Effect of Physical Training on Hemodynamic Response during Submaximal and Maximal Exercise in 11–13-Year Old Boys

Nine healthy boys, mean age 11.7 years (11.0–13.0), height 150.4 cm and weight 45.1 kg, were examined with determinations of maximal oxygen uptake (1.85 1×min^-1), heart volume (499 ml) and total hemoglobin (391 g). Cardiac output was determined at rest and during exercise, including maximal exercise, using the dye-dilution technique and i.a. pressures were recorded. Cardiac output was approximately 2 1×min^-1 lower and the systemic a-v oxygen difference (AVD) was correspondingly higher than for young adult men at the same sub-maximal oxygen uptake. At maximal exercise cardiac output was 12.5 1×min^-1, stroke volume 67 ml, AVD 14.2 ml × 100 ml^-1, systolic, diastolic and mean blood pressure 160, 71 and 105 mm Hg respectively and total peripheral resistance 8.6 mm Hg×1–¹×min. After a training period of 4 months a normal increase in height was found in all boys, but body weight was unchanged. Maximal oxygen uptake increased to 2.21 1×min^-1 (p < 0.01), almost entirely due to increased stroke volume (80 ml), resulting in a maximal cardiac output of 14.6 1×min^-1. No significant increase in AVD was found. Mean blood pressure at maximal exercise increased significantly, total peripheral resistance was unchanged. Both heart volume and total hemoglobin showed minor increases, but the changes found were not significantly larger than expected from body growth. The hemoglobin concentration was normal (13 g%) for the age and unaffected by training.     

Enzyme Activities and Muscle Strength after “Sprint Training” in Man

Sprint type strength training was performed 3–4 times a week for 8 healthy male students (16–18 yrs). The training was carried out on a treadmill at high speed and with high inclination. Muscle biopsies were obtained from vastus lateralis before and after the training period for histochemical classification of slow and fast twitch muscle fibres and for biochemical determination of metabolites and enzyme activities. Muscle fibre type distribution was unchanged. whereas fibre area indicated an increase for both fibre types in 3 subjects after training. The muscle enzyme activities of Mg²⁺ stimulated ATPase, myokinase and creatine phosphokinase increased 30, 20, and 36 percent, pespectively. Muscle concentration of ATP and creatine phosphate (CP) did not change with training. Sargent's jump increased with on average 4 cm (from 47 to 51 cm), maximal voluntary contraction (MVC) with 19 kp (from 165 to 184 kp), andurance at 50 percent of MVC with 9 s (from 47 to 56 s), respectively. After training all subjects showed a gain in body weight (mean 1.4 kg) and in thigh circumference (mean 1.5 cm) indicating a larger leg muscle volume and consequently also an increase in total ATP and CP.     

Effect of Strength Training on Enzyme Activities and Fibre Characteristics in Human Skeletal Muscle

Progressive strength training was performed 3 times a week for 8 weeks by 14 healthy male students (19–31 yrs). The training program consisted mainly of dynamic exercises for the leg extensors with maximal or close to maximal loads. The training caused significant improvements in dynamic and isometric strength. One repetition maximum in squats increased with 67%, Sargent jump with 22%, and maximal voluntary isometric contraction (MVC) with 13 %, respectively. Body weight and leg muscle circumferences remained unchanged after training, whereas total body potassium, lean body mass and calculated total muscle mass increased, suggesting a change in body composition with training. Muscle biopsies were obtained from vastus lateralis for fibre analyses and determination of enzyme activities. There were no changes in muscle fibre composition or fibre area with training. The activities of Mg²⁺ stimulated ATPase, creatine phosphokinase and phosphofructokinase remained unchanged, whereas myokinase activity was increased after training (from 1.41 to 1.52 moles × 10^-4× g^-1× min^-1, p > 0.05). After training significant correlations (p > 0.01) were demonstrated between Mg²⁺ stimulated ATPase activity and % fast twitch fibres (% FT) (r = 0.67), as well as between myokinase activity and % FT (r=0.86).     

Learned persistence at 11–12 days but not at 10–11 days in infant rats

In 2 experiments using milk-suckling from an anesthetized dam as the reinforcer, evidence is presented that the transitional age in rat pups for learning of persistence as a result of appetitive partial reinforcement is between 11 and 12 days of age. In Experiment I, pups 12–13 days of age showed the partial reinforcement extinction effect (PREE) whereas 10–11-day olds did not. In Experiment II, pups trained at 11–12 days and tested at Day 13 did show a PREE at Day 13 but those trained at 10–11 days did not.     

t(10;11)(p13–14;q14–21): A New Recurrent Translocation in T-Cell Acute Lymphoblastic Leukemias

A workshop held by the ?Groupe Français de Cytogénétique Hématologique”? has identified a t( 10; 11)(p13–14;q14–21) in four acute lymphoblastic leukemias of T-cell lineage. The immunophenotypes were consistent with immature thymocytes. This translocation is therefore a new candidate for a recurrent translocation in early T-cell leukemia. A similar translocation has been reported as a rare change in early pre-B lymphoid leukemias and also in myeloid leukemias. It is not known whether the similar cytogenetic changes involve different molecular breakpoints or whether the same rearrangement affects a multipotential stem cell capable of lymphoid and myeloid differentiation.     

Deletion of chromosome 15 (q11 – 13) in a Prader-Labhart-Willi syndrome clinic population

Deletion of the long arm of chromosome 15 has recently been reported in a number of patients with the Prader-Labhart-Willi syndrome who were studied with prometaphase banding. We performed cytogenetic analysis on 12 patients with this disorder in whom the clinical diagnosis was certain. A specific cytogenetic anomaly, del(15q11 – 13) was found in all of the 12 patients. In nine of the 12, the deletion was noted in all cells examined; in two, there was mosaicism, some cells having the deletion and others being normal; one patient had a 7;15 translocation. No clinical differences were evident between individuals with mosaicism for the translocation and those with the typical deletion in all cells examined. The finding that all of our patients with Prader-Labhart-Willi syndrome have a cytogenetic anomaly, with some patients having mosaicism, distinguishes the results of this study from those of previous reports. Prometaphase chromosome analysis is recommended in all individuals clinically suspected of having Prader-Labhart-Willi syndrome and should be considered in hypotonic infants without a specific diagnosis.     

Genetic linkage analysis of schizophrenia using chromosome 11q13–24 markers in Israeli pedigrees

It is generally agreed that there is a genetic component in the etiology of schizophrenia which may be tested by the application of linkage analysis to multiply-affected families. One genetic region of interest is the long arm of chromosome 11 because of previously reported associations of genetic variation in this region with schizophrenia, and because of the fact that it contains the locus for the dopamine D2 receptor gene. In this study we have examined the segregation of schizophrenia with microsatellite dinucleotide repeat DNA markers along chromosome 11q in 5 Israeli families multiply-affected for schizophrenia. The hypothesis of linkage under genetic homogeneity of causation was tested under a number of genetic models. Linkage analysis provided no evidence for significant causal mutations within the region bounded by INT and D11S420 on chromosome 11q. It is still possible, however, that a gene of major effect exists in this region, either with low penetrance or with heterogeneity. © 1995 Wiley-Liss, Inc.     

Presence of antibodies to human papillomavirus virus-like particles (VLPs) in 11–13-year-old schoolgirls

To allow meaningful approaches to vaccine development, it is important to know the extent of exposure to human papillomavirus (HPV) within the general population, and particularly the age at which the at risk population is infected. The humoral response to human papillomavirus is directed largely to conformationally-dependent epitopes on the whole virion. Virus-like particles (VLPs) of HPV types 1, 2, and 16 were produced using a baculovirus expression system, and were used in the intact state as antigen in an indirect ELISA. Anonymised serum samples from a cohort of Edinburgh schoolgirls were tested for the presence of IgG antibodies directed against the VLPs. The reproducibility of the ELISA was assured by repeated testing of control samples, and by testing all samples in duplicate and, where possible, on several occasions. Of 1,192 tested with the HPV16 VLPs, 90 (7.6%) were classified as clearly positive, and a further 87 (7.3%) were positive but close to the cutoff calculated by comparison with a group of consistently negative sera. Antibodies to HPV2 were detected in 37.5% (407/1,139) and antibodies to HPV 1 in 51.9% (558/1,076) of the schoolgirls. Antibodies to both HPV1 and HPV2 were found frequently, being present in 29.7% (295/993) of samples tested; 40 samples had antibodies to all three types. The significance of these results is discussed. J. Med. Virol. 56:210–216, 1998. © 1998 Wiley-Liss, Inc.     

Maternal origin of 15q11–13 deletions in Angelman syndrome suggests a role for genomic imprinting

Six persons with the classical Angelman syndrome (AS) phenotype and de novo deletions of chromosome 15q11-q13 were studied to determine the parental origin of the chromosome deletion. Four of the 6 patients had informative cytogenetic studies and all demonstrated maternal inheritance of the deletion. These findings, together with other reported cases of the origin of the chromosome 15 deletion in AS, suggest that deletion of the maternally contributed chromosome leads to the AS phenotype. This contrasts with the Prader-Willi syndrome (PWS) in which a similar deletion of the paternally contributed chromosome 15 is observed. In deletion cases, a parental gamete effect such as genomic imprinting may be the best model to explain why apparently identical 15q11-q13 deletions may develop the different phenotypes of AS or PWS.