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Biomedical subjects

B Brady

Publications and source records attributed to B Brady.

13 recordsLinked to original sources
PubMed2000

Binaural-beat induced theta EEG activity and hypnotic susceptibility.

Six participants varying in degree of hypnotizability (2 lows, 2 mediums, and 2 highs) were exposed to 3 20-minute sessions of a binaural-beat sound stimulation protocol designed to enhance theta brainwave activity. The Stanford Hypnotic Susceptibility Scale, Form C (SHSS:C) was used for pre- and post-stimulus measures of hypnotic susceptibility. A time-series analysis was utilized to evaluate anterior theta activity in response to binaural-beat sound stimulation over baseline and stimulus sessions. The protocol designed to increase anterior theta activity resulted in a significant increase in percent theta for 5 of 6 participants. Hypnotic susceptibility levels remained stable in the high-susceptible group and increased significantly in the low and medium-susceptible groups.

Acoustic Stimulation↗
PubMed1999

Health-promoting lifestyles and exercise: a comparison of older African American women above and below poverty level.

The purpose of this study was to compare the health-promoting behaviors and exercise behaviors of older African American women above and below poverty level. Fifty-eight African American women completed a demographic form and the Health Promoting Lifestyle Profile (HPLP). Results indicated that African American women living above the poverty level had higher overall scores on the total HPLP and higher scores on the exercise subscale of the HPLP than women living below poverty level. Implications include teaching culturally specific, practical, and inexpensive exercise activities in primary care and community settings.

Black or African American↗
PubMed1996

DSK1, a novel kinesin-related protein from the diatom Cylindrotheca fusiformis that is involved in anaphase spindle elongation.

We have identified an 80-kD protein that is involved in mitotic spindle elongation in the diatom Cylindrotheca fusiformis. DSK1 (Diatom Spindle Kinesin 1) was isolated using a peptide antibody raised against a conserved region in the motor domain of the kinesin superfamily. By sequence homology, DSK1 belongs to the central motor family of kinesin-related proteins. Immunoblots using an antibody raised against a non-conserved region of DSK1 show that DSK1 is greatly enriched in mitotic spindle preparations. Anti-DSK1 stains in diatom central spindle with a bias toward the midzone, and staining is retained in the spindle midzone during spindle elongation in vitro. Furthermore, preincubation with anti-DSK1 blocks function in an in vitro spindle elongation assay. This inhibition of spindle elongation can be rescued by preincubating concurrently with the fusion protein against which anti-DSK1 was raised. We conclude that DSK1 is involved in spindle elongation and is likely to be responsible for pushing hal-spindles apart in the spindle midzone.

Anaphase↗
PubMed1993

Costimulation of T-cell activation and virus production by B7 antigen on activated CD4+ T cells from human immunodeficiency virus type 1-infected donors.

Infection with the human immunodeficiency virus type 1 (HIV-1) requires T-cell activation. Recent studies have shown that interactions of the T-lymphocyte receptors CD28 and CTLA-4 with their counter receptor, B7, on antigen-presenting cells are required for optimal T-cell activation. Here we show that HIV-1 infection is associated with decreased expression of CD28 and increased expression of B7 on CD4+ T-cell lines generated from seropositive donors by alloantigen stimulation. Loss of CD28 expression was not seen on CD4+ T-cell lines from seronegative donors, but up-regulation of B7 expression was observed upon more prolonged culture. Both T-cell proliferation and interleukin 2 mRNA accumulation in HIV-1-infected cultures required costimulation with exogenous B7 because these events were blocked by CTLA4Ig, a soluble form of CTLA-4 that binds B7 with high avidity. In contrast, levels of HIV-1 RNA were not affected by CTLA4Ig, indicating that regulation of virus transcription in these cultures did not depend upon CD28-B7 engagement. Infected T cells could present alloantigen to fresh, uninfected CD4+ T cells, leading to increased proliferation and virus spread to the activated cells. Both of these events were blocked by CTLA4Ig. Thus, chronic activation of HIV-1-infected CD4+ T cells reduces expression of CD28 and increases expression of B7, thereby enabling these T cells to become antigen-presenting cells for uninfected CD4+ T cells; this might be another mechanism for HIV-1 transmission via T-cell-T-cell contact.

Abatacept↗
PubMed1989

The perfect job.

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Aged↗
PubMed1988

Infection of a human leukemia K-562 cell line with Semliki Forest virus.

Infection of the human leukemia hematopoietic stem cell line, K-562, with Semliki Forest virus (SFV) can be characterized by three stages: (1) an early virus-proliferating stage lasting 1 to 4 days post-infection (pi) in which infectious virus is produced in high titers (10(3)pfu/cell) but in which there is minimal cytopathic effect. All cells appear viable by trypan blue dye exclusion, although they do not proliferate, and DNA and cell protein synthesis decrease to less than 3% of uninfected controls within 24 hours; (2) an intermediate stage extending from day 5 to about day 24-30 pi in which the amount of infectious virus declines to low levels. During this stage, viral protein synthesis decreases to undetectable levels, although viral gylcoproteins are readily demonstrated by immunofluorescence and by immunoblot; however, capsid protein appears to degrade within 21 days pi. Cell numbers remain constant but the viability of the non-proliferating cells determined by trypan blue exclusion could not be determined with confidence; (3) a final long-term stage in which viral glycoproteins, E1 and E2, are detectable by immunoblots and immunofluorescence for many months but the cells are metabolically inactive and do not synthesize viral proteins. These non-viable cells do not lyse for as long as 2 years.

Antigens, Viral↗
PubMedDate not supplied

Why am I a trustee?

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Community-Institutional Relations↗