julilili42/papers huggingface dataset:
Fibrocytes induce an angiogenic phenotype in cultured endothelial cells and promote angiogenesis in vivo
2001-10-01

Angiogenesis is an ordered process requiring the inter‐play of numerous cellular and humoral factors. Studies over the past 20 years have identified several growth factors, cytokines, and enzymes that promote blood vessel formation. Most have revealed how individual factors promote an angiogenic phenotype in endothelial cells in vitro or contribute to blood vessel formation in vivo. However, the fundamental question that remains unanswered is how the cellular microenvironment contributes to angiogenesis. Fibrocytes are a recently characterized mesenchymal cell type isolated from peripheral blood that rapidly enter subcutaneously implanted wound chambers and sites of tissue injury. Here we describe the induction of an angiogenic phenotype in microvascular endothelial cells in vitro and promotion of angiogenesis in vivo by cultured fibrocytes. Fibrocytes constitutively secrete extracellular matrix‐degrading enzymes, primarily matrix metalloproteinase 9, which promotes endothelial cell invasion. In addition, fibrocytes secrete several proangiogenic factors including VEGF, bFGF, IL‐8, PDGF, and hematopoietic growth factors that promote endothelial cell migration, proliferation, and/or tube formation. By contrast, they do not produce representative antiangiogenic factors. Finally, both autologous fibrocytes and fibrocyte‐conditioned media were found to induce blood vessel formation in vivo using the Matrigel angiogenesis model.—Hartlapp, I., Abe, R., Saeed, R. W., Peng, T., Voelter, W., Bucala, R., Metz, C. N. Fibrocytes induce an angiogenic phenotype in cultured endothelial cells and promote angiogenesis in vivo. FASEB J. 15, 2215–2224 (2001)
Tectonic erosion and consequent collapse of the Pacific margin of Costa Rica: Combined implications from ODP Leg 170, seismic offshore data, and regional geology of the Nicoya Peninsula
2001-10-01

The convergent margin off the Pacific coast of the Nicoya Peninsula of Costa Rica exhibits evidence for subduction erosion caused by the underthrusting Cocos plate. Critical evidence for efficacy of this process was recovered at the Ocean Drilling Program (ODP) drilling Site 1042 (Leg 170), positioned ∼7 km landward of the Middle America trench axis off the Nicoya Peninsula. The primary drilling objective at this site was to identify the age and origin of a regionally extensive and prominent seismic discontinuity, the so‐called base‐of‐slope sediment (BOSS) horizon or surface. The BOSS horizon, which can be traced landward from near the trench to the Nicoya coastal area and parallel to it for hundreds of kilometers, separates a low‐velocity (∼ 2.0–2.5 km s −1 ) sequence of slope sediment, from an underlying sequence of much higher‐velocity (&gt;4–4.5 km s −1 ) rock. Site 1042 reached the acoustically defined BOSS horizon at a below sea level depth of ∼ 3900 m and yielded a carbonate‐cemented calcarenitic breccia of early‐middle Miocene age. Sedimentological, geochemical, paleontological, and cement paragenesis data document that the breccia accumulated in a shallow water depositional environment. On the basis of coastal exposures, the BOSS horizon, as a margin‐wide geologic interface, can be temporally and lithostratigraphically correlated to a regional angular unconformity. This unconformity, known as the Mal Pais unconformity, separates Neogene and younger shelf‐to‐littoral beds from the underlying mafic units of the Mesozoic Nicoya Complex and Cretaceous and early Tertiary sedimentary sequences. At Site 1042 it is inferred that tectonism caused the vertical subsidence of the early Neogene breccia from a shallow to a deep water setting. The Mal Pais unconformity of the BOSS horizon thus connects the rock fabric of the outermost part of margin to that of coastal Nicoya and implies that in the early Neogene the Nicoya shelf extended seaward to near the present trench axis. This circumstance requires that the early Neogene trench axis was at least 50 km seaward of where it is now located. The long‐term effects of subduction erosion, similar to those described for the scientifically drilled Japan, Tonga, and Peru margins, best account for offshore and onshore evidence for a post‐Paleogene history of crustal thinning and landward trench migration of Costa Rica's Pacific margin. During the past 16–17 Myr the calculated mass removal and landward migration rates are 34–36 km3 Myr −1 km −1 of margin, and 3 km Myr −1 , respectively. These values are similar to those found for other Pacific margins dominated by nonaccretionary subduction zone processes.
Phthalocyanines as Active Materials for Optical Limiting
2001-10-01

This work gives an overview concerning the optical limiting processes in phthalocyanines. In particular, the synthesis and the relevant optical properties of a series of axially substituted indium(III)− and titanium(IV)−phthalo- and -naphthalocyanines are described. Several techniques, such as transient absorption, Z-scan, and degenerate four-wave mixing, have been used for assessing the optical properties and optical limiting performance of the investigated compounds.
A Polyketide Synthase in Glycopeptide Biosynthesis
2001-10-01

Balhimycin, a vancomycin-type antibiotic from Amycolatopsis mediterranei, contains the unusual amino acid (S)-3,5-dihydroxyphenylglycine (Dpg), with an acetate-derived carbon backbone. After sequence analysis of the biosynthetic gene cluster, one gene, dpgA, for a predicted polyketide synthase (PKS) was identified, sharing 20-30% identity with plant chalcone synthases. Inactivation of dpgA resulted in loss of balhimycin production, and restoration was achieved by supplementation with 3,5-dihydroxyphenylacetic acid, which is both a possible product of a PKS reaction and a likely precursor of Dpg. Enzyme assays with the protein expressed in Streptomyces lividans showed that this PKS uses only malonyl-CoA as substrate to synthesize 3,5-dihydroxyphenylacetic acid. The PKS gene is organized in an operon-like structure with three downstream genes that are similar to enoyl-CoA-hydratase genes and a dehydrogenase gene. The heterologous co-expression of all four genes led to accumulation of 3,5-dihydroxyphenylglyoxylic acid. Therefore, we now propose a reaction sequence. The final step in the pathway to Dpg is a transamination. A predicted transaminase gene was inactivated, resulting in abolished antibiotic production and accumulation of 3,5-dihydroxyphenylglyoxylic acid. Interestingly, restoration was only possible by simultaneous supplementation with (S)-3,5-dihydroxyphenylglycine and (S)-4-hydroxyphenylglycine, indicating that the transaminase is essential for the formation of both amino acids.
Role of KCNE1-Dependent K+ Fluxes in Mouse Proximal Tubule
2001-10-01

The electrochemical gradient for K+ across the luminal membrane of the proximal tubule favors K+ fluxes to the lumen. Here it was demonstrated by immunohistochemistry that KCNE1 and KCNQ1, which form together the slowly activated component of the delayed rectifying K+ current in the heart, also colocalize in the luminal membrane of proximal tubule in mouse kidney. Micropuncture experiments revealed a reduced K+ concentration in late proximal and early distal tubular fluid as well as a reduced K+ delivery to these sites in KCNE1 knockout (-/-), compared with wild-type (+/+) mice. These observations would be consistent with KCNE1-dependent K+ fluxes to the lumen in proximal tubule. Electrophysiological studies in isolated perfused proximal tubules indicated that this K+ flux is essential to counteract membrane depolarization due to electrogenic Na+-coupled transport of glucose or amino acids. Clearance studies revealed an enhanced fractional urinary excretion of fluid, Na+, Cl-, and glucose in KCNE1 -/- compared with KCNE1 +/+ mice that may relate to an attenuated transport in proximal tubule and contribute to volume depletion in these mice, as indicated by higher hematocrit values.
Substances with estrogenic activity in effluents of sewage treatment plants in southwestern Germany. 2. Biological analysis
2001-10-01

Abstract The proliferation test with human estrogen receptor-positive MCF-7 breast cancer cells (E-Screen assay) was applied for quantitative determination of total estrogenic activity in 24-h composite effluent samples from 16 municipal and two industrial sewage treatment plants (STPs) in the state of Baden-Württemberg, southwestern Germany. The estrogenic efficacy relative to the positive control, 17β-estradiol, was between 26 and 74% (median, 48%) for the 16 municipal STPs. Estradiol equivalent concentrations (EEQs) were between 0.2 and 7.8 ng/L (median, 1.6 ng/L) and, thereby, were lower than those found in a pilot study, which revealed EEQs of greater than 10 ng/L in the effluents of two other STPs. The EEQs in 14 of the 16 effluent samples were very similar (0.9–3.3 ng/L), indicating a rather constant input of estrogenic substances via STPs into rivers. Additional activated charcoal filtration turned out to be very efficient in further eliminating estrogenic activity from effluents. The EEQs of the E-Screen assay and those calculated from the results of extensive chemical analysis using the estradiol equivalency factors determined for 13 natural and synthetic estrogenic substances were comparable for most of the effluent samples. 17β-Estradiol, 17α-ethinylestradiol, and, to a lesser extent, estrone contributed to 90% or more of the EEQ value.
Precursor‐Derived Si‐B‐C‐N Ceramics: Oxidation Kinetics
2001-10-01

The oxidation behavior of three precursor‐derived ceramics—Si 4.46 BC 7.32 N 4.40 (AMF2p), Si 2.72 BC 4.51 N 2.69 (AMF3p), and Si 3.08 BC 4.39 N 2.28 (T2/1p)—was investigated at 1300° and 1500°C. Scale growth at 1500°C in air can be approximated by a parabolic rate law with rate constants of 0.0599 and 0.0593 μm 2 /h for AMF3p and T2/1p, respectively. The third material does not oxidize according to a parabolic rate law, but has a similar scale thickness after 100 h. The results show that at least within the experimental times these ceramics develop extremely thin scales, thinner than pure SiC or Si 3 N 4 .
Influence of motoneuron firing synchronization on SEMG characteristics in dependence of electrode position
2001-10-01

The frequency content of the surface electromyography (SEMG) signal, expressed as median frequency (MF), is often assumed to reflect the decline of muscle fiber conduction velocity in fatigue. MF also decreases when motor unit firings synchronize, and we hypothesized that this effect can explain the electrode-dependent pattern in our previous recordings from the trapezius muscle. An existing motoneuron (MN) model describes the afterhyperpolarization following a spike as an exponential function on which membrane noise is superimposed. Splitting the noise into a common and an individual component extended the model to a MN pool with a tunable level of firing synchrony. An analytical volume conduction model was used to generate motor unit action potentials to simulate SEMG. A realistic level of synchrony decreased the MF of the simulated bipolar SEMG by ∼30% midway between endplate position and tendon but not above the endplate. This is in accordance with experimental data from the biceps brachii muscle. It was concluded that the pattern of decrease of MF during sustained contractions indeed reflects MN synchronization.
Yersinia enterocolitica invasin triggers phagocytosis via beta1 integrins, CDC42Hs and WASp in macrophages
2001-10-01

The Yersinia outer surface protein invasin binds to beta1 integrins on target cells and has been shown to trigger phagocytic uptake by macrophages. Here, we investigated the role of the actin regulator Wiskott-Aldrich syndrome protein (WASp), its effector the Arp2/3 complex and the Rho-GTPases CDC42Hs, Rac and Rho in invasin/beta1 integrin-triggered phagocytosis. During uptake of invasin-coated latex beads, the alpha5beta1 integrin, WASp and the Arp2/3 complex were recruited to the developing actin-rich phagocytic cups in primary human macrophages. Blockage of beta1 integrins by specific antibodies, inhibition of Arp2/3 function by microinjection of inhibitors or the use of WASp knockout macrophages inhibited phagocytic cup formation and uptake. Furthermore, microinjection of the dominant negative GTPase mutants N17CDC42Hs, N17Rac or the Rho-specific inhibitor C3-transferase into macrophages greatly attenuated invasin-induced formation of cups. These data suggest that during invasin-triggered phagocytosis beta1 integrins activate actin polymerization via CDC42Hs, its effector WASp and the Arp2/3 complex. The contribution of Rac and Rho to phagocytic cup formation also suggests a complex interplay between different Rho GTPases during phagocytosis of pathogens.
Genetic evidence for a microtubule‐destabilizing  effect of conventional kinesin and analysis of its consequences for the control of nuclear distribution  in Aspergillus nidulans
2001-10-01

Conventional kinesin is a microtubule‐dependent motor protein believed to be involved in a variety of intracellular transport processes. In filamentous fungi, conventional kinesin has been implicated in different processes, such as vesicle migration, polarized growth, nuclear distribution, mitochondrial movement and vacuole formation. To gain further insights into the functions of this kinesin motor, we identified and characterized the conventional kinesin gene, kinA , of the established model organism Aspergillus nidulans. Disruption of the gene leads to a reduced growth rate and a nuclear positioning defect, resulting in nuclear cluster formation. These clusters are mobile and display a dynamic behaviour. The mutant phenotypes are pronounced at 37°C, but rescued at 25°C. The hyphal growth rate at 25°C was even higher than that of the wild type at the same temperature. In addition, kinesin‐deficient strains were less sensitive to the microtubule destabilizing drug benomyl, and disruption of conventional kinesin suppressed the cold sensitivity of an α‐tubulin mutation ( tubA4 ). These results suggest that conventional kinesin of A. nidulans plays a role in cytoskeletal dynamics, by destabilizing microtubules. This new role of conventional kinesin in microtubule stability could explain the various phenotypes observed in different fungi.
The Prevalent Gly1057Asp Polymorphism in the Insulin Receptor Substrate-2 Gene Is Not Associated with Impaired Insulin Secretion
2001-10-01

Disruption of the insulin receptor substrate-2 was shown to cause type 2 diabetes in mice. This could be largely attributed to abnormalβ -cell development. In humans, a prevalent polymorphism in insulin receptor substrate-2 (Gly1057Asp) was not found be associated with type 2 diabetes in linkage and association studies. We tested the hypothesis that an extreme challenge of the β cell might reveal subtle abnormalities in carriers of this polymorphism undetected by conventional insulin secretion tests. Therefore, in addition to assessing β-cell function by oral glucose tolerance testing (n = 318, normal glucose tolerance), we measured the secretory response to maximal stimulation by hyperglycemia (10 mm), glucagon-like peptide-1, and arginine administered in an additive fashion (n = 77, nondiabetic). The allelic frequency of the Asp allele was ∼37%. Neither the β-cell function indices from the oral glucose tolerance test nor the secretory response during the hyperglycemic clamp differed measurably between carriers and controls. Moreover, maximal plasma C-peptide concentrations in response to the combined glucose, glucagon-like peptide-1, and arginine stimulus was not different between Gly/Gly (10,745 ± 1,186 pmol/liter) and X/Asp (10,800 ± 490 pmol/liter, P = 0.99). In conclusion, our findings strongly suggest that the Gly1057Asp polymorphism in insulin receptor substrate-2 is not associated withβ -cell dysfunction. The normal maximal insulin secretory response makes it unlikely that this common polymorphism results in abnormalβ -cell development.
Trefoil Factor Family–Peptides Promote Migration of Human Bronchial Epithelial Cells
2001-10-01

A process termed "restitution" enables rapid repair of the respiratory epithelium by migration of neighbouring cells. Mucin-associated TFF-peptides (formerly P-domain peptides or trefoil factors) are typical motogens enhancing migration of cells in various in vitro models mimicking restitution of the intestine. The human bronchial epithelial cell line BEAS-2B was used as a model system of airway restitution. The motogenic activities of recombinant human TFF2 as well as porcine TFF2 were demonstrated by in vitro wound healing assays of BEAS-2B cells. TFF2 did not induce phosphorylation of the epidermal growth factor (EGF) receptor. EGF was capable of enhancing the motogenic effect of human TFF2 at a concentration of 3 x 10(-10) M whereas EGF itself (i.e., in the absence of TFF2) did not stimulate migration at this low concentration. Furthermore, TFF2 as well as monomeric and dimeric forms of TFF3 enhanced migration of BEAS-2B cells in Boyden chambers. Motogenic activity of TFF2 was also shown for normal human bronchial epithelial (NHBE) cells in Boyden chambers. These results suggest that TFF-peptides act as motogens in the human respiratory epithelium triggering rapid repair of damaged mucosa in the course of airway diseases such as asthma.
Dermatoscopy Turns Histopathologist's Attention to the Suspicious Area in Melanocytic Lesions
2001-10-01

Specific dermatoscopic patterns of malignancy can be found in highly suspicious areas, eg, broadened networks, radial streaming, pseudopods, or dots located at the periphery. The dermatoscopic-histopathologic correlation can improve the diagnosis of melanoma. Therefore, the clinician should point to the most suspicious area with a drawing or image, and the suspected diagnosis of melanoma and the history of the lesion should be also mentioned.
Thyroid Hormone-deficient Period Prior to the Onset of Hearing Is Associated with Reduced Levels of β-Tectorin Protein in the Tectorial Membrane
2001-10-01

The genes for alpha- and beta-tectorin encode the major non-collagenous proteins of the tectorial membrane. Recently, a targeted deletion of the mouse alpha-tectorin gene was found to cause loss of cochlear sensitivity (). Here we describe that mRNA levels for beta-tectorin, but not alpha-tectorin, are significantly reduced in the cochlear epithelium under constant hypothyroid conditions and that levels of beta-tectorin protein in the tectorial membrane are lower. A delay in the onset of thyroid hormone supply prior to onset of hearing, recently described to result in permanent hearing defects and loss of active cochlear mechanics (), can also lead to permanently reduced beta-tectorin protein levels in the tectorial membrane. beta-Tectorin protein levels remain low in the tectorial membrane up to one year after the onset of thyroid hormone supply has been delayed until postnatal day 8 or later and are associated with an abnormally structured tectorial membrane and the loss of active cochlear function. These data indicate that a simple delay in thyroid hormone supply during a critical period of development can lead to low beta-tectorin levels in the tectorial membrane and suggest for the first time that beta-tectorin may be required for development of normal hearing.
Follow-up in Neuroblastoma: Comparison of Metaiodobenzylguanidine and a Chimeric Anti-GD2 Antibody for Detection of Tumor Relapse and Therapy Response
2001-10-01

Early and correct diagnosis of local tumor recurrence, occurrence of metastases, and therapy response are essential in patients with neuroblastoma stage IV. The aim of the study was to evaluate the diagnostic value of metaiodobenzylguanidine (mIBG) and a chimeric GD2 antibody in the follow-up of patients with neuroblastoma. In a prospective study, mIBG (N = 31 scans) and immunoscintigraphy were compared with a chimeric antiganglioside antibody, ch14.18 (MAb) (N = 31 scans), labeled with technetium Tc 99m in the follow-up of 18 patients with stage IV neuroblastoma. The findings were compared with histologic findings, other imaging examinations, and clinical changes over the course of 4 to 6 years. For the diagnosis of local tumor recurrences, sensitivity was 80% for MAb and 70% for mIBG. Specificity was 93% for MAb and 72% for mIBG. The MAb was superior for the detection of skeletal metastases, with a sensitivity of 82% compared with 72% for mIBG. Specificity was 100% for both techniques. Also, for soft tissue/lymph node metastases, sensitivity for MAb was higher (50%) than for mIBG (31%). Specificity was 100% for each technique. In sequential studies, metastases were detected earlier with MAb (mean: 2.3 m for skeletal metastases, 3.6 m for soft tissue metastases) than with mIBG. After therapy, tumor uptake was visualized longer with mIBG (mean 6.3 m) than with MAb. The chimeric antibody ch14.18 is likely to be valuable for follow-up examinations and for assessment of therapy response because of earlier detection of new metastases.
Chemical Composition and Crystal Lattice Defects of Bi2Te3 Peltier Device Structures
2001-10-01

The microstructure of p-type (Bi,Sb)2Te3 and n-type Bi2(Te,Se)3 Peltier devices was investigated by scanning electron microscopy, energy-dispersive X-ray spectroscopy, electron probe microanalysis and transmission electron microscopy, in the bulk and close to the metal–semiconductor interface. The substitution of Sb for Bi in the p-type material varies about 1 at% or 3 × 1020 atoms cm—3 on the micrometer scale. The same behaviour was found for Se and Te in the n-type material. From these results it can be ruled out that Bi and Sb and Se and Te are statistically distributed in the crystal structure. Models for the Bi/Sb and Se/Te disorder are discussed. No evidence for the presence of antisite defects was found by electron probe microanalysis. The investigated materials were highly textured and contained large dislocation densities of 109 cm—2. In the bulk, straight dislocations, loops and half-loops were observed that are 10 nm in size. Under the electron beam elongated mobile dislocations move in the basal plane by successive hopping from pinning sites. The role of the observed extended lattice defects for accommodating local non-stoichiometry is discussed. The lattice defects might primarily affect the low-temperature electronic transport properties and the lattice heat conductivity. At the metal–Bi2Te3 interface, characteristic defect structures were identified, that extend up to between 2 and 20 μm into the Bi2Te3.