic Parkinson's disease (PD) occurs less frequently in persons who have smoked cigarettes for many years than among age-matched non-smokers. Since PD might be caused by neurotoxins chemically similar to N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we explored the possible protective effect of repeated exposure to cigarette smoke against MPTP neurotoxicity in the C57 black mouse. Mice given MPTP and exposed to cigarette smoke suffered just as great a depletion of striatal dopamine as did mice treated only with MPTP. We discovered also that different lots of C57 black mice obtained from a single supplier can have markedly different sensitivities to MPTP.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Amino acids, glutathione, and glutathione transferase activity in the brains of patients with Alzheimer's disease.

We measured the contents of amino acids and related amino compounds in autopsied brain from 22 patients with Alzheimer's disease (AD) and in cortical biopsy specimens from 2 other patients. The diagnosis of AD was established neuropathologically in all 24 patients by the presence of both neurofibrillary tangles and neuritic plaques in neocortex. The mean contents of gamma-aminobutyric acid (GABA), and of the GABA dipeptide homocarnosine, were significantly reduced in frontal and occipital cortices and in hippocampus of the autopsied brains of AD patients compared to control patients without neurological disease. However, GABA contents were normal in frontal cortex in biopsy samples from 2 patients. Phosphoethanolamine contents were significantly reduced at autopsy in frontal and occipital cortex, and in the substantia innominata. We found no evidence of a deficiency of glutamate, aspartate, or taurine in AD brain, as has been claimed. Glutathione contents and glutathione transferase activities were normal in frontal cortex and substantia innominata. The mechanism of neuronal death in patients with AD is unlikely to involve either insufficient synthesis of glutathione or failure to conjugate free radicals with glutathione.

Adolescent↗
PubMed1987

Tissue culture evidence for a circulating neurotoxin in Huntington's chorea.

We explored with tissue culture techniques the possibility that a circulating neurotoxin might cause the premature loss of certain populations of neurons that characterizes Huntington's chorea (HC). Explants of striatum from newborn rats were grown in culture media containing 30% by volume of serum from drug-free HC patients or from healthy control subjects. Glutamic acid decarboxylase (GAD), the enzyme which synthesizes gamma-aminobutyric acid (GABA), was later assayed in these explants as an indicator of the health of GABAergic striatal neurons. The sera of 7 of 8 HC patients decreased GAD activity markedly when present as 30% of the tissue culture medium. When present in lower concentration (15%), HC sera either decreased or increased GAD activity in explants. Deproteinization of sera with perchloric acid did not abolish these effects on GAD activity. A depressant effect on GAD activity was detected in the cerebrospinal fluid of 1 of 4 HC patients tested. These experiments suggest the presence of a circulating neurotoxin, possibly excitotoxic to GABAergic striatal interneurons, and probably a small molecule. Identification of this substance could lead to an effective preventive treatment for persons genetically at risk for HC.

Adolescent↗