julilili42/papers huggingface dataset:
Regimes of youth transitions
2006-04-12

In a context of de-standardized transitions to work, young people are required to take more individual decisions, a process in which their subjectivities become increasingly important for social integration. While it can be assumed that this is a general trend, this article seeks to analyse the impact of different ‘transition regimes’ upon young people’s biographical experiences. Based on three comparative studies related to young people’s transitions to work, firstly, different ‘transition regimes’ are outlined, and secondly, the extent to which regime characteristics are reflected in young people’s accounts of their experiences is analysed; simultaneously, the underlying question of the extent to which young people perceive the possibilities of making subjectively meaningful choices is addressed, along with how this decision-making process is facilitated by flexibility and secured against the risk of failure and exclusion.
The inhibitor-of-apoptosis protein Bir1p protects against apoptosis in S. cerevisiae and is a substrate for the yeast homologue of Omi/HtrA2
2006-04-12

Inhibitor-of-apoptosis proteins (IAPs) play a crucial role in the regulation of metazoan apoptosis. IAPs are typically characterized by the presence of one to three baculovirus IAP repeat (BIR) domains that are essential for their anti-apoptotic activity. Bir1p is the sole BIR-protein in yeast and has been shown to participate in chromosome segregation events. Here, we show that Bir1p is a substrate for Nma111p, which is the homologue of the human pro-apoptotic serine protease Omi/HtrA2 and which is known to mediate apoptosis in yeast. Bir1p is a cytoplasmic and nuclear protein, and yeast cells lacking bir1 are more sensitive to apoptosis induced by oxidative stress. Consistently, overexpression of Bir1p reduces apoptosis-like cell death, whereas this protective effect can be antagonized in vivo by simultaneous overexpression of Nma111p. Moreover, chronologically aged cells that constitutively overexpress Bir1p show a delayed onset of cell death. Therefore, Bir1p, like its closest metazoan homologues deterin and survivin, has dual functions: it participates in chromosome segregation events and cytokinesis and exhibits anti-apoptotic activity.
Leptin down‐regulates insulin action through phosphorylation of serine‐318 in insulin receptor substrate 1
2006-04-12

Insulin resistance in skeletal muscle is found in obesity and type 2 diabetes. A mechanism for impaired insulin signaling in peripheral tissues is the inhibition of insulin action through serine phosphorylation of insulin receptor substrate (Irs) proteins that abolish the coupling of Irs proteins to the activated insulin receptor. Recently, we described serine-318 as a protein kinase C (PKC)-dependent phosphorylation site in Irs1 (Ser-318) activated by hyperinsulinemia. Here we show in various cell models that the adipose hormone leptin, a putative mediator in obesity-related insulin resistance, promotes phosphorylation of Ser-318 in Irs1 by a janus kinase 2, Irs2, and PKC-dependent pathway. Mutation of Ser-318 to alanine abrogates the inhibitory effect of leptin on insulin-induced Irs1 tyrosine phosphorylation and glucose uptake in L6 myoblasts. In C57Bl/6 mice, Ser-318 phosphorylation levels in muscle tissue were enhanced by leptin and insulin administration in lean animals while in diet-induced obesity Ser-318 phosphorylation levels were already up-regulated in the basal state, and further stimulation was diminished. In analogy, in lymphocytes of obese hyperleptinemic human subjects basal Ser-318 phosphorylation levels were increased compared to lean individuals. During a hyperinsulinemic euglycemic clamp, the increment in Ser-318 phosphorylation observed in lean individuals was absent in obese. In summary, these data suggest that phosphorylation of Ser-318 in Irs1 mediates the inhibitory signal of leptin on the insulin-signaling cascade in obese subjects.
4D measurement system for automatic location of anatomical structures
2006-04-14

Orthopedics and neurosciences are fields of medicine where the analysis of objective movement parameters is extremely important for clinical diagnosis. Moreover, as there are significant differences between static and dynamic parameters, there is a strong need of analyzing the anatomical structures under functional conditions. In clinical gait analysis the benefits of kinematical methods are undoubted. In this paper we present a 4D (3D + time) measurement system capable of automatic location of selected anatomical structures by locating and tracing the structures' position and orientation in time. The presented system is designed to help a general practitioner in diagnosing selected lower limbs' dysfunctions (e.g. knee injuries) and also determine if a patient should be directed for further examination (e.g. x-ray or MRI). The measurement system components are hardware and software. For the hardware part we adapt the laser triangulation method. In this way we can evaluate functional and dynamic movements in a contact-free, non-invasive way, without the use of potentially harmful radiation. Furthermore, opposite to marker-based video-tracking systems, no preparation time is required. The software part consists of a data acquisition module, an image processing and point clouds (point cloud, set of points described by coordinates (x, y, z)) calculation module, a preliminary processing module, a feature-searching module and an external biomechanical module. The paper briefly presents the modules mentioned above with the focus on the feature-searching module. Also we present some measurement and analysis results. These include: parameters maps, landmarks trajectories in time sequence and animation of a simplified model of lower limbs.
Total internal reflection energy transfer (TIRET) microscopy for analysis of focal adhesions in living cells
2006-04-14

Total internal reflection fluorescence microscopy (TIRFM) is used to measure non-radiative energy transfer between membrane associated proteins in living cells. Measurements are concentrated on focal contacts and their associated proteins focal adhesion kinase (FAK) and Paxillin (Pax) which play major roles with respect to cell migration, growth, and survival. These proteins are visualized after fusion with variants of green fluorescent protein (ECFP and EYFP), and an intermolecular energy transfer ECFP -> EYFP is deduced from fluorescence spectra as well as from fluorescence decay kinetics of single cells.
Control of leaf vascular patterning by polar auxin transport
2006-04-15

The formation of the leaf vascular pattern has fascinated biologists for centuries. In the early leaf primordium, complex networks of procambial cells emerge from homogeneous subepidermal tissue. The molecular nature of the underlying positional information is unknown, but various lines of evidence implicate gradually restricted transport routes of the plant hormone auxin in defining sites of procambium formation. Here we show that a crucial member of the AtPIN family of auxin-efflux-associated proteins, AtPIN1, is expressed prior to pre-procambial and procambial cell fate markers in domains that become restricted toward sites of procambium formation. Subcellular AtPIN1 polarity indicates that auxin is directed to distinct “convergence points” in the epidermis, from where it defines the positions of major veins. Integrated polarities in all emerging veins indicate auxin drainage toward pre-existing veins, but veins display divergent polarities as they become connected at both ends. Auxin application and transport inhibition reveal that convergence point positioning and AtPIN1 expression domain dynamics are self-organizing, auxin-transport-dependent processes. We derive a model for self-regulated, reiterative patterning of all vein orders and postulate at its onset a common epidermal auxin-focusing mechanism for major-vein positioning and phyllotactic patterning.
BCR/ABL Oncogene Directly Controls MHC Class I Chain-Related Molecule A Expression in Chronic Myelogenous Leukemia
2006-04-15

Abstract MHC class I chain-related molecules (MIC) participate in immune surveillance of cancer through engagement of the NKG2D-activating receptor on NK and T cells. Decreased NKG2D expression and function upon chronic exposure to NKG2D ligands and/or soluble forms of MIC (sMIC) may participate in immune escape. In chronic myeloid leukemia, a malignancy caused by the BCR/ABL fusion oncoprotein, we showed cell surface expression of MICA on leukemic, but not healthy, donor hemopoietic CD34+ cells. At diagnosis, chronic myeloid leukemia patients had abnormally high serum levels of sMICA and weak NKG2D expression on NK and CD8+ T cells, which were restored by imatinib mesylate (IM) therapy. In the BCR/ABL+ cell line K562, IM decreased both surface MICA/B expression and NKG2D-mediated lysis by NK cells. Silencing BCR/ABL gene expression directly evidenced its role in the control of MICA expression. IM did not affect MICA mRNA levels, but decreased MICA protein production and release. Sucrose density gradient fractionation of K562 cytoplasmic extracts treated with IM showed a shift in the distribution of MICA mRNA from the polysomal toward the monosomal fractions, consistent with decreased translation. Among the major pathways activated by BCR/ABL that regulate translation, PI3K and mammalian target of rapamycin were shown to control MICA expression. These data provide evidence for direct control of MICA expression by an oncogene in human malignancy and indicate that posttranscriptional mechanisms may participate in the regulation of MICA expression.
Prospective memory failures as an unexplored threat to patient safety: results from a pilot study using patient simulators to investigate the missed execution of intentions
2006-04-15

This study investigated failures of prospective memory (PM) as a relevant but neglected error type in medicine. A patient simulator was used to investigate PM failures. The influence of subjective importance (high, low) and type of intention (educational, internal, external) on the (missed) execution of intention was investigated in a 2 x 2 design. The effects on missed executions by importance (high < low) and type of intention (educational < external < internal) were hypothesized. Of 73 valid intentions in 40 prepared simulator scenarios 19 (26%) were missed overall. A total of 64% of unimportant and 80% of important intentions were executed 79% of educational 67% of external and 72% of internal intentions were executed. Neither difference was statistically significant using chi(2) tests. Interaction was significant for missed executions (p = 0.025; n = 19; df = 2; chi(2) = 7.41) and for executions (p = 0.002; n = 54; df = 2; chi(2) = 12.50). Despite low statistical support and some methodological limitations, it was possible to show that PM failures are relevant to patient safety and that patient simulators are a suitable but so far unused tool for their investigation.
Platelets secrete stromal cell–derived factor 1α and recruit bone marrow–derived progenitor cells to arterial thrombi in vivo
2006-04-17

The accumulation of smooth muscle and endothelial cells is essential for remodeling and repair of injured blood vessel walls. Bone marrow–derived progenitor cells have been implicated in vascular repair and remodeling; however, the mechanisms underlying their recruitment to the site of injury remain elusive. Here, using real-time in vivo fluorescence microscopy, we show that platelets provide the critical signal that recruits CD34+ bone marrow cells and c-Kit+ Sca-1+ Lin− bone marrow–derived progenitor cells to sites of vascular injury. Correspondingly, specific inhibition of platelet adhesion virtually abrogated the accumulation of both CD34+ and c-Kit+ Sca-1+ Lin− bone marrow–derived progenitor cells at sites of endothelial disruption. Binding of bone marrow cells to platelets involves both P-selectin and GPIIb integrin on platelets. Unexpectedly, we found that activated platelets secrete the chemokine SDF-1α, thereby supporting further primary adhesion and migration of progenitor cells. These findings establish the platelet as a major player in the initiation of vascular remodeling, a process of fundamental importance for vascular repair and pathological remodeling after vascular injury.
Suppression of Prostaglandin E2by Malaria Parasite Products and Antipyretics Promotes Overproduction of Tumor Necrosis Factor–α: Association with the Pathogenesis of Childhood Malarial Anemia
2006-04-18

Cytokines and effector molecules are important immunoregulatory molecules in human malaria. Tumor necrosis factor (TNF)-alpha limits malaria parasitemia but also promotes pathogenesis at high concentrations, whereas prostaglandin E2 (PGE2) inhibits TNF-alpha production and is reduced in childhood malaria, at least in part, through suppression of cyclooxygenase (COX)-2 following the ingestion of Plasmodium falciparum hemozoin (pfHz; malarial pigment) by peripheral blood mononuclear cells (PBMCs). Although molecular interactions between TNF-alpha and PGE2 are largely unexplored in human malaria, results presented here show that pfHz-induced suppression of PBMC COX-2 gene products induces overproduction of TNF-alpha. Moreover, addition of exogenous PGE2 to pfHz-treated PBMCs dose-dependently decreased TNF-alpha production, whereas experimental COX inhibitors and antipyretics used during human malaria generated increased TNF-alpha production. Healthy, malaria-exposed children had elevated levels of circulating bicyclo-PGE2/TNF-alpha, compared with children with malarial anemia (P<.01), with systemic bicyclo-PGE2 and TNF-alpha significantly associated with hemoglobin concentrations (r=0.745; P<.01). The results of the present study illustrate that pfHz-induced suppression of PGE2 promotes overproduction of TNF-alpha, which is associated with enhanced malarial anemia.
Direct Protein Identification from Nonspecific Peptide Pools by High‐Accuracy MS Data Filtering
2006-04-18

Validate your results! High-accuracy mass spectrometric analysis and composition-based de novo sequencing (CBS) combined with database(DB)-assisted protein identification allows for the rapid production of validated analytical results in proteome research. A simplified sample preparation scheme is sufficient to provide for reliable identification of proteins even when following nonspecific and unknown degradation processes.
Antinociceptive and anti-Inflammatory effects of the standardized oil of Indian <i>Callistemon lanceolatus</i> leaves in experimental animals
2006-04-20

The effect of Callistemon lanceolatus (Syn. C. citrinus curtis; Family: Myrtaceae) leaf oil was studied for the antinociceptive and anti-inflammatory activity in experimental animals. C. lanceolatus, 25 – 100 mg/kg administered orally for 3 days exhibited graded dose response equivalent to 21.95% - 89.90% protection in the tail flick latent test in rat. The C. lanceolatus oil (50 and 100 mg/kg, given orally for 3 days) was effective in hot plate reaction time (64.05% and 112.97%, p
MreB of Streptomyces coelicolor is not essential for vegetative growth but is required for the integrity of aerial hyphae and spores
2006-04-21

Summary MreB forms a cytoskeleton in many rod‐shaped bacteria which is involved in cell shape determination and chromosome segregation. PCR‐based and Southern analysis of various actinomycetes, supported by analysis of genome sequences, revealed mreB homologues only in genera that form an aerial mycelium and sporulate. We analysed MreB in one such organism, Streptomyces coelicolor . Ectopic overexpression of mreB impaired growth, and caused swellings and lysis of hyphae. A null mutant with apparently normal vegetative growth was generated. However, aerial hyphae of this mutant were swelling and lysing; spores doubled their volume and lost their characteristic resistance to stress conditions. Loss of cell wall consistency was observed in MreB‐depleted spores by transmission electron microscopy. An MreB–EGFP fusion was constructed to localize MreB in the mycelium. No clearly localized signal was seen in vegetative mycelium. However, strong fluorescence was observed at the septa of sporulating aerial hyphae, then as bipolar foci in young spores, and finally in a ring‐ or shell‐like pattern inside the spores. Immunogold electron microscopy using MreB‐specific antibodies revealed that MreB is located immediately underneath the internal spore wall. Thus, MreB is not essential for vegetative growth of S. coelicolor , but exerts its function in the formation of environmentally stable spores, and appears to primarily influence the assembly of the spore cell wall.
Patterns of SPARC expression and basement membrane intactness at the tumour–brain border of invasive meningiomas
2006-04-21

The matricellular glycoprotein SPARC (secreted protein, acidic and rich in cysteine), also termed osteonectin, has been found to regulate the invasive behaviour of several tumour types by interacting with basement membrane constituents. Brain invasive meningiomas are supposed to disrupt the pial‐glial basement membrane. In the present study we aimed at determining the relationship of basement membrane intactness and SPARC protein expression at the meningioma–brain border. Sections of 51 brain‐invasive meningiomas (31 meningothelial meningiomas WHO grade I, 11 atypical WHO grade II, and nine anaplastic WHO grade III tumours) were immunolabelled with antibodies against SPARC, epithelial membrane antigen (EMA), collagen IV and glial fibrillary acidic protein (GFAP). Twenty‐two non‐invasive WHO grade I meningothelial meningiomas were included in the study for comparison. At the tumour–brain border of invasive meningiomas, spindle‐shaped tumour cells expressed SPARC. The number of tumours containing SPARC+ spindle cells did not differ significantly between WHO grades. By contrast, the number of WHO grade I tumours expressing collagen IV (15/31) was highly significantly elevated when compared with WHO grade II (1/11) and WHO grade III (0/9) (both P &lt; 0.0001). There was an inverse relationship of the presence of SPARC+ spindle cells and basement membrane material. In conclusion, the destruction of the basement membrane is correlated with meningioma malignancy grade whereas the expression of SPARC protein at the tumour–brain border is not. Destruction of the basement membrane and appearance of SPARC+ spindle cells are not coincident during the course of brain invasion by meningiomas.
Synthesis and Studies of Lanthanide Oxide Nitrates LnONO3 (Ln: Pr, Nd, and Sm—Yb).
2006-04-21

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF.
Small Molecular anti‐Cytokine Agents
2006-04-21

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract, please click on HTML or PDF.
Scotoma mapping by semi‐automated kinetic perimetry: the effects of stimulus properties and the speed of subjects' responses
2006-04-23

Abstract. Purpose: The study aimed firstly to determine the effects of stimulus variables on the detection of a scotoma border and, secondly, to study the reproducibility of the method during semi‐automated kinetic perimetry. Methods: The size of the physiological blind spot in 18 young normal subjects was measured with a video‐campimetric device, the Tübingen computer campimeter (TCC). Kinetic stimuli of two different sizes and at four different levels of luminance were presented. Examinations were repeated within 2 weeks. Measurements were corrected for individual response times and the area of the blind spot was computed. The effects of stimulus strength and size and the repeatability of blind spot measurements were evaluated by an analysis of variance. Results: The physiological blind spot showed significant inter‐ and intraindividual variations in size (least square means ranging from 17 to 49 square degrees), with a standard deviation of 6.8 square degrees. The measured size of the blind spot increased as a function of decreasing stimulus value, by reducing either the relative brightness or the size of stimuli. Use of a correction for each subject's speed of responses nearly halved the level of random variance. The temporal sequence of measurements (the order in which they were performed) had no apparent effect on the calculated values of blind spot size. Conclusions: Semi‐automated kinetic perimetry can determine the size of the physiological blind spot with good repeatability in young, normal subjects. Determination of each individual's speed of response and inclusion of this variable in the calculations reduced variance of the measure significantly. This study confirmed the presence of considerable interindividual differences in the size of the physiological blind spot.
LACK‐reactive CD4+ T cells require autocrine IL‐2 to mediate susceptibility to Leishmania major
2006-04-24

Abstract Mice from most inbred strains are resistant to infection with Leishmania major whereas mice from BALB strains are highly susceptible. Resistance and susceptibility result from the development of Th1 or Th2 cells, respectively. In this report, we document an IL‐2 mRNA burst, preceding the reported early IL‐4 response, in draining lymph nodes of susceptible mice infected with L. major. Neutralization of IL‐2 during the first days of infection redirected Th1 cell maturation and resistance to L. major , through interference with the rapid IL‐4 transcription in Leishmania homolog of mammalian RACK1 (LACK)‐reactive CD4 + cells. A burst of IL‐2 transcripts also occurred in infected C57BL/6 mice that do not mount an early IL‐4 response. However, although the LACK protein induced IL‐2 transcripts in susceptible mice, it failed to trigger this response in resistant C57BL/6 mice. Reconstitution experiments using C.B.‐17 SCID mice and LACK‐reactive CD4 + T cells from IL‐2 –/– BALB/c mice showed that triggering of the early IL‐4 response required autocrine IL‐2. Thus, in C57BL/6 mice, the inability of LACK‐reactive CD4 + T cells to express early IL‐4 mRNA transcription, important for disease progression, appears due to an incapacity of these cells to produce IL‐2.
Functional Unity of the Ponto-Cerebellum: Evidence That Intrapontine Communication Is Mediated by a Reciprocal Loop With the Cerebellar Nuclei
2006-04-26

The majority of cerebral signals destined for the cerebellum are handed over by the pontine nuclei (PN), which thoroughly reorganize the neocortical topography. The PN maps neocortical signals of wide-spread origins into adjacent compartments delineated by spatially precise distribution of cortical terminals and postsynaptic dendrites. We asked whether and how signals interact on the level of the PN. Intracellular fillings of rat PN cells in vitro did not reveal any intrinsic axonal branching neither within the range of the cells' dendrites nor farther away. Furthermore, double whole cell patch recordings did not show any signs of interaction between neighboring pontine cells. Using simultaneous unit recording in the PN and cerebellar nuclei (CN) in rats in vivo, we investigated whether PN compartments interact via extrinsic reciprocal connections with the CN. Repetitive electrical stimulation of the cerebral peduncle of ≤40 Hz readily evoked rapid sequential activation of PN and CN, demonstrating a direct connection between the structures. Stimulation of the PN gray matter led to responses in neurons ≤600 μm away from the stimulation site at latencies compatible with di- or polysynaptic pathways via the CN. Importantly, these interactions were spatially discontinuous around the stimulation electrode suggesting that reciprocal PN-CN loops in addition reflect the compartmentalized organization of the PN. These findings are in line with the idea that the cerebellum makes use of the compartmentalized map in the PN to orchestrate the composition of its own neocortical input.