PubMed Health⌕ Search

Biomedical subjects

F Tabatabai

Publications and source records attributed to F Tabatabai.

5 recordsLinked to original sources
PubMed2000

PROFILE: Wetland Mitigation Banking: A Framework for Crediting and Debiting.

/ Wetland mitigation banking as a resource management tool has gained popular support for its potential to provide an ecologically effective and economically efficient means to fulfill compensatory mitigation requirements for impacts to aquatic resources. Although this management tool has been actively applied within the past 10 years (C. Short, 1988, Mitigation banking, in Biological Report 88(41):1-103), assessment of credits and determination of a compensation ratio that reflects existing and/or potential functional condition in a mitigation bank has been a formidable task. This study presents a framework for a systematic approach for determination of credits and debits and subsequently the compensation ratio. A model for riparian systems is developed based on this framework that evaluates credits and debits for spatial and structural diversity, contiguity of habitats, invasive vegetation, hydrology, topographic complexity, characteristics of flood-prone areas, and biogeochemical processes. The goal of developing this crediting and debiting framework is to provide an alternative to the current methods of determining credits and debits in a mitigation bank and assigning mitigation ratios, such as best professional judgement or use of preset ratios. The purpose of this crediting and debiting framework is to develop a method that (1) can be tailored to evaluate ecological condition based on the target resources of a specific mitigation bank, (2) is flexible enough to be used for evaluation of existing or potential ecologic condition at a mitigation bank, (3) is a structured and systematic way to apply data and professional judgment to the decision-making process, (4) has an ecologically defensible basis, (5) has ease of use such that the level of expertise and time required to employ the method is not a deterrent to its application, and (6) provides a semiquantitative measure of the condition of aquatic resources that can be translated to a mitigation ratio.

Journal Article↗
PubMed1989

Papillomavirus-associated inductions of cellular proteins in mouse C127 cells: correlation with the presence of open reading frame E2.

Bovine papillomavirus type 1 (BPV-1) readily transforms mouse C127 cells, conferring the ability to grow in soft agar and to form tumors in athymic (nu/nu) mice. Electrophoresis of total cellular proteins from these BPV-transformed lines on ultra-high resolution, giant two-dimensional gels displays the presence of novel, papillomavirus-related protein phenotypes. Analysis of the established BPV-1-transformed C127 cell lines, ID13 and ID14, reveals a set of six proteins which are either absent or synthesized at extremely low levels in the parental cell line. One of these proteins is also present in v-ras-transformed C127 cells, but none of the others are found in cells transformed by a variety of viral oncogenes, including the polyomavirus middle T, v-mos, or v-fes. The genome of BPV-1 contains two separate open reading frames (ORFs), E5 and E6, which can act independently to transform C127 cells. In addition, trans-activator and repressor proteins encoded respectively by the full-length and carboxy-terminal E2 ORF regulate the level of expression of other BPV-1 genes. We examined 34 cell lines transformed by intact and subgenomic recombinant DNAs of BPV-1. Cells harboring BPV-1 DNAs engineered to eliminate the expression of ORFs E4, E5, E6, or E7 display five of the PV-associated proteins, but these proteins are not seen in lines lacking the full E2 ORF. Moreover, G418-selected nontransformed cells expressing E2 cDNA from an SV40 promoter exhibit these proteins at high levels. Surprisingly, these proteins are also present in cells containing BPV-1 DNAs with amino-terminal E2 deletions, suggesting that these PV-associated proteins represent novel cellular responses to a factor encoded within the E2-C gene region.

Animals↗
PubMed1987

Transcriptional regulation of the human papillomavirus-16 E6-E7 promoter by a keratinocyte-dependent enhancer, and by viral E2 trans-activator and repressor gene products: implications for cervical carcinogenesis.

The transcriptional promoter of the candidate E6-E7 transforming gene region of human papillomavirus (HPV)-16 (P97) was active in transiently transfected cervical carcinoma cells when linked to the HSV-1 tk or bacterial cat genes. Sequences 5' to P97 contain a short enhancer element responding to cellular factor(s) in uninfected human foreskin keratinocytes and in cervical carcinoma cells, but not in human or animal fibroblasts. The E2 trans-activator products of HPV-16 or of the related bovine papillomavirus (BPV)-1 further elevated HPV-16-driven transcripts in co-transfections, and required the presence of E2-binding ACC(N)6GGT cores in cis. A 'short E2' C-terminal repressor gene product (sE2) of HPV-16 or the BPV-1 sE2 repressor not only inhibited viral E2 trans-activation, but also suppressed enhancer response to keratinocytic factors. Suppression by the sE2 products was abolished by deletion of the E2-binding cores in cis or by a mutation in the sE2 DNA binding domain. The keratinocyte-dependent enhancer is likely to contribute to the epithelial cell tropism of HPV-16, and may direct persistent E6-E7 gene transcription in response to cellular factors in cervical carcinoma cells in which the viral E2 genes are inactive.

Animals↗