Kinetics of hula hooping: an inverse dynamics analysis.

This paper involved a biomechanical analysis of lower limb joint coordination during hula hooping. A lower extremity inverse dynamics model that incorporated kinematic input and force platform data was developed to compute the angular velocities, moments about and powers produced at the lower extremity joints. The abductor moments and powers were discovered to be paramount in maintaining hoop oscillations, as demonstrated consistently in the three study participants. However, hula hooping was demonstrated to be variable in terms of the involvement of flexor and extensor moments and powers of the ankle, knee and hip joints, resulting in the adoption of varying strategies by each of the three participants.

Rehabilitation improves walking kinematics in children with a knee varus: Randomized controlled trial.

BACKGROUND: Previous studies have demonstrated increased medial stresses in knee varus alignment. Selecting a suitable treatment strategy for individuals with knee malalignment should be a priority. OBJECTIVES: We aimed to investigate the effects of a 16-week corrective exercise continuum (CEC) program on 3-D joint angles of the dominant and non-dominant lower limbs in children with genu varus during walking. METHODS: Overall, 28 male children with genu varus (age range 9-14 years) volunteered to participate in this study. They were randomly divided into 2 equal groups (experimental and control). The participants of the experimental group received CEC for 16 weeks. 3-D gait analysis involved using a Vicon Motion System. Paired and independent sample t-tests were used for within- and between-group comparisons, respectively. RESULTS: For the experimental group, comparison of pre- and post-test joint kinematics of the dominant lower limb revealed that CEC decreased the peak ankle dorsiflexion angle by 26% (P=0.020), peak foot internal rotation angle by 53% (P=0.001), peak knee internal rotation angle by 40% (P=0.011), peak hip abduction by 47% (P=0.010), and peak hip external rotation angle by 60% (P=0.001). In contrast, peak knee external rotation angle of the dominant limb was increased after the training program by 46% (P=0.044). For the non-dominant lower limb, CEC decreased the peak ankle inversion by 63% (P<0.01), peak ankle eversion by 91% (P<0.01), peak foot internal rotation by 50% (P<0.01), peak knee internal rotation by 29%; P=0.042), peak hip abduction angle by 38% (P<0.01), and peak hip external rotation angle by 60% (P<0.01). CONCLUSIONS: CEC therapy reduced excessive foot and knee internal rotations as well as excessive hip external rotation during walking in children with genu varus.

Do different methods for measuring joint moment asymmetry give the same results?

Gait asymmetry is defined as a loss of perfect agreement between the dominant and non-dominant lower limbs. Conflicting results from gait asymmetry studies may be due to different definitions of asymmetry, different research methods, and/or different variables and formulas used for asymmetry calculation. As a result, this makes it difficult to compare joint asymmetry values between studies. An accurate and precise understanding of asymmetry during human walking is an important step towards developing enhanced rehabilitation protocols for pathological gait. This study examined bilateral lower extremity joint moment asymmetry during the stance phase of walking using three different methods. Fourteen male children (with flat feet) aged 8-14 years participated in this study. The three-dimensional lower limb kinetics was evaluated during a comfortable gait. Then, right and left lower limb joint moments were used to calculate the joint moment asymmetry via three different methods (Lathrop-Lambach method: equation used by Lathrop-Lambach et al. (2014); Su method: equation used by Su et al. (2015); Nigg method: equation used by Nigg et al. (2013)). Repeated-measures ANOVAs (α = 0.05) were used to compare the values of net joint moment asymmetry calculated by the three methods. The results of the statistical analyses found that the amounts of moment symmetry between limbs calculated by the first two methods were significantly greater than that of using the Nigg method (except for the values of the frontal ankle moment computed by the Lathrop-Lambach method). Furthermore, in comparison of the first two methods, using the Su method showed a reduction in moment asymmetry for all joints and for all moments (p < 0.05). We conclude that, although all of three common methods for determining asymmetry between limbs have documented merit, they sometimes differ dramatically in results.

The effect of time restricted visual sensory input on asymmetry of ground reaction force components in female children.

The association between visual sensory and the asymmetry index of sit-to-stand ground reaction force characteristics is not fully understood. Therefore, the purpose of this study was to investigate asymmetry index of sit-to-stand ground reaction forces, their times-to-peak, vertical loading rate, impulses, and free moment in blind and sighted children. 15 female children with congenital blindness and 30 healthy girls with no visual impairments volunteered to participate in this study. The girls with congenital blindness were placed in one group and the girls with no visual impairments were randomly divided into two groups of 15. The two condition groups consisted of, one eyes open and the other, eyes closed. The participants in the eyes closed group were asked to close their eyes for 20 min before the test, whereas those in the eyes open group kept their eyes open. Kinematic and kinetic data were collected using an eight-camera motion analysis system synchronized with two force plates embedded in the floor. A MANOVA test was run for between-group comparisons. There were no distinctive biomechanical alternations in all axes of ground reaction forces and their times-to-peak, vertical loading rate, impulses and free moments in congenital blindness and eyes closed groups compared with the eyes open group. However, eyes closed was associated with increased total time and second phase duration of sit-to-stand performance by 69% (p = 0.008) and 62% (p = 0.008), respectively. These findings reveal that individuals who are visually restricted in the short term, do not develop stereotypical movement strategies for sit-to-stand.

Adaptation Behavior of Skilled Infant Bouncers: Leg Movements and Mechanisms of Control.

Rhythmic behavior in nonlinear systems can be described as limit cycles or attractors. System perturbations may result in shifts between multiple attractors. We investigated individual cycle-to-cycle leg movement kinematics of three prewalking skilled infant bouncers (10.6 ±0.91 months) during four different spring frequencies (0.9, 1.15, 1.27 and 1.56 Hz). A novel visual analysis phase-plane methodology was introduced to analyze the lower body joint kinematics. It was found that as infants' bounce frequency increased to match the natural frequency of the system, their joint ranges of motion decreased and lower extremity dynamics shifted from forced to simple harmonic motion. All infants produced highly synchronized and coordinated movements, as supported by moderate to high inter- and intralimb correlations. This study extends from previous work (Habib Perez et al., 2015) by focusing on the lower extremity kinematic movements, joint coordination and the occurrence of different movement patterns for individual bounce cycles over four spring conditions.

Nutrition and somatomedin XXIX. Molecular regulation of IGFBP-1 in hepatocyte primary culture.

The insulinlike growth factors (IGFs) circulate in association with insulinlike growth factor binding proteins (IGFBPs) that modulate IGF action, but mechanisms of IGFBP regulation are poorly understood. We investigated the regulation of IGFBPs in primary cultures of rat hepatocytes, measuring the appearance of export proteins by ligand blotting after separation via SDS/PAGE, and evaluating mRNA with cDNA probes. Northern blotting studies revealed that IGFBP-1 was expressed at high levels in cultured hepatocytes, in which sustained release of both insulinlike growth factor I and albumin marks preservation of differentiated status. In contrast, transcripts of IGFBP-3 and IGFBP-2 were not detected. Release of IGFBP-1 was unaffected by exposure to glucose (20-500 mg/dl) or to provision of amino acids (0.25-6.25 times normal rat arterial plasma levels). Hormonal studies revealed little effect of glucagon, inhibition by insulin, stimulation by dexamethasone, and blunting of dexamethasone effects by added insulin. Adding dexamethasone provided progressive stimulation: 5-, 11-, and 26-fold at 10(-9), 10(-8), and 10(-7) M, all P less than 0.01; increases in IGFBP-1 protein (ligand blot) and IGFBP-1 mRNA (Northern blot) were highly correlated (r = 0.62, P less than 0.001). In contrast, adding insulin resulted in progressive suppression of both IGFBP-1 protein and IGFBP-1 mRNA, 43% at 10(-10) M, 74% at 10(-9) M, and 83% (maximal) at 10(-8) M; ED50 of approximately 10(-10) M is within the physiological range of insulin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of insulin-like growth factor-I (IGF-I) and IGF-binding protein 1 gene transcription by hormones and provision of amino acids in rat hepatocytes.

Synthesis of insulin-like growth factor-I (IGF-I) and IGF binding protein-1 (IGFBP-1) is altered in diabetes and malnutrition, but underlying processes are poorly understood. To study molecular mechanisms, we examined regulation of IGF-I and IGFBP-1 gene transcription in primary cultures of rat hepatocytes. Transcription of the IGF-I and IGFBP-1 genes was measured as incorporation of [alpha-32P]UTP into preinitiated message in isolated nuclei. IGFBP-1 gene transcription was not sensitive to reduction in amino acid concentration from 5x to 0.5x rat arterial plasma levels. However, IGF-I gene transcription fell 60-70% in response to reduced provision of amino acids. Culture with 10(-9) M insulin lowered IGFBP-1 gene transcription 50% below control levels (10-11 M) but did not affect IGF-I gene transcription; 10(-6) M insulin raised IGF-I gene transcription 2-fold. After an acute reduction in insulin concentration, IGFBP-1 transcription began to rise within 30 min, but IGF-I gene transcription was unchanged over 120 min. Similarly, 3-6 h were required for stimulation of IGF-I gene transcription by insulin, but a 40% decrease in IGFBP-1 gene transcription could be detected within 15 min after adding 10(-6) M insulin, and suppression of IGFBP-1 transcription by insulin was unaffected by the presence of cycloheximide. Effects of insulin on IGFBP-1 gene transcription were not mimicked or antagonized by phorbol ester.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth hormone modulates insulin regulation of hepatic insulin-like growth factor binding protein-1 transcription.

Hepatic transcription of insulin-like growth factor-binding protein-1 (IGFBP-1) is enhanced in hypophysectomized (hypox) rats and can be rapidly down-regulated by GH administration. Here we examined the effect of insulin on IGFBP-1 messenger RNA abundance in hypox rats and the effects of insulin and GH on IGFBP-1/chloramphenicol acetyltransferase (CAT) reporter plasmids transiently transfected into isolated hepatocytes from pituitary-intact and hypox rats. Unlike GH, administration of insulin to hypox rats in doses of 10 or 50 micrograms/100 g BW had no effect on hepatic IGFBP-1 messenger RNA abundance. Insulin at 10(-7) M resulted in a 42.1 +/- 9.8% suppression of CAT activity in hepatocytes from pituitary-intact animals transfected with a CAT reporter plasmid containing 1671 bp of the 5'-flanking region of the rat IGFBP-1 gene. In the same assay, GH at a concentration of 2.3 x 10(-8) M significantly reduced CAT activity. In contrast, insulin had no effect on CAT activity in hepatocytes from hypox rats, whereas GH resulted in comparable suppression of CAT activity in hepatocytes from hypox rats and pituitary-intact rats, 13.6 +/- 2.3% vs. 18.2 +/- 3.2%. Deletional analysis and mobility shift assays were used to identify the GH-responsive regions in the IGFBP-1 gene. GH suppression of CAT activity was lost when the IGFBP-1 5'-flanking region was deleted down to -277 bp, whereas insulin suppression was retained for all but the smallest fragment of the IGFBP-1 gene. Mobility shift assays were used to compare nuclear extracts from sham-operated, hypox, and GH-treated hypox rats. When hepatic nuclear extracts from hypox rats were incubated with the -277 to -82 and the -556 to -368 bp fragments, retarded bands were apparent that were not present in the extracts from sham-operated rats. GH treatment of hypox rats 15 or 30 min before death completely normalized the retardation pattern seen with the -277 to -82 bp fragment, but did not affect the pattern seen with the -556 to -368 bp fragment. A 20-bp fragment corresponding to the previously identified insulin response element, -108 to -89 bp, was also analyzed. An additional retarded band, not seen with nuclear extracts from sham-operated rats, was apparent when nuclear extracts of hypox rats or GH-treated hypox rats were used. These data provide the first in vitro evidence that GH directly regulates transcription of IGFBP-1 expression. In addition, our findings suggest that GH modulates insulin regulation of IGFBP-1 transcription, possibly by altering the milieu of trans-acting factors that interact with both the insulin response element and distinct upstream sites.

Hepatic microsomal induction profile of carbamic acid [[2,6-bis(1- methylethyl)phenoxy] sulfonyl]-2,6-bis(1-methylethyl) phenyl ester, monosodium salt (PD138142-15), a novel lipid regulating agent.

Induction of hepatic microsomal cytochrome P450 produced by carbamic acid [2,6-bis(1-methylethyl)phenoxy]sulfonyl]-2,6-bis(1-methylethyl) phenyl ester, monosodium salt (PD138142-15), a novel water-soluble inhibitor of acyl-CoA: cholesterol acyltransferase, was examined in male and female rats, dogs, and monkeys, and in male guinea pigs. Relative to control, PD138142-15 increased hepatic microsomal total spectral P450 in all species examined. Hepatic microsomal ethoxyresorufin-O-deethylase, pentoxyresorufin-O-dealkylase, and peroxisomal carnitine acetyltransferase activities and cyanide-insensitive Beta-oxidation were affected only marginally. Erythromycin-N-demethylase activity was increased (2- to 6-fold) in all three species in which it was examined (rat, dog and pig). Marked increases in immunoreactive P450 3A were noted in the rats and dogs, while slight increases were seen in monkeys. Pharmacokinetic studies of PD138142-15 in rats and dogs revealed pronounced decreases (80-90%) in plasma Cmax and AUC within 2 weeks of initiation of daily dosing. In spite of the marked decline in plasma drug levels, efficacy in dogs, as determined by serum cholesterol levels, was maintained for up to 6 weeks with continued dosing. Potential acid (gastric) breakdown products of PD 138142-15 were examined for their hepatic cytochrome P450 induction profiles in rats adn were found to differ both quantitatively and qualitatively from profiles produced by the parent compound. This suggested that induction observed in rats was due to parent PD138142-15 and not to any of the known potential acid breakdown products. The cumulative data establish that PD 138142-15 is an inducer of P450 3A in rats and dogs. The results also suggest that P450 3A is induced in monkeys and pigs as well, although the data are less definitive. Decreases in plasma drug levels imply that the compound may be an autoinducer in dogs and rats. The maintenance of efficacy in spite of decreased drugs levels in dogs suggests that the effects on serum cholesterol are due to a metabolite or that cholesterol lowering effects occur before the compound is metabolized by the liver.

Preclinical safety evaluation of avasimibe in beagle dogs: an ACAT inhibitor with minimal adrenal effects.

Avasimibe, a novel inhibitor of acyl coenzyme A:cholesterol acyltransferase (ACAT), is currently being developed as an antiatherosclerotic agent. The preclinical safety and toxicokinetics of the compound were assessed in beagle dogs in an escalating-dose study and in repeated-dose studies of 2-, 13-, and 52-week duration. Oral (capsule) doses up to 1000 mg/kg b.i.d. were assessed in the escalating dose study and once-a-day doses up to 300 mg/kg, 1000 mg/kg, and 1000 mg/kg were assessed in the 2-, 13-, and 52-week studies, respectively. Avasimibe was found to be a substrate and inducer of hepatic CYP 3A, producing pronounced decreases in plasma drug concentrations subsequent to Day 1. Plasma drug concentrations plateaued markedly at doses above 100 mg/kg. Significant toxicologic findings were restricted to the higher doses (> or =300 mg/kg) and included emesis, fecal consistency changes, salivation, body weight loss, microscopic and clinical pathologic evidence of hepatic toxicity, and red blood cell (RBC) morphology changes. Mortality occurred at 1000 mg/kg due to hepatic toxicity. Toxicity was more closely associated with the exaggerated pharmacodynamic effects of the compound (e.g., marked serum cholesterol decreases) seen at the high doses of avasimibe used in these studies rather than with measures of systemic exposure (Cmax or AUC). Adrenal effects were noted only in the 52-week study and consisted of minimal to mild cortical cytoplasmic vacuolization and fibrosis at doses > or =300 mg/kg, with no change in adrenal weight. In conclusion, avasimibe is an ACAT inhibitor that has minimal adrenal effects in dogs, with dose-limiting toxicity defined by readily monitored and reversible changes in hepatic function.

Metabonomics: evaluation of nuclear magnetic resonance (NMR) and pattern recognition technology for rapid in vivo screening of liver and kidney toxicants.

The purpose of this study was to evaluate the feasibility of metabonomics technology for developing a rapid-throughput toxicity screen using 2 known hepatotoxicants: carbon tetrachloride (CCl(4)) and alpha-naphthylisothiocyanate (ANIT) and 2 known nephrotoxicants: 2-bromoethylamine (BEA) and 4-aminophenol (PAP). In addition, the diuretic furosemide (FURO) was also studied. Single doses of CCl(4) (0.1 and 0.5 ml/kg), ANIT (10 and 100 mg/kg), BEA (15 and 150 mg/kg), PAP (15 and 150 mg/kg) and FURO (1 and 5 mg) were administered as single IP or oral doses to groups of 4 male Wistar rats/dose. Twenty-four-h urine samples were collected pretest, daily through Day 4, and on Day 10 (high dose CCl(4) and BEA only). Blood samples were taken on Days 1, 2, and 4 or 1, 4, and 10 for clinical chemistry assessment, and the appropriate target organ was examined microscopically. NMR spectra of urine were acquired and the data processed and subjected to principal component analyses (PCA). The results demonstrated that the metabonomic approach could readily distinguish the onset and reversal of toxicity with good agreement between clinical chemistry and PCA data. In at least 2 instances (ANIT and BEA), PCA analysis suggested effects at low doses, which were not as evident by clinical chemistry or microscopic analysis. Furosemide, which had no effect at the doses employed, did not produce any changes in PCA patterns. These data support the contention that the metabonomic approach represents a promising new technology for the development of a rapid throughput in vivo toxicity screen.

Metabonomic assessment of vasculitis in rats.

The vasculitides are a heterogeneous group of lesions characterized by inflammation and necrosis of the vascular wall and have proven to be a disconcerting dilemma in the development of several classes of therapeutics. Metabonomics is an emerging technology having great potential for rapid noninvasive assessment of toxicity in vivo and providing identification of peripheral surrogate markers of toxicity. Metabonomic evaluation of CI-1018, a selective type 4 phosphodiesterase inhibitor associated with vasculitis in rats, was undertaken. Two experiments were performed in which CI-1018 was administered for up to 4 d to groups of male Wistar rats at doses up to 3000 mg/kg. Urine was collected from all animals pretest and daily for metabonomic analysis. Eleven of 38 CI-1018-treated animals were found to have vascular injury of varying severity at doses = or > 750 mg/kg. Principal component analysis produced a clear pattern separation among 8 of 11 animals with lesions and 36 of 37 animals without lesions in samples collected on d 3 or 4. These data demonstrate that the metabonomics approach has significant potential for developing a noninvasive method for identifying vasculitis in rats. It remains to be seen if urinary analyte patterns identified in this study are reproducible and whether a biomarker pattern for vasculitis can be established.

Species differences in response to photohemolytic agents.

Species differences in red blood cell susceptibility to the photohemolytic agents chlorpromazine, menadione and tetracycline were examined in mouse, rat, dog, and human blood. Menadione and tetracycline (25 microM) hemolyzed mouse but not dog, rat, or human red blood cells (RBC) when irradiated with UV light but not in the dark. Chlorpromazine (25 microM) produced a photohemolytic response in all four species with mouse and rat RBC lysing fastest followed by human then dog cells. Investigations into the nature of these species differences suggested that the size of mouse RBC may contribute to its high sensitivity to photohemolytic agents. An investigation of the effect of UV light on key antioxidant enzymes revealed species differences in enzyme inactivation. These data suggest that mouse RBC may be particularly vulnerable to phototoxic agents, especially those compounds which produce active oxygen species and, therefore, may prove more useful than human RBC as a model for predicting phototoxic potential of some chemical entities.

DFP-induced elevation of strength-duration threshold in hen peripheral nerve.

Previous research has indicated that organophosphorus agents which induce a delayed neuropathy also elevate the strength-duration threshold during the progression of the neuropathy. To establish further the correlation between strength-duration changes and delayed neuropathy, the purpose of the present study was to investigate the biochemical and electrophysiological effects of two additional agents: diisopropylflourophosphate (DFP) and phosphonothioc acid, methyl-[2-(dimethylamino)-ethyl]O-ethyl ester (VX). DFP-treated hens exhibited clinical signs of toxicity at the time of electrophysiologic recording and biochemical analysis. DFP treatment also resulted in significantly elevated thresholds of the strength-duration curves of both the sciatic and tibial nerves. The VX-treated animals exhibited no clinical signs, despite aggressive dosing, and there were no significant changes in the electrophysiologic characteristics (conduction velocity, relative refractory period, strength-duration threshold) of either peripheral nerve. Acetylcholinesterase activities of the brain and skeletal muscle were significantly reduced in the VX- and DFP-treated hens, whereas creatine phosphokinase activities in these tissues were unaffected. These results are consistent with the view that elevation of the strength-duration threshold in peripheral nerves is among the earliest indicators of organophosphorus-induced delayed neuropathy.

Biochemical alterations in guinea pig adrenal cortex following administration of PD 132301-2, an inhibitor of acyl-CoA:cholesterol acyltransferase.

To assess whether previously reported ultrastructural alterations of adrenocortical mitochondria induced by the acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor PD 132301-2 are accompanied by functional deficits in tissue energy stores, phosphorylated adenine nucleotide levels in guinea pig adrenal cortex were quantitated. Adrenals of male guinea pigs were obtained at 1, 2, 6, or 24 hours after oral administration of 100 mg/kg PD 132301-2 or 0.5% methylcellulose vehicle. In treated animals, ATP levels and ATP/ADP ratios were decreased approximately 50% with concurrent increases in AMP. Calculated energy charge was also decreased; these decreases were maximal by 6 hours. Cholesterol esterification in adrenal cortex was inhibited, resulting in progressive accumulation of free cholesterol up to 3-fold over control by 24 hours, consistent with the ACAT inhibitory activity of the drug. These data suggest that PD 132301-2 distributes to the adrenal cortex where early alterations of tissue bioenergetics occur in a time frame consistent with ultrastructural alterations of mitochondria.

Atorvastatin is not cataractogenic in beagle dogs.

PURPOSE: Atorvastatin (Lipitor) was developed as an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase for treatment of serum lipid disorders. Other reductase inhibitors (RIs) induce cataracts in dogs exposed to relatively high levels of the drugs for extended periods of time. The purpose of these studies was to assess the cataractogenic potential of atorvastatin, when administered for up to 2 years in beagle dogs. METHODS: Atorvastatin was administered at doses up to 150 mg/kg/day in 2-week, 13-week or 104-week studies. A 52-week interim sacrifice and a reversal group in which dosing was terminated at week 52 and the dogs sacrificed at week 64, was included in the 104-week study. RESULTS: Serum cholesterol was significantly lowered in all studies. No clinical or histologic evidence of drug-induced cataracts was found in any study. Lens biochemical analyses in the 13-week study revealed no statistically significant changes in lenticular weight, reduced or oxidized glutathione content, adenosine nucleotide content, glucose-6-phosphate dehydrogenase activity or phosphofructokinase activity in any treatment group. Modest (11-17%) and transient decreases in lens protein, potassium and glucose content were noted in the 13-week study and at week 52 (glucose only) in the 104-week study, at the doses > or = 40 mg/kg. CONCLUSIONS: These studies demonstrated that, in spite of marked reduction in serum cholesterol, atorvastatin was not cataractogenic in dogs at any tested dose. We conclude that atorvastatin differs from other RIs in this regard.

NMR of biofluids and pattern recognition: assessing the impact of NMR parameters on the principal component analysis of urine from rat and mouse.

The ability to interpret metabolic responses to toxic insult as expressed in altered urine composition and measured by NMR spectroscopy is dependent upon a database of proton NMR spectra of urine collected from both control and treated animals. Pattern recognition techniques, such as principal component analysis (PCA), can be used to establish whether the spectral data cluster according to a dose response. However, PCA will be sensitive to other variables that might exist in the data, such as those arising from the NMR instrument itself. Thus, studies were conducted to determine the impact that NMR-related variables might impart on the data, with a view towards understanding and minimizing variables that could interfere with the interpretation of a biological effect. This study has focused on solvent suppression methods, as well as instrument-to-instrument variability, including field strength. The magnitude of the NMR-induced variability was assessed in the presence of an established response to the nephrotoxin bromoethanamine. Changes caused by the model toxin were larger and easily distinguished from those caused by using different solvent suppression methods and field strengths.

Electrophysiologic characteristics of tibial and sciatic nerves in the hen.

The peripheral nerve of the hen has become an increasingly important animal model in studies of peripheral neuropathy, especially that induced by organophosphorus agent exposure. However, few electrophysiologic studies have been performed, and few data on normal peripheral nerve function exist. The purpose in the present study was to measure the characteristics of the compound action potential of peripheral nerves of the healthy hen. The results showed that conduction velocities of the tibial and the sciatic nerves were 41 m/s and 60 m/s, respectively. The relative refractory period was slightly shorter in the sciatic nerve. The tibial nerve exhibited a lower threshold for stimulation and a significantly shorter chronaxie (19 microseconds) than did the sciatic nerve (25 microseconds). Variability between animals was relatively small. These data should provide useful reference points on studies in which peripheral neuropathy is induced or suspected.

Comparison of methyl bromide and other nematicides for control of nematodes in peanut.

The efficacy of methyl bromide for control ofMeloidogyne arenaria and to increase yields of 'Florunner' peanut (Arachis hypogaea) was studied in a field at the Wiregrass Substation near Headland, Alabama. Methyl bromide was applied in the row at a depth of 35 cm using a subsoiler-bedder 2 weeks before planting at rates of 0, 34, 50, 67, 101, and 118 kg a.i./ha. Methyl bromide treatments of 67 kg a.i./ha or higher resulted in significant (P = 0.05) yield increases similar to those obtained in the same experiment with at-plant applications of aldicarb (2.2 kg a.i./ha), EDB (1.55 ml a.i./m row), or 1,3-D (5.10 ml a.i./m row). The relation between yield (Y) and methyl bromide rate (x) was described (R(2) = 0.97**) by the exponential function: Y = 2,302.963eb, where b = (- 1.901 - ln x)(2)/169.482. M. arenaria juvenile populations in soil in mid-August were too low to permit establishment of a relation between application rate of methyl bromide and size of the population.

Soybean-Peanut Rotations for the Management of Meloidogyne arenaria.

Rotating soybean (Glycine max cv. Kirby) with peanut (Arachis hypogaea cv. Florunner) for managing Meloidogyne arenaria race 1 was studied for 3 years (1985-87) in a field near Headland, Alabama. Each year soybean plots had lower soil numbers of M. arenaria second-stage juveniles (J2) at peanut harvest than did plots in peanut monocnlture. Peanut following either 1 or 2 years of soybean resulted in approximately 50% reduction in J2 soil population densities and a 14% (1-year soybean) or 20% (2-year soybean) increase in yields compared with continuous peanut. The soybean-peanut rotation increased peanut yield equal to or higher than the yield obtained with continuous peanut treated with aldicarb at 0.34 g a.i./mL.