Script training treatment for adults with apraxia of speech.

Purpose: Outcomes of script training for individuals with apraxia of speech (AOS) and mild anomic aphasia were investigated. Script training is a functional treatment that has been successful for individuals with aphasia but has not been applied to individuals with AOS. Principles of motor learning were incorporated into training to promote long-term retention of scripts.

Differences in tongue strength across age and gender: is there a diminished strength reserve?

Maximum tongue strength was investigated and compared to mean swallowing pressure elicited by the anterior tongue to calculate the percentage of maximum tongue strength used during swallowing in 96 participants with normal swallowing, divided into three 20-year age groups. The purposes of this investigation were to investigate normal swallowing physiology and to determine whether tongue strength reserves diminished according to age or gender. The results of the study yielded significant maximum tongue strength differences between the youngest and oldest and middle and oldest age groups; the oldest group had the weakest tongues.

Implications of an advice-giving and teacher role on language production in adults with dementia.

Purpose: The purpose of the two studies described in this paper was to assess whether adults with dementia could assume an advice-giving role (Study 1) and a teacher role (Study 2) despite their cognitive impairments. So far, no research on adults with dementia has compared language production in a social conversation condition with that in an advice-giving condition. Moreover, there are no data on language production in cognitively intact adults and in adults with dementia in a teaching situation (e.

Use of chemiluminescent DNA probes in the rapid detection of oxacillin resistance in clinically isolated strains of Staphylococcus aureus.

Chemiluminescent DNA probes (AccuProbe, species specific; and FlashTrack, bacterial generic) were used to determine oxacillin resistance in Staphylococcus aureus. Ribosomal RNA was measured at designated intervals in the presence and absence of antibiotic. A total of 48 (AccuProbe assay) and 24 (FlashTrack) S.

Calcific deposits in the heart.

Four case reports are presented which illustrate various patterns of calcific deposits in the heart. Valvular, myocardial, intracavitary, and coronary calcific deposits are illustrated, with emphasis on pathology and clinicopathologic-radiologic correlation. "Dystrophic" and "metastatic" calcifications are terms used to describe calcific deposits in abnormal and normal soft tissues, respectively.

Effect of metabolic inhibitors on the formation of antibody to sheep erythrocytes, on development of delayed hypersensitivity, and on the immune response to infection with Mycobacterium tuberculosis in mice.

The effect of a number of metabolic inhibitors was determined on: (i) the production of cellular immunity to infection with Mycobacterium tuberculosis in mice by vaccination with mycobacterial ribonucleic acid (RNA), (Ii) the production of cellular immunity to infection with M. tuberculosis in mice with viable H37Ra cells, (iii) the induction of antibody formation to sheep erythrocytes, and (iv) the induction of delayed hypersensitivity in mice to purified protein derivative. The pattern of inhibition produced by metabolic inhibitors on cellular immunity to infection with M.

Lack of protection afforded by ribonucleic acid preparations from Mycobacterium tuberculosis against Mycobacterium leprae infections in mice.

Mycobacterial ribonucleic acid preparations from H37Ra, an attenuated strain of Mycobacterium tuberculosis, provide their usual marked protection against M. tuberculosis challenge; however, they provided no protection against Mycobacterium leprae challenge. Suspensions of intact H37Ra were not effective against M.

Mycobacterial ribonucleic acid: comparison with mycobacterial cell wall fractions for regression of murine tumor growth.

Mycobacterial ribonucleic acid (RNA) and cell wall skeleton fraction isolated from H37Ra caused P-815 mastocytoma regression in DBA/2 mice provided the animals were presensitized with freshly harvested living H37Ra cells. In the absence of presensitization, only the RNA fraction inhibited. Cell wall skeleton fraction, under these conditions, stimulated tumor growth.

Mycobacterial RNA. A comparison with intact mycobacteria for suppression of murine tumor growth.

Our experimental data imply the following: (1) An RNA-rich fraction isolated from H37Ra, and intact H37Ra, are effective agents for suppression of tumor growth. (2) For suppression of two chemically-induced tumors with both RNA and H37Ra, direct contact with tumor is necessary. This may not be the case with other tumors in different strains of syngeneic mice.

Effect of rifampin on immunity to tuberculosis and on delayed hypersensitivity to purified protein derivative.

Mice vaccinated with mycobacterial ribonucleic acid (RNA) produced a high immune response and did not develop delayed hypersensitivity to purified protein derivative (PPD), and rifampin had no effect on the immune response. Mice vaccinated with viable H37Ra cells produced a high immune response and did develop delayed hypersensitivity to PPD. Rifampin had no effect on this immune response, but reduced the footpad reactions to PPD.

Macrophage migration inhibitory activity of mycobacterial growth inhibitory factor and the effect of a number of factors on mycobacterial growth inhibitory factor activity.

Mycobacterial growth inhibitory factor (MycoIF), which inhibits the intracellular multiplication of virulent tubercle bacilli within normal peritoneal macrophages in vitro, was tested for its ability to inhibit the migration of normal peritoneal exudate cells. The migration of peritoneal exudate cells was not inhibited by MycoIF. It was also shown that normal peritoneal macrophages infected with virulent Mycobacterium tuberculosis, strain H37Rv, required 72 h of incubation with spleen cell culture supernatant fluids containing MycoIF in order to inhibit intracellular bacillary multiplication.

Molecular weight and other characteristics of mycobacterial growth inhibitory factor produced by spleen cells obtained from mice immunized with viable attenuated mycobacterial cells.

Exposure of mycobacterial growth inhibitory factor (MycoIF) to trypsin, chymotrypsin, or neuraminidase decrease its ability to produce intracellular inhibition of mycobacterial growth within macrophages, suggesting that MycoIF was a glycoprotein. MycoIF was unaffected by deoxyribonuclease or ribonuclease. Supernatant fluids from antigenically stimulated H37Ra-immunized mouse spleen cells exposed to puromycin were unable to produce significant intracellular inhibition.

Conditions for production, and some characteristics, of mycobacterial growth inhibitory factor produced by spleen cells from mice immunized with viable cells of the attenuated H37Ra strain of Mycobacterium tuberculosis.

Mycobacterial growth inhibitory factor (MycoIF), found in supernatant fluids of mouse spleen cell cultures that have been stimulated in vitro with homologous antigen, inhibited the intracellular multiplication of virulent tubercle bacilli within normal mouse peritoneal macrophages in vitro. Antigenically stimulated H37Ra-immunized mouse spleen cells required 72 h of incubation to produce supernatant fluids that would cause intracellular inhibition. Supernatant fluids from 48-h mouse spleen cell cultures were not able to produce intracellular inhibition.

The induction of delayed hypersensitivity in guinea pigs to poly U and poly A:U.

Guinea pigs were sensitized to poly U and poly A:U so that subsequent stimulation of spleen cells from these immunized animals with poly U and poly A:U resulted in the production of migration inhibitory factor (MIF). MIF was also produced when spleen cells from animals immunized with poly A:U were cultured in the presence of mycobacterial RNA or whole viable H37 Ra cells. Negative dermal reactions were observed when guinea pigs immunized with poly A, poly A:U were skin tested wtih these same synthetic nucleotides.

The adjuvant activity of mycobacterial RNA preparations and synthetic polynucleotides for induction of delayed hypersensitivity to purified protein derivative in guinea pigs.

The adjuvant activity of mycobacterial RNA and synthetic polynucleotides for the induction of delayed hypersensitivity to PPD was determined. It was shown that when mycobacterial RNA or synthetic polynucleotides are injected together with purified protein derivative (PPD), delayed hypersensitivity to PPD developed as compared to no detectable delayed response when PPD was administered alone without adjuvant into guinea pigs. Four different criteria were employed to detect delayed hypersensitivity responses.

Nonspecific inhibition of growth of intracellular Listeria monocytogenes by lymphocyte culture products.

Supernatant fluids from mycobacteria-immune and mitogen-stimulated lymphocyte cultures were able to inhibit the intracellular growth of listeria in listeria-infected macrophages.

Relationship between tuberculin hypersensitivity and cellular immunity to infection in mice vaccinated with viable attenuated Mycobacterial cells or with Mycobacterial ribonucleic acid preparations.

The migration inhibition technique has been used to study delayed hypersensitivity in vitro by using peritoneal exudate cells and splenic lymphocytes from mice vaccinated with viable cells of the attenuated H37Ra strain of Mycobacterium tuberculosis and from mice vaccinated with ribonucleic acid (myc RNA) preparations obtained from viable mycobacterial cells of the same strain. Inhibition of macrophage migration was noted when purified protein derivative (PPD) or viable H37Ra cells were added to peritoneal exudate cells obtained from mice immunized with viable H37Ra cells and not from mice immunized with myc RNA. Splenic lymphocyte cultures were exposed to the same antigens in vitro.

Inhibition of migration of mouse macrophages by tuberculin-sensitive mouse lymphocytes and by mouse migration inhibitory factor.

The guinea pig migration inhibition technique, an accepted in vitro correlate of delayed hypersensitivity, has been adapted to a murine system. Peritoneal exudate cells from CF-1 mice vaccinated with viable cells of the H37Ra strain of Mycobacterium tuberculosis were inhibited in vitro by purified protein derivative (PPD) or whole H37Ra microorganisms. Peritoneal exudate cells from the inbred C57Bl/6 mice immunized with H37Ra cells also were inhibited in vitro by PPD or whole H37Ra microorganisms.