Biomedical subjects

T Wadden

Publications and source records attributed to T Wadden.

6 recordsLinked to original sources

PubMed1998

A neuro-mechanical model of legged locomotion: single leg control.

Most models of legged locomotion have concentrated on properties of either the mechanical or the neural system. Here a combined neuro-mechanical model of stepping in a single leg is presented, as the first step in the process of modeling and building a fast and dynamically stable quadruped. It is based on general principles of legged animals with special reference to vertebrates. The mechanical leg was first studied separately in order to take advantage of its inherent mechanical properties and avoid over-control during stepping generation. As a part of the design strategy it uses elastic actuators to increase shock tolerance and energy efficiency. The neural controller consists of a neural phase generator (NPG), a system of fast feedback pathways, and a single control neuron representing descending drive from higher centers in the brain. Sensory information directly influences the movements through the fast feedback pathways, but also entrains the NPG. The NPG has its own description of the state of the leg, which then enables it to set the feedback pathways so that only actions appropriate for the particular stage of the step cycle are undertaken. This preprogramming benefits from the NPG's ability to filter out any inconsistencies or gaps in the afferent input. In this way the model unites the use of central pattern generators and peripheral feedback systems for the generation of stepping movements. The neuro-mechanical system produced stable stepping patterns over a large velocity range and was adaptable to different body weights and landing from varying heights.

Animals↗

PubMed1998

Tumor necrosis factor-alpha in sera of obese patients: fall with weight loss.

In view of the recent demonstration that obesity in animals and humans is associated with an increase in tumor necrosis factor-alpha (TNFalpha) expression, that this expression falls with weight loss, and that TNFalpha may specifically inhibit insulin action, the possibility that TNFalpha may be a mediator of insulin resistance has been raised. We have undertaken this study to investigate whether serum TNFalpha concentrations are elevated in obese subjects, whether they fall after weight loss, and whether this fall parallels the fall in insulin release after glucose challenge. Obese patients (age range: 25-54, weight mean +/- SD: 96.4 +/- 13.8 kg, body mass index: 35.7 +/- 5.6 kg/m2) were started on a diet program. The mean weight fell to 84.5 +/- 11.3 (P < 0.0001) and body mass index to 31.3 +/- 4.9 (P < 0.0001). Plasma TNFalpha concentrations were markedly elevated in the obese (3.45 +/- 0.16 pg/mL), when compared with controls (0.72 +/- 0.28 pg/mL), and fell significantly (2.63 +/- 1.40 pg/mL) after weight loss (P < 0.02). The magnitude of insulin release after glucose (75 g) challenge (area under the curve) also fell significantly (P < 0.01) after weight loss. The magnitude of weight loss and fall in TNFalpha were related to basal body weight (r = 0.57, P < 0.001) and basal TNFalpha (r = 0.55, P < 0.001) concentrations, respectively, but not to each other or to the glucose-induced insulin release (area under the curve). We conclude that obesity is associated with increased plasma TNFalpha concentrations, which fall with weight loss. Because circulating TNFalpha may mediate insulin resistance in the obese, a fall in TNFalpha concentrations may contribute to the restoration of insulin resistance after weight loss, Thus, TNFalpha may be an important circulating cytokine, which may provide a potentially reversible mechanism for mediating insulin resistance.

Adult↗

PubMed1996

Binge eating disorder and the night-eating syndrome.

OBJECTIVE: To determine in three samples of obese women the prevalence of two eating disorders--binge eating disorder and the night-eating syndrome. METHOD: Interviews utilizing standard criteria. For binge eating disorder: the consumption of large amounts of food in a discrete period of time together with a subjective sense of loss of control and no vomiting or laxative abuse. For the night-eating syndrome: morning anorexia, evening hyperphagia and insomnia. Determining the rate of binging among patients receiving a placebo. SUBJECTS: (1) 102 viewers of a television show describing binge eating disorder; (2) 50 participants in a trial of medication for this disorder and (3) 79 participants in a weight reduction program. RESULTS: In the television sample 19.6% of respondents and in the weight reduction sample 7.6% met criteria for binge eating disorder; all subjects in the medication sample met criteria. During a 4-week placebo period average binge frequency fell from 6.0 to 1.7 binges per week. The night-eating syndrome was manifested by 13.7% of the television sample, 8.9% of the weight reduction sample and 15.0% in the medication trial sample. There was little overlap between the two disorders. CONCLUSIONS: Binge eating disorder is far less frequent than has been believed on the basis of questionnaire studies and it is highly responsive to placebos. Frequency of the night-eating syndrome is comparable to that of binge eating disorder. Future studies should assess binge eating disorder by interview rather than by self-administered questionnaire.

Adult↗

PubMed1993

Binge eating disorder: its further validation in a multisite study.

Binge eating disorder (BED) is a new eating disorder that describes the eating disturbance of a large number of individuals who suffer from recurrent binge eating but who do not regularly engage in the compensatory behaviors to avoid weight gain seen in bulimia nervosa. This multisite study of BED involved 1,785 subjects drawn from 18 weight control programs, 942 subjects from five nonpatient community samples, and 75 patients with bulimia nervosa. Approximately 29% of subjects in weight control programs met the criteria for BED. In the nonpatient community samples BED was more common than purging bulimia nervosa. The validity of BED was supported by its strong association with (1) impairment in work and social functioning, (2) overconcern with body/shape and weight, (3) general psychopathology, (4) significant amount of time in adult life on diets, (5) a history of depression, alcohol/drug abuse, and treatment for emotional problems.

Adolescent↗

PubMed1993

Binge eating disorder should be included in DSM-IV: a reply to Fairburn et al.'s "the classification of recurrent overeating: the binge eating disorder proposal".

Extensive recent research supports a proposal that a new eating disorder, binge eating disorder (BED), be included in DSM-IV. BED criteria define a relatively pure group of individuals who are distressed by recurrent binge eating who do not exhibit the compensatory features of bulimia nervosa. This large number of patients currently can only be diagnosed as eating disorder not otherwise specified (EDNOS). Recognizing this new disorder will help stimulate research and clinical programs for these patients. Fairburn et al.'s critique of BED fails to acknowledge the large body of knowledge that indicates that BED represents a distinct and definable subgroup of eating disordered patients and that the diagnosis provides useful information about psychopathology, prognosis, and outcome (Fairburn, Welch, & Hay [in press]. The classification of recurrent overeating: The "binge eating disorder" proposal. International Journal of Eating Disorders.) Against any reasonable standard for adding a new diagnosis to DSM-IV, BED meets the test.

Anorexia Nervosa↗

PubMed1990

Childhood onset (age less than 10) obesity has high familial risk.

We assessed risk for obesity in 1743 first-degree relatives (parents and siblings) of 566 obese patients at three sites in the USA and one in Argentina. Onset of obesity prior to adulthood, and especially by age 10, significantly increased relative risk (2.14) for obesity in adult first-degree relatives. This increase in risk was consistent across four different patient samples from two different countries. Higher levels of obesity in patients were also associated with increased familial risk. Age of onset of obesity may be used to select obese adults with high genetic loading--an approach that should facilitate the identification of specific genes for human obesity. The enhanced ability to identify persons at high genetic risk for obesity provided by this study should increase the effectiveness of efforts to prevent obesity.

Adolescent↗