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Biomedical subjects

J B Watson

Publications and source records attributed to J B Watson.

66 records · Page 4Linked to original sources
PubMed1984

Specific termination of in vitro transcription by calf thymus RNA polymerase III.

In vitro transcription of cleaved SV40 DNA with calf thymus RNA polymerase reveals a discrete transcript. The pattern of resistance to the inhibitor alpha-amanitin identifies the RNA as a product of RNA polymerase III transcription. The RNA is shown to initiate artificially near a DNA terminus created by cleavage and to terminate specifically near a cluster of 8 thymidine residues within the SV40 control region. Faithfully initiated transcripts cannot be detected using the calf thymus enzyme, supporting the idea that polymerase III termination can be accomplished by an initiation-deficient enzyme. Transcription of SV40 DNA in a HeLa cell lysate also leads to specific polymerase III transcription. When PvuII-cleaved DNA is the template, the same RNA is produced as with the calf thymus enzyme. At the lowered lysate concentration known to activate certain AluI-family transcripts, a collection of SV40 polymerase III transcripts is also produced. These do not depend on restriction cleavage of the DNA and thus arise from transcription of intact DNA.

Amanitins↗
PubMed1982

Mechanism of hypoalbuminemia in the 7/8-nephrectomized rat with chronic renal failure.

Hypoalbuminemia has been observed consistently in patients and experimental animals with chronic renal failure (CRF). A defect in albumin synthesis, catabolism, or distribution has been invoked as the cause, but there is no agreement as to which, if any, of these disorders results from the uremic state. We studied albumin homeostasis in 7/8-nephrectomized rats with CRF. Serum albumin concentration was lower in CRF (29.6 +/- 4.59 mg/ml) than in sham-operated control rats (36.3 +/- 4.3 mg/ml). Albumin synthesis, determined directly by measuring incorporation of 14CO2 into arginine in albumin, was increased in CRF rats as was total albumin clearance, measured using 125I-albumin disappearance. Rats with CRF were albuminuric. Albumin synthesis was increased by the amount necessary to replace urinary losses, but net albumin catabolism was the same as in control animals. Albuminuria was prevented by addition of excess tryptophan to the diet. Total albumin clearance and albumin synthesis were the same in these tryptophan-fed CRF animals as in CRF sham-operated animals, but these CRF rats were still hypoalbuminemic (33.6 +/- 5.27 vs. 36.3 +/- 4.3 mg/ml). Rats with CRF were plasma volume expanded. Institution of a low-sodium diet at the time of partial nephrectomy prevented plasma volume expansion and albuminuria as well. Serum albumin concentration, albumin distribution, pool sizes, and total albumin clearance remained the same as in CRF sham-operated animals. Hypoalbuminemia in CRF rats is due to two factors. Plasma volume expansion with pool dilution contributes 40% of the decrease and external albumin losses resulting from albuminuria contribute the other 60%. Albumin synthesis, catabolism, and distribution are intact.

Albuminuria↗
PubMed1980

Respiratory patterns and risk of sudden unexpected death in infancy.

The overnight respiratory patterns of 25 infants at high risk and 42 infants at low risk of sudden unexpected death were studied during the first 6 months of life. 'Risk' was determined using the birth scoring criteria of Carpenter and Emery. Recordings were made at home using a twin-channel radar chest movement detector which was designed to avoid the need for contact with the infant. The recordings were analysed for respiratory frequency, total duration of apnoea, periodic breathing, duration of regular breathing, and amount of body movement. The high risk group of infants showed respiratory frequencies that were significantly higher than those of the low risk group. None of the other parameters showed significant differences between the groups. These findings do not support the widespread use of home apnoea monitors for infants.

Humans↗
PubMed1980

Nonaccidental poisoning: the elusive diagnosis.

Although nonaccidental poisoning in childhood is now more often recognised, it is still difficult to establish a diagnosis despite correct investigative procedures. In 1978 we were unable, initially, to establish the cause of intermittent episodes of loss of consciousness in a boy admitted to Sheffield Children's Hospital. Subsequently it was conclusively shown that his mother systematically poisoned him with Tuinal (amylobarbitone and quinalbarbitone) both before admission and while he was being treated in the hospital.

Amobarbital↗
PubMed1980

Anion-stimulated phosphohydrolase activity of intestinal alkaline phosphatase.

Phosphohydrolase activity of a highly enriched commercial preparation of calf intestinal alkaline phosphatase was stimulated in the presence of HCO3. SO4, Cl, SCN, and acetate did not stimulate hydrolysis, whereas SO3 exhibited a bimodal effect, stimulating at low (25mM) concentration but inhibiting at high (100 mM) concentration. The pH optimum of this stimulation by HCO3 or SO3 was 8.5--9.0 and was maximal at a Mg concentration of 0.5 mM. HCO3 increased the Vmax of the reaction without changing the Km for ATP. ATP, GTP, UTP, and xanthosine triphosphate were equally effective as substrates, whereas AMP and p-nitrophenyl phosphate were much less effective. Alkaline phosphatase activity was inhibited by L-cysteine and L-phenylalanine, compounds that also inhibited the HCO3-ATPase activity of the preparation. Passage of the commercial preparation through an anion-exchange column yielded a fraction with enriched alkaline phosphatase and HCO3-ATPase activities; this fraction proved to be a single protein on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, on isoelectric focusing, and by immunologic techniques. These studies strongly suggest that alkaline phosphatase and anion-stimulated phosphohydrolase activities are properties of the same protein in small intestine. It is possible that alkaline phosphatase may function as a HCO3-ATPase involved in intestinal absorption and secretion.

Adenosine Triphosphatases↗
PubMed1979

Nonaccidental poisoning in childhood.

A boy aged 7 years 10 months was admitted to hospital on several occasions in an unconscius state with twitching and apnoeic episodes. Initial investigations failed to show a specific cause. During his time in hospital he had recurrent episodes of loss of consciousness and, on the last occasion, hypotension and ventricular tachycardia. A diagnosis of imipramine poisoning was established by the presence of imipramine in stomach washings and blood. The drug was being given to the child, both at home and in hospital, by his mother. The possibility of nonaccidental poisoning must be considered if there is no obvious cause for a child's illness. In this case the mother responded to psychiatric treatment.

Child↗
PubMedDate not supplied

Diabetes mellitus in childhood cystic fibrosis.

Since 1984, five patients in the cystic fibrosis (CF) clinic at Cork Regional Hospital have developed diabetes mellitus (DM) and were treated with Insulin. None had received systemic corticosteroids but two had high calorie naso-gastric feeding regimes. Two died from lung disease. A fifteen year old boy developed bilateral cataracts. In nine other paediatric CF clinics in the Republic of Ireland (total: 420 patients), three patients have DM, two receiving Insulin. Abnormal glucose tolerance is becoming more common in CF as patients survive longer. The possible role of corticosteroid treatment and intensive carbohydrate feeding regimes in development of glucose intolerance must be considered. DM in CF differs from the usual childhood DM. Regular screening and early Insulin supplementation may be beneficial.

Adolescent↗