[Yoghurt and skimmed milk are not suitable for infants].
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Biomedical subjects
Publications and source records attributed to M Seip.
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"Programming" may be defined as a process whereby a stimulus or an insult applied during a "critical" or "sensitive" period of development can result in a long-term or permanent effect in the organism, with consequences for a number of metabolic, developmental and pathologic processes. The effect may sometimes occur after a long period of latency. Foetal life and infancy are such critical periods in man. Five examples of such programming are described from experiments in rats and baboons, after which the author discusses how nutritional deficiencies in foetal life and in infancy, either alone or combined with other adverse environmental factors, may have important consequences in later life.
Broadly speaking, infant nutrition in Norway is good during the first six months. Fortunately breast feeding is very common. In the second half of the first year, however, our infant nutrition is not quite in accord with recent research. The iron intake is less than recommended, and in many infants the iron status at one year of age is not satisfactory, although serious degrees of iron deficiency anemia are rare. Many infants are given cow's milk from six months of age, and thus receive more protein and electrolytes than desirable. This represents an unnecessary load on metabolism, fluid balance and kidneys, with too high "potential renal solute load". Insulin secretion is stimulated to a higher degree than with breast milk, and there is also some blood loss in the stools. The author emphasizes the importance of essential unsaturated fatty acids, particularly the fatty acids in marine oils (cod liver oil), and proposes a simple and inexpensive adjustment of Norwegian infant nutrition.
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The activities of pyrimidine 5'-nucleotidase (P5N) and the nucleotide pools in the erythrocytes from 19 members of a Dutch family with P5N deficiency were measured. In the erythrocytes of 5 (out of 6) apparent heterozygotes (based on P5N activities), an increased amount of UDP-N-acetylhexosamines was found. This increase was also found in the erythrocytes of 2 (out of 3) questionable heterozygotes (P5N activity below normal range, but not below normal mean--2 X SD) and not in the erythrocytes of family members with a normal P5N activity nor in erythrocytes from healthy donors. We conclude that analysis of the ribonucleotide patterns, in combination with determination of P5N activity, allows a more accurate diagnosis of heterozygosity for P5N.
Two hundred and thirty children with standard risk acute lymphoblastic leukemia (ALL) were diagnosed during a period of 3 years from July 1, 1981 to June 30, 1984 in the five Nordic countries. Criteria for standard risk ALL were age above 2.0 and below 10 years, WBC less than or equal to 20 x 10(9)/l, no evidence of CNS-involvement, mediastinal mass or T- or B-cell leukemia. The children were treated without prophylactic CNS irradiation, the majority (200 patients) according to two treatment programs. Follow-up of the entire group after a minimum of 30 months showed 64% of the children living in complete continuous remission with a probability of event-free survival of 0.60. The treatment results are not entirely satisfactory and intensification of therapy is required. A subgroup of patients with WBC between 10 and 20 x 10(9)/l and with adverse prognosis was identified, justifying a change of the present criteria for risk grouping.
We have fully characterized two alpha thalassaemia mutants that occur in Southeast Asia, - -THAI and - -FIL. Each mutant is due to a deletion that removes the entire zeta-alpha-globin gene complex. Localization of the 5' breakpoints described here, allows the identification of unique fragments that are specific for each of the two mutations. This information can be used to assess the frequency of these mutants in Southeast Asia and will be of value in prenatal testing for alpha thalassaemia in this area.
Two siblings with Diamond-Blackfan anaemia (DBA) and several congenital malformations were first treated with corticosteroids and blood transfusions. High steroid doses were needed, but in spite of this haemoglobin values periodically fell below acceptable levels. Cyclosporine was then given in addition to prednisolone. A slow increase in haemoglobin levels was observed over 2-3 months, and the prednisolone doses could be reduced gradually. Two short communications in the literature report similar experiences. Cyclosporine could be tried in DBA when reasonable corticosteroid doses do not give a satisfactory response. Since the main effect of cyclosporine is a specific inhibition of T-lymphocytes, the observed therapeutic effect in DBA indicates that T-lymphocytes may play an important role in the pathogenesis of this disease.
In a retrospective study of 84 children with standard-risk acute lymphoblastic leukemia diagnosed in 1981-1986, mean white cell count (mWBC) during maintenance chemotherapy (MT) was found to be significantly related to risk of hematological relapse, giving patients with the higher mWBC the poorer outcome. The only other significant relapse-related risk factor was white-cell count at diagnosis. mWBC was not significantly related to white cell count at diagnosis, sex, age, or dose of methotrexate or mercaptopurine. Patients with low mWBC also had relatively low white-cell counts after cessation of therapy when compared with patients with high mWBC.
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Six hundred and fifty-six children with acute lymphoblastic leukemia (ALL) have been diagnosed in the five Nordic countries (Denmark, Finland, Iceland, Norway and Sweden) during the period from July 1981 through June 1985. Annual incidence of ALL was 3.6/100,000 children aged less than 15 years, with an incidence for males of 3.8 and for females of 3.4 respectively. Half of the children were younger than 5 years of age at diagnosis, with a peak incidence between 2-3 years of age. The leukemias were classified as Standard Risk (SR), Intermediate Risk (IR) or High Risk (HR) leukemia according to prognostic criteria at diagnosis. The remission rate was 95%. In children greater than or equal to 1 year of age with non-B-cell ALL at diagnosis, the Event-Free Survival (EFS) was 0.58; 0.65 for SR-children, 0.51 for IR-children and 0.52 for HR-children. WBC count at diagnosis was the most important prognostic factor and a WBC count of 11-20 X 10(9)/l was associated with the worst prognosis of all WBC values (EFS = 0.30), independent of other prognostic factors. Male sex was the second most important adverse prognostic criterion. The follow-up in January 1986 (observation time 6-54 months), showed that 442 of the 656 children (67%) were in complete continuous remission. The total results indicate a possibility to improve the prognosis for most of the risk groups of ALL with a more intensive treatment.
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One hundred fifty-three children with ALL were diagnosed in Norway in the period August 1975-December 1980. One hundred thirty-two of them received 3 infusions of methotrexate as consolidation therapy combined with methotrexate intrathecally as CNS prophylaxis. Eleven (44%) of the total 25 methotrexate cases with WBC above 50 X 10(9)/L were in CCR after 4 1/2-10 years. Two more cases had discontinued therapy, while in second remission. The event-free survival of all diagnosed 32 children in Norway with WBC above 50 X 10(9)/L was 37%. Seven infants below the age of 1 year are included in the 32 cases.
Because cardiomegaly has been observed in lipodystrophic patients we studied cardiac morphology and function with one- and two-dimensional echocardiography in addition to general cardiologic examination in a series of seven patients. Muscular hypertrophy with increased chamber size and myocardial indentations were found. Two patients had asymmetrical septal hypertrophy (ASH), and two patients demonstrated systolic anterior movement (SAM) of the mitral valve. Wall motion analysis showed anomalities in four patients during contraction, in three during the early relaxation phase. Since pathological findings, probably increasing with age, were made in the majority of the patients, these findings add an additional unfavourable aspect to the syndrome.
A boy, born in 1975, developed severe aplastic anaemia in 1982. Treatment with oxymetholone plus corticosteroids and later bolus methylprednisolone was ineffective. Following a 5-d course with antithymocyte globulin, a partial remission was achieved, but thrombocytopenia necessitating platelet transfusions every 10-14 d persisted. Under treatment with cyclosporine A the thrombocytopenia improved markedly, and there is no need for further transfusions. These observations combined with those reported in another case of aplastic anaemia by Stryckmans et al (1) indicate that cyclosporine A may be of value in some cases of aplastic anaemia.
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