Search PubMed⌕ Search

Biomedical subjects

B Sims

Publications and source records attributed to B Sims.

17 recordsLinked to original sources
PubMed2001

How urban African American young adolescents spend their time: time budgets for locations, activities, and companionship.

The time budgets of a population of youth provide important information about their daily experience and socialization. This study reports data on the time budgets of a sample of 253 urban African American poor to working- and middle-class 5th-8th graders in Chicago. These youth were found to spend less time in school than other postindustrial adolescent populations, but spent no less time doing homework than White suburban U.S. young adolescents. They spent large quantities of time at home and with their families--at rates comparable to rates for young adolescents in a society with collectivist values like India. Unlike with other populations, early adolescence was not associated with major age changes in time allocations. Amount of time in schoolwork did not differ by grade, and amount of time with family did not show the decline with age that has been found for European American suburban adolescents.

Adolescent↗
PubMed1999

Regulation of AMP deaminase by phosphoinositides.

AMP deaminase (AMPD) converts AMP to IMP and is a diverse and highly regulated enzyme that is a key component of the adenylate catabolic pathway. In this report, we identify the high affinity interaction between AMPD and phosphoinositides as a mechanism for regulation of this enzyme. We demonstrate that endogenous rat brain AMPD and the human AMPD3 recombinant enzymes specifically bind inositide-based affinity probes and to mixed lipid micelles that contain phosphatidylinositol 4,5-bisphosphate. Moreover, we show that phosphoinositides specifically inhibit AMPD catalytic activity. Phosphatidylinositol 4,5-bisphosphate is the most potent inhibitor, effecting pure noncompetitive inhibition of the wild type human AMPD3 recombinant enzyme with a K(i) of 110 nM. AMPD activity can be released from membrane fractions by in vitro treatment with neomycin, a phosphoinositide-binding drug. In addition, in vivo modulation of phosphoinositide levels leads to a change in the soluble and membrane-associated pools of AMPD activity. The predicted human AMPD3 sequence contains pleckstrin homology domains and (R/K)X(n)(R/K)XKK sequences, both of which are characterized phosphoinositide-binding motifs. The interaction between AMPD and phosphoinositides may mediate membrane localization of the enzyme and function to modulate catalytic activity in vivo.

AMP Deaminase↗
PubMed1990

Nucleolar organiser regions: new prognostic variable in breast carcinomas.

Nucleolar organiser regions (NORs), which are important for regulating protein synthesis, were identified in 20 breast carcinomas by means of a silver (Ag) staining technique. Infiltrating neoplasms with metastases in four or more axillary lymph nodes possessed, on average, a greater number of AgNORs per cell nucleus compared with neoplasms without nodal disease, or with one to three positive lymph nodes. The size, morphology, and distribution of AgNORs within the nucleus were also different in the two study groups. Overall, these findings suggest that breast carcinomas with multiple, irregular, and widely dispersed AgNORs tend to be of high grade malignancy.

Breast Neoplasms↗
PubMed1986

Stability of aspirin in solid mixtures.

It has been shown that the degradation of aspirin in mixtures may be monitored by thermal analytical techniques. The methodology employed differential scanning calorimetry and thermal gravimetric analysis by standard techniques providing simple and rapid analysis for screening the stability of aspirin in mixtures. The degradation was found to depend on the nature of the additive but, in particular, the presence of acidic or basic groups within its structure.

Aspirin↗
PubMedDate not supplied

Elevated adenosine monophosphate deaminase activity in Alzheimer's disease brain.

Abnormal elevations in ammonia have been implicated in the pathogenesis of Alzheimer's disease. However, the biochemical mechanism(s) leading to increased ammonia in Alzheimer's disease have not yet been identified. A potential source of increased ammonia production is adenosine monophosphate (AMP) deaminase, an important enzyme in the regulation of the purine nucleotide cycle and adenylate energy charge. AMP deaminase activity is expressed in human brain and converts AMP to inosine monophosphate with the release of ammonia. We have investigated AMP deaminase activity in postmortem brain tissue from Alzheimer's disease subjects and age-matched controls. Compared to control brain, Alzheimer's disease brain AMP deaminase activity is 1.6- to 2.4-fold greater in the regions examined--the cerebellum, occipital cortex, and temporal cortex. Similar increases in AMP deaminase protein and mRNA levels are observed in Alzheimer's disease brain. These results suggest that increased AMP deaminase activity may augment ammonia levels in the brain in Alzheimer's disease.

AMP Deaminase↗