Treatment with ganirelix effectively prevents premature LH rises, luteinization in subjects undergoing stimulated IUI. Low-dose rFSH regimen combined with a GnRH antagonist may be an alternative treatment option for subjects with previous proven luteinization or in subjects who would otherwise require insemination when staff are not working.

The urinary excretion of seven selected low molecular weight organic acids in normal neonates was measured by gas chromatography. First and third to fourth day of life excretion of the following compounds was significantly unchanged: 3-OH-butyric acid (less than 13 mumol/mmol creatinine), succinic acid (approx. 43 mumol/mmol creatinine), adipic acid (approx. 12 mumol/mmol creatinine), 2-OH-glutaric acid (approx. 23 mumol/mmol creatinine), 3-OH-3-Me-glutaric acid (approx. 25 mumol/mmol creatinine) and citric acid (approx. 115 mumol/mmol creatinine). The excretion of 4-OH-phenyl-acetic acid increased during the first four days of life (from less than 8 mumol/mmol creatinine to approx. 20 mumol/mmol creatinine). It is postulated that urinary orgainc acid excretion in the neonate, which is clearly different from the adult urinary pattern, is a reflection of the specific neonatal metabolic situation, including a high fatty acid utilisation and a low protein catabolism.

Summary.A highly polymorphic locus flanking the human insulin gene contains two major size classes of DNA restriction fragments, which segregate in families as stable genetic elements. The L-allele, i.e. fragments with an average size of about 600 base-pairs seems to be a weak genetic marker for Type 1 (insulin-dependent) diabetes mellitus, whereas the Uallele, i.e. fragments of an average size of about 2500 basepairs hitherto has been associated with Type 2 (non-insulindependent) diabetes mellitus and diabetic hypertriglyceridaemia. The most recent reports on this subject do not confirm an association between the U-allele and Type 2 diabetes. Our own studies indicate that the U-allele is a fairly strong marker for the development of atherosclerosis (relative risk for U-cartiers 3.36). The putative functions of the polymorphic region in atherogenesis and the relation of this region to other genetic markers for atherosclerosis are not known.

24 hour ambulatory electrocardiography was performed in a representative group of people born in 1897. Out of 73 people included in the study, 22 were without known heart disease, 15 had definite ischaemic heart disease (IHD) and 36 symptoms of possible cardiac origin. An R-R interval in excess of 2000 ms was seen in only 3 subjects and Wenckebach A-V block in only one. One subject without a history of syncope had a nocturnal episode of complete A-V block with an escape interval of 8000 ms. The most striking difference between healthy subjects and patients with IHD was the higher number of patients with more than 1000 ventricular premature beats (VPBs) per 24 hour and ventricular couplets compared with the number of healthy subjects with such findings. At follow-up two years later 11% had died, with the highest mortality in patients with IHD (33%), and out of 8 patients with IHD who had more than 1000 VPBs per 24 hour, 4 (50%) had died compared with only one (14%) of those with less than 1000 VPBs. Our results seem to indicate that more than 1000 VPBs per 24 hour is a very unusual finding in healthy 85 year old individuals. When it occurs in very old people, it is usually in connection with IHD, and in this setting it signifies a poor prognosis.

Iron status, including S-ferritin, S-iron, S-total iron binding capacity (TIBC), TIBC saturation, haemoglobin (Hb) and dietary iron intake, was assessed in a population study comprising 92 healthy 85-year-old subjects (32 males, 60 females). S-iron, S-TIBC, TIBC saturation and S-ferritin values were not significantly different in the two sexes. Males had a geometric mean S-ferritin of 130 micrograms/l, females of 98 micrograms/l. Ferritin levels less than 15 micrograms/l (i.e. depleted iron stores) were found in one female (1.6%); and in one male (3.1%), who in addition had iron deficiency anaemia. None of the females displayed latent iron deficiency (i.e. S-ferritin less than 15 micrograms/l and S-TIBC saturation less than 15%) or iron deficiency anaemia. Arithmetic mean Hb was 145 +/- 13 (SD) g/l (9.0 +/- 0.8 mmol/l) in males and 139 +/- 11 g/l (8.6 +/- 0.7 mmol/l) in females (p less than 0.02). Median nutritional iron intake was 10 mg/day (range 3-17), higher in males (median 12) than in females (median 9) (p less than 0.0001). Iron intake showed significant correlations to S-iron, S-TIBC and TIBC saturation, but not to S-ferritin.

The excretion of C6-C10-dicarboxylic acids, i.e. adipic, suberic and sebacic acids, was measured during the three first days of life in 3 fasting newborns, 2 newborns fed with isocaloric glucose and 2 newborns given mothers'-milk. On the second and third day of life the starved children excreted 27-84 mmol adipic acid/mol creatinine, 6-22 mmol suberic acid/mol creatinine and 4-7 mmol sebacic acid/mol creatinine. The excretion of C6-C10-dicarboxylic acids in the neonates given glucose or mothers'-milk was, for the first three days of life, 0-9 mmol adipic acid/mol creatinine, 0-10 mmol suberic acid/mol creatinine and 0-4 mmol sebacic acid/mol creatinine. The latter amounts are equivalent to the excretion of dicarboxylic acids in older children. It is argued that the detected dicarboxylic acids are formed by omega-oxidation of long-chain monocarboxylic acids followed by beta-oxidation, and that the excreted amounts reflect omega-oxidation activity. It is speculated that the substantial omega-oxidation activity in the starving newborn serve to provide succinyl-CoA-substrate for the citric acid cycle and for gluconeogenesis.

OBJECTIVES: To examine how the slimming drug, Letigen 1 , containing ephedrine (E) 20 mg and caffeine (C) 200 mg (E C), affects blood pressure in normotensive and hypertensive patients treated with adrenergic b-receptor blocking drugs and/or other antihypertensive agents, during a period of six weeks. DESIGN: A double-blind, randomised, placebo controlled study of ®ve parallel groups of overweight patients from general practices. SUBJECTS: One hundred and thirty-six patients with Body Mass Index (BMI) b 25 kg/m 2 were included consecutively by 25 general practitioners in Denmark and randomized into ®ve groups: (1) Hypertensive patients treated with betablockers and E C; (2) Hypertensive patients treated with antihypertensive agents other than betablockers, and E C; (3) Normotensive patients treated with E C; (4) Hypertensive patients under any antihypertensive treatment placebo; and (5) Normotensive patients placebo. All patients were instructed in a 1200 kcal ( 5040 kj) diet. RESULTS: Of a total of 136 patients aged 20±74 y, 112 completed the study protocol. Fluctuations in systolic and diastolic blood pressure were seen in all groups. The systolic blood pressure was reduced signi®cantly (5.5 mmHg) in the patients treated with antihypertensive agents other than betablockers, plus E C. In the other hypertensive groups the reduction in blood pressure was not signi®cant. In normotensive patients treated with E C, the systolic and the diastolic blood pressure declined signi®cantly (4.4/3.9 mmHg). At the end of the treatment period heart rate had increased signi®cantly (4.9 beats/min) in the group of normotensive patients treated with E C. Blood pressure and heart rate measured by the patient at home showed similar¯uctuations from baseline prior to and during treatment with E C or placebo.A mean loss of weight of approximately 4 kg in 6 weeks was signi®cant for all the groups. There was no signi®cant difference between the groups during this short period of treatment. In 56% of the patients treated with E C complaints/side-effects related to the medical treatment were found at questioning. Corresponding complaints occurred in 21% of the placebo treated patients. In the E C treated group 7% dropped out due to side-effects. In the placebo group there were no drop-outs. CONCLUSIONS: This study does not support the assumption that E C should cause rises in blood pressure, acutely or during shortterm treatment, in either normotensive or hypertensive obese patients. The antihypertensive effect of the betablockers was not reversed by E C.

VariationsIn the DNA sequence flanking the 5' region of the human Insulin gene (U-and L-alleles) were studied in relation to atherosclerosis, lipid levels, and age In three groups of atherosclerotic Individuals and in nonatherosclerotlc controls. The atherosclerotic groups comprised a postmyocardlal infarction group with a mean age of 48 years, a group of Individuals operated on for carotid stenosis with a mean age of 62 years, and a group of 85-year-olds with clinical coronary disease, peripheral arterial disease, or both. All 331 individuals were unrelated Caucasians of Danish ancestry. There were no significant differences (p>0.05) In genotype distribution or allele frequencies between atherosclerotic and nonatherosclerotlc Individuals, but In the 85-year-olds, there was evidence (p<0.10) for a lower U-allele frequency in nonatherosclerotlc women compared to atherosclerotic women. In nonatherosclerotlc women, there was a significant decrease In U-allele frequency with age (60 to 85 years). This decrease does not prove conclusively, but Is compatible with, the hypothesis that the U-allele predisposes to, or the L-allele protects against, atherosclerosis. The possible effect of the U-allele on the development of atherosclerosis does not seem to be mediated through conventional risk factors. (Arteriosclerosis 10:372-378, May/June 1990)