Miracle-dz/UniFAR-FTUs huggingface dataset:
Adolescent Intermittent Alcohol Exposure: Dysregulation of Thrombospondins and Synapse Formation are Associated with Decreased Neuronal Density in the Adult Hippocampus.

BACKGROUND Adolescent intermittent alcohol exposure (AIE) has profound effects on neuronal function. We have previously shown that AIE causes aberrant hippocampal structure and function that persists into adulthood. However, the possible contributions of astrocytes and their signaling factors remain largely unexplored. We investigated the acute and enduring effects of AIE on astrocytic reactivity and signaling on synaptic expression in the hippocampus, including the impact of the thrombospondin (TSP) family of astrocyte-secreted synaptogenic factors and their neuronal receptor, alpha2delta-1 (α2δ-1). Our hypothesis is that some of the influences of AIE on neuronal function may be secondary to direct effects on astrocytes. METHODS We conducted Western blot analysis on TSPs 1 to 4 and α2δ-1 from whole hippocampal lysates 24 hours after the 4th and 10th doses of AIE, then 24 days after the last dose (in adulthood). We used immunohistochemistry to assess astrocyte reactivity (i.e., morphology) and synaptogenesis (i.e., colocalization of pre- and postsynaptic puncta). RESULTS Adolescent AIE reduced α2δ-1 expression, and colocalized pre- and postsynaptic puncta after the fourth ethanol (EtOH) dose. By the 10th dose, increased TSP2 levels were accompanied by an increase in colocalized pre- and postsynaptic puncta, while α2δ-1 returned to control levels. Twenty-four days after the last EtOH dose (i.e., adulthood), TSP2, TSP4, and α2δ-1 expression were all elevated. Astrocyte reactivity, indicated by increased astrocytic volume and area, was also observed at that time. CONCLUSIONS Repeated EtOH exposure during adolescence results in long-term changes in specific astrocyte signaling proteins and their neuronal synaptogenic receptor. Continued signaling by these traditionally developmental factors in adulthood may represent a compensatory mechanism whereby astrocytes reopen the synaptogenic window and repair lost connectivity, and consequently contribute to the enduring maladaptive structural and functional abnormalities previously observed in the hippocampus after AIE.
Traffic classification on mobile core network considering regularity of background traffic

Recent widespread use of smartphones and rich multimedia contents has brought a considerable increase in mobile traffic. Therefore, the characteristics of smartphone traffic need to be considered when designing mobile core networks. Smartphone traffic is categorized by whether it is generated from user interaction (foreground (FG) traffic) or not (background (BG) traffic), and such traffic types can be managed differently to efficiently maintain the communication quality in the case of network congestion. However, it is difficult to distinguish such traffic types and their characteristics solely by IP addresses/port numbers. In addition, the increase in HTTPS traffic makes application-level packet inspection difficult. In this paper, we propose a traffic classification method on a mobile core network. The proposed method captures packets on the mobile core network, constructs TCP flows, and labels each flow by considering the regularity of BG traffic and the randomness of FG traffic using a Support Vector Machine (SVM) classifier with selected feature indexes obtained from the TCP/IP layer. Also, we attempt to restrict the indexes that can be obtained in the observation of the initial part of each TCP flow in order to reduce the calculation cost. The proposed method is evaluated in terms of the classification accuracy using experimental data through the Wi-Fi connections of smartphones. The full-index classifier using 40 indexes classifies FG and BG traffic with 97.2% accuracy and the shortcut-index classifier using restricted 36 indexes also indicates 94.4% accuracy.
A mutation in the XPB/ERCC3 DNA repair transcription gene, associated with trichothiodystrophy.

Trichothiodystrophy (TTD) is a rare, autosomal recessive disorder characterized by sulfur-deficient brittle hair and nails, mental retardation, impaired sexual development, and ichthyosis. Photosensitivity has been reported in approximately 50% of the cases, but no skin cancer is associated with TTD. Virtually all photosensitive TTD patients have a deficiency in the nucleotide excision repair (NER) of UV-induced DNA damage that is indistinguishable from that of xeroderma pigmentosum (XP) complementation group D (XP-D) patients. DNA repair defects in XP-D are associated with two additional, quite different diseases; XP, a sun-sensitive and cancer-prone repair disorder, and Cockayne syndrome (CS), a photosensitive condition characterized by physical and mental retardation and wizened facial appearance. One photosensitive TTD case constitutes a new repair-deficient complementation group, TTD-A. Remarkably, both TTD-A and XP-D defects are associated with subunits of TFIIH, a basal transcription factor with a second function in DNA repair. Thus, mutations in TFIIH components may, on top of a repair defect, also cause transcriptional insufficiency, which may explain part of the non-XP clinical features of TTD. Besides XPD and TTDA, the XPB gene product is also part of TFIIH. To date, three patients with the remarkable conjunction of XP and CS but not TTD have been assigned to XP complementation group B (XP-B). Here we present the characterization of the NER defect in two mild TTD patients (TTD6VI and TTD4VI) and confirm the assignment to X-PB. The causative mutation was found to be a single base substitution resulting in a missense mutation (T119P) in a region of the XPB protein completely conserved in yeast, Drosophila, mouse, and man. These findings define a third TTD complementation group, extend the clinical heterogeneity associated with XP-B, stress the exclusive relationship between TTD and mutations in subunits of repair/transcription factor TFIIH, and strongly support the concept of "transcription syndromes. "
Multicenter evaluation of a new immunoassay for procalcitonin measurement on the Kryptor® System

Abstract We compared the manually performed LUMItest® procalcitonin (PCT) assay with the newly developed fully mechanized Kryptor® PCT assay and determined the essential assay characteristics of this assay. The new Kryptor® PCT assay was evaluated according to modified NCCLS EP-10/EP-6 protocols in five different laboratories. Samples from 696 patients were assayed using the original LUMItest® PCT assay and the new Kryptor® PCT assay. Possible interference by hemoglobin, triglycerides and bilirubin was evaluated by spiking patient plasma with the appropriate substances. The functional assay sensitivity (FAS) was determined by analyzing samples with low PCT concentrations. The FAS of the new Kryptor® PCT assay was 0.04 ng/ml and the imprecision within- and between-series below 5% and below 10%, respectively. Within the smallest range of determination, from 0.3 ng/ml to 50 ng/ml, common to the LUMItest® PCT assay (x) and the Kryptor® PCT assay (y) the values correlated well: y=0.64+0.94x, s.xy=2.78 ng/ml. The performance characteristics of the Kryptor® PCT assay are fully compatible with the intended clinical use. The assay allows determination of PCT in a turnaround time (TAT) of about 20 minutes and thus is adequate for STAT analyses.
Sleepwalking into Catastrophe: Cognitive Biases and Corporate Climate Change Inertia

Despite the consensus that climate change will have huge consequences not just for the planet but also on corporate operations, businesses continue to fail to adjust their strategic decision-making processes to become more sustainable. One of the silent culprits behind climate change inertia lies in the cognitive biases at play in corporate decision making. This article builds on existing strategic decision-making models to explain how biases prevent managers from accurately identifying the moral dimensions of climate change. It also presents a broad range of practical interventions for how this constraint can be overcome.
TGF-β Induces Growth Arrest in Burkitt Lymphoma Cells via Transcriptional Repression of E2F-1*

Transforming growth factor-β (TGF-β) is a potent regulator of tissue homeostasis and can act as both a tumor suppressor and a tumor promoter. The ability to induce cell cycle arrest is a major component of the tumor suppressor function of TGF-β. Lung, mammary, and skin epithelial cells exhibit a common minimal cytostatic program in response to TGF-β signaling involving the repression of the growth-promoting factors c-MYC, Id1, Id2, and Id3. Loss of c-MYC expression is a pivotal event in this process, resulting in derepression of the cyclin-dependent kinase inhibitors CDKN1A (p21) and CDKN2B (p15) and ultimately leading to growth arrest. It is not clear, however, which responses are necessary for TGF-β-mediated growth arrest in other cell types. Here, in human Burkitt lymphoma cells transformed by deregulated c-MYC expression, we demonstrate that efficient TGF-β-induced cytostasis can occur despite both maintenance of c-MYC levels and a lack of p21 and p15 induction. TGF-β treatment also results in induction, rather than repression, of Id1 and Id2 expression. In this context, growth arrest correlates with transcriptional repression of E2F-1, and overexpression of E2F-1 in Burkitt lymphoma cells largely overcomes the TGF-β-mediated G1 arrest phenotype. These data indicate that deregulation of c-MYC in lymphoma cells does not overcome the tumor suppressor function of TGF-β and that repression of E2F-1 transcription is sufficient for the efficient induction of cytostasis.
Application of laser capture microdissection combined with two‐dimensional electrophoresis for the discovery of differentially regulated proteins in pancreatic ductal adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is the most lethal of all the common malignancies and markers for early detection or targets for treatment of this disease are urgently required. The disease is characterised by a strong stromal response, with cancer cells usually representing a relatively small proportion of the cells in the tumor mass. We therefore performed laser capture microdissection (LCM) to enrich for both normal and malignant pancreatic ductal epithelial cells. Proteins extracted from these cells were then separated by two‐dimensional gel electrophoresis (2‐DE). The limited amounts of protein in the LCM procured samples necessitated the detection of 2‐DE resolved proteins by silver staining. Consequently, loading equivalent amounts of protein onto gels was essential. However, we found that conventional means of measuring total protein in the samples were not sufficiently accurate. We therefore adopted a strategy in which the samples were first separated by one‐dimensional sodium dodecyl sulphate‐polyacrylamide gel electrophoresis, stained with silver stain and subjected to densitometry. Evaluation of the staining intensity was then used to normalise the samples. We found that the protein profiles from undissected normal pancreas and LCM‐acquired non‐malignant ductal epithelial cells from the same tissue block were different, underpinning the value of LCM in our analysis. The comparisons of protein profiles from nonmalignant and malignant ductal epithelial cells revealed nine protein spots that were consistently differentially regulated. Five of these proteins showed increased expression in tumor cells while four showed diminished expression in these cells. One of the proteins displaying enhanced expression in tumor cells was identified as the calcium‐binding protein, S100A6. To determine the incidence of S100A6 overexpression in pancreatic cancer, we carried out immunohistochemical analysis on sections from a pancreas cancer tissue array containing 174 duplicate normal and malignant pancreatic tissue samples, from 46 pancreas cancer patients. Normal pancreatic ductal epithelia were either devoid of detectable S100A6 or showed weak expression only. Moderately or poorly differentiated tumors, by contrast, showed a higher incidence and a higher level of S100A6 expression. These observations indicate that the combination of LCM with 2‐DE provides an effective strategy to discover proteins that are differentially expressed in PDAC.
Supply-side policy coordination in the European Union

Summary Europe’s overall economic performance has been depressing for more than a decade. The reasons are well known, as are the solutions. The problem lies squarely with the supply side. While some countries have been able to undertake the necessary reforms, others have not. Can the solution come from outside, through more centralization, formal or informal, at the EU level of government? Our answer is negative. Centralization works by exploiting externalities and increasing returns, but it cannot substitute for domestic policy failures. With few exceptions, chiefly research and higher education, the supply side displays no significant externalities and no increasing returns. Is the Open Method of Coordination, which lies at the heart of the Lisbon strategy, an alternative to centralization? Here again, our answer is negative. We view the strategy as misguided in its ambitions, muddled in its endless list of priorities, undercut by the illusory precision of its quantitative targets, and flawed in its reliance on improbable peer pressure. We make three main proposals. First, in order to complete the single market, held up by powerful interest groups, we suggest increasing the powers of the Commission or, preferably setting up independent agencies. Second, in those countries where the labor markets need politically difficult reforms, we recommend that national parliaments be required to debate the conclusions of European Council meetings. Third, to overcome Europe’s scientific innovation failures, we propose that the EU’s research budget be primarily used to provide matching grants for setting up new universities and research centers.
A novel method for underwater image segmentation based on M-band wavelet transform and human psychovisual phenomenon(HVS)

Underwater image segmentation becomes a difficult and challenging task due to various perturbations present in the water. In this paper we propose a novel method for underwater image segmentation based on M-band wavelet transform and human psychovisual phenomenon(HVS). The M-band wavelet transform captures the texture of the underwater image by decomposing the image into sub bands with different scales and orientations. The proper sub bands for segmentation are selected depending on the HVS. The HVS imitates the original visual technique of a human being and it is used to divide each sub band into Weber, De-Vries Rose and Saturation regions. A sub band is selected for segmentation depending on those three regions. The performance of the proposed method is found to be superior than that of the stare-of-the-art methods for underwater image segmentation on standard data set.
Joint use of multi-orbit high-resolution SAR interferometry for DEM generation in mountainous area

SAR interferometry has long been regarded as an effective tool for wide-area topographic mapping in hilly and mountainous areas. However, quality of InSAR DEM product is usually affected by atmospheric disturbances and decorrelation-induced voids, especially for data acquired in repeat-pass mode. In this paper, we proposed an approach for improved topographic mapping by optimal fusion of multi-orbit InSAR DEMs with correction of atmospheric phase screen (APS). An experimental study with high-resolution TerraSAR-X and COSMO-SkyMed datasets covering a mountainous area was carried out to demonstrate the effectiveness of the proposed approach. Validation with a reference DEM of scale 1:50,000 indicated that vertical accuracy of the fused DEM can be better than 5 m.
Phorbol esters can persistently replace interleukin‐2 (IL‐2) for the growth of a human IL‐2‐dependent T‐cell line

A selected clone from an IL‐2‐dependent human T‐cell line was persistently propagated in the presence of phorbol esters with the ability to activate protein kinase C (PKC), such as 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) or phorbol‐12,13‐dibutylate (PDBu). Thus, a TPA(PDBu)‐dependent T‐cell line, designated TPA‐Mat, was established from IL‐2‐dependent T cells. The TPA‐dependency of TPA‐Mat was not lost during cultivation for more than a year in the presence of TPA, and TPA‐Mat cells still showed IL‐2‐dependent growth. However, the TPA (PDBu)‐dependent growth of TPA‐Mat did not seem to be mediated by an autocrine mechanism of IL‐2 or by any other growth factor production, because these factors were not detected in TPA‐Mat cell supernatants. Therefore, the phorbol esters substituted for IL‐2 and may be directly involved in transduction of growth signals in TPA‐Mat cells. Although activity of PKC was down‐regulated, messenger ribonucleic acid (mRNA) of the PKC β‐gene was detected in TPA‐Mat cells was stimulated not only by phorbol esters but also by nonphorbol ester tumor promoters with the ability to activate PKC. These observations suggest that the sustained activation of PKC by the phorbol esters could induce continuous growth of the IL‐2‐dependent TPA‐Mat cells.
Differences between cellular integration sites of transcribed and nontranscribed Rous sarcoma proviruses

Transcribed Rous sarcoma proviruses in Rat-1 DNA tend to integrate closely 3' to C-G-rich restriction enzyme sites, and 2 of 13 such proviruses were found to have inserted at the same locus. However, most integrated proviruses were transcriptionally silent insertions at sites indistinguishable from random. We conclude that Rous sarcoma proviruses in rat cells usually fail to integrate in a favorable site for transcription, in contrast to studies on proviral integration in permissive hosts.
Ultrastructural Observations on Mitochondria and Microvesicles in Renal Oncocytoma, Chromophobe Renal Cell Carcinoma, and Eosinophilic Variant of Conventional (Clear Cell) Renal Cell Carcinoma

On light microscopic examination, the morphologically overlapping features of granular eosinophilic cytoplasm in renal oncocytoma and the eosinophilic variants of chromophobe renal cell carcinoma and conventional (clear cell) renal cell carcinoma may pose difficulties in diagnosis. We investigated the ultrastructure of 5 renal oncocytomas, 7 eosinophilic variants of chromophobe renal cell carcinoma, and 5 eosinophilic variants of conventional (clear cell) renal cell carcinoma. Special attention was paid to mitochondria and microvesicles and interrelations thereof. The electron microscopic features were correlated with the light microscopic findings. All of the tumors had abundant mitochondria. Although abundant microvesicles were present in all of the chromophobe renal cell carcinomas, scant numbers of microvesicles were also sometimes present in renal oncocytomas (2 of 5) and in the eosinophilic variant of conventional (clear cell) renal cell carcinoma (1 of 5). The mitochondria in all three types of renal neoplasms studied differed in morphology, being predominantly uniform and round with predominantly lamellar cristae in renal oncocytoma, variable in shape and size with predominantly tubulocystic cristae in chromophobe renal cell carcinoma, and swollen and pleomorphic with rarefied matrix and attenuated cristae in the eosinophilic variant of conventional (clear cell) renal cell carcinoma. Variable numbers of mitochondria in all of the chromophobe renal cell carcinomas had outpouchings of the outer membranes, some of which carried parts of inner membrane within them. These outpouchings closely resembled the nearby cytoplasmic microvesicles, as did the tubulocystic cristae of the mitochondria. Some microvesicles contained homogeneous, electron-dense, finely granular matrix, similar to that seen in mitochondria. In one of seven chromophobe renal cell carcinomas, microvesicles were present in rough endoplasmic reticulum, and in two others, mitochondria were present within some vesicles. These features strongly suggest a close relationship between the microvesicles and mitochondria. Based on the role of vesicle formation in normal mitochondriogenesis, and some of our observations, we propose that defective mitochondriogenesis may be the source of microvesicles in chromophobe renal cell carcinomas.
Quantitative Gene Expression Profiles of Human Liver-Derived Cell Lines Exposed to Moderate Hypoxia

Aims: To obtain better understanding of molecular events following critical oxygen shortage in liver tissue, we performed a large-scale comparison of gene expression profiles in four human liver cell lines, Chang, Hep3B, HuH7, and HepG2. Methods: We used Atlas cDNA expression arrays from Clontech for initial screening, and quantitative real-time RT-PCR to assess the statistical significance of observed changes. Results: RT-PCR analysis confirmed significantly changed levels of 24 transcripts after 24 hours incubation in 1% O2. Among the genes most robustly up-regulated were plasminogen activator inhibitor-1 (PAI-1), insulin-like growth factor binding protein–3, and glyceraldehyde-3-phosphate dehydrogenase. Only PAI-1 was concordantly up-regulated in all four cell lines. Conversely, most down-regulated were the stress response genes, including several heat shock proteins, yet only the expression of flap endonuclease-1 was significantly decreased in all cell lines. When comparing individual cell lines, the HepG2 cells displayed a pattern of general down-regulation (83%), followed by Hep3B with 58% of genes down-regulated. In the Chang and HuH7 cells, however, the expression of most genes, 50% and 67%, respectively, remained unchanged. Conclusion: These studies provide information that is of importance for improved insight into the responses of not only liver tumor cells but also normal liver tissue in the conditions where physiological oxygenation is severely impaired.
Evaluation of the Marginal Fit of CAD/CAM Crowns Fabricated Using Two Different Chairside CAD/CAM Systems on Preparations of Varying Quality.

PURPOSE This study evaluated the marginal gap of crowns fabricated using two new chairside computer-aided design/computer-aided manufacturing systems on preparations completed by clinicians with varying levels of expertise to identify whether common preparation errors affect marginal fit. The null hypothesis is that there is no difference in the mean marginal gaps of restorations of varying qualities and no difference in the mean marginal gap size between restorations fabricated using the PlanScan (D4D, Richardson, TX, USA) and the CEREC Omnicam (Sirona, Bensheim, Germany). MATERIAL AND METHODS The fit of 80 lithium disilicate crowns fabricated with the E4D PlanScan or CEREC Omnicam systems on preparations of varying quality were examined for marginal fit by using the replica technique. These same preparations were then visually examined against common criteria for anterior all-ceramic restorations and placed in one of four categories: excellent, good, fair, and poor. Linear mixed modeling was used to evaluate associations between marginal gap, tooth preparation rating, and fabrication machine. RESULTS The fit was not significantly different between both systems across all qualities of preparation. The average fit was 104 μm for poor-quality preparations, 87.6 μm for fair preparations, 67.2 μm for good preparations, and 36.6 μm for excellent preparations. CONCLUSION The null hypothesis is rejected. It can be concluded that preparation quality has a significant impact on marginal gap regardless of which system is used. However, no significant difference was found when comparing the systems to each other. CLINICAL SIGNIFICANCE Within the limitations of this in vitro study, it can be concluded that crown preparation quality has a significant effect on marginal gap of the restoration when the clinician uses either CEREC Omnicam or E4D PlansScan.