Evaluation of reduced-tillering (tin) wheat lines in managed, terminal water deficit environments.

Small or shrivelled wheat kernels (screenings) that reduce crop value are commonly produced in terminal drought environments. The aim of this study was to establish whether the incorporation of the tiller inhibition (tin) gene would contribute to maintenance of kernel weight and reductions in screenings under terminal water deficit. Five Silverstar near-isogenic lines contrasting in high and low tiller potential and their recurrent Silverstar parent were established at two plant densities under managed terminal water deficit (mild and severe) and irrigated conditions. With irrigation (grain yield of 5.6 t ha(-1)), kernels of all lines weighed ~31 mg, with restricted-tillering (R-tin) lines producing an average 15% lower grain yield. Under both mild and severe terminal water deficit (4.1 t ha(-1) and 2.8 t ha(-1)), free-tillering lines had relatively high screenings ranging from 11.9% to 16.2%. Compared with free-tillering lines, R-tin lines maintained large kernel weight (~29 mg kernel(-1)) and had 29% and 51% fewer screenings under the two stresses, and a significantly greater (+11%) grain yield under mild stress. Higher kernel weights in tin lines were realized even with the greater kernel number per spike. The higher kernel weight of the R-tin lines under stress conditions was associated with greater anthesis biomass and increased stem water-soluble carbohydrates, ensuring more assimilate for later translocation to filling grain. The incorporation of the tin gene into genetic material adapted to the target environments provides scope for improvement in both grain yield and kernel weight, and a reduction in screenings in terminal water deficit environments.

Objective assessment of telesurgical robot systems: Telerobotic FLS.

The Society of American Gastrointestinal Endoscopic Surgeons (SAGES) Fundamentals of Laparoscopic Surgery (FLS) program contains curriculum that includes both a cognitive and psychomotor skills. In this research the use of FLS Block Transfer task is used to evaluate the performance of surgeons' teleoperating the University of Washington Surgical robot. The use of the FLS Trainer Box and accessories kit provides a well-defined series of tasks that can be repeated by any researchers working in the field of surgical robotics so that systems can be evaluated using a common method.

Effect of hemodialysis on left ventricular function. Dissociation of changes in filling volume and in contractile state.

Prior studies of the effect of hemodialysis on left ventricular function have not distinguished between the removal of uremic toxins and the change in cardiac filling volume. To separate these effects, left ventricular function was examined by serial echocardiography in five stable hemodialysis patients before and after three different dialysis procedures: (a) hemodialysis with volume Loss, (b) ultrafiltration (volume loss only), and (c) hemodialysis without volume loss. The patients were similarly studied under control conditions and after increased (5 degrees of head-down tilt for 90 min) and decreased (lower body negative pressure) cardiac filling volume. After hemodialysis with volume loss, end-diastolic volume (EDV) decreased from 167 to 128 ml (P less than 0.001) and end-systolic volume (ESV) decreased from 97 to 51 ml (P less than 0.001) without a change in stroke volume (SV). Ejection fraction increased from 42 to 52% (P less than 0.001) and mean velocity of circumferential fiber shortening (VCF) increased from 0.61 to 1.04 circumferences (circ)/s (P less than 0.001). After ultrafiltration, EDV decreased from 167 ml to 124 ml (P less than 0.001) and SV from 73 ml to 39 ml (P less than 0.001), without significant changes in ESV or VCF. In contrast to the maneuvers in which volume loss occurred, after hemodialysis without volume loss ESV decreased from 95 to 66 ml (P less than 0.001) and SV increased from 74 ml to 97 ml (P less than 0.001) without changes in EDV. EF increased from 44 to 59% (P less than 0.001) and VCF increased from 0.64 to 1.26 circ/s (P less than 0.001). Ventricular function curves plotted from data obtained under conditions of altered cardiac filling volume before and after the three dialysis maneuvers demonstrate that ultrafiltration produced a pure Frank-Starling effect, while hemodialysis with or without volume loss produced a shift in the ventricular function curves, which demonstrated an increase in the contractile state of the left ventricle. The changes in left ventricular function produced by regular hemodialysis are the combined effects of a decrease in EDV and an increase in the contractile state of the left ventricle.

Influence of acute myocardial depression on left ventricular stiffness and its elastic and viscous components.

The influence of acute myocardial depression on ventricular stiffness and on its elastic and viscous components was studied in 19 dogs. After the animals were placed on cardiopulmonary bypass, stiffness was measured by sinusoidally injecting volume changes of 0.5 ml (deltaV) at 22 Hz into paced, isovolumically (deltaP) of the sinusoidal pressure response. Stiffness was linearly related to pressure (P) throughout the cardiac cycle, so that deltaP/delta V = alpha P + beta, where alpha and beta are constants. Myocardial depression was induced in one of three different ways: by coronary artery ligation, by administration of propranolol (Inderal), or by administration of pentobarbital. All three interventions caused significant increases in the slope, alpha, of the stiffness-pressure relationship, while the intercept, beta, remained unchanged. Release of the coronary occlusion or administration of acetylstrophantidin partially reversed depression and the change in alpha; Approximation of the mechanical nature of the left ventricle in terms of a linear second-order mechanical system permitted the division of stiffness into its elastic and viscous components. Like total stiffness, both the elastic and the viscous components were linearly related to ventricular pressure. Elastic stiffness was not changed, but the slope of the line relating viscous stiffness to pressure was significantly increased during ischemic depression, indicating that a change in viscosity was primarily responsible for the increase in total ventricular stiffness.

Telesurgery via Unmanned Aerial Vehicle (UAV) with a field deployable surgical robot.

Robotically assisted surgery stands to further revolutionize the medical field and provide patients with more effective healthcare. Most robotically assisted surgeries are teleoperated from the surgeon console to the patient where both ends of the system are located in the operating room. The challenge of surgical teleoperation across a long distance was already demonstrated through a wired communication network in 2001. New development has shifted towards deploying a surgical robot system in mobile settings and/or extreme environments such as the battlefield or natural disaster areas with surgeons operating wirelessly. As a collaborator in the HAPs/MRT (High Altitude Platform/Mobile Robotic Telesurgery) project, The University of Washington surgical robot was deployed in the desert of Simi Valley, CA for telesurgery experiments on an inanimate model via wireless communication through an Unmanned Aerial Vehicle (UAV). The surgical tasks were performed telerobotically with a maximum time delay between the surgeon's console (master) and the surgical robot (slave) of 20 ms for the robotic control signals and 200 ms for the video stream. This was our first experiment in the area of Mobile Robotic Telesurgery (MRT). The creation and initial testing of a deployable surgical robot system will facilitate growth in this area eventually leading to future systems saving human lives in disaster areas, on the battlefield or in other remote environments.

Optimization of a spherical mechanism for a minimally invasive surgical robot: theoretical and experimental approaches.

With a focus on design methodology for developing a compact and lightweight minimally invasive surgery (MIS) robot manipulator, the goal of this study is progress toward a next-generation surgical robot system that will help surgeons deliver healthcare more effectively. Based on an extensive database of in-vivo surgical measurements, the workspace requirements were clearly defined. The pivot point constraint in MIS makes the spherical manipulator a natural candidate. An experimental evaluation process helped to more clearly understand the application and limitations of the spherical mechanism as an MIS robot manipulator. The best configuration consists of two serial manipulators in order to avoid collision problems. A complete kinematic analysis and optimization incorporating the requirements for MIS was performed to find the optimal link lengths of the manipulator. The results show that for the serial spherical 2-link manipulator used to guide the surgical tool, the optimal link lengths (angles) are (60 degrees, 50 degrees). A prototype 6-DOF surgical robot has been developed and will be the subject of further study.

Control system architecture for a minimally invasive surgical robot.

As the field of surgical robotics continues to evolve, it is important to keep patient safety in mind. This paper describes a safety control architecture aimed at moving an experimental system in the direction of intrinsically safe operation. The system includes safety features such as: a small number of states, Programmable Logic Controller (PLC) state transition control, active enable, brakes, E-STOP, and a surgeon foot pedal.

Hybrid analysis of a spherical mechanism for a minimally invasive surgical (MIS) robot--design concepts for multiple optimizations.

Several criteria exist for determining the optimal design for a surgical robot. This paper considers kinematic performance metrics, which reward good kinematic performance, and dynamic performance metrics, which penalize poor dynamic performance. Kinematic and dynamic metrics are considered independently, and then combined to produce hybrid metrics. For each metric, the optimal design is the one that maximizes the performance metric over a specific design space. In the case of a 2-DOF spherical mechanism for a surgical robot, the optimal design determined by kinematic metrics is a robot arm with link angles (alpha(12)=90 degrees , alpha(23)=90 degrees ). The large link angles are the most dextrous, but have the greatest risk of robot-robot or robot-patient collisions and require the largest actuators. The link lengths determined by the dynamic metrics are much shorter, which reduces the risk of collisions, but tend to place the robot in singularities much more frequently. When the hybrid metrics are used, and a restriction that the arm must be able to reach a human's entire abdomen, the optimal design is around (alpha(12)=51 degrees, alpha(23)=54 degrees). The hybrid design provides a compromise between dexterity and compactness.

A 30-year follow-up of the Dallas Bedrest and Training Study: I. Effect of age on the cardiovascular response to exercise.

BACKGROUND: Cardiovascular capacity declines with aging, as evidenced by declining maximal oxygen uptake (VO(2)max ), with little known about the specific mechanisms of this decline. Our study objective was to assess the effect of a 30-year interval on body composition and cardiovascular response to acute exercise in 5 healthy subjects originally evaluated in 1966. METHODS AND RESULTS: Anthropometric parameters and the cardiovascular response to acute maximal exercise were assessed with noninvasive techniques. On average, body weight increased 25% (77 versus 100 kg) and percent body fat increased 100% (14% versus 28%), with little change in fat-free mass (66 versus 72 kg). On average, VO(2)max decreased 11% (3.30 versus 2.90 L/min). Likewise, VO(2)max decreased when indexed to total body mass (43 versus 31 mL. kg(-1). min(-1)) or fat-free mass (50 versus 43 mL/kg fat-free mass per minute). Maximal heart rate declined 6% (193 versus 181 bpm) and maximal stroke volume increased 16% (104 versus 121 mL), with no difference observed in maximal cardiac output (20.0 versus 21.4 L/min). Maximal AV oxygen difference declined 15% (16.2 versus 13.8 vol%) and accounted for the entire decrease in cardiovascular capacity. CONCLUSIONS: Cardiovascular capacity declined over the 30-year study interval in these 5 middle-aged men primarily because of an impaired efficiency of maximal peripheral oxygen extraction. Maximal cardiac output was maintained with a decline in maximal heart rate compensated for by an increased maximal stroke volume. Most notably, 3 weeks of bedrest in these same men at 20 years of age (1966) had a more profound impact on physical work capacity than did 3 decades of aging.

A 30-year follow-up of the Dallas Bedrest and Training Study: II. Effect of age on cardiovascular adaptation to exercise training.

BACKGROUND: Aerobic power declines with age. The degree to which this decline is reversible remains unclear. In a 30-year longitudinal follow-up study, the cardiovascular adaptations to exercise training in 5 middle-aged men previously trained in 1966 were evaluated to assess the degree to which the age-associated decline in aerobic power is attributable to deconditioning and to gain insight into the specific mechanisms involved. Methods and Results-- The cardiovascular response to acute submaximal and maximal exercise were assessed before and after a 6-month endurance training program. On average, VO(2max) increased 14% (2.9 versus 3.3 L/min), achieving the level observed at the baseline evaluations 30 years before. Likewise, VO(2max) increased 16% when indexed to total body mass (31 versus 36 mL/kg per minute) or fat-free mass (44 versus 51 mL/kg fat-free mass per minute). Maximal heart rate declined (181 versus 171 beats/min) and maximal stroke volume increased (121 versus 129 mL) after training, with no change in maximal cardiac output (21.4 versus 21.7 L/min); submaximal heart rates also declined to a similar degree. Maximal AVDO(2) increased by 10% (13.8 versus 15.2 vol%) and accounted for the entire improvement of aerobic power associated with training. CONCLUSIONS: One hundred percent of the age-related decline in aerobic power among these 5 middle-aged men occurring over 30 years was reversed by a 6-month endurance training program. However, no subject achieved the same maximal VO(2) attained after training 30 years earlier, despite a similar relative training load. The improved aerobic power after training was primarily the result of peripheral adaptation, with no effective improvement in maximal oxygen delivery.

Effects of static and rhythmic twitch contractions on the discharge of group III and IV muscle afferents.

Although both static and rhythmic twitch contractions of the hindlimb muscles of anaesthetised cats have been shown to reflexly evoke pressor responses, the increase in arterial pressure evoked by the former type of contraction has been shown to be substantially larger than that evoked by the latter. We have therefore recorded the impulse activity of single group III and IV muscle afferents, whose activation reflexly increases arterial pressure, while we both statically and rhythmically twitch-contracted the triceps surae muscles of anaesthetised cats. We found that group III afferents (n = 17) discharged significantly more impulses in response to static contraction than in response to rhythmic contraction. By contrast, group IV afferents (n = 18) fired approximately the same number of impulses in response to the two types of contraction. In addition, we found that many of the group III but only a few of the group IV afferents displayed discharge properties suggestive that these afferents were mechanoreceptors. We conclude that the discharge of group III afferents are likely to be responsible for the difference in the magnitudes of the reflex pressor responses evoked by static and rhythmic contraction.

Selenoenzyme expression in thyroid and liver of second generation selenium- and iodine-deficient rats.

The stimulation of thyroid hormone synthesis in iodine deficiency may increase the requirement for the selenoproteins which are involved in thyroid hormone synthesis in the thyroid gland. Selenoenzyme activity and expression were investigated in the thyroid and liver of second generation selenium-and/or iodine-deficient rats. Selenium deficiency caused substantial decreases in hepatic selenium-containing type I iodothyronine deiodinase (ID-I) and cytosolic glutathione peroxidase (cGSHPx) activities and mRNA abundances, but phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activity was only 55% of selenium-supplemented control levels, despite the absence of change in its mRNA abundance. Selenoenzyme mRNA concentrations were maintained at control levels in thyroid glands from the selenium-deficient rat pups. Despite this, a differential effect was observed in selenoenzyme activities: ID-I activity was decreased to 61%, cGSHPx activity to 45% and phGSHPx to 29% of that in selenium-adequate controls. In iodine-deficient thyroid glands, mRNA levels were increased 2.2, 5.0 and 2.8 times for ID-I, cGSHPx and phGSHPx respectively. ID-I and cGSHPx enzyme activities were also increased but the activity of phGSHPx was decreased despite the high mRNA abundance. Thyroid selenoprotein mRNA levels were also increased in combined selenium and iodine deficiency but again there were differential effects on enzyme activities, with ID-I activity increased, cGSHPx unchanged and phGSHPx decreased. Thus, iodine deficiency may produce an oxidant stress on the thyroid gland, increasing the requirement for selenium to maintain selenoenzyme activity. When dietary supplies of selenium are limiting, thyroid selenoprotein mRNA levels are increased to compensate for overall lack of the micronutrient. Furthermore, there is a preferential supply of available selenium to ID-I and cGSHPx to allow maintenance of thyroid function.

Selenoprotein expression and brain development in preweanling selenium- and iodine-deficient rats.

Selenium deficiency causes further impairment of thyroid hormone metabolism in iodine-deficient rats and therefore could have a role in the aetiology of both myxoedematous and neurological cretinism in humans. Thyroidal type I iodothyronine deiodinase (ID-I), cytosolic glutathione peroxidase and phospholipid hydroperoxide glutathione peroxidase activities were increased in iodine-deficient adult rats and their offspring at 11 days of age. Thyroidal ID-I activity was unchanged and thyroidal cytosolic glutathione peroxidase activity was decreased by more than 75% by combined selenium and iodine deficiency in 11-day-old rats, indicating that, while the thyroid retained an ability to produce 3,3',5-triiodothyronine (T3), the gland was probably more susceptible to peroxidative damage caused by increased hydrogen peroxide concentrations driven by increased thyrotrophin. Thyroidal atrophy, common in myxoedematous cretinism, did not occur in iodine- or selenium and iodine-deficient rat pups. Iodine deficiency increased brain type II iodothyronine deiodinase activity 1.5-fold in 4-day-old rats and 3-fold in 11-day-old rats, regardless of selenium status. Thus rats were able to activate compensatory mechanisms in brain that would maintain T3 concentrations in selenium and iodine deficiencies. Surprisingly, however, selenium deficiency had a greater effect than iodine deficiency on markers of brain development in rat pups. Expression of the brain-derived neurotrophic factor (BDNF) mRNA was decreased in selenium deficiency in 4- and 11-day-old pups and in combined selenium and iodine deficiency in 4-day-old pups. Iodine deficiency caused an increase in BDNF expression in 11-day-old pups but had no effect on 4-day-old pups. Myelin basic protein mRNA expression in brain was decreased by combined selenium and iodine deficiency in 11-day-old rats.

Contraction-sensitive skeletal muscle afferents inhibit arterial baroreceptor signalling in the nucleus of the solitary tract: role of intrinsic GABA interneurons.

Arterial baroreceptor and skeletal muscle receptor afferents relay sensory information to the nucleus of the solitary tract (NTS) during exercise. Previous studies have suggested that skeletal muscle afferent input inhibits baroreflex function; however, detailed information on the role of muscle afferents and GABAergic mechanisms in the NTS is limited. Furthermore, identification of specific afferent modalities that activate GABAergic neurons in the NTS remains unknown. In the present study, we examined the neuroanatomical and physiological interactions between spinal dorsal horn cells that transmit contraction-sensitive input from skeletal muscle and GABAergic interneurons in the NTS. Biotinylated dextran amine (BDA, 10%, 25-100 nL) microinjection into dorsal horn of the cervical spinal cord was combined with glutamate decarboxylase (GAD) immunohistochemistry to visualize the nature of the relationship of BDA-labeled fibers in the NTS with GAD immunoreactivity (GAD-ir). BDA-labeled axons and terminal processes were localized in the medial, commissural, dorsomedial and dorsolateral subdivisions of the caudal NTS. Moreover, BDA-labeled fibers were observed in close proximity to GAD-ir structures throughout these regions of the NTS. The physiological interaction between skeletal muscle receptor and arterial baroreceptor afferents was investigated using an arterially perfused, decerebrate rat preparation. Activation of skeletal muscle afferents by electrically evoked twitch contraction of the forelimb attenuated baroreflex responsiveness (BR, calculated as the ratio of changes in heart rate to systemic pressure) from -1.5+/-0.3 bpm.mm Hg(-1) to -0.1+/-0.1 bpm.mm Hg(-1) (control versus contraction, P<0.05, n=15). However, forelimb contraction failed to inhibit the reflex bradycardia evoked by activation of peripheral chemoreceptor afferents, indicating a reflex-specific action. Bilateral microinjection of bicuculline methiodide (BIC, 10 microM, 40-60 nL) into the caudal NTS restored baroreflex responsiveness during contraction (-1.6+/-0.2 versus -0.1+/-0.1 versus -1.5+/-0.2 bpm.mmHg(-1), control versus contraction versus contraction+BIC P<0.05, n=8). We conclude that activation of ascending spinal neurons from the cervical dorsal horn by contraction-sensitive skeletal muscle afferents selectively inhibits arterial baroreceptor signaling in the NTS via activation of a GABAergic mechanism.

Cardiovascular control during exercise: central and reflex neural mechanisms.

Both reflex neural and central command mechanisms have been postulated to explain the cardiovascular responses that occur during exercise. The 2 mechanisms appear to affect the same neural circuits and to be capable of working either in conjunction with one another or independently.

Left ventricular mass as determined by magnetic resonance imaging in male endurance athletes.

Although many studies of the effect of dynamic exercise training on left ventricular (LV) mass have been reported, controversy continues to exist. Previous work has been criticized because of the techniques used for measuring LV mass, the variable level of training of the subjects recruited and the methods used to normalize the data. In an attempt to resolve this controversy, LV mass was determined using the very accurate and reproducible technique of magnetic resonance imaging (MRI). Highly trained competitive athletes including cross-country skiers, endurance cyclists and long distance runners (VO2max = 77 +/- 1, 72 +/- 2 and 75 +/- 2 ml (kg X min)-1, respectively) were examined. The data were normalized for body weight, body surface area and lean body mass. LV mass was significantly greater in skiers (239 +/- 9 g), runners (244 +/- 10 g) and cyclists (258 +/- 11 g) when compared with nonathletic control subjects (189 +/- 6 g) (p less than 0.001), which represents percent differences of 26, 29 and 37%, respectively. LV mass remained greater in the athletes, regardless of the method used to normalize the data. In addition, there was a good correlation between LV mass and VO2max (r = 0.80, p less than 0.001). It was concluded that LV mass is significantly greater in highly trained competitive endurance athletes and that normalizing LV mass with respect to body weight, body surface area or lean body mass does not alter this relation.

Ventricular performance in human hearts aged 61 to 73 years.

The effects of increasing and decreasing cardiac preload by 15% on the left ventricular (LV) performance of 11 carefully screened normal subjects aged 61 to 73 years were examined. Comparisons were made with 11 subjects aged 21 to 28 years. Two-dimensional echocardiograms were obtained before and at the termination of 5 degrees of head-down tilt for 90 minutes and at the termination of graded lower body negative pressure to -40 mm Hg. Heart rates and blood pressures were unchanged after physiologic interventions. Changes in LV end-diastolic and stroke volumes were similar but of a smaller magnitude in the older subjects compared with changes in younger subjects. When LV end-diastolic volumes obtained at each extreme of preload variation were compared, the range of mean change was less in the older (23 ml, 26%) than in the younger subjects (31 ml, 41%). Control LV end-diastolic and end-systolic volumes were greater in the older subjects. This study shows that despite larger control LV volumes, alterations in preload produce changes in the LV end-diastolic and stroke volumes of these older subjects that conform to the normal LV function curve, but that these responses are diminished compared with changes in younger subjects, suggesting an age-related change in diastolic stiffness.

Effect of increasing heart rate on left ventricular performance in patients with normal cardiac function.

The influence of an increase in heart rate on left ventricular (LV) contractile performance was assessed in patients with normal LV function. In 19 patients (3 men, 16 women) ages 55 +/- 9 years (mean +/- standard deviation) with normal global and segmental LV function and normal coronary arteries, LV dP/dt max was measured at baseline heart rate and during atrial pacing at baseline +5, baseline +25 and baseline +45 beats/min. In 10 of the patients, intravascular volume was not altered during pacing and, as a result, echocardiographically measured LV end-diastolic dimension decreased (5.4 +/- 0.4 at baseline vs 4.9 +/- 0.5 cm at baseline +45 beats/min, p less than 0.05). In these patients, LV dP/dt max increased modestly (1,571 +/- 237 at baseline vs 1,760 +/- 199 mm Hg/s at baseline +45 beats/min, p less than 0.05). In the other 9 patients, intravascular volume was expanded rapidly (by saline infusion) during pacing and, as a result, LV end-diastolic dimension was held constant (5.2 +/- 0.6 at baseline vs 5.1 +/- 0.6 cm at baseline +45 beats/min, difference not significant). In these patients, LV dP/dt max increased substantially with pacing (1,505 +/- 228 at baseline vs 2,050 +/- 258 mm Hg/s at baseline +45 beats/min, p less than 0.05). Thus, an increase in heart rate induces a modest increase in LV dP/dt max in patients in whom LV preload (as reflected by end-diastolic dimension) is allowed to decrease; in contrast, it causes a marked increase in LV dP/dt max in those in whom LV preload is maintained constant.

Left ventricular dimensions and mass using magnetic resonance imaging in female endurance athletes.

Few published studies of left ventricular (LV) mass in female endurance athletes have been performed with M-mode echocardiography, which involves assumptions of LV geometry. Therefore, magnetic resonance imaging, a 3-dimensional technique, was used to examine LV mass, LV end-diastolic volume and mean wall thickness in female long distance runners (n = 13; mean age 29 years), cyclists (n = 12; mean age 26 years) and cross-country skiers (n = 11; mean age 24 years), and the findings were compared with sedentary control subjects (n = 10; mean age 27 years) matched for height and body weight. The physical characteristics for all subjects included height (mean 166 cm, and body weight (mean 56 kg). The percent body fat (mean 11.7) and maximal oxygen uptake (VO2max, mean 63 ml.kg-1.min-1) were similar (p greater than 0.05) among all athletic groups, but significantly different from the control group (body fat, mean 22.5%; VO2max, mean 35 ml.kg-1.min-1). LV mass (mean 159 kg), LV end-diastolic volume (mean 122 ml), and mean wall thickness (mean 11.5 mm) were also similar among the athletic groups and significantly larger than the following control values: LV mass (mean 115 g), LV end-diastolic volume (mean 93 ml) and mean wall thickness (mean 9.8 mm). Ratios of LV mass to lean body weight were similar among all athletic groups, although athletic groups had larger ratios (p less than 0.05) than the sedentary control subjects. LV mass/LV end-diastolic volume ratio was similar (p greater than 0.05) among all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Selenium and iodine deficiencies: effects on brain and brown adipose tissue selenoenzyme activity and expression.

Adequate dietary iodine supplies and thyroid hormones are needed for the development of the central nervous system (CNS) and brown adipose tissue (BAT) function. Decreases in plasma thyroxine (T4) concentrations may increase the requirement for the selenoenzymes types I and II iodothyronine deiodinase (ID-I and ID-II) in the brain and ID-II in BAT to protect against any fall in intracellular 3,3',5 tri-iodothyronine (T3) concentrations in these organs. We have therefore investigated selenoenzyme activity and expression and some developmental markers in brain and BAT of second generation selenium- and iodine-deficient rats. Despite substantial alterations in plasma thyroid hormone concentrations and thyroidal and hepatic selenoprotein expression in selenium and iodine deficiencies, ID-I, cytosolic glutathione peroxidase (cGSHPx) and phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activities and expression remained relatively constant in most brain regions studied. Additionally, brain and pituitary ID-II activities were increased in iodine deficiency regardless of selenium status. This can help maintain tissue T3 concentrations in hypothyroidism. Consistent with this, no significant effects of iodine or selenium deficiency on the development of the brain were observed, as assessed by the activities of marker enzymes. In contrast, BAT from selenium- and iodine deficient rats had impaired thyroid hormone metabolism and less uncoupling protein than in tissue from selenium- and iodine-supplemented animals. Thus, the effects of selenium and iodine deficiency on the brain are limited due to the activation of the compensatory mechanisms but these mechanisms are less effective in BAT.