The Distribution of Attention Across Auditory Input Channels: An Assessment Using the Human Evoked Potential

In order to determine the extent to which distraction disrupts performance when attention is divided, the distribution of attention across five auditory input channels was assessed using the N1 component of the human auditory evoked potential. In addition, the possibility that methylphenidate (Ritalin) affects the distribution of attention across input channels was tested. Sixteen subjects performed a tone discrimination task under conditions of focused attention and divided attention, both with and without the presence of stimuli interposed between the points to be attended. The subjects performed in two sessions during which they received either methylphenidate (10 mg) or a placebo in a double-blind design. The results showed that the interposed stimuli were receiving some attention resulting in a disruption of performance. Methylphenidate did not affect the distribution of attention as reflected in the N1 wave. The data are interpreted as showing that: 1) distraction plays a major role in producing performance deficits observed with divided attention; and 2) methylphenidate does not appreciably affect the distribution of attention across input channels.     

A human recessive neurosensory nonsyndromic hearing impairment locus is a potential homologue of the murine deafness (dn) locus

A locus for recessive neurosensory nonsyndromic hearing impairmentmaps to chromosome 9q13–q21 in two regionally separateconsanguineous families from India. Each family demonstratesa LOD score greater than 4.5 to this region. D9S15, tightlylinked to the Friedreich's ataxia locus, a region that has beendefined with over 1 Mb of YAC contig information and severalexpressed sequences, is one of the flanking markers. In mice,the deafness (dn) locus maps to mouse chromosome 19 and flankingloci are syntenic to human chromosome 9q11–q21. The dnmouse is a potential model for the hearing impairment foundin both these families.     

Curing efficiency and ocular hazards of dental photopolymerization sources

The spectral distributions of a range of dental photocuring sources were measured at the exit window and at a distance of 10 cm. The former enabled the evaluation of a newly proposed photocuring efficiency index which correlates well with the depth of cure of the photopolymerized resins, thus providing a basis for the comparison of different photocuring sources. The spectral irradiante of the sources obeyed the inversesquare law, allowing a comparison with the ACGIH threshold limit values. According to these criteria, no ocular hazard is posed to the patient or clinician by u.v.-A or u.v.-B radiation nor to the patient by the visible light when momentarily exposed to the sources. Similarly the ACGIH criterion indicates that the clinician does not risk chorioretinal injury provided the exposure is restricted to less than 140 s in a 3 h period.     

Phosphorylation of a C-SRC-related protein in macrophages activated in vitro with lymphokine

Treatment of proteose peptone elicited peritoneal macrophages from C3H/HeN mice or the macrophage cell line B6MP102 with a T-cell lymphokine preparation induces cytotoxicity for SV3T3 tumor cells. The Triton X-100 (TX-100) insoluble fractions from activated macrophages possessed kinase activity for an endogenous 53 kDa phosphoprotein (pp53) which was markedly greater than extracts from untreated macrophages. Addition of the tyrosine phosphatase inhibitor, Na₃,VO₄ to the cytotoxicity assay also enhanced tumor cell lysis and Na₃VO₄ treated macrophages showed increased phosphorylation of pp53. Moreover, addition of Na₃VO₄ to the cytoskeleton kinase assay enhanced the phosphorylation of pp53 in a dose dependent manner. Pp53 was immunoprecipitated from the in vitro phosphorylated TX-100 insoluble fraction with monoclonal antibody to pp60^v-src. Anti-pp60^v-src also precipitated a 53 and a 60 kDa phosphoprotein from whole cell extracts and from TX-100 cytoskeleton extracts of macrophages phosphorylated as viable intact cells. Addition of a known tyrosine kinase inhibitor, quercetin, to the macrophage cytoskeleton kinase assay inhibited phosphorylation of pp53, and the in vitro phosphorylated pp53 was resistant to 1 N NaOH hydrolysis, indicating phosphorylation of tyrosine residues. Immune complex kinase assays of anti-pp60^c-src precipitated TX-100 insoluble macrophage fractions revealed strong phosphorylation for α-casein which was inhibited by quercetin. These data suggest that macrophage pp53 is a c-src-related gene product that is inducible by stimuli that activate macrophages to cytotoxicity.     

Coping strategies,hostility, and depressive symptoms: A path model

Previous studies of coping, hostility, and depressive symptoms have highlighted the significant relations between all possible pairs of these 3 variables. To more completely explore the nature of depressive symptoms, we link them all together in this study by testing a coping→hostility→depressive symptoms path model. One hundred forty participants completed psychological questionnaires measuring coping strategies, hostility, and depressive symptoms. While controlling age and social class as covariates, SPSS stepwise regression analyses were used to examine relations among these 3 constructs. Results suggest that coping has a direct relation with depressive symptoms as well as an indirect relation mediated by hostility. Passive coping may lead to increased hostility, resulting in depressive symptoms. Active coping may have the opposite effect. These findings suggest that the inclusion of measures of both coping strategies and hostility yields a more thorough understanding of concomitants of depressive symptoms. From a clinical perspective, knowing what coping strategies a person uses and how much anger they experience and express may be useful in guiding the management of depressive symptoms.     

Recombination hotspot activity of hypervariable minisatellite DNA requires minisatellite DNA binding proteins

Hypervariable minisatellite DNA repeats are found at tens of thousands of loci in the mammalian genome. These sequences stimulate homologous recombination in mammalian cells [Cell60:95–103]. To test the hypothesis that protein-DNA interaction is required for hotspot functionin vivo, we determined whether a second protein binding nearby could abolish hotspot activity. Intermolecular recombination between pairs of plasmid substrates was measured in the presence or absence of thecis-acting recombination hotspot and in the presence or absence of the secondtrans-acting DNA binding protein. Minisatellite DNA had hotspot activity in two cell lines, but lacked hotspot activity in two closely related cell lines expressing a site-specific helicase that bound to DNA adjacent to the hotspot. Suppression of hotspot function occurred for both replicating and non-replicating recombination substrates. These results indicate that hotspot activityin vivo requires site occupancy by minisatellite DNA binding proteins.     

A voltage-dependent K+ current contributes to membrane potential of acutely isolated canine articular chondrocytes

The electrophysiological properties of acutely isolated canine articular chondrocytes have been characterized using patch-clamp methods. The 'steady-state' current–voltage relationship ( I–V ) of single chondrocytes over the range of potentials from −100 to +40 mV was highly non-linear, showing strong outward rectification positive to the zero-current potential. Currents activated at membrane potentials negative to −50 mV were time independent, and the I–V from −100 to −60 mV was linear, corresponding to an apparent input resistance of 9.3 ± 1.4 GΩ ( n = 23). The outwardly rectifying current was sensitive to the K⁺ channel blocking ion tetraethylammonium (TEA), which had a 50% blocking concentration of 0.66 m m (at +50 mV). The 'TEA-sensitive' component of the outwardly rectifying current had time- and membrane potential-dependent properties, activated near −45 mV and was half-activated at −25 mV. The reversal potential of the 'TEA-sensitive' current with external K⁺ concentration of 5 m m and internal concentration of 145 m m , was −84 mV, indicating that the current was primarily carried by K⁺ ions. The resting membrane potential of isolated chondrocytes (−38.1 ± 1.4 mV; n = 19) was depolarized by 14.8 ± 0.9 mV by 25 m m TEA, which completely blocked the K⁺ current of these cells. These data suggest that this voltage-sensitive K⁺ channel has an important role in regulating the membrane potential of canine articular chondrocytes.