Association between fibrinogen levels and insulin resistance.
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Biomedical subjects
Publications and source records attributed to J Mercier.
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Orthodontic preparation before orthognatic surgery must straighten teeth alignment to enable correct adaptation of the upper and lower arches. It must also rectify dento-alveolar abnormalities partially responsible for the dysmorphosis and which can hinder smooth articulation of the bones. Thus before and after the operation, the orthodontist will have to prepare and monitor the surgical splints used in posterior deficiencies.
Since iron deficiency is associated with abnormal erythrocyte rheology, we investigated relationships between plasma ferritin and blood rheology in 36 male elite sportsmen (age: 22.38+/-0.9 years). On the whole, ferritin was negatively correlated with blood viscosity (r = -0.36, p < 0.05). When 23 subjects with low ferritin levels suggesting mild iron deficiency were compared with 13 matched sportsmen with normal ferritin levels, iron-deficient sportsmen were shown to have a higher blood viscosity at 1000 s(-l) (3.17+/-0.09 vs. 2.85+/-0.06 mPas, p < 0.05), explained by a higher plasma viscosity (1.38+/-0.02 vs. 1.31+/-0.02 mPa s, p < 0.05), while hematocrit and RBC rigidity index Tk were similar in the two groups. RBC aggregability index M (4.59+/-0.58 vs. 2.95+/-0.43 mPas, p < 0.05) and M1 (8.46+/-0.58 vs. 6.07+/-0.55, p < 0.01) were higher in iron-deficient subjects. Serum zinc was lower in iron-deficient sportsmen (0.73+/-0.02 vs. 0.83+/-0.02 mg/l, p < 0.01), but the score of early signs of overtraining was higher in this group (10.84+/-1.61 vs. 4.08+/-1.11, p < 0.01). These data suggest that mild iron deficiency as commonly seen in athletes, before anemia occurs, is associated with an increase in plasma viscosity and RBC aggregation, together with an increased subjective feeling of exercise overload.
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While it is well established that blood viscosity is decreased in sportsmen and related to fitness, the involvement of fibrinogen in this relationship is less well defined. Relationships among fitness, rheology and fibrinogen were investigated in 32 football players (age 17-33 years: 19 professionals and 13 leisure players). A submaximal 25 min exercise-test was performed and allowed the calculation of aerobic working capacity. Aerobic working capacity (W170 and VO2 max) was negatively correlated to fibrinogen (r = -0.531, p < 0.01 and r = -0.623, p < 0.01), while on the whole sample the correlation to viscosity and erythrocyte aggregation was not significant. When subjects were divided into two subgroups according to their plasma fibrinogen concentration, the aerobic working capacity (either expressed as W170 or VO2 max) is higher when plasma fibrinogen level is lower than 2.7 g/l. Thus, there is a highly significant negative correlation between fibrinogen and fitness in these sportsmen, independent of blood rheology. These data suggest that rheology and fibrinogen are to some extent separate determinants of an individual's fitness.
A genomic clone of RbcS was isolated from an alfalfa (Medicago sativa L. cv. Apica) genomic library and characterized. Although this clone has structural features similar to a functional gene, the second exon is interrupted by a stop codon and thus is not fully translatable in the plant. Sequence analysis of the 5' and 3' noncoding regions of RbcSK-1A showed a high sequence homology to the flanking sequences of the RbcS-3A gene from pea. The regions of homology contain many important cis-regulatory elements shown to be essential for regulation of the RbcS-3A gene in pea. The promoter of this alfalfa rubisco clone was used in a translational fusion to test its ability to control the expression of the GUS reporter gene in an homologous nuclear background. High levels of GUS enzyme activity were recorded. These strong levels are comparable to some exceptionally high levels produced in other studies following the use of photosynthesis gene promoters in fusions with the GUS reporter gene.
We studied genotype-phenotype correlations in a group of 100 patients with typical Friedreich ataxia (FRDA), and in three groups of patients with atypical clinical presentations, including 44 Acadian FRDA, 8 late-onset FRDA (LOFA), and 6 FRDA with retained reflexes (FARR). All patients, except 3 with typical FRDA, carried two copies of the FRDA-associated GAA triplet repeat expansion. Overall, the phenotypic spectrum of FRDA appeared to be wider than defined by the currently used diagnostic criteria. Our study indicated the existence of several sources of variability in FRDA. Patients with larger GAA expansions tended to have earlier onset and were more likely to show additional manifestations of the disease. Mitotic instability of the expanded GAA repeats may partially account for the limited degree of correlation between expansion sizes as determined in lymphocytes and clinical parameters. Some clinical variants associated with specific FRDA haplotypes, such as Acadian FRDA and FARR, turned out to be unrelated to expansion sizes. No polymorphism in the frataxin coding sequence could be associated with these clinical variants.
We investigated metabolic and hormonal responses during repeated bouts of brief and intense exercise (a force-velocity test; Fv test) and examined the effect of glucose ingestion on these responses and on exercise performance. The test was performed twice by seven subjects [27 (2) years] according to a double-blind randomized crossover protocol. During the experimental trial (GLU), the subjects ingested 500 ml of glucose polymer solution containing 25 g glucose 15 min before starting the exercise. During the control trial (CON), the subjects received an equal volume of sweet placebo (aspartame). Exercise performance was assessed by calculating peak anaerobic power (W(an,peak)). Venous plasma lactate concentration increased significantly during the Fv test (P < 0.001), but no difference was found between CON and GLU. Blood glucose first decreased significantly from the beginning of exercise up to the 6-kg load (P < 0.001) and then increased significantly at W(an,peak) and for up to 10 min during the recovery period (P < 0.001) in both CON and GLU. Insulin concentrations decreased significantly in both groups, but were higher at W(an,peak) in GLU compared with CON (P < 0.05). Glucagon and epinephrine did not change significantly in either group, but epinephrine was significantly lower in GLU after glucose ingestion (P < 0.05) and at W(an,peak) (P < 0.05). W(an,peak) was not significantly different between CON and GLU. In conclusion, blood glucose and insulin concentrations decreased during repeated bouts of brief and intense exercise, while blood lactate concentration increased markedly without any significant change in glucagon and epinephrine concentrations. Glucose ingestion altered metabolic and hormonal responses during the Fv test, but the performance as measured by W(an,peak) was not changed.
The aims of the present study were: (1) to assess aerobic metabolism in paraplegic (P) athletes (spinal lesion level, T4-L3) by means of peak oxygen uptake (VO2peak) and ventilatory threshold (VT), and (2) to determine the nature of exercise limitation in these athletes by means of cardioventilatory responses at peak exercise. Eight P athletes underwent conventional spirographic measurements and then performed an incremental wheelchair exercise on an adapted treadmill. Ventilatory data were collected every minute using an automated metabolic system: ventilation (l x min[-1]), oxygen uptake (VO2, l x min[-1], ml x min[-1] x kg[-1]), carbon dioxide production (VCO2, ml x min[-1]), respiratory exchange ratio, breathing frequency and tidal volume. Heart rate (HR, beats x min[-1]) was collected with the aid of a standard electrocardiogram. VO2peak was determined using conventional criteria. VT was determined by the breakpoint in the VCO2 - VO2 relationship, and is expressed as the absolute VT (VO2, ml x min[-1] x kg[-1]) and relative VT (percentage of VO2peak). Spirometric values and cardioventilatory responses at rest and at peak exercise allowed the measurement of ventilatory reserve (VR), heart rate reserve (HRr), heart rate response (HRR), and O2 pulse (O2 P). Results showed a VO2peak value of 40.6 (2.5) ml x min(-1) x kg(-1), an absolute VT detected at 23.1 (1.5) ml x min(-1) x kg(-1) VO2 and a relative VT at 56.4 (2.2)% VO2peak. HRr [15.8 (3.2) beats min(-1)], HRR [48.6 (4.3) beat x l(-1)], and O2 P [0.23 (0.02) ml x kg(-1) x beat(-1)] were normal, whereas VR at peak exercise [42.7 (2.4)%] was increased. As wheelchair exercise excluded the use of an able-bodied (AB) control group, we compared our VO2peak and VT results with those for other P subjects and AB controls reported in the literature, and we compared our cardioventilatory responses with those for respiratory and cardiac patients. The low VO2peak values obtained compared with subject values obtained during an arm-crank exercise may be due to a reduced active muscle mass. Absolute VT was somewhat comparable to that of AB subjects, mainly due to the similar muscle mass involved in wheelchair and arm-crank exercise by P and AB subjects, respectively. The increased VR, as reported in patients with chronic heart failure, suggested that P athletes exhibited cardiac limitation at peak exercise, and this contributed to the lower VO2peak measured in these subjects.
PURPOSE: The authors analyze the advantages and disadvantages of mandibular reconstruction with a fibula free flap in a retrospective study of 29 cases, and make comparisons with the iliac free flap and the lateral brachial free flap. MATERIAL AND METHODS: Twenty-nine patients (22 male, 7 female) aged 5 to 70 years were studied. Functional and esthetic evaluations were performed together with radiologic examination of the bony calluses. RESULTS: The fibula free flap has advantages for mandibular reconstruction, such as the length of bone available, low morbidity of the donor site, and the possibility of using a skin paddle. However, there is the disadvantage of not being able to reconstruct large soft tissue defects. In addition, bone vascularization is reduced when a large number of osteotomies are required. CONCLUSION: This reconstruction technique is satisfactory for mandibular defects measuring over 20 cm.
The aim of this mixed cross-sectional longitudinal study covering a total age range of 11-17 years, i.e. the entire pubertal growth period, was (1) to specify the changes in maximal breathing pattern during incremental exercise; (2) to determine what parts of the changes are due to anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength; and (3) to determine if the role of these variables is identical before, during and after pubertal growth spurt. This study was conducted in 44 untrained schoolboys separated into three groups, with an initial age of 11.2 +/- 0.2 years for group A, 12.9 +/- 0.25 years for group B, and 14.9 +/- 0.26 years for group C. These children were subsequently followed for 3 years, during the same time period each year. The maximal inspiratory and expiratory pressures (PI max and PE max) were used as an index of the respiratory muscle strength. During an incremental exercise test, maximal ventilation (VE max), tidal volume (VT max), breathing frequency (fmax), inspiratory and expiratory times (tI max and tE max) and mean inspiratory flow (VT/tI max) were measured at maximal oxygen uptake (VO2max). Our study showed that there was a marked increase with age in VE max, VT max, and VT/tI max, and no significant changes in fmax, tI max and tE max. PI max and PE max showed a general trend towards an increase between 11 and 17 years. The study of the linear correlations between maximal breathing pattern and the anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength showed that, in the three groups of children, (1) lean body mass was the major determinant of VE max, VT max and VT/tI max and the relationships were significantly different before, during and after the pubertal growth spurt; (2) physical fitness was the main determinant of tI max, tE max and fmax before and after the pubertal growth spurt; and (3) maximal respiratory strength did not play a significant role. In conclusion, this mixed cross-sectional longitudinal study showed, at maximal exercise, a significant increase in VE max during growth due only to a significant increase in VT max and VT/tI max, and that the relationships of anthropometric characteristics and physical fitness with maximal breathing pattern change during growth.
Whole-mount immunocytochemistry was used to map the location of FMRFamide-like peptides in the crayfish (Procambarus clarkii) stomatogastric nervous system. This system contains the pyloric and gastric mill central pattern generators, which receive modulatory inputs from projection neurons with somata located primarily in other ganglia of the stomatogastric nervous system. Our studies revealed stained somata in the commissural and esophageal ganglia. A pair of stained somata was located in the inferior ventricular nerve, and another pair of somata was located in the stomatogastric nerve where it is joined by the two superior esophageal nerves. The stomatogastric ganglion contained no stained somata, but the neuropil was brightly stained and 2-4 axons projected laterally in small nerves directly from the ganglion. These results indicate that FMRFamide or related peptides may act as neuromodulators in the crayfish stomatogastric nervous system. To test this hypothesis, we studied the effects of FMRFamide and four related peptides (DF2, NF1, F1 and LMS) on the pyloric motor pattern. DF2, NF1 and F1 all excited certain pyloric cells, especially the lateral pyloric (LP) and ventricular dilator (VD) neurons, and enhanced pyloric cycling frequency in most actively rhythmic preparations. FMRFamide had no detectable effects on pyloric cells, and LMS had inhibitory effects, causing disruption of the pyloric rhythm in actively cycling preparations and reducing tonic activity in non-rhythmic preparations.
The authors present a case of osteoma of the tongue. This tumor was discovered without any functional symptom. Surgical resection with histological examination gives the diagnostic. This choristoma is rare, benign and clinically poor. Osteoma of the tongue is a heterotopic bone tissue and his main differential diagnosis are lingual thyroid and thyroglossal cyst. There are several opinions concerning the histogenesis of this choristoma, but an embryological anomaly is probable. Surgical removal of the tumor is curative, without any reported local recurrence.
During muscular exercise, adenosine triphosphate (ATP) must be resynthesized in order to allow subsequent muscle contraction. ATP can be immediately resynthesized from adenosine diphosphate (ADP) and from creatine phosphate (CP). However, such resynthesis from phosphorylated compounds is not possible in very short-duration exercise. For further exercise an energy source, mainly carbohydrates and lipids, is needed. While anaerobic (glycolysis and glycogenolysis) and aerobic (mitochondrial oxidation) pathways are used for carbohydrates, lipids can only undergo oxidation. Carbohydrates are used preferentially with rising exercise intensity because of increased muscle uptake, progressive recruitment of type II fibers and catecholamine release. Lipid oxidation rises with the duration of exercise and falls with increasing intensity. The observation that training plays an important role in the use of these energy substrates has led to the development of the crossover theory by which the use of carbohydrates and lipids in all individuals depends at all times on the combined effect of training and exercise intensity. Training facilitates lipid oxidation but, by allowing higher intensity, also implies inevitable use of carbohydrates. Thus there is an exercise level, or a crossover point, at which carbohydrate energy predominates over lipid energy. Beyond this point, increasing energy requirements are satisfied by preferential use of carbohydrates. Finally, although it was incorrectly thought that proteins play a very minor role, actually amino acids coming from the voluminous tissue mass provide an important source of energy during prolonged exercise.
The main objective of the maximal exercise test is to measure a patient's exercise limit and to identify the cause. The test to be interpreted is evaluated first by judging exercise tolerance on the basis of maximal oxygen consumption (VO2max or symptom-limited VO2(VO2 SL). Intolerance is moderate if VO2 is under 85% of the theoretical level and severe when it is under 60%. Interpretation then consists in identifying the cause of the limitation. Ventilatory reserve is the main element for determining whether the limitation is due to ventilatory or cardiac impairment. In case of a ventilatory limitation, ventilatory reserve falls and the ventilatory pattern and gasometric values orient the diagnosis to emphysema, diffuse interstitial lung disease or bronchopneumopathy. If the ventilatory reserve rises, the limitation has cardiac as origin and in this case the oxygen pool is decreased. Persistence of chronotrope reserve can indicate coronary artery disease while the VD/VT ratio is useful for differentiating cardiac and vascular limitations. Peripheral limitations usually produce an early major increase in blood lactate, a high lactate/pyruvate ratio, with lactate or ventilatory thresholds under 40% of theoretical VO2max, especially in case of muscle pain and low watt equivalent. Nevertheless, these parameters cannot be used to confirm a precise diagnosis. The only positive diagnosis given by the exercise test concerns glycogenolysis disorders (por example McArdle's disease) seen as a total absence of increased lactate level. In conclusion, the exercise test is a means of assessing a patient's exercise tolerance and provides arguments for determining the origin of the limitation. However, as no one argument is truly pathognomonic, the diagnosis hypothesis must be based on all the elements available from clinical examination and complementary explorations.
The gene for Friedreich ataxia (FRDA), an autosomal-recessive neurodegenerative disease, remains elusive. The current candidate region of about 150 kb lies between loci FR2 and F8101 near the D9S15/D9S5 linkage group at 9q13-21.1. Linkage homogeneity between classical FRDA and a milder, slowly progressive Acadian variant (FRDA-Acad) has been demonstrated. An extended D9S15-D9S5 haplotype (C6) predominates in FRDA-Acad chromosomes from Louisiana. We studied 10 Acadian families from New Brunswick, Canada. In eight families, affected individuals conformed to the clinical description of FRDA-Acad; in one, 2 sibs presented with spastic ataxia (SPA-Acad). In the last family, 2 sibs had FRDA-Acad, and one had SPA-Acad. We found that SPA-Acad is linked to the FRDA gene region. The C6 haplotype and a second major haplotype (B7) were identified. The same ataxia-linked haplotypes segregated with both FRDA-Acad and SPA-Acad in two unrelated families. The parental origins of these haplotypes were different. Our observation of different phenotypes associated with the same combination of haplotypes may point to the influence of the parent of origin on gene expression, indicate the effect of modifier genes, or reflect the presence of different mutations on the same haplotypes. Our findings underline the need to investigate families with autosomal-recessive ataxias for linkage to the FRDA region, despite lack of key diagnostic manifestations such as cardiomyopathy or absent deep-tendon reflexes.
Nager acrofacial dysostosis (NAFD) combines the facial anomalies of mandibulofacial dysostosis (Treacher-Collins-Francescetti) with hypoplastic/aplastic or triphangeal thumbs. The MURCS association consists of Müllerian duct aplasia, renal aplasia, cervicothoracic somite dysostosis with Klippel-Feil anomaly, and often defects of the facio-auriculo-vertebral (Goldenhar) spectrum. We describe a child with NAFD, MURCS anomaly (Klippel-Feil anomaly, vertebral synostoses, left renal agenesis), and left pulmonary agenesis. Our proband appears to express a unique anomaly of blastogenesis, simultaneously affecting the acrorenal, the mandibulofacial, and the cervicothoracic developmental fields, combining clinical manifestations of the MURCS, NAFD, VACTERL, and pulmonary agenesis associations. All anomalies may be traced back to abnormal blastogenesis, occurring during the third or the fourth week of embryonic development, and show that NAFD is a polytopic developmental field defect.