Effects of vitamin A on growth of vitamin A-deficient children: field studies in Nepal

Inconsistencies have been observed in the impact of vitamin A (VA) supplementation on early child growth. To help clarify this issue, a cohort of 3377 rural Nepalese, nonxerophthalmic children 12-60 mo of age were randomized by ward to receive vitamin A [60,000 microg retinol equivalents (RE)] or placebo-control (300 RE) supplementation once every 4 mo and followed for 16 mo. VA had no impact on annual weight gain or linear growth. However, arm circumference (AC) and muscle area (MA) growth improved in VA recipients, by 0.13 cm and 25 mm2, respectively, over controls. Growth of children with xerophthalmia, who were treated with >/= 120, 000 RE at base line, was also compared to that of nonxerophthalmic children, stratified by initial wasting status, and adjusted for sex, baseline age and measurement status. Among initially nonwasted children (AC >/= 13.5 cm), VA-treated xerophthalmic children (n = 86) gained 0.7 cm more in linear growth than nonxerophthalmic children. Among initially wasted children (AC < 13.5 cm), VA-treated children (n = 34) gained additional weight (672 g), height (approximately 1 cm), muscle (76 mm2) and fat (79 mm2) areas, and subscapular skinfold (1.3 mm) compared to changes observed in nonxerophthalmic children. Relative increments in soft tissue growth occurred within 4 mo of VA treatment, while the effect on linear growth was gradual. Moderate-to-severe VA deficiency, marked by xerophthalmia, is likely to impair normal physical growth, but milder stages of deficiency may not have this effect in rural South Asia.     

Integration of local inputs in visual cortex

In mammalian visual cortex, local connections are ubiquitous, extensively linking adjacent neurons of all types. In this study, optical maps of intrinsic signals and responses from single neurons were obtained from the same region of cat visual cortex while the effectiveness of the local cortical circuitry was altered by focally disinhibiting neurons within a column of known orientation preference. Maps of intrinsic signals indicated that local connections provide strong and functional subthreshold inputs to neighboring columns of other orientation preferences, altering the observed orientation preference to that of the disinhibited column. However, measuring the suprathreshold response using single-cell recordings revealed only mild changes of preferred orientation over the affected region. Because strongly tuned subthreshold inputs from cortex only marginally affect the tuning of a cortical cell's output, it is concluded that local cortical inputs are integrated weakly compared to geniculate inputs. Such circuitry potentially allows for the normalization of responses across a wide range of input activity through local averaging.     

Identification and characterisation of serogroup M among Nepalese isolates of Dichelobacter nodosus, the transmitting agent of footrot in small ruminants

One thousand and sixty three isolates of Dichelobacter nodosus cultured between 1992 and 1996 from cases of footrot in sheep and goats of migratory flocks of Nepal were characterised by agglutination test using prototype antisera of the Australian classification system. Of those, sixty six isolates could not be classified into any of the nine serogroups (A-I). This study was therefore undertaken to characterise these isolates. It was established that they were agglutinated by antiserum against serotype M of an alternative classification system. The distinct antigenic character of these isolates was further confirmed by DNA sequence analysis of the gene for the fimbrial subunit protein of two of them. At a molecular level, these isolates were closer to the prototype of serogroup F, VCS 1017. However, when compared with VCS 1017, the number of amino acid substitutions (28) in the fimbrial protein of these isolates was similar to that expected between isolates of different serogroups. Because these isolates are antigenically similar to 'serotype' M, but meet all the criteria to be classified into an independent serogroup, it is proposed that these isolates together with isolates previously classified as serotype M be classified as 'serogroup M'.     

Microglial activation in multiple system atrophy: a potential role for NF-kappaB/rel proteins

Microglial activation is a prominent feature of affected brain areas in multiple system atrophy. Microglia express proinflammatory peptides, which may be a result of activation of nuclear factor-KB. We investigated the nuclear presence of RelA, the 65 kDa subunit of the NF-KB/RelA family in striatum and brain stem of patients with multiple system atrophy. Affected brain areas of patients with multiple system atrophy showed a marked immunoreactivity for nuclear Rel A p65, which was almost exclusively localized in activated microglia. Interestingly nuclear translocation of Rel A was not detected in striatal tissue of controls and Parkinson disease patients. Thus, NF-kappaB/Rel A complexes may play a role in mediating microglial activation in multiple system atrophy.     

Characterization of novel set of membrane antigens associated with axonal growth. III: Expression in the regenerating goldfish optic nerve and tectum

In the preceding two papers in this series, a polyclonal antiserum (3070) and several monoclonal antibodies (MAbs 4 and 199) were used to define a novel set of laminin-binding membrane antigens in chick brain. In chick brain, 3070 and MAb 4 antigens stained growing axons and migrating nascent neurons transiently; though projection neurons were intensely labelled at all stages, normal glial cells were stained faintly or not at all. To learn if these antigens are associated more generally with active states of nerve growth, the present paper examined the expression of 3070 and MAb 4 antigens during regeneration of the goldfish optic nerve. Only a few optic fibers or glial cells were stained by 3070 antiserum in the resting (uninjured) optic nerve, but 10 days following a unilateral nerve crush, when the growth response is maximal in these fish, distal regenerating neuritic sprouts and glial cell bodies and processes were profusely labelled. The intensity of labelling was diminished by 135 days post-crush, when most active growth was completed. Since 3070/MAb 4 antigens exhibit properties expected for functional laminin receptors, these findings suggest several possible roles that they could play to aid nerve regeneration.     

Spinal morphine/clonidine antinociceptive synergism: involvement of G proteins and N-type voltage-dependent calcium channels

When morphine and clonidine are coadministered into the spinal cord (intrathecally) the resulting antinociception is greater than would be expected if the drug responses were additive; thus, a synergistic interaction. The mechanism for this synergistic interaction was investigated using agents which alter calcium channel function and G protein function. Drugs were administered intrathecally to mice and antinociception was measured using the tail flick test. The L-type calcium channel antagonists nifedipine (15 micrograms) and verapamil (15 micrograms) and the N-type antagonist omega-conotoxin GVIA (3 and 30 ng) decreased ED50 values for both morphine and clonidine three-to five-fold. The L-type calcium channel activator Bay K 8644 had a biphasic effect; 1.7 ng increased, although 170 ng decreased, morphine and clonidine ED50 values. None of the calcium channel modifiers affected the morphine/clonidine synergism. In mice pretreated with pertussis toxin (PTX, one, 10-ng dose 21 days previously), the morphine ED50 value increased two-fold, although the clonidine ED50 value was not changed. PTX pretreatment did not alter the morphine/clonidine synergism. Also, in PTX-pretreated mice, nifedipine and 1.7 ng Bay K 8644 did not alter the morphine/clonidine synergism. However, in PTX-pretreated animals omega-conotoxin GVIA (3 ng) changed the morphine/clonidine synergism to an additive interaction. Thus, both N-type calcium channels and PTX-sensitive G proteins are likely involved in spinal morphine/clonidine synergism.