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PubMed1989

Evidence for limits on the acceptability of lowest-tar cigarettes.

The sales of the lowest yield cigarettes (1-3 mg tar) seem to have been particularly resistant to the effects of promotion and advertising, while the sales of other low-yield cigarettes (4-9 mg tar) seem to have been increased by promotional efforts. This finding is consistent with the existence of a boundary of tar and nicotine acceptability below which consumers in general are not prepared to go. Use of lower tar cigarettes may be helpful for those who cannot stop smoking, but, since 1979, the percentage of cigarettes under 16 mg tar has changed little.

Advertising↗

PubMed1990

Information on tar and nicotine yields on cigarette packages.

We examined information on tar and nicotine yields on the packages of 160 cigarette brands, 58 percent of the 275 brands for which tar and nicotine yields were listed in a recent Federal Trade Commission report. The tar yield was indicated on 14 percent, the nicotine yield was indicated on 11 percent. As tar yield increased among brands, the yield was progressively less likely to be shown on the package and was not disclosed on the package of any cigarette yielding 11 mg or more of tar.

Humans↗

PubMed1996

Coal tar therapy. Is it carcinogenic?

Epidemiological studies indicate that occupational exposure to coal tar may lead to an increased risk of lung, scrotum and skin cancer. Furthermore, studies with laboratory rodents show carcinogenicity of coal tar after dermal application. This effect may be attributable to polycyclic aromatic hydrocarbons (PAH), which are ubiquitous coal tar constituents. Absorbed PAH can be metabolised to reactive derivatives that bind to DNA. These PAH-DNA binding products are thought to be involved in PAH-induced carcinogenesis. However, no clearly increased skin cancer incidences have been reported in psoriasis patients who have been exposed to therapeutically high doses of coal tar. To determine whether patients treated with coal tar actually have an altered risk of cutaneous malignancies, we suggest that further controlled studies and experiments are necessary. Future research should also focus on the possibility of increased risks of developing internal malignancies.

Animals↗

PubMed1990

Biological monitoring of human exposure to coal tar. Urinary mutagenicity assays and analytical determination of polycyclic aromatic hydrocarbon metabolites in urine.

The mutagenicity of urine extracts from anode plant workers exposed to coal tar pitch volatiles and non-smoking psoriatic patients treated with coal tar applications and UV light (Goeckermann regimen), was determined by the plate incorporation assay and the fluctuation test employing Salmonella typhimurium strain TA98 in the presence of rat liver post-mitochondrial fractions and deconjugating enzymes. The levels of total polycyclic aromatic hydrocarbons (PAHs) and of a marker metabolite of pyrene (1-hydroxypyrene) were determined in the urine of the same subjects. Both the occupational and in particular the therapeutic exposure to coal tar resulted in clear increases in urinary levels of PAH metabolites as compared to unexposed subjects. The level of 1-hydroxypyrene in the urine samples was comparable to or even greater than the corresponding level of total PAHs, indicating a poor recovery of PAH metabolites for this method. Following treatment with coal tar, most of the psoriatic patients excreted clearly increased levels of mutagens in their urine, while non-smoking anode plant workers showed no increase in urinary mutagenicity. The minimum levels of PAH metabolites corresponding to a significant increase in urinary mutagenicity varied from sample to sample, presumably depending on interfering factors present in different amounts in the extracts. Nonetheless the urine samples which were clearly mutagenic presented elevated levels of PAH metabolites, suggesting that the mutagenicity assays lack sufficient sensitivity to allow their application in the biological monitoring of most occupational exposures to coal tar.

Coal Tar↗

PubMed1988

The benefits, costs and risks of topical tar preparations in the treatment of psoriasis: considerations of cost effectiveness.

Cost-effectiveness analysis provides an analytical framework for comparing the costs, benefits, and risks of treatment. Using these techniques we evaluated topical tar in the treatment of psoriasis. Topical tar has, at most, a small benefit in accelerating the clearing of psoriasis. There is no systematic evidence to suggest that using topical tar during clearing extends the length of a remission. This analysis suggests that using topical tar may increase costs of therapy three-to thirteen-fold without substantial clinical benefits. Adequate data to support tar as a cost-effective agent in the treatment of psoriasis is lacking.

Administration, Topical↗

PubMed1987

The separate effects of tar and nicotine on the cigarette smoking manoeuvre.

The separate effects of tar and nicotine on the cigarette smoking manoeuvre were investigated. Each of ten asymptomatic habitual smokers smoked three different commercially available cigarettes in a randomised order. The brands were chosen such that two had the same tar yield (10 mg) and two had the same nicotine yield (1.4 mg). The volume of smoke inhaled into the lungs was measured by tracing the smoke with the inert gas 81Krm. Puffing indices were recorded using an electronic smoking analyser and flowhead/cigarette holder. There was no difference in the total volume of smoke puffed from each of the cigarette brands. With cigarettes of the same tar level, the total inhaled smoke volume was lower with the higher nicotine cigarette (P less than 0.05): by contrast, with cigarettes of the same nicotine level, the total inhaled smoke volume was lower with the lower tar cigarette (P less than 0.02). Tar and nicotine appear to exercise independent control over the volume of smoke inhaled.

Adult↗

PubMed1978

Crude coal tar plus near ultraviolet light suppresses DNA synthesis in epidermis.

Crude coal tar and a refined product, when they are combined with near ultraviolet (UV) light (UVA, 320-400 nm), depress DNA synthesis in vivo in normal and proliferating skin of the hairless mouse. Near ultraviolet light alone does not interfere with DNA synthesis, but coal tar without UVA does have an inhibitory effect on DNA synthesis of normal skin. This effect of coal tar without UVA is not as great as the effect of the combination of UVA and coal tar. Between 0.9 and 1.6 joules/sq cm of UVA are required for its biologic effect on DNA synthesis in coal-tar-treated skin.

Animals↗

PubMed1983

[Tar treatment in dermatology].

There is a controversial discussion of the carcinogenic action of coal tar used as a therapeutic agent in dermatologic practice. The carcinogen benzo(a)pyrene is present in most coal tar preparations, and it is a potent inducer of the aryl hydrocarbon hydroxylase activity in liver and skin after topical application. The formation of the most reactive metabolite of benzo(a)pyrene is catalyzed by aryl hydrocarbon hydroxylase hydroxylase. Topically used coal tar alters the mutagenicity of the urine indicating a systemic effect. These experimental data recommend to be very cautious in using coal tar as a therapeutic agent although there are only a few case reports on tumors after treatment with coal tar.

Administration, Topical↗

PubMed1983

Tar burns in the southwest.

The burns which result from contact of human skin with hot tar may be quite serious in proportion to the body surface area involved. Although tending toward partial thickness burns, patchy areas of full thickness skin loss are commonly observed. The use of petrolatum-based ointments on the burn initially to dissolve the tar into the dressings seems like the most efficient and humane method of tar removal. Subsequently, care of the wound is like that of any other burn. Tar burns involving greater than 10 per cent of the body surface area are likely to be the most serious and require intravenous fluid resuscitation. Many tar burns appear to be preventable.

Accidents, Occupational↗

PubMed1981

Skin cancer in patients with psoriasis treated with coal tar. A 25-year follow-up study.

For many years, crude coal tar has been used for the treatment of psoriasis. The possible carcinogenic effect of crude coal tar and ultraviolet (UV) radiation (Goeckerman regimen), considered individually or in combination, has been of some concern to physicians. A 25-year follow-up study was completed on 280 patients with psoriasis who were hospitalized and treated with crude coal tar and UV radiation at the Mayo Clinic, Rochester, Minn, during the years 1950 through 1954. The results of this study suggest that the incidence of skin cancer is not appreciably increased above the expected incidence for the general population when patients are treated with coal tar ointments. It seems that the Goeckerman regimen (topical crude coal tar combined with UV radiation) can be used with minimal risk for skin cancer in the treatment of psoriasis.

Adult↗

PubMed1976

Ultraviolet light and tar in the Goeckerman treatment of psoriasis.

In an attempt to evaluate and improve the Goeckerman treatment of psoriasis, combinations of tar and ultraviolet (UV) light were studied. The effects of UV irradiation alone, of curde coal tar (CCT) ointment alone, and of UV irradiation with 1% CCT ointment and with 6% CCT ointment on psoriatic lesions were compared. The combinations of 1% CCT ointment with UV irradiation and of 6% CCT ointment with UV irradiation were found to be equally effective. The combination of UV irradiation with ointment had little effect on psoriatic lesions. In most cases, the combination of 1% CCT ointment and UV irradiation was superior to high-concentration (6%) tar ointment without UV irradiation. This study suggests that UV light is an important component of the Goeckerman treatment ant that tar and UV irradiation are superior to tar alone.

Adolescent↗

PubMed1986

Parent to child transmission of the thrombocytopenia absent radius (TAR) syndrome.

We report on cases of the thrombocytopenia absent radius syndrome (TAR) in a family with the first documented occurrence of parent-to-child transmission. At least three other families have been reported in which TAR has been transmitted across generations. The pattern of transmission in these cases is not consistent with the simple autosomal recessive mode of inheritance which has been proposed. TAR syndrome may be a genetically heterogeneous disorder of the result of one of a group of related alleles. Given the increasing evidence for genetic and causal heterogeneity in TAR together with its similarity to conditions such as Holt-Oram, WT Limb-Blood and SC-Roberts Phocomelia syndromes it may be reasonable to view TAR as a developmental field defect rather than a genetic syndrome. Genetic counseling of affected individuals and their families should be modified to reflect the possibility of a recurrence risk as high as 50%.

Adult↗

PubMed1990

TAR independent activation of the human immunodeficiency virus in phorbol ester stimulated T lymphocytes.

Multiple regulatory elements in the human immunodeficiency virus long terminal repeat (HIV LTR) are required for activation of HIV gene expression. Previous transfection studies of HIV LTR constructs linked to the chloramphenicol acetyltransferase gene indicated that multiple regulatory regions including the enhancer, SP1, TATA and TAR regions were important for HIV gene expression. To characterize these regulatory elements further, mutations in these regions were inserted into both the 5' and 3' HIV LTRs and infectious proviral constructs were assembled. These constructs were transfected into either HeLa cells, Jurkat cells or U937 cells in both the presence and absence of phorbol esters which have previously been demonstrated to activate HIV gene expression. Viral gene expression was assayed by the level of p24 gag protein released from cultures transfected with the proviral constructs. Results in all cell lines indicated that mutations of the SP1, TATA and the TAR loop and stem secondary structure resulted in marked decreases in gene expression while mutations of the enhancer motif or TAR primary sequence resulted in only slight decreases. However, viruses containing mutations in either the TAR loop sequences or stem secondary structure which were very defective for gene expression in untreated Jurkat cells, gave nearly wild-type levels of gene expression in phorbol ester-treated Jurkat cells but not in phorbol ester-treated HeLa or U937 cells. High level gene expression of these TAR mutant constructs in phorbol ester-treated Jurkat cells was eliminated by second site mutations in the enhancer region or by disruption of the tat gene.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Proteins↗

PubMed1995

Use of a polyethylene glycol-peptide conjugate in a competition gel shift assay for screening potential antagonists of HIV-1 Tat protein binding to TAR RNA.

Interference of binding of Tat protein to TAR RNA in HIV-1-infected cells may be a useful therapeutic strategy for AIDS. An electrophoretic assay to screen potential low-molecular-weight (< 2 kDa) Tat antagonists has been established. A radiolabeled TAR RNA fragment (delta TAR) is retarded in mobility when bound by a Tat peptide-polyethylene glycol conjugate (Tat-PEG), which is used in place of the Tat protein. The assay determines the ability of a potential antagonist to compete with Tat-PEG for binding to delta TAR, as measured by interference with the gel shift of delta TAR. To discriminate between specific and nonspecific interactions, the assay is done in the absence or the presence of a 250-fold molar excess of tRNA.

Amino Acid Sequence↗

PubMed1998

Construction of human chromosome 16- and 5-specific circular YAC/BAC libraries by in vivo recombination in yeast (TAR cloning).

Transformation-associated recombination (TAR) in yeast was exploited for the selective isolation of human DNAs as large circular yeast artificial chromosomes (YACs) from two rodent/human hybrid cell lines containing human chromosomes 5 and 16. TAR cloning vectors containing the F-factor origin of replication were constructed for use in these experiments. Presence of the F-factor origin in TAR vectors provides the capability of transferring the YACs generated by in vivo recombination in yeast into Escherichia coli cells and propagating them as bacterial artificial chromosomes (BACs). A high enrichment of human versus rodent YACs was observed during isolation of human DNA from the rodent/human hybrid cell lines. Although <3% of the DNA content in the hybrid cells was human, as many as 75% of the transformants contained human YACs. In contrast to the standard YAC cloning method based on in vitro ligation, no human/mouse chimeras were observed during TAR cloning. The constructed human chromosome 16 YAC library had approximately 2.6x coverage, represented by 4320 YAC clones with an average insert size of 80 kb. YAC clones generated from chromosome 16 were successfully converted into BACs by electroporation of DNA isolated from yeast transformants into E. coli. The BAC clones represent approximately 0.6x chromosomal coverage. Pilot YAC and BAC libraries of chromosome 5 have been also constructed. The chromosomal distribution of YAC/BACs from chromosome 5 and chromosome 16 was evaluated by fluorescence in situ hybridization (FISH). The distribution of FISH signals appeared random along the length of each chromosome. We conclude that TAR cloning provides an efficient means for generating representative chromosome-specific YAC/BAC libraries.

Animals↗

PubMed1993

Hydrogen-bonding contacts in the major groove are required for human immunodeficiency virus type-1 tat protein recognition of TAR RNA.

The binding site for tat on TAR RNA was analysed by preparing a series of model RNA substrates carrying site-specific functional group modifications. The test RNAs were prepared by annealing two short synthetic oligoribonucleotides to form a duplex structure with a U-rich bulge and flanking sequences identical to TAR RNA. Tat binds these duplex RNAs with approximately half the affinity for wild-type TAR RNA. Substitution at positions U23 or U25 by the base analogue, O4-methyl-dT, which is deficient in its ability to hydrogen-bond at the N3 position reduces tat affinity more than 20-fold. Modifications to purines in the stem of TAR RNA that affect hydrogen-bonding ability in either the major or the minor groove of duplex RNA were also tested. Removal of the nitrogen atom at either the N7 position of G26 or at the N7 position of A27 reduces tat affinity 10- to 20-fold. By contrast removal of the exocyclic amino group in the minor groove at position G26, by substitution with inosine, does not affect tat binding significantly. A single methylphosphonate substitution at the phosphate bond between A22 and U23 also leads to a significant loss of tat binding ability, whereas all other methylphosphonate substitutions in the U-rich bulge are not harmful to tat binding. We conclude that tat forms multiple specific hydrogen bonds to a series of dispersed sites displayed in the major groove of the TAR RNA molecule. These include the N3-H of U23, the N7 of G26, the N7 of A26 and the phosphate between A22 and U23.

Base Sequence↗

PubMed1996

Effect of the position of TAR on transcriptional activation by HIV-1 Tat in vivo.

Efficient expression of the human immunodeficiency virus (HIV) genome requires the viral-encoded transactivator Tat. Tat interacts with the highly structured trans-activation-response (TAR) RNA that is found at the 5' end of all viral transcripts, and mediates the formation of transcription complexes that are capable of elongation through the entire length of the viral genome. By placing TAR immediately downstream from the P2 promoter of the mouse c-myc gene, we have previously shown that Tat can also direct transcriptional elongation through potential sites of premature termination within c-myc in transfected HeLa cells. We now demonstrate that Tat can activate c-myc transcription when TAR is positioned internally within the c-myc transcript at distances up to 353 nt downstream from the P2 promoter. We show that Tat can also activate transcription from the c-myc P1 promoter, which is located 165 nt upstream from P2 in these hybrid gene constructs. These novel findings show that Tat can activate transcription in vivo when TAR is positioned at distances up to 518 nt downstream from the site of transcriptional initiation. The ability of TAR to mediate Tat-activated transcription over distances greater than previously appreciated has important implications for the mechanism of action of Tat.

Animals↗

PubMed1997

Solution structure of the HIV-2 TAR-argininamide complex.

The trans-activating region (TAR) RNA-Tat protein interaction is important for activation of transciption in the human immunodeficiency virus (HIV). A model complex for this interaction composed of the two base bulge HIV-2 TAR and the amide derivative of arginine was studied by multidimensional heteronuclear NMR. Because of the improved spectral properties of the HIV-2 TAR complex, a larger number of NOEs in the bulge region were observed than in earlier studies of the HIV-1 TAR-argininamide complex. A total of 681 NOE distance restraints were collected and used to determine the solution structure of the HIV-2 TAR-argininamide complex. As observed in the previously proposed model from this lab, the two A-form stems co-axially stack and the critical U23 and the argininamide are located in the major groove. Model calculations including non-experimental restraints indicate that U23 is within hydrogen bonding distance to A27 consistent with the formation of a U x A x U base-triple. Base-triple formation helps open the major groove to increase the accessibility of G26 to hydrogen bond donors from the guanidinium group of argininamide. Argininamide binding is stabilized by stacking of the guanidinium group between the bases of A22 and U23, forming an argininamide sandwich.

Arginine↗