PubMed Health⌕ Search

Biomedical subjects

E Faure

Publications and source records attributed to E Faure.

At least 19 recordsLinked to original sources
PubMed2006

Comparison of chaetognath mitochondrial genomes and phylogenetical implications.

Two complete mitochondrial genomes (mtDNAs) of chaetognaths, Spadella cephaloptera and Paraspadella gotoi, have been recently published. These genomes are highly unusual. They are the smallest metazoan mtDNAs so far known; atp6 and atp8 genes are missing; lastly, our reanalysis has evidenced that, contrarily to what has been previously published for one sequence, both contain a unique transfer RNA (tRNA(Met)) evidencing that both have the same gene content. Indeed, even if the gene order seems very different, two gene blocks are conserved. In addition, comparison of gene arrangement suggests phylogenetical relationships between chaetognaths and some lophotrochozoa like annelids and molluscs.

Animals↗
PubMed2005

Alternative peptide-fusion proteins generated by out-of-frame mutations, just upstream ORFs or elongations in mutants of human hepatitis B viruses.

By various means including out-of-frame mutations, just upstream ORFs and elongations, additional peptide fusions could be generated by mutants of Human Hepatitis B Virus (HBV). Numerous frameshift mutations inducing long alternative open reading frames have been evidenced in all HBV genes. Interestingly, these mutants are frequently detected in severe liver diseases, but seldom in asymptomatic carriers. The high level of conservation of some of these sequences in spite of the fact that they could be generated by different types of mutations, as their presence in mutants found on various continents, suggest that these mutations could play a role. These mutants could combine two advantages, that related to the loss of a part of a wild-type protein and that related to the putative advantage conferred by the additional sequences. In addition, in numerous Asian genomes (more than 300 to date) pre-X or pre-pre-S regions were found just upstream to, respectively, the X and the pre-S1 genes. These two regions are translated with their respective genes in frame and recent studies have evidenced the transactivating role of the corresponding proteins. With some exceptions, these regions are genotype- and serotype-specific (C/adr). In addition, these mutants have been found principally in patients with severe hepatitis diseases, for example, hepatocarcinoma in more than one third of the cases. As additional sequences generated by HBV variants may be relevant for viral life cycle, persistence and pathogenesis, further investigations are necessary to give a clearer picture of the subject.

Frameshift Mutation↗
PubMed2005

Multiple sclerosis and hepatitis B vaccination: could minute contamination of the vaccine by partial hepatitis B virus polymerase play a role through molecular mimicry?

Reports of multiple sclerosis developing after hepatitis B vaccination have led to the concern that this vaccine might be a cause of multiple sclerosis in previously healthy subjects. Some articles evidenced that minor Hepatitis B virus (HBV) polymerase proteins could be produced by alternative transcriptional or translational strategies. Their detection is very difficult because they are in minute concentration and probably enzymatically inactive, however, it was shown that they could be exposed on the outside of the virus particles and also be immunogenic. In addition, HBV polymerase shares significant amino acid similarities with the human myelin basic protein. We hypothesise that some of the apparent adverse reactions to the vaccine could be due to a process called of molecular mimicry, the HBV polymerase, which could be a contaminant in the recombinant or plasma-derived vaccines, could act as autoantigens and induce autoimmune demyelinating diseases such as multiple sclerosis.

Amino Acid Sequence↗
PubMed2002

Factors associated with early atrial fibrillation after ablation of common atrial flutter. A single centre prospective study.

BACKGROUND: The occurrence of early atrial fibrillation (< or = 6 months) after ablation of common atrial flutter is of clinical significance. Variables predicting this evolution in ablated patients without a previous atrial fibrillation history have not been fully investigated. OBJECTIVES: The aim of the present study was: (1) to identify predictive factors of early atrial fibrillation (< or = 6 months) in the overall population following atrial flutter catheter ablation; (2) to identify predictive variables of early atrial fibrillation following (< or = 6 months) atrial flutter catheter ablation within a subgroup of patients without documented prior atrial fibrillation. METHODS: This study prospectively included 96 consecutive patients (age 65 +/- 13 years; 18 women) over a 12-month period. Their counterclockwise flutter was ablated by radiofrequency, by the same operator, with an 8-mm-tip catheter. Clinical, electrophysiological and echocardiographic data were collected and 27 variables were retained for analysis: age; gender; type of atrial flutter (permanent vs paroxysmal); symptom duration (months +/- SD); pre-ablation history of atrial fibrillation; structural heart disease; left ventricular ejection fraction (%); left atrial size (mm); cava--tricuspid isthmus dimension; septal isthmus dimension; systolic pulmonary pressure > or < or = 30 mmHg; right atrial area; left atrial area; isthmus block; number of radiofrequency applications (+/- SD); antiarrhythmic drugs at discharge; left ventricular diastolic diameter; left ventricular systolic diameter; left ventricular telediastolic volume; left ventricular telesystolic volume; A-wave velocity (cm . s(-1)); E-wave velocity (cm . s(-1)); E/A; isovolumetric relaxation time; E-wave deceleration time; significant mitral regurgitation and flutter cycle length (ms). RESULTS: Of the 96 consecutive ablated patients, early atrial fibrillation was documented in 16 patients (17%). Atrial fibrillation occurred 30 +/- 46 days (range 1 to 171 days) after ablation. Univariate analysis associated an early occurrence of atrial fibrillation with: atrial fibrillation history, left ventricular ejection fraction, left atrial size, left ventricular telesystolic volume, A-wave velocity, significant mitral regurgitation and flutter cycle length. Multivariate analysis using a Cox model found that the only independent predictors of early atrial fibrillation were left ventricular ejection fraction and pre-ablation history of atrial fibrillation. In the subgroup without prior atrial fibrillation history (n=63; 66%), the only independent predictor of early atrial fibrillation was the presence of a significant mitral regurgitation. CONCLUSIONS: In a subgroup of patients without atrial fibrillation history, 8% of patients revealed an early atrial fibrillation. Mitral regurgitation is a strong predictive factor of early atrial fibrillation occurrence with 80% sensitivity, 78% specificity and 98% negative predictive value. These data should be considered in post-ablation management.

Adult↗
PubMed2001

Toll-like receptor-4 is expressed by macrophages in murine and human lipid-rich atherosclerotic plaques and upregulated by oxidized LDL.

BACKGROUND: Inflammation is implicated in atherogenesis and plaque disruption. Toll-like receptor 2 (TLR-2) and TLR-4, a human homologue of drosophila Toll, play an important role in the innate and inflammatory signaling responses to microbial agents. To investigate a potential role of these receptors in atherosclerosis, we assessed the expression of TLR-2 and TLR-4 in murine and human atherosclerotic plaques. METHODS AND RESULTS: Aortic root lesions of high-fat diet-fed apoE-deficient mice (n=5) and human coronary atherosclerotic plaques (n=9) obtained at autopsy were examined for TLR-4 and TLR-2 expression by immunohistochemistry. Aortic atherosclerotic lesions in all apoE-deficient mice expressed TLR-4, whereas aortic tissue obtained from control C57BL/6J mice showed no TLR-4 expression. All 5 lipid-rich human plaques expressed TRL-4, whereas the 4 fibrous plaques and 4 normal human arteries showed no or minimal expression. Serial sections and double immunostaining showed TLR-4 colocalizing with macrophages both in murine atherosclerotic lesions and at the shoulder region of human coronary artery plaques. In contrast to TLR-4, none of the plaques expressed TLR-2. Furthermore, basal TLR-4 mRNA expression by human monocyte-derived macrophages was upregulated by ox-LDL in vitro. CONCLUSIONS: Our study demonstrates that TLR-4 is preferentially expressed by macrophages in murine and human lipid-rich atherosclerotic lesions, where it may play a role to enhance and sustain the innate immune and inflammatory responses. Moreover, upregulation of TLR-4 in macrophages by oxidized LDL suggests that TLR-4 may provide a potential pathophysiological link between lipids and infection/inflammation and atherosclerosis.

Animals↗
PubMed2001

Decreased expression of Toll-like receptor-4 and MD-2 correlates with intestinal epithelial cell protection against dysregulated proinflammatory gene expression in response to bacterial lipopolysaccharide.

The lumenal surface of the colonic epithelium is continually exposed to Gram-negative commensal bacteria and LPS. Recognition of LPS by Toll-like receptor (TLR)-4 results in proinflammatory gene expression in diverse cell types. Normally, however, commensal bacteria and their components do not elicit an inflammatory response from intestinal epithelial cells (IEC). The aim of this study is to understand the molecular mechanisms by which IEC limit chronic activation in the presence of LPS. Three IEC lines (Caco-2, T84, HT-29) were tested for their ability to activate an NF-kappaB reporter gene in response to purified, protein-free LPS. No IEC line responded to LPS, whereas human dermal microvessel endothelial cells (HMEC) did respond to LPS. IEC responded vigorously to IL-1beta in this assay, demonstrating that the IL-1 receptor signaling pathway shared by TLRs was intact. To determine the reason for LPS hyporesponsiveness in IEC, we examined the expression of TLR4 and MD-2, a critical coreceptor for TLR4 signaling. IEC expressed low levels of TLR4 compared with HMEC and none expressed MD-2. To determine whether the low level of TLR4 expression or absent MD-2 was responsible for the LPS signaling defect in IEC, the TLR4 or MD-2 gene was transiently expressed in IEC lines. Transient transfection of either gene individually was not sufficient to restore LPS signaling, but cotransfection of TLR4 and MD-2 in IEC led to synergistic activation of NF-kappaB and IL-8 reporter genes in response to LPS. We conclude that IEC limit dysregulated LPS signaling by down-regulating expression of MD-2 and TLR4. The remainder of the intracellular LPS signaling pathway is functionally intact.

Antigens, Surface↗
PubMed2001

Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling.

Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. Here we report that HMEC are unresponsive to several additional biologically relevant TLR2 ligands, including, phenol-soluble modulin (PSM), a complex of three small secreted polypeptides from the skin commensal Staphylococcus epidermidis, soluble tuberculosis factor (STF), and Borrelia burgdorferi outer surface protein A lipoprotein (OspA-L). Expression of TLR2 renders HMEC responsive to all these ligands. We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Bacterial lipopolysaccharide activates HIV long terminal repeat through Toll-like receptor 4.

In HIV-infected patients, concurrent infections with bacteria and viruses are known to induce HIV replication as assessed by increases in plasma HIV RNA levels. In the present study, we determined the cell surface receptor and molecular mechanisms of enterobacterial LPS-induced HIV transcription. Human dermal microvessel endothelial cells (HMEC) were transfected with an HIV-long terminal repeat (LTR)-luciferase construct and subsequently stimulated with purified bacterial LPS. Our studies demonstrate that human Toll-like receptor 4 (TLR4) mediates LPS-induced NF-kappaB and HIV-LTR activation in HMEC through IL-1 signaling molecules, namely myeloid differentiation protein, IL-1R-associated kinase, TNFR-associated factor, and NF-kappaB-inducing kinase. Cotransfection of HMEC with HIV-LTR-luciferase and TLR4 cDNA from LPS-hyporesponsive C3H/HeJ mice abrogates LPS-induced HIV transcription as does the use of dominant-negative mutants of the IL-1 signaling molecules. Transfection of HMEC with an HIV-LTR-mutant that lacks the NF-kappaB binding site or pretreatment of cells with chemical inhibitors of the NF-kappaB pathway also blocked LPS-induced HIV-LTR transactivation. These data support the conclusion that TLR4 mediates enterobacterial LPS-induced HIV transcription via IL-1 signaling molecules and NF-kappaB activation plays an important role in HIV-LTR transactivation.

Animals↗
PubMed2001

Bacterial lipopolysaccharide and IFN-gamma induce Toll-like receptor 2 and Toll-like receptor 4 expression in human endothelial cells: role of NF-kappa B activation.

Toll-like receptor (TLR) 4 has been identified as the primary receptor for enteric LPS, whereas TLR2 has been implicated as the receptor for Gram-positive and fungal cell wall components and for bacterial, mycobacterial, and spirochetal lipoproteins. Vascular endothelial cell (EC) activation or injury by microbial cell wall components such as LPS is of critical importance in the development of sepsis and septic shock. We have previously shown that EC express predominantly TLR4, and have very little TLR2. These cells respond vigorously to LPS via TLR4, but are unresponsive to lipoproteins and other TLR2 ligands. Here we show that LPS, TNF-alpha, or IFN-gamma induce TLR2 expression in both human dermal microvessel EC and HUVEC. Furthermore, LPS and IFN-gamma act synergistically to induce TLR2 expression in EC, and LPS-induced TLR2 expression is NF-kappaB dependent. LPS and IFN-gamma also up-regulate TLR4 mRNA expression in EC. These data indicate that TLR2 and TLR4 expression in ECs is regulated by inflammatory molecules such as LPS, TNF-alpha, or IFN-gamma. TLR2 and TLR4 molecules may render EC responsive to TLR2 ligands and may help to explain the synergy between LPS and lipoproteins, and between LPS and IFN-gamma, in inducing shock associated with Gram-negative sepsis.

Cell Line↗
PubMed2001

Surgical treatment of active and sequelar forms of pulmonary tuberculosis.

BACKGROUND: The incidence of tuberculosis has risen since 1990, and in some countries, the resistant forms are becoming more and more frequent. Surgical treatment is once again needed to manage these problems. The purpose of this study was to analyze the indications and results of resection, which we performed for pulmonary tuberculosis. METHODS: From 1980 to 1997, 477 patients were operated on for thoracic or intrathoracic tuberculosis in Laennec Hospital, Paris (259 suffered lung diseases). There were 165 women and 94 men, aged 25 to 86 years (mean 46 years), from Europe (n = 148), North Africa (n = 65), Subsaharian Africa (n = 34), Asia (n = 7), and the West Indies (n = 5). This population was reviewed concerning the lung tuberculosis (sequelae or active lesions), the indications of lung resection, the type of resections performed, and the results at 1, 6, and 12 months. RESULTS: Active lesions were present in 97 cases and sequelae in 162. Surgery was performed for a therapeutic purpose in 104 patients with sequelae, and in 10 patients with active tuberculosis (pneumonectomy, n = 19; pleuropneumonectomy, n = 19; lobectomy, n = 54; and segmentectomy, n = 22). Surgery was performed for a diagnostic purpose in 54 patients with sequelae, and in 87 patients with active lesions (lobectomy, n = 32; segmentectomy, n = 19; wedge resection, n = 94, of which 11 performed by video-assisted thoracoscopy since 1991). One patient died after pleuropneumonectomy. We observed 25 complications: empyema, n = 7; hemothorax, n = 2; prolonged air leaks, n = 14; and pneumopathy, n = 2. All patients with active lesions subsequently were given antitubercular drugs. Follow-up was 100% at 1 month, 57% (n = 92) and 77% (n = 75) at 6 months for patients with sequelae and for patients with active lesions, respectively. All were asymptomatic with a normal chest roentgenogram. The number of operations for active lesions is increasing over the years, while it is decreasing for sequelar lesions. CONCLUSIONS: In our department, surgery is being performed more frequently to make a diagnosis in cases of active tuberculosis, and to treat complicated lesions in case of sequelae. Lung resection for active tuberculosis evolving under treatment or for drug resistance was rare. However, our study confirms the good results commonly obtained by surgery and supports the idea that surgery may help eradicate tuberculosis when social and economic circumstances render its medical management difficult or hazardous.

Adult↗
PubMed2001

Long-term follow-up of contralateral lobe in patients hemithyroidectomized for solitary follicular adenoma.

OBJECTIVES: Since there are no available conclusive studies on the long-term evolution of remnant thyroid tissue after hemithyroidectomy in patients who undergo surgery for solitary follicular adenomas, we searched for such cases in our records to elucidate this issue. DESIGN: Search criteria were as follows: (i) presence of a single palpable thyroid nodule with the remainder of the gland normal on palpation; (ii) clinically euthyroid status at the time of surgery; (iii) histological diagnosis of nodule as follicular adenoma; (iv) a hemithyroidectomy operation, sparing the contralateral lobe; (v) normal macroscopic aspect of the contralateral lobe at the time of surgery; and (vi) at least 4 years of postoperative follow-up. PATIENTS: Only 47 female cases were found to meet above criteria, with a mean age of 45.9 years (range: 23-79) at the time of surgery and a mean follow-up of 7.2 years (range: 4-32). Besides evaluating the presence or absence of antithyroid antibodies and the extranodular histology of tissue removed during surgery, a preoperative TRH test also allowed patients to be classified into two groups: normal extranodular thyroid (NET) (n = 32) and abnormal extranodular thyroid (AET) (n = 15). RESULTS: Eleven of the 15 patients with AET had thyroid autoimmunity, with or without overt histological thyroiditis, and the remaining four had subclinical hypothyroidism with negative antithyroid antibody titres. In the entire study population, only 28 patients received treatment with L-T4 immediately after surgery, none of whom had any alterations in the contralateral lobe. However, six of the nineteen patients not treated with T4 (31.6%) developed overt abnormalities in the contralateral lobe, including the only three with AET who had not received L-T4 treatment. The remaining three were two patients with NET, who showed postoperative TSH hyper-responsiveness to TRH (peak TSH > 25 mU/l), and one who developed a new follicular adenoma 32 years later. To date, none of the patients with NET, who had a normal TRH test after surgery, have developed any kind of alterations in the contralateral lobe, even those who received no L-T4 prophylactic treatment. CONCLUSIONS: The findings of this study suggest that: (i) there is a higher risk of follicular adenomas developing in a gland affected by thyroid autoimmunity than in a previously normal gland; (ii) L-T4 therapy may prevent the formation of new nodules or the development of goitre in the contralateral lobe; and (iii) in the absence of prophylactic treatment after surgery, the contralateral lobe of subjects with thyroid autoimmunity and/or previous subclinical hypothyroidism develops morphological abnormalities.

Adenoma↗
PubMed2001

Clinical characteristics, aetiological factors and long-term prognosis of myocardial infarction with an absolutely normal coronary angiogram; a 3-year follow-up study of 91 patients.

OBJECTIVES: The purpose of this study was to evaluate the clinical outcome of a large cohort of patients who suffered an acute myocardial infarction with absolutely normal epicardial coronary arteries at the post-myocardial infarction coronary angiogram. The aetiological and prognostic factors in this population were also analysed. BACKGROUND: Few data exist concerning the outcome, and aetiological and prognostic factors, of patients with myocardial infarction and angiographically absolutely normal coronary arteries. METHODS: Ninety-one patients (34 females/57 males; mean age 50+/-13 years, range 24--78 years) admitted with an acute myocardial infarction had absolutely normal coronary arteries at the angiogram performed 6.2+/-4 days (range 1--15 days) after the myocardial infarction, defined by smooth contours and no focal reduction (NC). Of the 91 NC patients, 71 were evaluated prospectively, alongside a systematic search of all aetiological factors reported in the literature. The NC patients were matched for age, sex, and the same period of myocardial infarction onset with a group of 91 patients with coronary artery stenosis (>50% diameter stenosis) at the angiogram performed 7.3+/-4 days (range 1--15 days) after the myocardial infarction (SC). RESULTS: The percent of smokers was similar between the two groups; higher prevalence rates of coronary heart disease family history, obesity, hypertension, hypercholesterolaemia and diabetes mellitus were found in SC (P=0.043 to 0.0001). In NC, coronary spasm was found in 15.5%, congenital coagulation disorders in 12.8%, collagen tissue disorders in 2.2%, embolization in 2.2%, and oral contraceptive use in 1.1%. Left ventricular ejection fraction at hospital discharge was higher in NC (60%+/-13%) than in SC (55%+/-13%, P=0.04). The mean follow-up was 35 months (range 1--100 months). Kaplan-Meier event-free survival, with the combined end-point defined as death, reinfarction, heart failure and stroke was 75% in NC vs 50% in SC (P<0.0001). Survival rate was 94.5% in NC compared to 92% in SC (ns). Univariate predictors of events in NC were left ventricular ejection fraction (P=0.03), age (P=0.02), diabetes (P=0.01), and smoking (P=0.03). Using Cox multivariate analysis, independent predictors of long-term outcome in NC patients were left ventricular ejection fraction (P=0.003) and diabetes (P=0.004). CONCLUSION: Aetiological factors, predominantly coronary spasm and inherited coagulation disorder, can be detected in only one third of the patients with myocardial infarction and absolutely normal coronary angiograms despite a systematic search in a prospective population. Mortality rates are similar but morbidity is lower in myocardial infarction patients with absolutely normal coronary angiography compared with those with coronary artery stenosis. The only two independent factors predictive of poor outcome in myocardial infarction patients with normal coronary arteries are left ventricular function and diabetes.

Adult↗
PubMed2001

Abnormal function of astroglia lacking Abr and Bcr RacGAPs.

Experiments in cultured cells have implicated the molecular switch Rac in a wide variety of cellular functions. Here we demonstrate that the simultaneous disruption of two negative regulators of Rac, Abr and Bcr, in mice leads to specific abnormalities in postnatal cerebellar development. Mutants exhibit granule cell ectopia concomitant with foliation defects. We provide evidence that this phenotype is causally related to functional and structural abnormalities of glial cells. Bergmann glial processes are abnormal and GFAP-positive astroglia were aberrantly present on the pial surface. Older Abr;Bcr-deficient mice show spontaneous mid-brain glial hypertrophy, which can further be markedly enhanced by kainic acid. Double null mutant astroglia are hyper-responsive to stimulation with epidermal growth factor and lipopolysaccharide and exhibit constitutively increased phosphorylation of p38 mitogen-activated protein kinase, which is regulated by Rac. These combined data demonstrate a prominent role for Abr and Bcr in the regulation of glial cell morphology and reactivity, and consequently in granule cell migration during postnatal cerebellar development in mammals.

Animals↗
PubMed2000

Bacterial lipopolysaccharide activates NF-kappaB through toll-like receptor 4 (TLR-4) in cultured human dermal endothelial cells. Differential expression of TLR-4 and TLR-2 in endothelial cells.

A missense mutation in the cytoplasmic domain of the Toll-like receptor-4 (TLR-4) has been identified as the defect responsible for lipopolysaccharide (LPS) hyporesponsiveness in C3H/HeJ mice. TLR-4 and TLR-2 have recently been implicated in LPS signaling in studies where these receptors were overexpressed in LPS non-responsive 293 human embryonic kidney cells. However, the signaling role of TLR-4 or TLR-2 in human cells with natural LPS response remains largely undefined. Here we show that human dermal microvessel endothelial cells (HMEC) and human umbilical vein endothelial cells express predominantly TLR-4 but very weak TLR-2 and respond vigorously to LPS but not to Mycobacterium tuberculosis 19-kDa lipoprotein. Transient transfection of non-signaling mutant forms of TLR-4 and anti-TLR-4 monoclonal antibody inhibited LPS-induced NF-kappaB activation in HMEC, while a monoclonal antibody against TLR-2 was ineffective. In contrast to LPS responsiveness, the ability of HMEC to respond to 19-kDa lipoprotein correlated with the expression of TLR-2. Transfection of TLR-2 into HMEC conferred responsiveness to 19-kDa lipoprotein. These data indicate that TLR-4 is the LPS signaling receptor in HMEC and that human endothelial cells (EC) express predominantly TLR-4 and weak TLR-2, which may explain why they do not respond to 19-kDa lipoprotein. The differential expression of TLRs on human EC may have important implications in the participation of vascular EC in innate immune defense mechanisms against various infectious pathogens, which may use different TLRs to signal.

Animals↗
PubMed2000

Differential expression of TGF-beta isoforms during postlactational mammary gland involution.

After cessation of lactation, the mammary gland undergoes involution, which is characterized by a massive epithelial cell death and proteolytic degradation of the extracellular matrix. Whereas the expression patterns and also the function of TGF-beta isoforms during mammary gland branching morphogenesis and lactation are well understood, their expression during postlactational involution and therefore a possible role in this process is poorly known. In this study we show that TGF-beta3 expression is dramatically induced (>fivefold) during mouse mammary gland involution when compared to that of virgin mouse, reaching a maximal expression level at day 4 after weaning. In contrast, other TGF-beta isoforms do not display significant increase in expression during involution (TGF-beta1, 1.3-fold and TGF-beta2, <1.5-fold) when compared to that of virgin or lactating mice. During mammary gland involution, TGF-beta3 is expressed in the epithelial layer and particularly in myoepithelial cells. A comparison of the kinetics of TGF-beta3 expression to that of programmed cell death and degradation of the basement membrane suggests that TGF-beta3 functions in the remodeling events of the extracellular matrix during the second stage of involution.

Animals↗
PubMed2000

Molecular phylogeography of western Mediterranean dusky grouper Epinephelus marginatus.

Intraspecific sequence variation in a portion of the gene coding for cytochrome b in the dusky grouper (Epinephelus marginatus Lowe 1834), an endangered fish species in various regions of the Mediterranean sea, was examined in 29 individuals from the western Mediterranean sea. Sixty-four phylogenetically informative nucleotide positions were present in a 353-base pair cytochrome b sequence, amplified using the polymerase chain reaction. Statistical analysis of the sequence data using a variety of tree-building algorithms separated the taxa into one group of dusky groupers corresponding to some of the Algerian individuals and another regrouped set of fishes originating in France, Tunisia and the remaining Algerian specimens. Although, on the basis of their morphology, E. marginatus are now considered as a single species, our results suggest that a subgroup of the Algerian dusky grouper constitutes a cryptic (undescribed) species. These results suggest that morphological and genetic evolution may be uncoupled in dusky grouper, resulting in morphological similarity between species despite extensive genetic divergence. In addition, we cannot rule out the possibility of gene introgression with other species of grouper. A more in depth phylogenetic analysis (i.e. between and within the different Epinephelus species) would likely affect many conservation management decisions about this assemblage of groupers.

Animals↗