Growth hormone in birds: a comparative perspective.
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Biomedical subjects
Publications and source records attributed to R Campbell.
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Policies about place of delivery have tended to be formulated without either looking at existing evidence or doing new research into the relative safety for women and babies of delivery in different settings. This article reviews published research on the subject, and finds that many of the data required have not been collected. Furthermore, many analyses fail to take account of selection biases or differences in the birthweight distribution and the incidence of congenital malformations among babies born in different settings. Nevertheless, some tentative conclusions can be drawn. The available evidence does not support claims that, for the baby, the iatrogenic risks of obstetric intervention outweigh the possible benefits. At the same time, there is no evidence to support the claim that the shift to hospital delivery is responsible for the decline in perinatal mortality in England and Wales nor the claim that the safest policy is for all women to be delivered in hospital.
Fibrin deposition and removal is a feature common to major pathological processes such as wound healing, chronic inflammation and tumour invasion: processes involving the ingrowth of new blood vessels. Low molecular weight fibrin degradation products (MW less than 50,000) are now shown to induce angiogenesis in the chick chorioallantoic membrane (CAM). This effect has also been shown by new quantitative assays to be associated with stimulation of both DNA and protein synthesis. Autoradiography indicates that all cell types in the CAM are stimulated to divide, and it is proposed that fibrin degradation products are a pathological growth factor.
A case of hepatic fructose-1,6-diphosphatase deficiency is described. She presented with congenital bilateral cataracts, failure to thrive, hypoglycaemia and hyperlactacidaemia. A liver biopsy revealed normal levels of gluconeogenic enzymes except fructose-1,6-diphosphatase which was present at 30% of the level of the lower control values. The residual activity had a normal affinity for fructose-1,6-diphosphate, a decreased sensitivity for inhibition by fructose-2,6-diphosphate and an increased resistance toward conversion to the AMP-insensitive form of the enzyme. As a result of this mutation, the residual FDPase will always be maintained in the AMP-inhibited form.
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Only one of six patients in whom a clinical diagnosis of rejection was confirmed by both biopsy and FNA benefited from a switch from cyclosporine to azathioprine. Nine patients, in whom nephrotoxicity and rejection could not be separated and in whom the biopsy was positive but the FNA negative, improved when converted to cyclosporine. This improvement was, however, followed by subsequent rejection episodes in four of these patients. This study suggests caution in changing from CsA therapy in patients with unstable function.
A survey was carried out of all 8856 births occurring at home in England and Wales in 1979. Of these births, 67% had been booked for delivery at home, 21% had been booked for delivery in hospital, 3% had not been booked, and for 9% the intended place of delivery was unknown. The perinatal mortality varied almost 50-fold according to the intended place of delivery, ranging from 4.1/1000 births in those booked for delivery at home to 196.6/1000 unbooked births. Deliveries that occurred at home but had been booked for a hospital consultant unit were associated with a perinatal mortality of 67.5/1000. Births that had been booked for delivery at home included the smallest proportion of babies of low birth weight: 2.5% weighed 2500 g or less compared with 18% of those booked for consultant units and 29% of those not booked. Within these low birthweight groups there were noticeable differences in perinatal mortality; births booked to occur at home had the lowest mortality and unbooked births had the highest. Perinatal mortality among babies who weighed more than 2500 g was generally low irrespective of the intended place of delivery; the only exception was in babies whose delivery had not been booked. In all groups perinatal mortality was considerably higher in nulliparous than parous women. Women booking a delivery at home are clearly a selected group, and some may have been transferred to hospital during labour and were thus not included in the survey. Nevertheless, these data suggest that the perinatal mortality among births booked to occur at home is low, especially for parous women.
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The impact of the increased T3 production induced by overfeeding is likely to be lessened if overfeeding also decreases the free fraction of thyroid hormones. Therefore, we examined the effect of 17 to 20 days of carbohydrate overfeeding of five men on total serum T4 and T3 concentrations, the free fraction of these hormones, and serum concentrations of thyroid-hormone binding proteins, TBG, TBPA, and albumin. Total serum T4 concentrations were unchanged by overfeeding and total serum T3 concentrations increased 42%. However, the free fraction of both T4 and T3 decreased during the overfeeding period, so that free T3 concentrations increased only 21% and free T4 concentrations decreased 17%. There was an increase in serum concentrations of both TBG (12%) and TBPA (20%), but no change in the concentration of albumin. We conclude that there is an increase in free T3 concentrations during overfeeding, in spite of a decrease in the free fraction of T3. However, the physiological effects of this increase in free T3 concentrations may be diminished by the decrease in free T4 concentrations.
The effect of alpha, beta, or combined sympathetic blockade on the increase in energy expenditure and concentrations of norepinephrine, glucose, and insulin following oral intake of 100 g of glucose was studied in lean subjects. Alpha blockade with intravenous (IV) phentolamine (n = 5) infusion increased oxygen consumption after glucose ingestion but no more than it increased the oxygen consumption when no glucose was given. Beta blockade with IV propranolol (n = 13) and combined alpha and beta blockade (n = 6) did not affect basal metabolic rate or the increase in metabolic rate after glucose ingestion. Phentolamine or combined propranolol plus phentolamine administration markedly increased plasma norepinephrine concentrations. Basal glucose and insulin concentrations were not affected by any of the infused drugs. Glucose-stimulated insulin concentrations were unchanged by propranolol and combined blockade, whereas there was a trend (P = 0.07) toward an increased response to glucose during phentolamine administration. These data do not support a role for the sympathetic nervous system in the increase in metabolic rate following glucose ingestion. The increase in metabolic rate during phentolamine administration can be attributed to beta adrenergic stimulation.
Clinical, operative and pathological findings in a series of 18 patients with aldosterone producing adrenal cortical adenomas are reviewed. All patients presented with hypertension and hypokalaemia. The main challenges in preoperative diagnosis were to differentiate primary aldosteronism from other causes of hypokalaemia, such as diuretic therapy, to establish the presence of a discrete adenoma and to localize the tumour to the left or right adrenal gland. A high rate of success was achieved in predicting a surgical diagnosis of aldosterone-producing adenoma. This was attributed to thorough biochemical evaluation of the underlying metabolic state by measurement of renal potassium handling and by determining the responses of the renin-aldosterone axis to changes in sodium balance. Preoperative tumour localization, using adrenal phlebography or scintiscanning, was accomplished in only eight cases. Our experience suggests that the transabdominal approach is preferable for cases in which a unilateral lesion is not clearly identified by imaging techniques.
Short term (48 h) in vivo administration of either T3 or T4 was associated with an increase in hepatic glycogen synthase activity in the rat. Administration of 0.25 mg T3/kg BW 48, 24, and 2 h before enzyme preparation increased the total glycogen synthase activity by approximately 50% and increased the percentage of synthase in the I or active form from 19 +/- 1% to 63 +/- 3%. These effects of thyroid hormones on glycogen synthase were rapid (expressed within 24 h) and dose dependent with respect to T3 or T4. Fasting rats for 24 h increased hepatic glycogen synthase levels in control but not thyroid hormone-treated rats. Total glycogen synthase activity of rats administered thyroid hormone and fasted for 24 h remained 1.4-fold greater than that of their fasted euthyroid controls. The percentage of synthase in the I form was 79 +/- 4% for the fasted T3-treated rats compared to 51 +/- 2% for their fasted euthyroid counterparts. Thus, both total hepatic glycogen synthase activity and the percentage of synthase in the I form are increased by short term administration of thyroid hormones in vivo.
This study examined the effect of overeating on plasma norepinephrine concentrations and urinary norepinephrine excretion in man, since overeating sucrose or fat increases norepinephrine turnover in rodents. Five normal subjects were overfed by 50% for 20 days, without substantially changing the proportions of protein, fat, and carbohydrate in the diet, after a control period of normal feeding. Sodium intake remained constant throughout the study. There was no effect of overfeeding on plasma norepinephrine concentrations when subjects were resting supine either before or after a meal. However, plasma norepinephrine concentrations after 10 min of orthostasis were 40% lower (P less than 0.05) at the end of overfeeding. Plasma norepinephrine concentrations during slow walking also tended to be lower during overfeeding, but this effect was not statistically significant. Mean 24-h norepinephrine and epinephrine excretion were not altered. These data do not support the hypothesis that overeating increases sympathetic nervous system activity in man.
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The symptoms which immediately follow envenomation by many crotalid snakes include hypotension, hypovolemia, hemoconcentration, and shock. We have isolated and characterized two proteases (EI and EII) from the venom of Crotalus atrox which may be involved in the onset of these symptoms. EI and EII have molecular weights of 27,500 and 29,200 and isoelectric points of 4.7 and 4.3, respectively. Specific esterolytic activities of EI and EII on N alpha-p-tosyl-L-arginine methyl ester are 51.5 mumol min-1mg-1 and 48.1 mumol min-1 mg-1, respectively. Both enzymes are rather specific in their substrate requirements in that neither was demonstrated to have any proteolytic activity against either of the oxidized chains of insulin, or glucagon. Neither enzyme was shown to have plasmin or fibrinolytic activity. Both enzymes are able to cleave a kininogen analog to release bradykinin. This proteolytic activity is inhibited by aprotinin and phenylmethanesulfonyl fluoride but not by ethylenediaminetetraacetate. The enzymes are active upon the kallikrein substrates S2666 and S2302. The Km values of the enzymes with these substrates are similar to those reported for kallikrein. Structural similarity between the two enzymes was demonstrated by ultraviolet and circular dichroic spectroscopy, and amino acid analysis. Tryptic peptide mapping of the two native enzymes also suggested a large degree of structural similarity. Furthermore, sequence studies on the NH2-terminal regions of the enzymes indicate that they share a significant degree of sequence homology with porcine kallikrein and crotalase, a kallikrein-like enzyme from Crotalus adamanteus. The main physical difference between the two kallikreins reported here appears to be due to the carbohydrate moieties on the enzymes. At present the in vivo role of venom kallikreins in envenomation pathology is uncertain; however, it is possible that they play an important part in giving rise to the initial symptoms of hypotension and shock.
Thirteen patients developed gastric ulcers between 6 months and 8.5 years after Nissen fundoplication. Eight patients presented with epigastric pain alone, 3 with bleeding alone and 2 with both pain and bleeding. Nine ulcers (69 per cent) were high on the lesser curve, close to the fundoplication and 7 of these patients had recurrent hernias. Anatomical distortion produced by fundoplication is probably the most important aetiological factor, though gastric distention, bile reflux gastritis and ischaemia may be contributory.
Two experiments show that the spelling of a nonword that is heard (i.e., /prein/) is influenced by the spelling of a word that is heard earlier (i.e., "brain" greater than prain and "crane" greater than prane). This is a robust effect and inspection of the pattern of results suggests that, under these conditions, both words and nonwords are lexically analyzed. A patient with an aquired reading disorder characterized as surface dyslexia was unaffected by such lexical influences in his spelling of nonwords. Moreover, his spelling suggested a defective ability to generate phonemically acceptable spellings of nonwords. Taken together with other reports of neurologically caused spelling impairments these results suggest that skill at assigning letters to sounds never becomes independent of lexical skill in adult readers. An analogical, lexically based parsing system for the reading and spelling of new (nonwords, as suggested by Marcel (1980) appears to be the best fit to these data.