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Abstract: The balance of intimate relationships between plants and seed-eating pollinators can depend on pollinator behaviour in relation to floral characters, such as flower size and flower number. Here, we examined how pollinator oviposition in relation to these traits affected annual fitness (seed output) of single- and multi-flowered Trollius europaeus along altitudinal gradients in subarctic Sweden and the French Alps. Small flies (Chiastocheta spp.) pollinate T. europaeus and their larvae feed on developing seeds. Assuming that late flowers in multi-flowered plants attracted flies to the earliest flower on the same plant, we expected more eggs and higher seed predation in early multiple flowers than in single flowers. Relative seed predation would thereby increase with flower number. Both in Sweden and the Alps, more eggs were placed on large flowers. Early multiple flowers were slightly larger than single flowers, and about twice the size of secondary flowers. As a result, and possibly combined with the effects of secondary flowers, early multiple flowers attracted more ovipositing flies and experienced relatively higher seed predation. However, this did not generally result in higher seed predation of multi-flowered hosts. Multiple flowers had greater seed output than single flowers at all altitudes, also in the high alpine and subarctic sites, where single flowers were more abundant. We hypothesise that the distribution of multiple flowers generally is enforced by environmental factors, rather than by fly-host plant interactions, because only very rarely (in triple-flowered alpine plants) was seed predation disproportionate, and the relationship skewed to the disadvantage of the host. The outcome of the mutualistic interaction was often similar in alpine and subarctic populations, but the underlying factors were different. Subarctic flowers had high abortion and low predation rates, while alpine flowers experienced the reversed situation. The higher fly abundance in the Alps suggests a more intense mutualistic interaction than in Sweden. Despite varying ecological and environmental conditions at these sites, the mutualistic relationship was generally in balance. However, when it was unbalanced, this could be explained by fly behaviour in response to floral traits, and by differences in fly abundance.

Apolipoprotein E polymorphism and the relationships of physical fitness to plasma lipoprotein-lipid levels in men and women. Med. Sci. Sports Exerc.,Vol. 31, No. 5, pp. 692-697, 1999.

Catecholamine-induced lipolysis was investigated in 32 obese subjects (14 men and 18 premenopausal women), aged 36-50 years, whose body mass index ranged from 30 to 42 kg/m(2). Isolated subcutaneous (subc) abdominal and femoral adipocytes were studied before and after a 15-week weight reducing program, during which mean body weight loss averaged 9 vs. 10 kg in women and men, respectively (P < 0.0001). Participants were re-examined when they were weight-stable. Fat cell weight decreased by about 15;-20% in both depots (P values ranging from 0.01 to 0.05). Epinephrine (mixed alpha2-/beta-adrenoceptor (AR) agonist) induced antilipolysis at low concentrations and a net lipolytic response at higher doses, irrespective of subjects' fatness and anatomic location of fat. Basal lipolysis, maximal lipolytic responses to isoprenaline (beta-AR agonist), dobutamine and procaterol (beta1- and beta2-AR agonists, respectively) as well as maximal antilipolytic effects of epinephrine or UK-14304 (alpha2-AR agonist) were similar before and after weight reduction. However, both beta- and beta2-AR lipolytic sensitivities and the beta-AR density were increased in both genders after weight reduction, this effect being more marked in subc abdominal than in femoral adipocytes (P values ranging from 0.001 to 0.05). The alpha2-AR antilipolytic sensitivity was reduced in adipose cells from both regions in women, but only in subc abdominal adipocytes in men (P < 0.05), although the alpha2-AR density remained unchanged after weight reduction. In conclusion, a moderate weight loss leads to a higher adipose cell lipolytic efficiency which is associated with changes at receptor levels (mainly an increased beta2- and a decreased alpha2-AR sensitivities), in both genders.

TREMBLAY, ANGELO, ERIC DOUCET, PASCAL IMBEAULT, PASCALE MAURIÈGE, JEAN‐PIERRE DESPRÉS, AND DENIS RICHARD. Metabolic fitness in active reduced‐obese individuals. Obes Res. Objective: To verify whether a physical activity‐low‐fat diet follow‐up could normalize the metabolic risk profile of reduced‐obese men and women having undergone considerable weight loss through energy restriction and drug therapy. Research Methods and Procedures: Twenty obese individuals (12 men, 8 women) participated in a weight‐reducing program that included two phases. In the first phase, a non‐macronutrient‐specific dietary restriction of about 700 kcal/day was prescribed to induce weight loss over 15 weeks, with either fenfluramine or placebo. The second phase consisted of a physical activity‐low‐fat diet follow‐up that was maintained as long as subjects did not experience resistance to further body weight and fat loss. Resistance to lose fat occurred after a mean cumulative fat loss of 14 and 8 kg in men and women, respectively. Results: Despite this substantial decrease in body fat, subjects' adiposity remained much higher at the end of this protocol than values observed in lean control subjects. However, fasting plasma levels of insulin, cholesterol, high‐density lipoprotein‐cholesterol, low‐density lipoprotein‐cholesterol, and triglyceride as well as the response of insulin and glucose to oral glucose were normalized at the end of the physical activity‐low‐fat diet follow‐up. Discussion: These results indicate that further weight and fat losses may not be justified when a moderate body weight loss resulting in a highly favorable improvement of metabolic risk profile is achieved in patients who would have still been diagnosed as overweight or obese on the basis of criteria currently promoted by public health agencies.

Seven pairs of young adult male identical twins completed a negative energy balance protocol during which they exercised on cycle ergometers twice a day, 9 out of 10 days, over a period of 93 days while being kept on a constant daily energy and nutrient intake. The total energy deficit caused by exercise above the estimated energy cost of body weight maintenance reached 244 ± 9.8 MJ (Mean ± SEM). Baseline energy intake was estimated over a period of 17 days preceding the negative energy balance protocol. Mean body weight loss was 5.0 kg (SEM = 0.6) (p <0.001) and it was entirely accounted for by the loss of fat mass (p <0.001). Fat‐free mass was unchanged. Body energy losses reached 191 MJ (SEM = 24) (p <0.001) which represented about 78% of the estimated energy deficit. Subcutaneous fat loss was slightly more pronounced on the trunk than on the limbs as estimated from skinfolds, circumferences, and computed tomography (CT). The reduction in CT‐assessed abdominal visceral fat was quite striking, from 81 cm2(SEM = 5) to 52 cm2(SEM = 6) (p <0.001). At the same submaximal power output level, subjects oxidized more lipids than carbohydrates after the program as indicated by the changes in the respiratory exchange ratio (p <0.05). Intrapair resemblance was observed for the changes in body weight (p <0.05), fat mass (P <0.01), percent fat (p <0.01), body energy content (p <0.01), sum of 10 skinfolds (p <0.01), abdominal visceral fat (p <0.01), fasting plasma triglycerides (p <0.05) and cholesterol (p <0.05), maximal oxygen uptake (p <0.05), and respiratory exchange ratio during submaximal work (p <0.01). We conclude that even though there were large individual differences in response to the negative energy balance and exercise protocol, subjects with the same genotype were more alike in responses than subjects with different genotypes particularly for body fat, body energy, and abdominal visceral fat changes. High lipid oxidizers and low lipid oxidizers during sub‐maximal exercise were also seen despite the fact that all subjects had experienced the same exercise and nutritional conditions for about three months.

Several investigations have suggested that body fat distribution is influenced by nonpathologic variations in the responsiveness to Cortisol. Genetic variations in the glucocorticoid receptor (GRL) could therefore potentially have an impact on the level of abdominal fat. A restriction fragment length polymorphism (RFLP) has previously been detected with the BelI restriction enzyme in the GRL gene identifying two alleles with fragment lengths of 4.5 and 2.3 kb. This study investigates whether abdominal fat areas measured by computerized tomography (CT) are associated with this polymorphism in 152 middle‐aged men and women. The less frequent 4.5‐kb allele was found to be associated with a higher abdominal visceral fat (A VF) area independently of total body fat mass (4.5/4.5 vs. 2.3/2.3 kb genotype; men: 190.7 ± 30.1 vs. 150.7 ± 33.3 cm2, p=0.04; women: 132.7 ± 37.3 vs. 101.3 ± 34.5 cm2, p=0.06). However, the association with AVF was seen only in subjects of the lower tertile of the percent body fat level. In these subjects, the polymorphism was found to account for 41% (p=0.003) and 35% (p=0.007), in men and women, respectively, of the total variance in AVF area. The consistent association between the GRL polymorphism detected with BelI and AVF area suggests that this gene or a locus in linkage disequilibrium with the BelI restriction site may contribute to the accumulation of AVF.

RICE, TREVA, JP DESPRÉS, LOUIS PÉRUSSE, JACQUES GAGNON, ARTHUR S LEON, JAMES S SKINNER, JACK H WILMORE, DC RAO, CLAUDE BOUCHARD. Segregation analysis of abdominal visceral fat: The HERITAGE Family Study. A major gene hypothesis for abdominal visceral fat (AVF) level, both before and after adjustment for total body fat mass, was investigated in 86 white families who participated in the HERITAGE Family Study. In this study, sedentary families were tested for a battery of measures (baseline), endurance exercise trained for 20 weeks, and then remeasured again. The baseline measures reported here are unique in that the variance due to a potentially important environmental factor (activity level) was limited. AVF area was assessed at L4 to L5 by the use of computerized tomography scan, and total body fat mass was assessed with underwater weighing. For fat mass, a putative locus accounted for 64% of the variance, but there was no evidence of a multifactorial component (i.e., no polygenic and/or common familial environmental effects). For AVF area, both a major gene effect accounting for 54% of the variance and a multifactorial component accounting for 17% of the variance were significant. However, after AVF area was adjusted for the effects of total level of body fat, the support for a major gene was reduced. In particular, there was a major effect for fat mass‐adjusted AVF area, but it was not transmitted from parents to offspring (i.e., the three transmission probabilities were equal). The importance of this study is twofold. First, these results confirm a previous study that suggested that there is a putative major locus for AVF and for total body fat mass. Second, the findings from the HERITAGE Family Study suggest that the factors underlying AVF area in sedentary families may be similar to those in the population at large, which includes both sedentary and active families. Whether the gene(s) responsible for the high levels of AVF area is the same as that which influences total body fat content remains to be further investigated.

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BASIC fibroblast growth factor (bFGF)-like localization was studied immunohistochemically in the lower auditory tract of neonatal and adult rats. During the neonatal period, bFGF-like immunoreactivity is present in the cytoplasm of inner hair cells, spiral ganglion cells, Scarpa's ganglion cells, in auditory brain stem nuclei and in vestibular nuclei. At the adult stage, bFGF-like protein is widely distributed in the auditory brain stem but was not found in the cochlea. These results suggest that bFGF could be implicated in the development as well as in the neuronal maintenance and plasticity of the auditory system.

ACSM Position Stand on The Recommended Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory and Muscular Fitness, and Flexibility in Adults. Med. Sci. Sports Exerc.,Vol. 30, No. 6, pp. 975-991, 1998. The combination of frequency, intensity, and duration of chronic exercise has been found to be effective for producing a training effect. The interaction of these factors provide the overload stimulus. In general, the lower the stimulus the lower the training effect, and the greater the stimulus the greater the effect. As a result of specificity of training and the need for maintaining muscular strength and endurance, and flexibility of the major muscle groups, a well-rounded training program including aerobic and resistance training, and flexibility exercises is recommended. Although age in itself is not a limiting factor to exercise training, a more gradual approach in applying the prescription at older ages seems prudent. It has also been shown that aerobic endurance training of fewer than 2 d·wk−1, at less than 40-50% of VO2R, and for less than 10 min−1is generally not a sufficient stimulus for developing and maintaining fitness in healthy adults. Even so, many health benefits from physical activity can be achieved at lower intensities of exercise if frequency and duration of training are increased appropriately. In this regard, physical activity can be accumulated through the day in shorter bouts of 10-min durations.

Most computed tomography (CT) scanners used today are able to accurately measure adipose tissue (AT) areas at any site of the body. However, first generation CT scanners used by some medical centers are not equipped with appropriate software allowing the measurements of AT areas. The aim of this study was to validate a technique of AT area measurements independent from CT scanner software. Abdominal AT areas were recorded with CT in a sample of 30 men. Areas were thereafter calculated using the standard CT software technique. Total and visceral AT areas were then remeasured using another technique for which X‐ray film of each subject's scan was analysed by a system completely independent from the CT scanner (imaging densitometer and NIH image analysis software). Correlations between measurements obtained with the two techniques were very strong for both total (n = 0.99; SEE = 11.7 cm2) and visceral AT areas (r = 0.99; SEE = 5.3 cm2). Values obtained with the image analysis method were generally higher than with the conventional CT software technique (cross‐sectional areas of AT were overestimated by 4.7% for total abdominal and 8.5% for visceral AT respectively). In conclusion, the results indicate that measurements obtained with this image analysis technique would be adequate to correctly rank subjects according to levels of total or visceral AT areas. However, since this method appears to slightly overestimate AT areas, a standardized correction should be performed before comparing subjects with AT areas measured with this technique to subjects whose AT areas have been obtained with the conventional CT software technique. Am. J. Hum. Biol. 11:61–68, 1999. © 1999 Wiley‐Liss, Inc.

Using the technique of homologous recombination in embryonic stem cells, we generated mice bearing a targeted disruption of the gene encoding the neurofilament light (NF-L) protein. The absence of NF-L protein in mice resulted in dramatic declines of ≈20-fold in the levels of neurofilament medium and heavy proteins in the brain and sciatic nerve while increases were detected for other cytoskeletal proteins such as tubulin and GAP-43. Despite a lack of neurofilaments and hypotrophy of axons, the NF-L knockout mice develop normally and do not exhibit overt phenotypes. However, in both NF-L −/− and NF-L +/− mice, the regeneration of myelinated axons following crush injury of peripheral nerves was found to be abnormal. In the second week after axotomy, the number of newly regenerated myelinated axons in the sciatic nerve and facial nerve of NF-L −/− mice corresponded to only ≈25 and ≈5% of the number of myelinated axons found in normal mice, respectively. At this early postaxotomy stage, electron microscopy of nerve segments distal to the crush site in NF-L −/− mice revealed abundant clusters of axonal sprouts that were indicative of retarded maturation of regenerating fibers. The analysis of the distal sciatic nerve at 2 months after crush indicated that neurofilament-deficient axons have the capacity to regrow for a long distance and to remyelinate, albeit at a slower rate. These results provide the first direct evidence for a role of neurofilaments in the maturation of regenerating myelinated axons.

The aim of the present study was to investigate the associations between total adiposity, body fat distribution, and plasma lipoprotein levels within groups of women defined on the basis of apolipoprotein E phenotypes, in order to verify whether apoE polymorphism could modify these associations. In women having only apolipoprotein E3 isoforms (n = 24), body fat mass, the waist: hip circumference ratio, and computed tomography-derived total and intra-abdominal fat areas were all positively correlated with very low density lipoprotein (VLDL) and low density lipoprotein (LDL) lipids and apolipoprotein B concentrations. These body fatness variables were also negatively correlated with plasma high density lipoprotein (HDL) cholesterol concentration. These associations were, however, altered in the groups of women carrying either apoE2 or E4 isoforms. Indeed, in women carrying the apoE2 isoform (n = 22), body fatness variables were predominantly associated with VLDL components concentration (0.05 greater than P less than 0.01) and with LDL triglyceride content. No association was found between adiposity and LDL cholesterol or apolipoprotein B levels in these women. In contrast, no relationship was found between total adiposity, regional fat accumulation, and VLDL fraction in women carrying the apolipoprotein E4 isoform (n = 17). In this latter group, computed tomography-measured total abdominal fat accumulation was positively correlated with LDL apolipoprotein B (r = 0.58, P less than 0.05) concentration, whereas intra-abdominal fat accumulation was positively correlated with both LDL cholesterol and apolipoprotein B concentrations (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Amyotrophic lateral sclerosis (ALS) is an adult‐onset neurological disorder of multiple etiologies that affects primarily motor neurons in the brain and spinal cord. Abnormal accumulations of neurofilaments (NFs) in motor neurons and a down‐regulation of mRNA for the NF light subunit (NF‐L) are associated with ALS, but it remains unclear to what extent these NF perturbations contribute to human disease. Transgenic mouse studies demonstrated that overexpression of normal and mutant NF proteins can sometimes provoke a motor neuronopathy characterized by the presence of abnormal NF accumulations resembling those found in ALS. Remarkably, the motor neuronopathy in transgenic mice overexpressing human NF heavy (NF‐H) sub‐units was rescued by the co‐ expression of a human NF‐L transgene at levels that restored a correct stoichiometry of NF‐L to NF‐H subunits. Transgenic approaches have also been used to investigate the role of NFs in disease caused by Cu/Zn superoxide dismutase (SOD1) mutations, which is responsible for ˜2% cases of ALS. Studies with transgenic mice expressing low levels of a fusion NF‐H/lacZ protein, in which NFs are withheld from the axonal compartment, suggested that axonal NFs are not toxic intermediates required for SOD1 ‐mediated disease. On the contrary, overexpression of human NF‐H proteins was found to confer an effective protection against mutant SOD1 toxicity in transgenic mice, a phenomenon that may be due to the ability of NF proteins to chelate calcium. In conclusion, transgenic studies showed that disorganized NFs can sometimes have noxious effects resulting in neuronopathy. However, in the context of motor neuron disease caused by mutant SOD1, there is emerging evidence that NF proteins rather play a protective role.

Obesity is a heterogeneous condition and not every obese patient is at increased risk of cardiovascular diseases (CVD). It is now well established that the regional distribution of body fat is a critical correlate of the metabolic complications of obesity. Studies that have assessed adipose tissue distribution by imaging techniques such as computed tomography have demonstrated the importance of the intra-abdominal (visceral) fat depot as a marker of a cluster of metabolic abnormalities which include glucose intolerance, insulin resistance, hyperinsulinemia, hypertriglyceridemia, elevated number of apo B-carrying lipoproteins as well as hypoalphalipoproteinemia. Although the association between visceral obesity and metabolic complications can hardly be questioned, it has been suggested that it may not necessarily represent a causal relationship. For instance, concomitant alterations in sex steroid levels have been found in both men and women with abdominal (visceral) obesity which have also been reported to be significantly correlated with the insulin resistant-dyslipidemic state found in abdominal obese subjects. In women, abdominal obesity is associated with increased free testosterone concentrations and reduced sex hormone binding globulin (SHBG) levels, whereas in men this condition is associated with reduced testosterone and adrenal C19steroid (dehydroepiandrosterone, androstenedione, androstene-3β, 17β-diol) levels as well as decreased SHBG concentrations. These altered steroid and SHBG levels have been reported to be independent correlates of the metabolic complications of visceral obesity although they cannot solely account for the increased CVD risk found in these patients. In this regard, intervention studies are clearly warranted to better quantify the respective contribution of excess visceral adipose tissue and of the concomitant alterations in sex steroid levels as modulators of metabolic disturbances increasing CVD risk in obesity.Journal of Endocrinology(1996) 150,S155–S164

J.P. Després, C. Bouchard, A. Tremblay, R. Savard, and M. Marcotte. Effects of aerobic training on fat distribution in male subjects. Med. Sci. Sports Exerc., Vol. 17, No. 1, pp. 113–118, 1985. To investigate the effects of aerobic training on adipose tissue morphology and fat distribution, several indicators of body fatness (percent body fat, seven subcutaneous skinfolds, fat cell weight) were assessed in 13 sedentary male subjects (SS) submitted to a 20-wk aerobic training program and in 20 male long-distance runners (LDR). The LDR subjects had a mean ± SD Cmaxof 65.9 ± 6.5 ml±mhr-1·kg-1and averaged 120 km·wk-1. Training increased the O2maxvalues of the SS group significantly (pre: 41.9 ± 7.0 vs post: 53.4 ± 6.4 ml-kg-1min-1; P< 0.001) and decreased significantly percent body fat (P< 0.01), sum of skinfolds (P< 0.01), and fat cell weight (P< 0.05). Trunk skinfolds were more altered by training than extremity skinfolds, with reductions of 22 and 12.5, respectively. Significant correlations were found between fat cell weight and percent body fat in SS before and after training (r= 0.75; P< 0.01), while no significant relationship was noted in the LDR group. Moreover, using the sum of skinfolds divided by percent fat or by fat mass to reflect the proportion of subcutaneous fat to total fat, the LDR subjects exhibited less subcutaneous fat than the SS group (P< 0.01) and training did not alter these ratios in the SS group. These results suggest that 20 wk of aerobic training can alter body fatness in men but that the induced fat loss does not seem to deplete preferentially subcutaneous fat.

This paper reviews the recently published literature on obesity, body fat distribution and lipid metabolism. Studies have emphasized the importance of visceral fat as a correlate of alterations in plasma lipid transport observed in abdominal obesity. Some of the mechanisms in the relation of fat distribution to lipid metabolism have been identified, but additional studies are needed.

OBJECTIVE: To investigate the possibility that leptin levels may be predictive of the risk of ischemic heart disease (IHD) through the relationship of leptin to body fat. RESEARCH DESIGN AND METHODS: The Quebec Cardiovascular Study cohort consisted of 2,103 French-Canadian men without IHD in 1985 who were followed until 1990, by which time 114 had experienced an IHD event. These 114 men were then individually matched for age, BMI, cigarette smoking, and alcohol intake with 114 subjects who were free of IHD at follow-up. After exclusion of diabetic patients and those in whom leptin levels could not be measured, we were able to compare the initial metabolic profiles of 86 men in the IHD group and of 95 control subjects. RESULTS: Plasma leptin concentrations were positively correlated with BMI (r = 0.67, P < 0.0001) and with fasting insulin concentrations (r = 0.46, P < 0.0001) in the overall sample. These significant associations were also observed when men with IHD and the control subjects were examined separately (control subjects: r = 0.68 for BMI and r = 0.45 for insulin; IHD subjects: r = 0.65 for BMI and r = 0.50 for insulin). With the exception of plasma triglyceride (r = 0.25, P < 0.001), no significant association was found between leptin and plasma lipoprotein and lipid concentrations. Furthermore, plasma insulin remained significantly associated with leptin levels even after adjustment for BMI (r = 0.22, P < 0.005). There was no difference in baseline leptin levels among men who developed IHD versus men who remained IHD-free during the 5-year follow-up (5.56 +/- 3.12 vs. 5.36 +/- 2.90 ng/ml, respectively). Thus, although significantly correlated with the BMI and fasting insulin levels, plasma leptin concentration was not a significant predictor of the 5-year incidence of IHD. This lack of a relationship to IHD was noted when leptin levels were analyzed as tertiles and when leptin concentration was analyzed as a continuous variable. CONCLUSIONS: These prospective results suggest that leptinemia, despite being a strong correlate of obesity, does not appear to be an independent risk factor for the development of IHD in men.

Objectives. This study was undertaken to determine whether lipoprotein(a) [Lp(a)] is an independent risk factor for ischemic heart disease (IHD) and to establish the relation of Lp(a) to the other lipid fractions.

Coronary heart disease (CHD) and type 2 diabetes mellitus represent two highly prevalent conditions in affluent societies. Although a dyslipidemic state is frequently found in type 2 patients with obesity, studies have shown that the high triglyceride, low high‐density lipoprotein (HDL) cholesterol dyslipidemia is also found in nondiabetic patients with insulin resistance. Studies that have used imaging techniques to assess the regional distribution of body fat have shown that an excess of visceral adipose tissue, that is, a high accumulation of fat in the abdominal cavity, was associated with a cluster of metabolic disturbances such as insulin resistance, hyperinsulinemia, glucose intolerance, hypertriglyceridemia, elevated apolipoprotein B (apoB) concentrations, small, dense low‐density lipoprotein (LDL) particles, as well as low HDL cholesterol levels. Prospective studies such as the Quebec Cardiovascular Study have shown that this cluster of metabolic abnormalities commonly found in patients with excess visceral adipose tissue substantially increases the risk of CHD. The high prevalence of visceral obesity in sedentary adult men and postmenopausal women is such that it may represent the most prevalent cause of atherogenic dyslipidemic states associated with CHD in our population.

Biopsies of adipose tissue were obtained from two subcutaneous regions (abdominal and femoral) in a sample of 54 men (32 obese and 22 lean subjects). Clonidine-induced antilipolysis in femoral adipose cells was similar in both groups, whereas subcutaneous abdominal adipocytes of obese individuals showed a higher alpha 2-adrenergic response than did subcutaneous abdominal adipose cells from lean subjects. In addition, epinephrine had a biphasic effect in subcutaneous abdominal adipocytes from obese individuals, as it induced antilipolysis at low concentrations, and a net lipolytic response at higher doses. In contrast, the physiological amine promoted lipolysis in subcutaneous abdominal adipose cells of lean subjects. Epinephrine- and clonidine-induced antilipolysis of subcutaneous abdominal adipocytes was positively associated with the level of subcutaneous abdominal fat measured by computed tomography (CT). Finally, men with a high alpha 2-adrenergic response of subcutaneous abdominal fat cells were fatter than those with a low alpha 2-adrenergic component. These results suggest that, in men with a wide range of body fatness, variations in the lipolytic response of subcutaneous abdominal adipose cells to epinephrine appear to involve changes in the functional balance between alpha 2- and beta-adrenoceptors.

We report here an immunohistochemical study of the distribution of intermediate filaments (neurofilament, peripherin) and a microtubules-associated protein, tau, in the human fetal cochlea at 27 weeks of gestation. Neurofilament immunoreactivity (160 and 200 KDa) was localized in afferent and efferent fibers of the cochlear innervation and restricted to a few small spiral ganglion neurons. Peripherin immunoreactivity was specifically distributed in some small ganglion neurons and in their central and peripheral extensions, particularly in fibers reaching the lower part of the outer hair cells. Double immunolabelling studies with these neurofilaments and peripherin antibodies show that only small neuron cell bodies were stained. Morpholometrical data indicate that immunostained neurons could be related to the Type II neuron population in the spiral ganglion. Tau protein was localized in intraganglionic spiral bundle fibers and in fibers that reach the lower part of hair cells. These observations suggest that neurofilament and peripherin antibodies stain a particular population of human spiral ganglion neurons with Type II characteristics. Moreover, the specificity of peripherin labelling in Type II cells and their processes suggest that peripherin could be used as a probe for the developmental study of this system in the human cochlea. On the other hand, tau antibody appeared as a marker for efferent fibers during development and could give information on the ontogenesis of efferent innervation

In order to study human fat cell morphology and metabolism in both sexes, with different levels of fatness and physical training, 53 subjects (14 women and 39 men), 25.9 ± 7.6 (mean ± SD) years of age, weighing 64.8 ± 10.8 kg and with 14.8 ± 4.7% body fat were submitted to a biopsy of subcutaneous adipose tissue in the supra-iliac region. Average fat cell diameter (ACD) was assessed measuring at least 500 cells per subject. Basal (BL), epinephrine sub-maximal (10-5 M) (ESML) and epinephrine maximal (10-4 M) (EML) stimulated lipolysis have been determined on collagenase isolated fat cells. Female subjects have larger ACD (83.4 ± 12.3 μm vs. 62.5 ± 1.9 μm) (P ≤ 0.001) and lower BL, ESML, and EML than men (P ≤ 0.05). After control over age and sex of subjects, there were significant and negative correlations between all fatness indicators (ACD, fat mass in kg, percent body fat, sum of 9 skinfolds) and BL, ESML and EML. A completely randomized factorial ANOVA design revealed a significant effect of fatness level on BL, ESML and EML, but a non-significant trend for the effect of physical training on the same variables. It is concluded that lipolytic activity is more related to body fatness than to the training status. However, training tends to accentuate lipolytic activity as shown values of BL, ESML and EML found in the lean highly trained subjects of the study.

The clinical performance of the Medtronic Intact porcine bioprosthesis was evaluated in 1,084 patients (mean age 66.4 years, range 9 to 91 years) who had a total of 1,099 implantations between 1985 and 1992, inclusive. There were 709 aortic valve replacements, 297 mitral valve replacements, and 80 multiple valve replacements. Concomitant procedures were performed in 432 (39.3%). The age group distribution (years) was 35 or younger in 20 patients, 36 to 50 in 64, 51 to 64 in 274, 65 to 69 in 225, 70 or older in 500. The total follow-up time was 2,741 patient-years (mean, 2.5 years) and was 97.5% complete. The early mortality rate was 7.1% and late mortality was 3.9% per patient-year. The overall patient survival at 7 years was 70% ± 3%. The freedom from major thromboembolism was 94% ± 1% at 7 years (p= not significant for valve positions). The freedom from reoperation at 7 years was 93% ± 1%; freedom from valve-related mortality was 89% ± 2%. The freedom from structural valve deterioration at 7 years was 97% ± 1% (aortic valve replacement 97% ± 1%; mitral valve replacement 97% ± 2%). The freedom from structural valve deterioration among age groups was not different for the overall population, aortic valve replacement, or mitral valve replacement. Hemodynamic assessment revealed obstructive properties for aortic valve replacement sizes of 21 and 23 mm and for mitral valve replacement sizes of 25 and 27 mm. The Medtronic Intact porcine bioprosthesis shows excellent freedom from structural failure at 7 years for all valve positions and age groups, but obstructive properties for small aortic and mitral valve sizes.

The yellow fever virus (YFV) cDNA segment coding for the part of the precursor polyprotein generating the structural proteins C (capsid), prM (precursor to the membrane protein M), and E (envelope) was expressed in vitro by using the T7 promoter-polymerase transcription system coupled to translation in rabbit reticulocyte lysates. A polypeptide of the expected molecular weight was observed to accumulate in the assay and was processed into proteins C, prM, and E only when dog pancreas microsomal membranes were added to the translation system. Proteins prM and E were translocated inside the endoplasmic reticulum, where prM underwent glycosylation. Regions essential for translocation of these proteins were localized to the 18- and 15-amino-acid C-terminal hydrophobic regions of proteins C and prM, respectively. Translocation of protein prM appeared to be less efficient than that of protein E. Maturation of these proteins followed different kinetics, indicating that the prM signal is probably cleaved off more slowly. A polypeptide composed of proteins C and prM, similar to the NVx polypeptide described in yellow fever virus-infected cells, was also produced in the in vitro system in the presence of membranes. No mature protein M was detected, suggesting that the cleavage of prM to M is a late processing event mediated by a protease different from endoplasmic reticulum signalases.

The concentrations of cefamandole, cloxacillin and fusicid acid were measured in the serum and heart tissue of 100 recipients of these drugs before cardiac surgery. During cardiopulmonary bypass, mean (+/- standard deviation) peak concentrations in serum of all patients were 63.0 +/- 34.0 micrograms of cefamandole per ml, 30.8 +/- 17.7 micrograms of cloxacillin per ml, and 32.4 +/- 10.8 micrograms of fusidic acid per ml. Mean (+/- standard deviation) concentrations in atrial appendages taken 1 h (+/- 15 min) after infusion were 21.3 +/- 11.0 micrograms of cefamandole per g, 23.8 +/- 17.3 micrograms of cloxacillin per g, and 10.7 +/- 4.2 micrograms of fusidic acid per g. No cloxacillin could be detected in 5 of 39 heart specimens. Mean tissue-to-serum ratios at 1 h for cefamandole, cloxacillin, and fusidic acid were respectively 0.35, 0.73, and 0.33. Fusidic acid, a drug which is highly effective in vitro against both methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis, was detectable in heart tissue in concentrations which were 12 times higher than the MICs of this agent against these resistant microorganisms.

This article presents an experiment of expertise capitalization in road traffic‐accident analysis. We study the integration of models of expertise from different members of an organization into a coherent corporate expertise model. We present our elicitation protocol and the generic models and tools we exploited for knowledge modeling in this context of multiple experts. We compare the knowledge models obtained for seven experts in accidentology and their representation through conceptual graphs. Finally, we discuss the results of our experiment from a knowledge capitalization viewpoint.

Strategies to measure metabolomics data in large cohorts capture not only genetic information, but also lifestyle habits and clinical outcomes, which could contribute to the identification of genetic and lifestyle biomarkers. Such an approach might pave the way for the development of personalized lifestyle medicine.

The Look AHEAD trial did not show that a lifestyle modification programme aimed at weight loss could reduce the incidence of cardiovascular disease events. We attempt to address why this trial was 'negative', and emphasize that further randomized lifestyle modification trials focusing on the effects of physical activity and exercise are needed.

Studies published in 2012 in the field of HDL research have provided further evidence suggesting that a low HDL-cholesterol level, in the absence of related lipid or nonlipid risk factors, is not associated with increased risk of coronary heart disease.

To evaluate the cardiometabolic outcomes associated with discordant visceral adipose tissue (VAT) and liver fat (LF) phenotypes in 2 cohorts.