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Biomedical subjects

R D Anderson

Publications and source records attributed to R D Anderson.

15 recordsLinked to original sources
PubMed1992

Transcriptional enhancer factor (TEF)-1 and its cell-specific co-activator activate human papillomavirus-16 E6 and E7 oncogene transcription in keratinocytes and cervical carcinoma cells.

The human papillomavirus (HPV)-16 oncogenes, E6 and E7, are transcribed preferentially in keratinocytes and cervical carcinoma cells due to a 5' enhancer. An abundant peptide binding to a 37 nt enhancer element was purified from human keratinocytes by sequence-specific DNA chromatography. This protein was identified as transcriptional enhancer factor (TEF)-1 by complex mobility, binding to wild-type and mutant SV40 and HPV-16 enhansons and antigenic reactivity with two anti-TEF-1 antibodies. TEF-1 is cell-specific, but its transactivation also depends on a limiting, cell-specific TEF-1 'co-activator'. We show that both TEF-1 and the TEF-1 co-activator are active in human keratinocytes and essential for HPV-16 transcription. TEF-1 binding in vivo was necessary for HPV-16 P97 promoter activity. Excess TEF-1 and chimeric GAL4-TEF-1 specifically inhibited the P97 promoter by 'squelching', indicating that HPV-16 transcription also requires a limiting TEF-1 co-activator. TEF-1 and the TEF-1 co-activator functions mirrored HPV-16 transcription by their presence in keratinocytes and cervical carcinoma cells and their absence from lymphoid B-cells, but also functioned in liver cells where the HPV-16 promoter is inactive. TEF-1 and its associated co-activator are thus part of a complex mechanism which determines the restricted cell range of the HPV-16 E6 and E7 oncogene promoter.

Antibodies↗
PubMed1992

Mirror to ASHP: 1942-1992.

Highlights from the history of ASHP are presented on the occasion of the Society's 50th anniversary. Efforts to organize a formal group representing hospital pharmacists, begun in the 1920s, resulted in the formation of a subsection on hospital pharmacy of the American Pharmaceutical Association in 1936. In 1942, ASHP became a distinct organization affiliated with APhA. The body's goals were to establish minimum standards for pharmaceutical services, ensure a supply of well-qualified hospital pharmacists by providing hospital internships, facilitate information exchange, and foster cost-effective use of medicines. The development of practice standards and periodic surveys of hospital pharmaceutical services, educational efforts and accreditation programs, publications, and ASHP's role in the development of principles for hospital formulary systems are described. ASHP's endorsement of unit dose drug distribution and systems for preparation of intravenous admixtures is discussed. The evolution of pharmacists' clinical roles, their increased involvement in drug therapy decisions and the provision of drug information to patients, and the expanded responsibility implicit in the pharmaceutical care concept are traced. Today's ASHP members can build on the work of yesterday's members to provide better pharmaceutical care.

History, 20th Century↗
PubMed1991

DNA sequence specificity of doxorubicin-induced mutational damage in uvrB- Escherichia coli.

In the absence of excision repair, doxorubicin caused a striking (41-fold) increase in the frequency of large deletion mutations extending from the lac operator (lacO) into the lac repressor gene (lacI) of Escherichia coli. In contrast, there was only a 2-fold increase in the frequency of small deletions despite a 3-fold increase in overall mutation frequency. The 5'-endpoints of doxorubicin-induced lacO and lacI/lacO deletions occurred at the DNA sequence 5'-pyTAA or 5'-AATpy (where py is pyrmidine) (16%), at runs of purines or pyrimidines (41%) and adjacent to 5'-dGdC or 5'-dCdG doublets (34%). Ninety % (27 of 30) of the doxorubicin-induced deletions involving the region of the lacO palindrome had 3'-endpoints within the palindrome sequence as compared with 40% (4 of 10) spontaneous deletions in an untreated set. Doxorubicin-induced single base substitutions were highly focused at one site (4 of 6) in the i-d region of lacI, in contrast to the spontaneous distribution of point mutations, where 16 mutants were recovered at 12 different sites. An increased frequency (3-fold) of highly focused base substitutions was also observed at 2 sites in the lac operator region (at lacO +6, which is a transition "hotspot" in the spontaneous spectra of both wild type and uvrB- organisms and at the adjacent +5 site). Notably, the frequency of 1- and 2-base frameshifts did not increase in the doxorubicin-induced spectrum, relative to the spontaneous mutation spectrum. These in vivo observations in E. coli suggest that in the absence of excision repair, doxorubicin causes highly focused deletions and base substitutions. These mutations occur adjacent to DNA sequences identified in previous in vitro studies as preferential sites of doxorubicin binding.

Base Sequence↗
PubMed1991

The association between pregnancy and human papilloma virus prevalence.

This study examined the effects of pregnancy on the prevalence of HPV infection, comparing 69 pregnant and 54 nonpregnant age-frequency matched female patients. HPV prevalence was detected by DNA hybridization using the ViraPap/ViraType dot blot procedure. The prevalence of HPV among pregnant women increased with gestational age from 8.0% in the first trimester, to 16.7% in the second, and 23.1% in the third trimester. This finding suggests that HPV infection may be activated by hormonal or other effects of pregnancy and may explain why number of pregnancies is known to be associated with increased risk of cervical dysplasia and cancer. Oncogenic HPV types 16/18 and 31/33/35 were identified with almost equal frequency in the study population whereas HPV 6/11 was seen rarely. The logistic regression models indicate that there were no significant differences between HPV positive and HPV negative groups by age, income, number of sex partners, age of first intercourse, average frequency of intercourse per month, number of pregnancies, oral contraceptive duration, or pregnancy status. There were no interaction effects. A current Pap result of cervical dysplasia (OR = 8.9; 95% confidence interval: 2.1, 38.8), oral contraceptive use (OR = 0.1; 0.03, 0.6), and education (OR = 1.4; 1.1, 1.8) were significant predictors of HPV status.

Adolescent↗
PubMed1990

Transcriptional activation of the human papillomavirus-16 P97 promoter by an 88-nucleotide enhancer containing distinct cell-dependent and AP-1-responsive modules.

The P97 promoter upstream of the oncogenic early genes of human papillomavirus (HPV)-16 is active in keratinocytes and in cervical carcinoma cells due to a 5' keratinocyte-dependent cis enhancer. In this study, we have mapped the main enhancer activity to an 88-nucleotide (nt) fragment composed of multiple cis elements. A 63-nt promoter-proximal enhancer core was sufficient for P97 activation in a human keratinocytic cell line, HaCaT, and in cervical carcinoma cells. Although the enhancer functioned poorly in hepatoma cells or in fibroblasts, nuclear extracts from different cells protected similar cis elements from DNase I digestion. Two protected half-palindromic NF-I/CTF sites within the 63-nt core were necessary for its function; one represents a "cytokeratin element" (CK), a previously described 8-nt sequence shared with cytokeratin gene promoters. Both sites formed complexes of the same apparent size and relative binding affinity with NF-I/CTF-like factor(s) present in all cells tested. Although cell-dependent P97 activation could be determined by similar, yet distinct NF-I/CTF-like proteins, adjacent cis elements in the enhancer core were also required for function, and may thus interact with additional transcription factors. A 25-nt distal module with two AP-1 sites increased enhancer activity and cooperated with cis elements of the proximal core. Each AP-1 site as well as a third AP-1 site near the promoter bound c-Jun and Jun/Fos in vitro, and was activated by c-Jun and c-Fos in transfections. In addition to cell type-dependent activation, HPV-16 P97 transcription may therefore respond to growth factors and oncogene products via the AP-1 pathway.

Base Sequence↗
PubMed1979

Grouping of streptococci by Streptex.

Streptex was compared to routine laboratory identification methods available. The results from Streptex sometimes required several attempts before final identification could be achieved. In the main, group D streptococci other than Strep. faecalis failed to group with the Streptex antisera, and this method cannot therefore be used exclusively as a means of identifying this group of streptococci.

Immune Sera↗
PubMed1978

Liver-kidney relationship in radioisotopic localization of retroheptic and subhepatic masses.

Combined liver-kidney scintigrams in 46 patients were obtained by administering two radiopharmaceuticals labeled with 99mTc. A mass in the right adrenal or subhepatic area was demonstrated as a void or absence of activity between the organs. Normally, the activity in the liver and right kidney blends together so visual separation of organs is not possible. Two clinical cases, including ultrasonic and angiographic studies for comparison, are presented.

Abdominal Neoplasms↗
PubMed1977

1976 Harvey A.K. Whitney lecture: the peril of deprofessionalization.

It is argued that American pharmacy is in great peril of being deprofessionalized, and that hospital pharmacy practice offers the best hope for restoring public confidence in the profession. Pharmacists are criticized for a failing sense of mission and a waning dependence on knowledge. It is observed that pharmacy has diminished control over practitioner education. Various threats to the professional association of hospital pharmacists, and the need for ethical codes enforced by the profession are discussed. The concept of an American School of Hospital Pharmacy is supported. Hospital pharmacists are urged to become drug experts; it is suggested that pharmacists in hospitals be required to develop expertise in specific categories of drugs. It is concluded that pharmacy must use its drug knowledge effectively to avoid the peril of deprofessionalization.

Education, Pharmacy↗
PubMed1976

Tortuosity of the cavernous carotid arteries causing sellar expansion simulating pituitary adenoma.

Tortuous, medially-displaced cavernous carotid arteries may cause sellar enlargement which simulates pituitary adenoma. Systemic hypertension appears to account for this tortuosity in some cases, while a congenital anomaly is probably responsible in others. Medical position of the carotid sulci may be demonstrated on sellar tomography. Cerebral arteriography provides the correct diagnosis. Surgery, particularly transsphenoidal hypophysectomy, should be avoided in such patients.

Adenoma↗
PubMed1975

B-Mode sonography as a screening procedure for asymptomatic carotid bruits.

Sixty-five B-mode carotid sonograms were obtained at random on patients undergoing cerebral arteriography. A 5 mHz transducer was used. The results were correlated with magnified cervical carotid arteriograms obtained on these patients. B-mode sonography was accurate in evaluating the carotid arteries for surgical stenosis in 72 per cent of the cases. The feasibility of using B-mode sonography as a screening test in patients with asymptomatic carotid bruits is discussed.

Angiography↗