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A Eichmann

Publications and source records attributed to A Eichmann.

At least 19 recordsLinked to original sources
PubMed1998

Paracrine and autocrine regulation of vascular endothelial growth factor during tissue differentiation in the quail.

The expression of vascular endothelial growth factor (VEGF) has been described to coincide both temporally and spatially with angiogenesis suggesting a role as a paracrine stimulator of endothelial cells. We have used digoxigenin labelled RNA probes to VEGF and the VEGF receptor-2 (Quek1) to investigate the relationship between VEGF expression and vascular events in quail embryos from day 1 to 13 of incubation. Furthermore, the effect of exogenously applied VEGF was studied in day 4 quail embryos using polyclonal anti-VEGF antibodies. Expression of VEGF mRNA was observed in day 1 and 2 embryos in regions of active angiogenesis and hemangiopoiesis. VEGF mRNA expression was found at high levels in the ventral aspect of the neural tube and Quek1 mRNA expression in the accompanying endothelial cells of day 3 embryos, suggesting a function in brain angiogenesis. However, in the neural tube, thyroid gland and cartilaginous skeleton VEGF mRNA was expressed at least 1 day before the ingrowth of vessels, suggesting that additional mechanisms are involved in control of angiogenesis. This is supported by the observation that application of VEGF165 into the midbrain induced dilatation of perineural vessels, while the intraneural vessels remained almost unaffected. Expression of VEGF mRNA was also observed at high levels in podocytes during all stages, indicative of its importance in glomerular development and function. The results of the present study indicate that as angiogenesis occurred in other tissues and organs (day 13 metanephros, dorsal third of the day 7 neural tube, skeletal muscle, and many mesodermal compartments), there was concurrent paracrine expression of VEGF mRNA and Quek1 mRNA. One noteable exception was the hepatocytes of the developing liver which appeared to remain VEGF-negative throughout the study. However, a small number of endothelial cells within liver sinuses, and additionally within the kidney and the elastic arteries, expressed VEGF mRNA. These results suggest that VEGF may also act as an autocrine mediator of angiogenesis, possibly as a result of localised tissue hypoxia.

Animals↗
PubMed1998

Avian VEGF-C: cloning, embryonic expression pattern and stimulation of the differentiation of VEGFR2-expressing endothelial cell precursors.

VEGF-C is a recently discovered secreted polypeptide related to the angiogenic mitogen VEGF. We have isolated the quail VEGF-C cDNA and shown that its protein product is secreted from transfected cells and interacts with the avian VEGFR3 and VEGFR2. In situ hybridization shows that quail VEGF-C mRNA is strongly expressed in regions destined to be rich in lymphatic vessels, particularly the mesenteries, mesocardium and myotome, in the region surrounding the jugular veins, and in the kidney. These expression sites are similar to those observed in the mouse embryo (E. Kukk, A. Lymboussaki, S. Taira, A. Kaipainen, M. Jeltsch, V. Joukov and K. Alitalo, 1996, Development 122, 3829-3837). We have observed VEGFR3-positive endothelial cells in proximity to most of the VEGF-C-expressing sites, suggesting functional relationships between this receptor-ligand couple. The comparison of the VEGF and VEGFR2 knockout phenotypes had suggested the existence of another ligand for VEGFR2. We therefore investigated the effect of VEGF-C on VEGFR2-positive cells isolated from the posterior mesoderm of gastrulating embryos. We have recently shown that VEGF binding triggers endothelial differentiation of these cells, whereas hemopoietic differentiation appears to be mediated by binding of a so far unidentified VEGFR2 ligand. We show here that VEGF-C also triggers endothelial differentiation of these cells, presumably via VEGFR2. These results indicate that VEGF and VEGF-C can act in a redundant manner via VEGFR2. In conclusion, VEGF-C appears to act during two different developmental phases, one early in posterior mesodermal VEGFR2-positive endothelial cell precursors which are negative for VEGFR3 and one later in regions rich in lymphatic vessels at a time when endothelial cells express both VEGFR2 and VEGFR3.

Amino Acid Sequence↗
PubMed1997

Ligand-dependent development of the endothelial and hemopoietic lineages from embryonic mesodermal cells expressing vascular endothelial growth factor receptor 2.

The existence of a common precursor for endothelial and hemopoietic cells, termed the hemangioblast, has been postulated since the beginning of the century. Recently, deletion of the endothelial-specific vascular endothelial growth factor receptor 2 (VEGFR2) by gene targeting has shown that both endothelial and hemopoietic cells are absent in homozygous null mice. This observation suggested that VEGFR2 could be expressed by the hemangioblast and essential for its further differentiation along both lineages. However, it was not possible to exclude the hypothesis that hemopoietic failure was a secondary effect resulting from the absence of an endothelial cell microenvironment. To distinguish between these two hypotheses, we have produced a mAb directed against the extracellular domain of avian VEGFR2 and isolated VEGFR2+ cells from the mesoderm of chicken embryos at the gastrulation stage. We have found that in clonal cultures, a VEGFR2+ cell gives rise to either a hemopoietic or an endothelial cell colony. The developmental decision appears to be regulated by the binding of two different VEGFR2 ligands. Thus, endothelial differentiation requires VEGF, whereas hemopoietic differentiation occurs in the absence of VEGF and is significantly reduced by soluble VEGFR2, showing that this process could be mediated by a second, yet unidentified, VEGFR2 ligand. These observations thus suggest strongly that in the absence of the VEGFR2 gene product, the precursors of both hemopoietic and vascular endothelial lineages cannot survive. These cells therefore might be the initial targets of the VEGFR2 null mutation.

Animals↗
PubMed1997

Expression of the avian VEGF receptor homologues Quek1 and Quek2 in blood-vascular and lymphatic endothelial and non-endothelial cells during quail embryonic development.

We have studied the expression of Quek1 and Quek2 (VEGFR-2 and VEGFR-3, respectively) in quail embryos from day 2 to day 16 by in situ hybridization with digoxigenin-labelled riboprobes on whole-mounts and paraffin sections. Parallel sections were also stained with the QH1 antibody to detect all endothelial cells and with an antibody against alpha-smooth-muscle-actin to reveal the media of blood vessels. Quek1/VEGFR-2 is a marker of blood-vascular and lymphatic endothelial cells throughout development. In 2-day-old embryos, it is expressed in the intra-embryonic vascular plexus, in cells (most probably angioblasts) located in the paraxial head mesoderm and in the somites, and caudo-laterally from Hensen's node. Thereafter, until about day 9, Quek1 is expressed in all endothelial cells. Cells positive and negative for Quek1 can later be found within the same vessel. Quek1 is additionally expressed in lymphatic endothelial cells. Occasionally, some non-endothelial cell types express Quek1. Quek2/VEGFR-3 is also a marker of endothelial cells; however, its expression pattern differs from that of Quek1. In 2-day-old embryos, Quek2 is expressed in the notochord and the intra-embryonic vascular plexus. Whereas all endothelial cells are Quek2-positive in 3-day-old embryos, expression is subsequently reduced to a subset of endothelial cells: arteries become Quek2-negative and then expression of Quek2 is limited to a few vessels that appear to be lymphatic. Endothelial cells of lymph nodes and the periaortal lymphatic vessels are Quek2-positive in later stages. A few non-endothelial cells express Quek2.

Animals↗
PubMed1997

The expression pattern of the mafB/kr gene in birds and mice reveals that the kreisler phenotype does not represent a null mutant.

The recessive mouse mutation kreisler affects hindbrain segmentation and inner ear development in homozygous mice. The mouse gene affected by the mutation was found to encode a basic domain leucine-zipper (bZIP)-type transcription factor of the Maf-family named kr (Cordes, S.P. and Barsh, G.S. (1994) Cell 79, 1025-1034). The avian bZIP transcription factor mafB, which shows high homology to kr, has been identified as an interaction partner of c-Ets 1 (Sieweke, M.H., Tekotte, M.H., Frampton, J. and Graf, T. (1996) Cell 85, 49-60). Here we demonstrate by Southern blot analysis that mafB is the avian homologue of kr, and present a detailed pattern of its expression during avian and murine embryonic development. Consistent with the kreisler phenotype, mafB is expressed in avians in the tissues which are affected by the mouse mutation: rhombomeres 5 and 6 (r5 and r6) and the neural crest derived from these rhombomeres. However, our analysis reveals a variety of additional expression sites: mafB/kr expression persists in vestibular and acoustic nuclei and is also observed in differentiating neurons of the spinal cord and brain stem. Restricted expression sites are found in the mesonephros, the perichondrium, and in the hemopoietic system. Since these expression sites are conserved between mouse and chicken we reexamined homozygous kreisler mice for unrevealed phenotypes in the hemopoietic system. However, peritoneal macrophages from homozygous kreisler mice were found to be functionally normal and still expressed mafB/kr. Other adult tissues examined from homozygous kreisler mice had also not lost mafB/kr expression. Our results thus indicate that the kreisler mutation involves a tissue specific gene inactivation and suggest additional roles for mafB/kr in later developmental and differentiation processes that are not revealed by the mutation.

Animals↗
PubMed1996

Molecular cloning of Quek 1 and 2, two quail vascular endothelial growth factor (VEGF) receptor-like molecules.

We have previously reported the cloning of two partial cDNAs corresponding to two quail (Coturnix coturnix japonica) receptor tyrosine kinases (RTKs), named Quek 1 and Quek 2, and their expression in endothelial cells of the early avian embryo. We here report the cloning of the full-size cDNAs for both molecules. Sequence comparison shows that Quek 1 and 2 share an overall amino acid (aa) identity of 49%. They both comprise seven extracellular immunoglobulin-like (Ig-like) domains, a single transmembrane domain, and an intracellular kinase domain split into two by a 70 aa insertion. These structural characteristics are shared by the members of the recently discovered VEGF receptor (VEGFR) family. We have compared the sequences of Quek 1 and 2 to the other VEGFRs. At the aa level, Quek 1 is most closely related to KDR/flk-1 (VEGFR 2) (aa identity of 69% and 71%, respectively). Quek 2 shows a similar degree of aa identity to fit-4 (VEGFR 3). Quek 1 and 2 display a lower homology to fit-1 (VEGFR 1) (about 45% aa identity). These data suggest that Quek 1 and 2 are the avian homologues of VEGFRs 2 and 3, respectively.

Amino Acid Sequence↗
PubMed1996

Endothelin-B receptor is expressed by neural crest cells in the avian embryo.

Disruptions of the genes encoding endothelin 3 (EDN3) and its receptor endothelin-B receptor (EDNRB) in the mouse result in defects of two neural crest (NC)-derived lineages, the melanocytes, and the enteric nervous system. To assess the mechanisms through which the EDN3/EDNRB signaling pathway can selectively act on these NC derivatives, we have studied the spatiotemporal expression pattern of the EDNRB gene in the avian embryo, a model in which NC development has been extensively studied. For this purpose, we have cloned the quail homologue of the mammalian EDNRB cDNA. EDNRB transcripts are present in NC cells before and during their emigration from the neural tube at all levels of the neuraxis. At later developmental stages, the receptor remains abundantly expressed in the peripheral nervous system including the enteric nervous system. In a previous study, we have shown that EDN3 enhances dramatically the proliferation of NC cells when they are at the pluripotent stage. We propose that the selective effect of EDN3 or EDNRB gene inactivation is due to the fact that both melanocytes and enteric nervous system precursors have to colonize large embryonic areas (skin and bowel) from a relatively small population of precursors that have to expand considerably in number. It is therefore understandable that a deficit in one of the growth-promoting pathways of NC cells has more deleterious effects on long-range migrating cells than on the NC derivatives which develop close to the neural primordium like the sensory and sympathetic ganglia.

Animals↗
PubMed1996

VEGF121 induces proliferation of vascular endothelial cells and expression of flk-1 without affecting lymphatic vessels of chorioallantoic membrane.

We have studied the effect of VEGF(121) homodimer and VEGF(121/165) heterodimer on the chorioallantoic membrane (CAM) of 13-day-old chick embryos. The factors were applied in doses of 2-4 micrograms and the effects were evaluated macroscopically after 2 and 3 days. Histological studies were performed on semi- and ultrathin sections. Proliferation was studied according to the BrdU-anti-BrdU method on whole mounts and sections. The labeling density was quantified in whole mounts. The fractal dimension, D, of the vascular tree was assessed as a value for vascular bifurcation density. Both forms of VEGF induce brush-like vessel formation in the precapillary region. New capillaries are found in the stroma of the CAM, which normally does not contain capillaries. Our results show that VEGF(121) is a specific endothelial cell mitogen. A fourfold increase of BrdU-labeled endothelial cells is found after VEGF(121) application. The fractal dimension of the vascular tree increases from 1.26 in the controls to 1.44 (VEGF(121)) and 1.41 (VEGF(121/165)). The endothelial cells of the newly formed capillaries possess many mitochondria and micropinocytotic vesicles, but no fenestrations. These capillaries are obviously formed by intussusceptive microvascular growth. Signs of sprouting are almost absent. An effect on the lymphatic vessels of the CAM is not detectable. Compared to VEGF(165) and VEGF(121/165), VEGF(121) diffuses over a slightly greater distance. Using in situ hybridization, VEGF receptor-2 (flk-1/Quek1) and the homologous flt-4 (Quek2) receptor were studied in the CAM of normal quail embryos and after VEGF(121) application on the CAM of 11-day-old quail embryos. During normal development, flk-1 expression becomes restricted to vascular endothelial cells of large vessels in the stroma of the CAM. VEGF(121) application induces expression of flk-1 in capillaries that normally do not express the receptor. In the normal development of the CAM, flt-4 becomes restricted to endothelial cells of vessels that appear to be lymphatic vessels. Application of VEGF(121) does not alter flt-4 expression.

Allantois↗
PubMed1996

[African histoplasmosis in a patient with HIV-2 infection].

9 months after immigration into Switzerland, a 38-year-old male patient from Liberia/West Africa developed granulomatous and subsequently ulcerative nodules in the face. The heterosexual patient, with no history of i.v. drug abuse, tested positive for HIV-2. Histology of a skin biopsy revealed superficial colonization by numerous fungal elements described as spores and hyphae that were compatible with the initial isolation of Candida parapsilosis. The definite diagnosis of African histoplasmosis was established 3 weeks later after review of the PAS-stained direct smear and after cultures had grown a cream-colored mold subsequently identified as Histoplasma capsulatum var. duboisii. There were no signs of disseminated disease. The lesions cleared under therapy with itraconazole (200 mg q 24h for 2 weeks, subsequently 100 mg q 24h) as well as ketoconazole and Aqua Dalibour (A. zinco-cuprica) locally for 2 months. Follow-up was not possible. Despite alarmingly increasing numbers of HIV-positive patients in Africa, the general incidence of African histoplasmosis seems to be stable with only a few cases per year. To our knowledge only four cases of disseminated African histoplasmosis have been reported in HIV-positive patients; localized cutaneous infection as in our patient, seems to be the exception. The low incidence of this infection is in contrast to the substantial number of HIV-positive patients with disseminated histoplasmosis by H. capsulatum var. capsulatum in the United States.

AIDS-Related Opportunistic Infections↗
PubMed1996

Chancroid.

Explore the source record for details and available documents.

Chancroid↗
PubMed1995

The angiogenic potentials of the cephalic mesoderm and the origin of brain and head blood vessels.

We have used two molecular markers to label blood vessel endothelial cells and their precursors in the early avian embryo. One marker, called Quek1, is the avian homologue of the mammalian VEGF receptor flk-1 and the other is the MB1/QH1 monoclonal antibody. Quek1 is expressed in a subset of mesodermal cells from the gastrulation stage. Quek1 positive cells later form blood vessel endothelial cells and express the MB1/QH1 antigen which is specific for endothelial and hemopoietic cells of the quail species. These two markers allowed us first to show that the cephalic paraxial mesoderm has angiogenic potentials which are much more extended than its trunk counterpart (the somites). Secondly, the origin of the endothelial cells lining the craniofacial and head blood vessels was mapped on the 3-somite stage cephalic mesoderm via the quail-chick chimera technique, in which well defined mesodermal territories are exchanged between stage-matched embryos of both species in a strictly isotopic manner. We found that the anterior region of the cephalic paraxial mesoderm is largely recruited to provide the forebrain and the upper face with their vasculature. This means that large volumes of tissues are vascularized by a discrete region of the cephalic mesoderm, the fate of which is otherwise to give rise to muscles. The widespread expansion of the angiogenic cells arising from the anterior paraxial mesoderm must be related to the high growth rate of the anterior region of the neural primordium, yielding the telencephalon and of the neural crest-derived facial structures which are themselves devoid of angiogenic potencies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

[Skin changes in HIV infections].

The spectrum of dermatologic findings related to human immunodeficiency virus includes a variety of cutaneous and mucocutaneous disorders. The most frequent diagnoses are oral candidiasis, seborrheic dermatitis, pyodermas and Kaposi's sarcoma. Distinctive skin lesions occur at various stages of HIV infection. Especially herpes zoster, seborrheic dermatitis and oral candidiasis may act as indicators, and their recognition is of particular importance for the early diagnosis of HIV infection and for the prevention of further opportunistic infections. In addition, some dermatologic findings as mollusca contagiosa and Kaposi's sarcoma occur mostly as late manifestations and may constitute a cutaneous correlate of advanced cellular immune deficiency.

AIDS-Related Opportunistic Infections↗
PubMed1994

Distinct developmental expression of a new avian fibroblast growth factor receptor.

We have cloned a new member of the fibroblast growth factor receptor family from avian embryonic RNA. The FREK (for fibroblast growth factor receptor-like embryonic kinase) primary transcript can be alternatively spliced in a tissue- and stage-specific manner to give rise to molecules containing either two or three Ig-like domains. During elongating primitive streak stages, FREK is expressed in the rostral and lateral epiblast and in the Hensen's node. From 2.5 days of development (E 2.5) on, it is expressed in various ectoderm- and mesoderm-derived structures. Most striking is FREK expression in the skeletal muscle lineage. It is highly expressed in the early myotome and, at later stages, in all skeletal muscles of the embryo. From E9 to hatching, FREK expression in the muscles decreases dramatically but is maintained in satellite cells of adult muscles. FREK transcript is elevated upon addition of basic fibroblast growth factor to serum-starved satellite cells. From this study, we conclude: (1) that the structure and pattern of expression of FREK set it apart from other cloned fibroblast growth factor receptors (FGFR) and suggest that FREK is a new member of that family; (2) that FREK may play multiple roles in early avian development, including a specialized role in the early differentiation of skeletal muscle.

Amino Acid Sequence↗
PubMed1993

[Sexually transmissible diseases following travel in tropical countries].

Travel to tropical countries is an important factor in the spread of sexually transmitted diseases. In spite of intensive anti-AIDS campaigns, some 30% of Swiss tourists have casual sexual contacts abroad. The prevalence of sexually transmitted diseases is higher in tropical countries than in western industrialized countries. More than 25% of cases of gonorrhea treated in Switzerland from 1989-1991 were imported from abroad. The penicillin producing Neisseria gonorrhoeae strains (PPNG) isolated in Switzerland from 1989-1991 are mainly imported from abroad (60%). The typical "imported sexually transmitted diseases" in Switzerland are chancroid, lymphogranuloma venereum and donovanosis. The clinical manifestations, laboratory and special examinations, and treatment of these diseases are described. The most frequent sexually transmitted disease from the so-called "imported tropical STD's" is chancroid. Chancroid is also a major risk factor for HIV infection.

Chancroid↗
PubMed1993

Two molecules related to the VEGF receptor are expressed in early endothelial cells during avian embryonic development.

We present the partial cloning and the expression patterns of two putative growth factor receptor molecules named Quek1 and Quek2 (for quail endothelial kinase) in chick and quail embryos from gastrulation to embryonic day 9 (E9). Quek1 and Quek2 show high homology to three interrelated murine and human genes, flk-1, KDR and flt. Flt was recently shown to be the receptor for the endothelial cell mitogen vascular endothelial growth factor (VEGF). In situ hybridization of Quek1 and Quek2 to sections of avian embryos showed that they are both expressed essentially by endothelial cells, that we identified with a monoclonal antibody (Mab) QH1 specific for endothelial and white blood cells of the quail. Quek1 is expressed in the mesoderm from the onset of gastrulation, whereas Quek2 message is first detected on QH1-expressing endothelial cells. The expression pattern of Quek1 suggests that it could identify the putative precursor of both endothelial and hematopoietic lineages, the hemangioblast. Quek1 and Quek2 are not expressed in all endothelial cells throughout life. At E9, after the initial phase of vasculogenesis, these genes are switched off in various compartments of the vascular network.

Animals↗