Neuropilin-1 is a placenta growth factor-2 receptor

Placenta growth factor (PlGF) belongs to the family of vascular endothelial growth factors (VEGFs). It binds to the flt-1 VEGF receptor but not to the KDR/flk-1 receptor which is thought to mediate most of the angiogenic and proliferative effects of VEGF. Three PlGF isoforms are produced by alternative splicing. PlGF-1 and PlGF-3 differ from PlGF-2 since they lack the exon 6 encoded peptide which bestows upon PlGF-2 its heparin binding properties. Cross-linking experiments revealed that 125I-PlGF-2 binds to two endothelial cell surface receptors in a heparin dependent fashion. The binding of 125I-PlGF-2 to these receptors was inhibited by an excess of PlGF-2 and by the 165-amino acid form of VEGF (VEGF165), but not at all by VEGF121 and very marginally if at all by PlGF-1. The apparent molecular weight and the binding characteristics of these receptors correspond to those of the recently identified VEGF165 specific receptor neuropilin-1, and we therefore conclude that neuropilin-1 is a receptor for PlGF-2. The binding of 125I-PlGF-2 as well as the binding of 125I-VEGF165 to these receptors was inhibited by a synthetic peptide derived from exon 6 of PlGF. Furthermore, the binding of 125I-PlGF-2, but not that of 125I-VEGF165, was also inhibited by a synthetic peptide derived from exon 7 of PlGF. These observations indicate that the peptides encoded by these exons probably participate in the formation of the domain which mediates the binding of PlGF-2 to these receptors. We have also determined, using chemically modified heparin species, that the presence of sulfate moieties on the glucosamine-O-6 and on the iduronic acid-O-2 groups of heparin was required for the potentiation of 125I-PlGF-2 binding to these receptors. To determine if PlGF-2 is able to induce biological responses that are not induced by PlGF-1, we compared the effects of PlGF-1 and PlGF-2 on the migration and proliferation of endothelial cells. Both PlGF forms induced migration of endothelial cells. However, there was no quantitative difference between the response to PlGF-2 and the response to PlGF-1. Furthermore, neither PlGF-1 nor PlGF-2 had any effect upon the proliferation of the endothelial cells.     

Preparation of P-47 scintillators for STEM

Uniform P-47 powder scintillators can be prepared with reproducible mass thicknesses by sedimenting the powder in an 0·01% solution of formvar in chloroform. A reflecting coating can be glued by floating a 60 nm aluminium film on the scintillation layer in an 0·1% solution of gelatine in water. The optimum thickness of P-47 for 20–100 keV electrons increases slower than the electron range due to the absorption and scattering of light with increasing thickness. An aluminium coating increases the light output by a factor 1·85 for 20 keV and 1·4 for 100 keV electrons. The noise of the emitted light quanta and the photomultiplier detection system shows a minimum for the optimum thickness of largest light output and is only a factor 1·3–1·6 larger than the calculated shot noise of the incident electron beam.     

A STEM/X-ray microanalytical study of the equilibrium segregation of bismuth in copper

Combined scanning transmission electron microscopy (STEM) and X-ray microanalysis have been used to detect the equilibrium segregation of bismuth to grain boundaries in copper. Quantification of the X-ray data gives grain boundary bismuth concentrations close to those reported previously by Auger electron spectroscopy (AES). Samples tempered at low temperatures (773,873 K) had detectable bismuth concentrations at more boundaries than those samples tempered at high temperature (1073 K). There is evidence that the degree of segregation varies strongly from boundary to boundary.     

The maternal and fetal levels of human chorionic gonadotropin, human placental lactogen and prolactin during the perinatal period (author's transl)

The levels of human chorionic gonadotropin (HCG), human placental lactogen (human choriosomatomamotropin HCS) and prolactin (PRL) were determined in the serum of 72 maternity patients and the serum of the newborn infants. The determinations were done with radioimmunologic tests (RIA). These three protein hormones were also determined in the amniotic fluid and in the maternal serum from 4-6 days prior to the delivery of the infant. The concentration of HCG or HCS in the serum of the newborn infants was a mean 0.43 or 0.37% of the level in the maternal serum. The concentration of PRL in the serum of the newborn was 118% and slightly higher than in the serum of the mothers. The concentration in the amniotic fluid was 1.5% for HCG, 5.8% for HCS, and 252% for PRL, compared to the corresponding levels in the maternal serum. The fact that the hormone concentrations in the amniotic fluid are significantly higher than in the serum of the newborn suggests excretion of the hormones from the fetal circulation via the fetal liver and the fetal kidney. The high levels of PRL in the maternal and the newborn serum may be caused by the high concentrations of estrogen or progesterone. Increased during the course of the pregnancy there was a significant sex linked difference in the level of HCG in the maternal serum correlated to the sex of the newborn infant.     

The possibilities and dangers of longterm infusion therapy in severely ill newborn and premature infants

The development of pediatric intensive medicine in the past 10 years has today made it possible to carry out specific longterm infusion therapy even in severely ill newborn and premature infants. The present study discusses the various technical possibilities and indications for the introduction of a caval catheter in newborn and premature infants. Although we only used a caval catheter for longterm parenteral nutrition in 9 newborn infants from 1965 to 1969, improved techniques have enabled us over the past 2 years to choose this method in 43 newborn and premature infants presenting with a wide variety of clinical conditions. We conclude that the use of caval catheters still requires a very strong indication.     

Cyclophosphamide and low-dose prednisone therapy in patients with systemic sclerosis (scleroderma) with interstitial lung disease

Fourteen patients with systemic sclerosis (SSc, scleroderma) and interstitial lung disease were treated with oral cyclophosphamide (1-2 mg/kg/day) and low dose prednisone (< 10 mg/day). There was a significant improvement in FVC after 6 months compared to entry values (2.21 +/- 0.19 l vs. 2.03 +/- 0.15 l, p < 0.02). Improvement was maintained at 12 months (2.27 +/- 0.27 l, p < 0.05) and 18-24 months (2.60 +/- 0.28 l, p < 0.001). In 12 cases followed for 18-24 months, FVC was stable or improved. No significant improvement or decline was noted for the DLCO. Side effects included cytopenia (2), infection (1), and hemorrhagic cystitis (2), and one possible related malignancy. A controlled prospective trial of cyclophosphamide is warranted in patients with SSc and active interstitial lung disease.     

Surgical repair of type A aortic dissection by the circulatory arrest-graft inclusion technique in sixty-six patients

During an 8-year period (1984 to 1991) 66 patients (mean age 59 years, range 26 to 84 years) with type A aortic dissection (60 ascending aorta tears, 6 arch tears; 35 acute, 31 chronic) had surgical repair by a continuous suture-graft inclusion technique. Hypothermic circulatory arrest (16 degrees C) was used in 58 patients (35/35 acute, 23/31 chronic; mean arrest time 26 minutes, range 10 to 55 minutes). Fifty-two patients had hemiarch repair and 6 had total arch replacement. Aortic valve disease necessitated treatment in 38 patients (1 valved conduit, 20 valve replacements, 17 valve repairs). Recently 11 patients had valve repair by reconstruction of the native aortic root, by means of techniques similar to those used for homograft valve insertion. Operative mortality was 9% (14% acute, 3% chronic). Stroke occurred in 2 patients (3%) and was fatal in both. Variables suggestive of increased operative risk by univariate analysis were acuteness (p = 0.12), visceral ischemia (p = 0.12), and preoperative shock (p = 0.13). No variable was significant by multivariate analysis. Overall actuarial survival at 48 months was 77%, with 3 late deaths from a ruptured distal aneurysm. Late computed tomography or magnetic resonance imaging scan was done in 28 patients at a mean interval of 33 months. These studies identified 1 patient with a pseudoaneurysm requiring reoperation and 3 patients with contained flow between the graft and the wrap. Three patients required late operation: 1 for pseudoaneurysm, 1 for arch dissection, and 1 for repair of a distal aneurysm.     

Monk seal mortality: virus or toxin?

During the past few months, more than half of the total population of about 300 highly endangered Mediterranean monk seals (Monachus monachus) on the western Saharan coast of Africa, died in a mysterious disease outbreak. Epizootiological and postmortem findings were reminiscent of similar outbreaks amongst pinniped and cetacean species in recent years, which were caused by an infection with newly discovered morbilliviruses (for review see osterhaus et al.). Virological, as well as toxicological, analysis performed on tissue samples collected from relatively fresh carcasses during the outbreak indicate that infection with a virus closely related to dolphin morbillivirus (DMV), possibly originating from affected dolphins in the same area, was the primary cause of the outbreak. Therefore it is concluded that vaccination with a safe and effective non-replicating vaccine should be considered as a management tool in the conservation of Mediterranean monk seals.