Effect of Working Memory Load and Typicality on Semantic Processing in Aphasia.

Purpose: This study evaluated the effects of a linguistic characteristic, typicality, and a processing variable, working memory on the abilities of people with aphasia (PWA) and neurologically intact adults to process semantic representations. This was accomplished using a newly developed assessment task, the Category Typicality Test, which was created for the Temple Assessment of Language and Short-Term Memory in Aphasia.

Method: A post hoc quasi-experimental design was used.

Caspase-1 processes IFN-gamma-inducing factor and regulates LPS-induced IFN-gamma production.

Interferon-gamma-inducing factor (IGIF, interleukin-18) is a recently described cytokine that shares structural features with the interleukin-1 (IL-1) family of proteins and functional properties with IL-12. Like IL-12, IGIF is a potent inducer of interferon (IFN)-gamma from T cells and natural killer cells. IGIF is synthesized as a biologically inactive precursor molecule (proIGIF).

Proteolytic activation of protein kinase C delta by an ICE/CED 3-like protease induces characteristics of apoptosis.

Recent studies have shown that protein kinase C (PKC) delta is proteolytically activated at the onset of apoptosis induced by DNA-damaging agents, tumor necrosis factor, and anti-Fas antibody. However, the relationship of PKC delta cleavage to induction of apoptosis is unknown. The present studies demonstrate that full-length PKC delta is cleaved at DMQD330N to a catalytically active fragment by the cysteine protease CPP32.

Proteolytic activation of protein kinase C delta by an ICE-like protease in apoptotic cells.

These studies demonstrate that treatment of human U-937 cells with ionizing radiation (IR) is associated with activation of a cytoplasmic myelin basic protein (MBP) kinase. Characterization of the kinase by gel filtration and in-gel kinase assays support activation of a 40 kDa protein. Substrate and inhibitor studies further support the induction of protein kinase C (PKC)-like activity.

Effects of long-term tracheostomy on spectral characteristics of vowel production.

This study investigated the effects of long-term tracheostomy on the development of speech. Eight children who underwent tracheotomy during the prelingual period were compared to matched controls on selected spectral parameters of the speech acoustic signal and standard measures of oral-motor, phonologic, and articulatory proficiency. Analysis of formant frequency values revealed significant between-group differences.

Impaired development of oral-motor functions required for normal oral feeding as a consequence of tube feeding during infancy.

The child who is tube fed during the first two years of life is at risk for impaired development of normal oral-motor patterns and coordination during feeding. In order to ensure as smooth a transition to oral feeding as possible, it is necessary to provide the tube-fed child with a framework of normal oral sensitization from which he can develop the level of trust in his own oral mechanism required to achieve the mature, coordinated oral movements essential to development of the normal bite-chew-suck-swallow sequence. While this can be a tedious and taxing process, an ongoing program of oral stimulation, training and development should be included in the overall management of every young child receiving tube feedings.

The myeloid blood cell differentiation-inducing protein MGI-2A is interleukin-6.

The mouse myeloid blood cell differentiation-inducing protein, macrophage and granulocyte inducer, type 2A (MGI-2A), was purified, and the amino acid sequence of a CNBr cleavage peptide (22 residues) was determined. This amino acid sequence is identical to the sequence found in positions 73 to 94 of mouse interleukin-6 (IL-6). Recombinant mouse IL-6 protein induces differentiation of mouse myeloid leukemic cells that are induced to differentiation by MGI-2, and monoclonal antimouse-MGI-2 antibody, which neutralizes MGI-2, also completely neutralizes this IL-6-induced differentiation.

The human hematopoietic colony-stimulating factors.

The complementary DNAs and genes encoding the four major human myeloid growth factors--granulocyte colony-stimulating factor, macrophage colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, and interleukin-3--have all been molecularly cloned. These DNA clones have proved valuable for studying the molecular biology of these important regulatory molecules as well as for the large-scale production of the recombinant growth factor proteins. These advances have led to a much better understanding of the role of the myeloid growth factors in regulating hematopoiesis in vivo that should soon find practical application in clinical medicine.

Immortalization of rat embryo fibroblasts by mutant polyomavirus large T antigens deficient in DNA binding.

We have identified a putative DNA-binding domain in polyomavirus large T antigen. Mutations introduced into the gene between amino acids 290 and 310 resulted in proteins that no longer bound to the high-affinity binding sites on the polyomavirus genome, showed no detectable nonspecific DNA binding, and were not able to initiate DNA replication from the viral origin. These mutant T antigen genes were introduced into rat embryo fibroblasts together with the neomycin resistance gene to allow selection for growth in the presence of G418.

A conserved AU sequence from the 3' untranslated region of GM-CSF mRNA mediates selective mRNA degradation.

The mRNAs of transiently expressed genes frequently contain an AU-rich sequence in the 3' untranslated region. We introduced a 51 nucleotide AT sequence from a human lymphokine gene, GM-CSF, into the 3' untranslated region of the rabbit beta-globin gene. Our experiments demonstrate that this caused the otherwise stable beta-globin mRNA to become highly unstable in vivo.

Stimulation of haematopoiesis in primates by continuous infusion of recombinant human GM-CSF.

Certain proteins are known to play an important part in the proliferation, differentiation and functional activation of haematopoietic progenitor cells in vitro. These proteins include erythropoietin and various colony-stimulating factors (CSFs), one of which is granulocyte-macrophage colony-stimulating factor (GM-CSF). Recently, both murine and human GM-CSF have been purified to homogeneity and complementary DNAs encoding them have been cloned.

Guanine nucleotide contacts within viral DNA sequences bound by polyomavirus large T antigen.

Essential nucleotide contacts between the polyomavirus large T antigen and its multiple specific binding regions within the regulatory sequences of the polyomavirus genome were determined in vitro by methylation interference. Methylation of any of the guanine residues of the 5'-G(A/G)GGC-3' pentanucleotide repeats in large-T-antigen-binding regions A, B, C, and 3 (A. Cowie and R.

Polyomavirus enhancer contains multiple redundant sequence elements that activate both DNA replication and gene expression.

Sequences that comprise the 244-base-pair polyomavirus enhancer region are also required in cis for viral DNA replication (Tyndall et al., Nucleic Acids Res. 9:6231-6250, 1981).

Multiple binding sites for polyomavirus large T antigen within regulatory sequences of polyomavirus DNA.

Polyomavirus large T antigen binds specifically to multiple sites within the regulatory region of the viral genome. Experiments done with crude extracts from wild-type virus-infected mouse cells and immunoprecipitation of protein-DNA complexes localized two high-affinity binding sites on the early region side of the DNA replication origin. Purification of the large T antigen by immunoaffinity chromatography made it possible to refine the analysis through application of DNase I footprinting.

Polyoma virus DNA replication requires an enhancer.

Sequences which activate polyoma virus DNA replication are located within a region that also includes the transcriptional enhancer. We demonstrate a cis involvement of enhancers in DNA replication by showing that this region can be replaced by other enhancers, in a position- and orientation-independent manner, and that an immunoglobulin gene enhancer confers tissue-specific replicatory ability.

Construction and functional characterization of polyomavirus genomes that separately encode the three early proteins.

Modified polyomavirus genomes that individually encode the large and small T proteins were constructed by exchanging restriction endonuclease fragments between cDNA copies of the respective mRNAs and cloned genomic DNA. The efficacies of the new constructs, and that of the middle T protein gene described previously (R. Treisman , U.

DNA binding activity of polyoma virus large tumor antigen.

Polyoma virus large tumor antigen from productively infected mouse cells has been purified to greater than 50% homogeneity by a simple immunoaffinity procedure using monoclonal antibodies. A radioimmunoreaction was devised for assaying purity. The purified large tumor antigen retained its antigenicity and its ability to bind DNA specifically.

Expression of the large T protein of polyoma virus promotes the establishment in culture of "normal" rodent fibroblast cell lines.

Transfer into mouse and rat embryo fibroblasts in primary culture of cloned polyoma virus genes encoding only the large T protein led to the establishment of flat colonies in sparse subcultures at a frequency equal to that of transformation by wild-type virus. Cell lines could be derived from such colonies and maintained in culture for large numbers of generations without entering crisis. They exhibited a normal phenotype, by the criteria of growth on plastic to a low saturation density and of anchorage dependency.

Regulation of polyoma virus transcription in murine embryonal carcinoma cells.

Undifferentiated murine embryonal carcinoma (EC) cells are resistant to infection with wild-type polyoma virus. The block appears to be located at the transcriptional level. Polyoma host range mutants capable of expressing early and late functions in EC cells have been isolated.

The roles of individual polyoma virus early proteins in oncogenic transformation.

The expression in normal rat cells of modified polyoma virus genomes, separately encoding large T, middle T or small T antigens, has allowed the investigation of the roles of these proteins in oncogenic transformation. Middle T is sufficient to transform cells of established lines but the transformants are serum dependent. Large T lacks intrinsic oncogenic potential but can relieve the serum dependence of normal and transformed cells.