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At least 163 records · Page 9Linked to original sources
PubMed1998

Principal stress analysis in LDA measurement of the flow field downstream of 19-mm Sorin Bicarbon heart valve.

Heart valve replacement has become, since many years, a common surgical practice. Along with the improvement that the patients' health has derived from it, however, a certain amount of risk could not be avoided, bound to the inevitable hemodynamic disturbances that an artificial device generates. A major shortcoming, often reported, is the formation of thrombus on the edge of the prosthetic valve, with a possible obstruction of the orifices through which blood should normally flow undisturbed. Hemolysis is another possible consequence of the implantation of a mechanical heart valve, generally correlated to turbulence downstream of prosthetic heart valves (PHV). As it is agreed upon by many researchers, the risk of thrombogenicity or hemolysis is higher in those valves that are more subject to promote turbulence and flow separation in the flow through them. In the following paper, we present a study of the turbulence-related shear stress downstream of a bileaflet valve of minimum size (19 mm external diameter) Sorin Bicarbon. This size was chosen, accordingly to the Food & Drug Administration (FDA) draft guidance suggestion to investigate the worst case in turbulence promoted by PHVs, in order to have the highest velocity gradients and shear stresses for the FDA-stated cardiac output (6 1/min), related to maximum Reynolds number conditions. Velocity data were collected with the two-dimensional laser Doppler anemometry (LDA) technique; whereas this approach does not investigate directly all three components of the flow field, in the present case (bileaflet valves) it is not a limitation to the assessment of the maximum turbulence shear stress (TSS), thanks to the two-dimensional flow nature downstream of bileaflet models. Data taken in coincident mode were elaborated in order to determine the maximum shear stress in the measured points in the flow field, using the 2D Principal Stress Analysis (PSA). The consequences of a variable principal normal stress direction all along the measured profile will be illustrated in terms of differences between measured and maximum shear stresses. Results show the need to estimate the maximum values for the TSS and the direction along which it is obtained to correctly define the turbulent flow field downstream of PHVs.

Blood Flow Velocity↗
PubMed2005

Complex biallelic IGH rearrangements in IgM-expressing Z-138 cell line: Involvement of downstream immunoglobulin class switch recombination.

Chromosomal translocations involving the immunoglobulin (Ig) receptor loci usually disrupt and silence these loci. On the basis of observations in follicular lymphoma (FL) with downstream Ig heavy chain (IGH) class switch recombination (CSR), we hypothesized that downstream CSR-mediated chromosomal translocations would leave the V(D)J-Cmu transcription unit intact, thereby still allowing IgM expression from the IGH allele involved in the translocation. To test this hypothesis, we analyzed biallelic IGH translocations in the IgM-expressing cell line Z-138 by interphase FISH, DNA fiber-FISH, long-distance vectorette PCR, and DNA sequencing. One IGH allele was involved in a t(11;14), showing a break in the JH region that juxtaposed the Emu enhancer and the 3' Calpha enhancers to the cyclin D1 gene. The other IGH allele contained a t(8;14) breakpoint involving the 3' end of a Sgamma region, whereas the reciprocal breakpoint at 8q24 was approximately 40 kb centromeric of MYC. Molecular analysis showed that this IGH allele harbored a normal V(D)J-Cmu complex, which is responsible for IgM expression. These data show that chromosomal breakpoints such as the t(8;14) can occur in downstream IGH constant regions and do not necessarily interfere with Ig expression.

3' Flanking Region↗
PubMed2005

beta-Catenin splice variants and downstream targets as markers for neoplastic progression of esophageal cancer.

This study characterizes the frequency of exon 3 CTNNB1 mutations and compares the expression of CTNNB1 transcript variants and downstream targets MYC and WAF1 (p21) across the neoplastic progression of esophageal squamous cell carcinomas (ESCCs). Mutational analysis was performed on 56 tumors and corresponding germline DNA, using primers to exon 3 of CTNNB1 and SSCP DNA sequencing gels. Quantitative Real Time RT-PCR was performed on 45 foci representing the histological spectrum from normal to invasive cancer, using specific primer sets for alternative splice variants that differ by the presence (16A) or absence (16B) of a 159-bp noncoding segment of exon 16 of CTNNB1, in conjunction with downstream targets MYC and WAF1. Two unique mutations were identified, S37F in the SxxxS repeat region, and a germline polymorphism, T59A. Thus, mutation of CTNNB1 exon 3 is a rare event in this population. RT-PCR analysis successfully confirmed the presence of both beta-catenin splice variants in histologically normal and preneoplastic squamous epithelium, and invasive tumors of the esophagus, and identified a significant reduction in the 16A/16B ratio (P = 0.014) and an accompanying significant increase in the MYC/WAF1 expression ratio (P = 0.001) with progression from normal mucosa to dysplasia. This represents the first identification of two CTNNB1 transcripts in histologically "normal" esophageal squamous cells, squamous dysplasia, and invasive ESCC. These results show an increase in the minor mRNA (16B) isoform and changes in the expression of downstream markers consistent with increased transcription during the histological progression from normal to squamous dysplasia.

Alternative Splicing↗
PubMed1994

The site of 3' end formation of histone messenger RNA is a fixed distance from the downstream element recognized by the U7 snRNP.

Two conserved elements direct the 3' end processing of histone messenger RNA: a stem-loop structure immediately upstream of the site of cleavage and the histone downstream element (HDE), located 12-19 nucleotides downstream of the stem-loop in the premessenger RNA. We studied the role of these two elements by systematically inserting up to 10 C residues between them in the mouse H2A-614 histone pre-mRNA. 3' End mapping of RNAs processed in vitro demonstrated that as the HDE is move downstream, the site of cleavage correspondingly moves 3'. In addition, the efficiency of processing declines. In the wild-type substrate, cleavage occurs 3' of an A residue; modest increases in the efficiency of processing of the insertion mutants were observed when an A residue was placed at the new cleavage site. The results of psoralen cross-linking studies and immunoprecipitations using anti-trimethylguanosine antibodies indicated that the decreased processing efficiency of the insertion mutants is not due to impaired binding of the U7 small nuclear ribonucleoprotein (snRNP). We conclude that the mammalian U7 snRNP acts as a molecular ruler, targeting enzymatic components of cleave histone pre-mRNAs a fixed distance from its binding site, the HDE.

Animals↗
PubMed2007

Connective tissue growth factor (CTGF/CCN2) is a downstream mediator for TGF-beta1-induced extracellular matrix production in osteoblasts.

Connective tissue growth factor (CTGF/CCN2) is a cysteine-rich, extracellular matrix (ECM) protein that acts as an anabolic growth factor to regulate osteoblast differentiation and function. Recent studies have identified CTGF as a downstream effector of transforming growth factor-beta1 (TGF-beta1) for certain functions in specific cell types. In this study, we examined the role of CTGF as a downstream mediator of TGF-beta1-induced ECM production and cell growth in osteoblasts. Using primary cultures, we demonstrated that TGF-beta1 is a potent inducer of CTGF expression in osteoblasts, and that this induction occurred at all stages of osteoblast differentiation from the proliferative through mineralization stages. TGF-beta1 treatment of osteoblasts increased the expression and synthesis of the ECM components, collagen and fibronectin. When CTGF-specific siRNA was used to prevent TGF-beta1 induction of CTGF expression, it also inhibited collagen and fibronectin production, thereby demonstrating the requirement of CTGF for their up-regulation. To examine the effects of TGF-beta1 on osteoblast cell growth, cultures were treated with TGF-beta1 during the proliferative stage. Cell number was significantly reduced and the cells exhibited a decrease in G1 cyclin expression, consistent with TGF-beta1-induced cell-cycle arrest. Cultures transfected with CTGF siRNA prior to TGF-beta1 treatment showed an even greater reduction in cell number, suggesting that TGF-beta1-induced growth arrest is independent of CTGF in osteoblasts. Collectively, these data demonstrate for the first time that CTGF is an essential downstream mediator for TGF-beta1-induced ECM production in osteoblasts, but these two growth factors function independently regarding their opposing effects on osteoblast proliferation.

Animals↗
PubMed2001

Identification of putative downstream genes of Oct-4 by suppression-subtractive hybridization.

As a step toward understanding how toti/pluripotence is maintained by Oct-4, we have first constructed a cell model with differentially expressed Oct-4 in embryonic stem cells, and then used suppression-subtractive hybridization (SSH) method to identify the downstream genes of Oct-4. Among the 384 clones we screened, 40 clones were detected as differentially expressed genes with colony hybridization, and 13 clones were confirmed as the putative downstream genes of Oct-4 by Northern blot analysis. Sequencing showed 12 different genes, 8 known genes (Oct-4, Rex-1, Sox-2, Creatine kinase B, Makorin 1, Importin beta, Histone H2A.Z, Ribosomal protein S7) and 4 new genes. Except Oct-4 and Rex-1, the other genes have not been reported to be regulated by Oct-4. These results showed that SSH provides a very efficient means to identify the downstream genes of transcription factor. Some known genes identified may provide new insight of the function of Oct-4 in stem cells.

Animals↗
PubMed2002

Targeted deletion of the MLC1f/3f downstream enhancer results in precocious MLC expression and mesoderm ablation.

The expression of skeletal muscle contractile proteins is tightly regulated during embryonic development. In the mouse, the myosin light chain (MLC) 1f/3f gene locus is not activated until E9.5, exclusively in skeletal muscle precursor cells. A potent enhancer downstream of the MLC1f/3f locus confers correct temporal and spatial activation of linked reporter gene in transgenic mouse embryos. To examine roles of the MLC downstream enhancer (MLCE) in its native context of the MLC1f/3f gene locus, we eliminated a 1.5-kb DNA segment containing the enhancer from the mouse genome by targeted deletion, leaving no exogenous sequences at the deletion site. Mouse embryos homozygous for the MLCE deletion were smaller and developmentally delayed, formed no mesoderm by E7.5, and were resorbed almost completely at E8.5. In situ hybridization and RT-PCR analyses of affected mutant embryos at E7.5 revealed ectopic MLC transcripts, whose products would be predicted to interfere with a variety of nonmuscle cell functions determining differentiation of mesoderm. These results suggest that the MLC downstream enhancer and its flanking sequences include negative regulatory elements which block precocious activation of MLC expression in mesodermal precursors during a critical window of development, as well as positive elements which subsequently permit tissue-restricted MLC transcription in differentiating skeletal muscles.

Animals↗
PubMed2002

lon-1 regulates Caenorhabditis elegans body size downstream of the dbl-1 TGF beta signaling pathway.

In Caenorhabditis elegans, two well-characterized TGF beta signaling cascades have been identified: the Small/Male tail abnormal (Sma/Mab) and Dauer formation (Daf) pathways. The Sma/Mab pathway regulates body size morphogenesis and male tail development. The ligand of the pathway, dbl-1, transmits its signal through two receptor serine threonine kinases, daf-4 and sma-6, which in turn regulate the activity of the Smads, sma-2, sma-3, and sma-4. In general, Smads have been shown to both positively and negatively regulate the transcriptional activity of downstream target genes in various organisms. In C. elegans, however, target genes have remained elusive. We have cloned and characterized lon-1, a gene with homology to the cysteine-rich secretory protein (CRISP) family of proteins. lon-1 regulates body size morphogenesis, but does not affect male tail development. lon-1 is expressed in hypodermal tissues, which is the focus of body size determination, similar to sma-2, sma-4, and sma-6. Using genetic methods, we show that lon-1 lies downstream of the Sma/Mab signaling cascade and demonstrate that lon-1 mRNA levels are up-regulated in sma-6-null mutant animals. This provides evidence that lon-1 is negatively regulated by Sma/Mab pathway signaling. Taken together, these data identify lon-1 as a novel downstream target gene of the dbl-1 TGF beta-like signaling pathway.

Amino Acid Sequence↗
PubMed2002

Distinct patterns of downstream target activation are specified by the helix-loop-helix domain of proneural basic helix-loop-helix transcription factors.

Both gain- and loss-of-function analyses indicate that proneural basic/helix-loop-helix (bHLH) proteins direct not only general aspects of neuronal differentiation but also specific aspects of neuronal identity within neural progenitors. In order to better understand the function of this family of transcription factors, we have used hormone-inducible fusion constructs to assay temporal patterns of downstream target regulation in response to proneural bHLH overexpression. In these studies, we have compared two distantly related Xenopus proneural bHLH genes, Xash1 and XNgnr1. Our findings indicate that both Xash1 and XNgnr1 induce expression of the general neuronal differentiation marker, N-tubulin, with a similar time course in animal cap progenitor populations. In contrast, these genes each induce distinct patterns of early downstream target expression. Both genes induce expression of the HLH-containing gene, Xcoe2, at early time points, but only XNgnr1 induces early expression of the bHLH genes, Xath3 and XNeuroD. Structure:function analyses indicate that the distinct pattern of XNgnr1-induced downstream target activation is linked to the XNgnr1 HLH domain, demonstrating a novel role for this domain in mediating the differential function of individual members of the proneural bHLH gene family.

Amino Acid Sequence↗
PubMed1997

Multiple downstream promoter modules regulate the transcription of the Drosophila melanogaster I, Doc and F elements.

The basal promoters of three Drosophila long interspersed nuclear elements (LINEs), the I factor and the F and Doc elements, have the same architecture. In each, transcription is directed by an initiator which is faithfully and efficiently recognized only when flanked 3' by a DNA segment approximately 20 bp in length called the B region. The B regions of the three promoters are interchangeable and have a complex structure, comprising three functionally distinct elements: de1, de2 and de3. While de2 is relatively conserved, fitting the consensus RGACGTGY, de1 and de3 vary among the three promoters. At different levels, each downstream element is able to ensure accurate recognition of the initiator. The de2 domain stimulates transcription of the F, I and Doc promoters to the same extent. In contrast, the I de1 domain stimulates transcription much more efficiently than the corresponding domains of the F and Doc elements. The finding that de2 is selectively required in order to detect full activity of enhancer sequences found in the F element suggests that de1 and de2 interact with different proteins. The B regions can be replaced by and synergize with a TATA element, can functionally substitute for downstream promoter sequences in the Drosophila hsp70 gene, and significantly activate the mouse terminal deoxynucleotidyl transferase initiator. Our data suggest that the B regions stimulate transcription by providing sites of interaction for the TFIID complex. Sequences homologous to the del to de3 array are found downstream from the transcription start site(s) both in TATA-less and TATA-containing promoters.

Animals↗
PubMed1998

Characterization of the initiator and downstream promoter elements of herpes simplex virus 1 late genes.

Previously identified cis-acting regulatory elements of herpes simplex virus (HSV) 1 late promoters include a TATA element upstream from the start of transcription, an initiator-like element at the start of transcription, and sequences downstream from the start of transcription. To determine whether these elements are functionally equivalent to similar elements from other eukaryotic genes, model late promoters were constructed using well-characterized regulatory elements from non-HSV genes. These modular promoters were then inserted into the viral genome upstream from a lacZ marker gene. Results showed that a eukaryotic initiator element, along with a TATA element, can function as a late HSV promoter. Several initiator sequences from both viral and nonviral genes were functionally similar to the initiator-like element in HSV-1 late promoters; however, a random sequence of the same size and a similarly located sequence from the HSV-1 early thymidine kinase promoter could not substitute for the initiator element. These results indicate that eukaryotic initiator elements are functionally equivalent to HSV-1 late promoter initiator elements. In addition, the downstream element of the late glycoprotein C promoter was further analyzed by construction of a series of small deletions and insertions. The presence of the downstream glycoprotein C region in a promoter consisting of a strong TATA and initiator element increased mRNA expression by a modest amount; this effect appeared to be sequence specific and dependent on its exact alignment with the upstream elements of the promoter.

Animals↗
PubMed2001

Hepatitis C virus core protein modulates the interferon-induced transacting factors of Jak/Stat signaling pathway but does not affect the activation of downstream IRF-1 or 561 gene.

Hepatitis C virus (HCV) has a propensity to cause chronic infection, with a low proportion of patients exhibiting a sustained response to interferon-alpha (IFNalpha) therapy. An earlier report suggested that HCV inhibits IFNalpha-induced signal transduction through the Jak/Stat pathway by preventing the formation of the transacting factor ISGF3 complex, although the effect on downstream pathway and the specific viral protein responsible for inhibition of IFNalpha-mediated signal transduction were not elucidated. HCV core protein displays a number of intriguing functional properties and has been implicated in virus-mediated pathogenesis. In this study, we have analyzed the effect of core protein upon IFNalpha- or IFNgamma-induced regulation of the Jak/Stat signaling pathway. HCV core protein expression exhibited a reduced Stat1 expression in IFN-treated mammalian cells. A gel retardation assay suggested a reduced level of formation of the transacting factors, GAF and ISGF3, in IFN-treated cells. Further studies from protein expression and RNase protection assay revealed that the reduced level of GAF or ISGF3 formation could be attributed to modulation of Stat1 protein expression, an important player for innate immunity in host defense mechanism. However, these modulatory effects did not interfere with the activation of the downstream effector genes, IRF-1 and 561, in IFN-treated cells. Stable transfectants of cells after introduction of a plasmid DNA encoding both the structural and the nonstructural proteins of HCV also exhibited a similar effect. Taken together, these results suggest that although expression of the core protein alone or with other HCV proteins modulate transacting factors of Jak/Stat signaling pathway, expression of the downstream effector genes IRF-1 and 561 remains unaffected upon IFN treatment and may contribute to host defense mechanism.

DNA-Binding Proteins↗
PubMed2005

Downstream processing in marine biotechnology.

Downstream processing is one of the most underestimated steps in bioprocesses and this is not only the case in marine biotechnology. However, it is well known, especially in the pharmaceutical industry, that downstreaming is the most expensive and unfortunately the most ineffective part of a bioprocess. Thus, one might assume that new developments are widely described in the literature. Unfortunately this is not the case. Only a few working groups focus on new and more effective procedures to separate products from marine organisms. A major characteristic of marine biotechnology is the wide variety of products. Due to this variety a broad spectrum of separation techniques must be applied. In this chapter we will give an overview of existing general techniques for downstream processing which are suitable for marine bioprocesses, with some examples focussing on special products such as proteins (enzymes), polysaccharides, polyunsaturated fatty acids and other low molecular weight products. The application of a new membrane adsorber is described as well as the use of solvent extraction in marine biotechnology.

Aquaculture↗
PubMed1994

A unique sequence located downstream from the rice mitochondrial atp6 may cause male sterility.

Asymmetric cell-fusion of the japonica cultivar of Oryza sativa (rice) with cytoplasmic-male-sterile (CMS) plants bearing cytoplasm derived from Chinsurah Boro II, resulted in two classes of cytoplasmic hybrids (cybrids), fertile and CMS. Southern-blot analysis of the mitochondrial DNA (mtDNA) indicates recombination events around a number of genes; however, the appearance of the CMS character is tightly correlated to reorganization around the atp6 gene, suggesting recombination downstream from the atp6 gene is involved in CMS. The nucleotide sequence downstream from atp6 contains a pseudogene which was probably created by recombination of the mitochondrial genome. Sense and antisense transcripts of the downstream region of atp6 were found in CMS- and restored CMS (fertile)-lines, but not in the normal (fertile) line. In the CMS line, several antisense transcripts of the atp6 gene were also found. However, in the restored line which contains a nuclear-encoded gene, Rf-1, the levels of these transcripts were lower than in the CMS line. These results suggest abnormal transcripts of the atp6 gene produced in the antisense direction may be involved in CMS, and that products of the nuclear-encoded restorer gene may reduce abnormal transcription in this region of the mitochondrial genome.

Base Sequence↗
PubMedDate not supplied

Steady flow velocity field and turbulent stress mappings downstream of a porcine bioprosthetic aortic valve in vitro.

Velocity profiles and Reynolds stresses downstream of heart valve prostheses are vital parameters in the study of hemolysis and thrombus formation associated with these valves. These parameters have previously been evaluated using single-point measurement techniques such as laser Doppler anemometry (LDA). The purpose of this study is to map the velocity vector fields and Reynolds stresses downstream of a porcine bioprosthetic heart valve in the aortic root region with particle image velocimetry (PIV) techniques in vitro under steady flow conditions. PIV is essentially a multipoint measurement technique that allows full-field measurement of instantaneous velocity vectors in a flow field, thus allowing us to map the entire velocity or stress field over the aortic root (where single-point measurements are difficult). Coupled with flow visualization techniques, the hydrodynamic consequences of introducing a porcine bioprosthetic heart valve into the aortic root was examined, and compared with data obtained from an empty aortic root and an aortic root with the valve mounting ring alone. From our velocity and stress mappings, we found that the valve mounting ring effectively diminishes the central orifice area, giving rise to a higher central axial flow with strong recirculating regions and a corresponding large pressure drop. This in turn produces an intermixing zone between the central jet and recirculating region further downstream from the valve, which contributes to the high-stress zone measured. The development of the flow is further restricted by the valve stents, giving rise to stagnation regions and wakes. High-velocity gradients were also measured at the interface of the jet and recirculating region in the sinus cavity. The overall view of the velocity and stress mappings helps to identify regions of flow disturbances that otherwise may be lost with single-point measuring systems. Although the PIV measurements may lack the accuracy of single-point measuring systems, the overall view of the flow in the aortic root region compensates for the shortcoming.

Animals↗
PubMed2006

Activated Src and Ras induce gefitinib resistance by activation of signaling pathways downstream of epidermal growth factor receptor in human gallbladder adenocarcinoma cells.

PURPOSE: Although gefitinib, a selective inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, has been demonstrated to exhibit its antitumor activity by the blockade of EGF receptor, the role of signaling pathways downstream of EGFR in gefitinib sensitivity remains unknown. In this study, we investigated the mechanistic role of Src and Ras, major oncogene products implicated in the pathogenesis of many human cancers in gefitinib sensitivity. METHODS: Using parental and v-src- or c-H-ras-transfected HAG-1 human gallbladder adenocarcinoma cell lines, effects of gefitinib on cytotoxicity, cell cycle purtubation and apoptosis, and tyrosine phosphorylation of EGFR, Akt, and Erk were determined by WST-1 assay, flow cytometry, and Western blots, respectively. RESULTS: Activated Ras and Src conferred a strong resistance to gefitinib by nearly 30-fold and 200-fold, respectively. Gefitinib induced accumulation of cells in the G0/G1 phase of the cell cycle at 24-h, with progressive expansion of apoptotic cell population in parental HAG-1 cells, but these effects were completely abolished in v-src- or c-H-ras-transfected cell line. Upon gefitinib treatment, EGFR activation and subsequent downstream activation through Erk and Akt were significantly inhibited in HAG-1 cells. By contrast, gefinitib failed to inhibit the activation of both Akt and Erk in v-src-transfected cells and Erk, but not Akt in c-H-ras-transfected cells, despite the blockade of EGFR activation in these respective cell lines. Treatment of v-src-transfected cells with herbimycin A, a Src tyrosine kinase inhibitor, partially reversed the gefitinib resistance, with concomitant inhibition of Akt and Erk. CONCLUSION: Our results suggest that activated Ras and Src could induce gefitinib resistance by activating either or both of Akt and Erk signaling pathways, thus providing a strategic rationale for assessment of these specific signaling molecules downstream of EGFR to customize treatment.

Antineoplastic Agents↗
PubMed2005

Translation enhancement by optimized downstream box sequences in Escherichia coli and Mycobacterium smegmatis.

The effect on translation of downstream box sequences optimized for binding to Mycobacterium smegmatis and Escherichia coli 16S rRNA in the absence of a Shine-Dalgarno (SD) region was investigated. The relative translational efficiency of each construct in either M. smegmatis or E. coli was determined. Eradication of the SD region in the absence of a downstream box abolished the translation activity. In contrast, optimized downstream box constructs resulted in a 13- and 18-fold increase in protein synthesis, relative to non-optimized DB controls in E. coli and M. smegmatis, respectively.

Base Sequence↗
PubMed1988

Application of fluorescence densitometry to the study of net albumin uptake by the rabbit aortic wall up- and downstream of intercostal ostia.

A method was developed for measuring levels of lissamine rhodamine B-labelled albumin in arterial walls with a spatial resolution of ca. 1 micron 3. The method was used to study variation in net macromolecular uptake up- and downstream of intercostal ostia in a small number of rabbit aortae. The physical and biological properties of the fluorescent tracer, including its stability, were compatible with its use in vivo. Tracer was injected into the ear vein of conscious rabbits. After 3 h the rabbits were anaesthetized and the thoracic aorta was fixed in situ at physiological pressure. The vessel was embedded in epoxy resin and longitudinal sections of the aortic wall were cut through the centre of the intercostal ostia. Photomicrographs were used to record fluorescence from these sections. The optical density across the photomicrographs was measured and related to the distribution of tracer in the wall. Mean intima-medial levels of tracer were greater downstream of ostia than upstream but were lower near the flow divider than further downstream. Higher levels of tracer were found in the adventitia than in the media and, in the latter, the distribution appeared to be related to the lamellar structure.

Animals↗