Inhibition of touch cell fate by egl-44 and egl-46 in C. elegans.

In wild-type Caenorhabditis elegans, six cells develop as receptors for gentle touch. In egl-44 and egl-46 mutants, two other neurons, the FLP cells, express touch receptor-like features. egl-44 and egl-46 also affect the differentiation of other neurons including the HSN neurons, two cells needed for egg laying. egl-44 encodes a member of the transcription enhancer factor family. The product of the egl-46 gene, two Drosophila proteins, and two proteins in human and mice define a new family of zinc finger proteins. Both egl-44 and egl-46 are expressed in FLP and HSN neurons (and other cells); expression of egl-46 is dependent on egl-44 in the FLP cells but not in the HSN cells. Wild-type touch cells express egl-46 but not egl-44. Moreover, ectopic expression of egl-44 in the touch cells prevents touch cell differentiation in an egl-46-dependent manner. The sequences of these genes and their nuclear location as seen with GFP fusions indicate that they repress transcription of touch cell characteristics in the FLP cells.

Screening for iron deficiency anemia by dietary history in a high-risk population.

BACKGROUND: Iron deficiency anemia (IDA) in young children is important to identify because of its adverse effects on behavior and development. Because of costs and inconvenience associated with blood test screening and the decline in prevalence of IDA, the Institute of Medicine and the Centers for Disease Control and Prevention recommend that blood test screening for IDA be targeted to children first identified by dietary and health history. OBJECTIVE: To evaluate a parent-completed dietary and health history as the first stage of 2-stage screening for IDA. DESIGN AND METHODS: A cross-sectional study was conducted in inner-city clinics in children 9 to 30 months old having routine anemia screening as part of a scheduled visit. Parents completed a questionnaire and children had venous blood sampling for complete blood count and ferritin. Anemia was defined as Hb <11.0 g/dL. Iron deficiency (ID) was defined as ferritin <10 microg/L or mean corpuscular volume <70 fL and red cell distribution width >14.5%. Children were categorized into 1 of 4 groups: iron-sufficient, not anemic (ISNA); iron-sufficient, anemic (ISA); iron-deficient, not anemic (IDNA); and iron-deficient anemic (IDA). The questionnaire consisted of 15 dietary items in domains of infant diet, intake of solid food, intake of beverages, and participation in the Special Supplemental Nutrition Program for Women, Infants, and Children together with 14 historical items in domains of birth history, recent illness, chronic medical conditions, history of anemia, and maternal history. Analysis was performed on individual items, domains, and combinations of selected items. RESULTS: In the 282 study subjects, the prevalence of anemia (35%), IDNA (7%), and IDA (8%) did not vary significantly by age. Among individual historical and dietary questions, maternal history of anemia and drinking >2 glasses of juice per day identified the highest proportion of children with IDA: 50% sensitivity (95% confidence interval [CI]: 16,81) and 77% sensitivity (95% CI: 54,89), respectively. However, specificities for these questions were 60% (95% CI: 55,65) and 22% (95% CI: 17,27), respectively. Domains of questions with the highest sensitivity for IDA were beverage intake (91%; 95% CI: 68,99) and intake of solid food (91%; 95% CI: 68,99). However, specificities of the domains were only 14% (95% CI: 10,18) and 29% (95% CI: 24,35), respectively. The dietary items used by Boutry and Needlman were 95% (95% CI: 77, 99) sensitive but only 15% (95% CI: 11,19) specific for IDA. The recommendations of the Centers for Disease Control and Prevention for health and dietary screening were 73% (95% CI: 56,92) sensitive and 29% (95% CI: 24,35) specific for IDA. The individual questions, domains of questions, and interdomain groups of questions had similar sensitivity and specificity for anemia and ID (IDA + IDNA). CONCLUSION: In this high-risk population, neither individual nor combinations of parental answers to dietary and health questions were able to predict IDA, anemia, or ID well enough to serve as a first-stage screening test.

Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls.

BACKGROUND: Up to 25% of adolescent girls in the USA are iron deficient. This double-blind, placebo-controlled clinical trial assessed the effects of iron supplementation on cognitive function in adolescent girls with non-anaemic iron deficiency. METHODS: 716 girls who enrolled at four Baltimore high schools were screened for non-anaemic iron deficiency (serum ferritin < or = 12 micrograms/L with normal haemoglobin). 98 (13.7%) girls had non-anaemic iron deficiency of whom 81 were enrolled in the trial. Participants were randomly assigned oral ferrous sulphate (650 mg twice daily) or placebo for 8 weeks. The effect of iron treatment was assessed by questionnaires and haematological and cognitive tests, which were done before treatment started and repeated after the intervention. We used four tests of attention and memory to measure cognitive functioning. Intention-to-treat and per-protocol analyses were done. FINDINGS: Of the 81 enrolled girls with non-anaemic iron deficiency, 78 (96%) completed the study (39 in each group). Five girls (three control, two treatment) developed anaemia during the intervention and were excluded from the analyses. Thus, 73 girls were included in the per-protocol analysis. Ethnic distribution, mean age, serum ferritin concentrations, haemoglobin concentrations, and cognitive test scores of the groups did not differ significantly at baseline. Postintervention haematological measures of iron status were significantly improved in the treatment group (serum ferritin 27.3 vs 12.1 micrograms/L, p < 0.001). Regression analysis showed that girls who received iron performed better on a test of verbal learning and memory than girls in the control group (p < 0.02). INTERPRETATION: In this urban population of non-anaemic iron-deficient adolescent girls, iron supplementation improved verbal learning and memory.

Release and spread of immunoreactive neurokinin A in the cat spinal cord in a model of acute arthritis.

Antibody microprobes were used to study the release of immunoreactive neurokinin A into the spinal cord of anaesthetised cats during and following injection of a knee joint with kaolin and carrageenan. A basal level of immunoreactive neurokinin A was detected prior to any noxious stimuli. Innocuous mechanical joint stimuli (flexion or pressure) did not alter this basal level of release. However, on injection of kaolin and carrageenan into a knee joint, evidence of release into the ipsilateral spinal cord was immediately observed. Initially, immunoreactive neurokinin A was detected in 2 regions: one at the dorsal surface of the spinal cord and the other centred on the superficial dorsal horn. Within 1 h of joint injection, however, immunoreactive neurokinin A was detected throughout the dorsal horn and the adjacent white matter. The extensive spread and persistence of immunoreactive neurokinin A in the spinal cord may underlie some of the prolonged excitability changes evoked by brief noxious stimuli and peripheral inflammation reported by other laboratories.

Morphine, naloxone and the responses of medial thalamic neurones of the cat.

Administered electrophoretically morphine depressed the firing of medial thalamic neurones. This effect was not antagonized by naloxone which itself was a depressant. A long lasting increase in sensitivity to L-glutamate followed ejection of both morphine and naloxone. Intravenous morphine, 0.5-1.5 mg/kg, had inconstant effects on spontaneous firing that evoked by electrical stimulation of the forepaws but in 7 of 10 experiments reduced the sensitivity of neurones to L-glutamate. This effect was reversed in all cases by intravenous naloxone, 0.3 mg/kg

Effects of opiate agonists and antagonists on central neurons of the cat.

Morphine, naloxone, nalorphine, levorphanol, dextrorphan and levallorphan were ejected electrophoretically from micropipettes near cholinoceptive and noncholinoceptive cells of the spinal cord, ventrobasal thalamus and cerebral cortex of decerebrate and barbiturate-anesthetized cats. Morphine excited those cells having nicotinic receptors for acetylcholine. Naloxone and nalorphine reduced the action of morphine and acetylcholine on these cells but not the effects of excitant amino acids. Levorphanol excited spinal neurons also excited by acetylcholine, an effect antagonized by naloxone, but also showed atropine-like activity when ejected for prolonged periods. Dextrorphan depressed the firing of both cholinoceptive and noncholinoceptive spinal neurons. Levallorphan reduced the effects of both acetylcholine and excitant amino acids on spinal neurons. The depressant effects of morphine and levorphanol on noncholinoceptive spinal neurons were not antagonized by naloxone.