Miracle-dz/UniFAR-FTUs huggingface dataset:
Assessment of the Myocardium on 2-Phase Cardiac Multidetector Computed Tomography: Does Cyclic Cardiac Contraction Influence Myocardial Attenuation?

Objective: To analyze changes in attenuation of non-contrast-enhanced and contrast-enhanced myocardium throughout the cardiac cycle and to determine the effect of myocardial location, cardiac phase, and dominant coronary perfusion type on myocardial attenuation to evaluate the impact of contraction-dependent factors on multidetector computed tomography (MDCT) perfusion studies. Material and Methods: Cardiac computed tomography imaging was performed on a 40-row MDCT scanner. Myocardial attenuation was assessed in 50 men during 20 cardiac phases. Ninety myocardial regions of interest were placed in the distribution of the right, left anterior descending, and left circumflex coronary arteries on contrast-enhanced MDCT. In 26 patients, myocardial attenuation was also assessed on non-contrast-enhanced MDCT. Myocardial attenuation was analyzed on isopycnic graphs. Attenuation changes due to myocardial contraction were evaluated on non-contrast-enhanced MDCT. The impact of cyclic perfusion on myocardial enhancement was determined on contrast-enhanced MDCT. Student t test and Pearson correlation were used. The influence of dominant coronary perfusion type, supplying coronary artery, and cardiac phase were evaluated using univariate general linear model analysis. Results: Isopycnic graphs revealed that myocardial contraction during systole led to significant increase in myocardial attenuation on non-contrast-enhanced MDCT [equation 1 = 33.2 vs equation 2 = 29.1, P < 0.001]. Reduction in myocardial perfusion during systole led to decrease in myocardial attenuation in contrast-enhanced MDCT [equation 1 = 92.4 vs equation 2 = 111.9, P < 0.001]. Systolic increase in attenuation due to myocardial contraction was far outweighed by the effects of intramyocardial contrast enhancement (correlation Pearson = 0.941). Dominant coronary perfusion did not lead to significant changes in contrast-enhanced myocardium (P = 0.299). Anatomical location and underlying cardiac phase represented significant factors in myocardial attenuation variation (P < 0.001). Conclusion: Myocardial attenuation is influenced by cardiac phase and myocardial location. These factors must be considered when analyzing myocardial perfusion with MDCT.
The umbilical cord: a study of 1,000 consecutive deliveries.

OBJECTIVE To establish base-line data on cord length among Igbo parturients of Eastern Nigeria, especially relationship between age and parity, gestation length, sex and weight of newborn, placental weight. DESIGN Retrospective analysis of 1,000 consecutive deliveries. SETTING Mission hospital. MATERIALS AND METHODS Placental length of umbilical cord, placental weight, and prenatal data. RESULTS Cord length varied between 15 cm and 130 cm (mean, 51.5 cm). No relationship found to parity, maternal age, or sex of baby. Increase in cord length with birthweight and gestational age, up to term. Correlation between umbilical length and placental weight, with a variation according to lie of the fetus: longest in cord encirclement and unstable lie, shortest in breech presentation, transverse lie, and twin birth.
Discretization Precision and Assessment Error

Continuous probability distributions are often discretized by assigning a weight to each of several percentiles (e.g., the 10th, 50th, and 90th percentiles). Previous work has analyzed the accuracy of various discretization methods. In practice, however, the assessed percentiles may not be precise. In this paper, we compare the performance of several discretization methods when the probability assessments are subject to error. Our results indicate that one should still strive to use the best discretization method even in the face of assessment error. This is particularly true if one is trying to preserve the variance and higher moments of the continuous distribution.
Secure multicast routing infrastructure : the network operator point of view. (Infrastructure sécurisée de routage multipoint : le point de vue de l'opérateur réseau)

Multicast is a promising technology for the distribution of streaming media, bulk data and many other added-value applications, yet the deployment of multicast still in its infancy. Providing security is still one of the main challenge that hinders the introduction of multicast in the existing infrastructure. It is therefore critical to provide sound security mechanisms that can protect the ISPs and the carriers infrastructure against multicast threats and allow them in the same time to get all the benefits of introducing multicast in their networks. This work considers one of the most challenging features of multicast deployment : the security of the multicast routing infrastructure. In this thesis we adopt the security from the multicast Network Operator's viewpoint. The kind of security required by a network operator, who manages and operates the multicast routing infrastructure, largely differs from that of end-toend security. More specifically, the operator is concerned by service continuity no matter what happens. In other words, the operator wants the group communication service provided to its clients (i.e. end users or other network operators with whom has peering relationships) must be operational at any time, in spite of anomalies in the multicast flows, no matter whether they are intentional (i.e. are the result of deliberate attacks) or not (e.g. are caused by a misbehaving component). While many theoretically ideal proposals have been done to secure the routing protocols, they have rarely been accepted by the operators community. For instance, because they require to modify existing and widely deployed protocols, or they introduce heavy authentication mechanisms, which is in practice almost impossible to deploy in legacy networks, and even infeasible, since a corrupted host may be the source of a DoS attack, even if it has been authenticated. In this thesis analyze in depth the threats to the multicast infrastructure. We show that the vulnerability of the multicast model comes largely from the edge. More specifically, several attacks arise from the use of group management protocols, IGMP for IPv4 and MLD for IPv6. In the light of this analysis, we introduce and evaluate a simple, yet efficient filtering approach to thwart some DoS attacks that are based on IGMP or MLD flooding, and that threaten the whole operator's infrastructure. A key feature of our proposal is that it follows a realistic and pragmatic approach, and in particular it does not require any modification to the existing, widely deployed protocols.
Increased carbonyl modification by lipids and carbohydrates in diabetic nephropathy.

BACKGROUND In diabetic nephropathy (DN), possible mediators of untoward effects of hyperglycemia include the advanced glycation end products (AGEs). Indeed, an AGE, carboxymethyllysine (CML), accumulates in expanded mesangial matrix and nodular lesions. An advanced lipoxidation end product (ALE), malondialdehyde-lysine (MDA-lysine), generated on proteins during lipid peroxidation also accumulates in these lesions. As both ALEs and AGEs are formed by carbonyl amine chemistry between protein and carbonyl compounds derived from autoxidation of lipids and carbohydrates, their colocalization suggests an increased carbonyl modification of proteins. METHODS To address this hypothesis, human diabetic renal tissues were examined to characterize carbonyl modification of proteins by lipids and carbohydrates: (a) ALEs, MDA-lysine and 4-hydroxynonenal (HNE) protein adduct, derived from lipids, and (b) AGEs, pentosidine and CML, derived from carbohydrates. Furthermore, to elucidate the biological effect of carbonyl modification on primary cultured human and rat mesangial cells, the intracellular protein phosphorylation was examined in the presence of various kinds of carbonyl compounds. RESULTS The ALE and AGE adducts examined were identified in expanded mesangial matrix and nodular lesions. The exposure of cultured mesangial cells to carbonyl compounds resulted in phosphorylation of tyrosine residues of a number of intracellular proteins. CONCLUSIONS These data suggest a broad derangement in nonenzymatic biochemistry involving both lipids and carbohydrates exists in diabetic glomerular lesions ("carbonyl stress").
Modeling Chlorophyll $a$ Concentration Affected by Artificial Upwelling in Qiandao Lake

Artificial upwelling of ocean water has been increasingly used to enhance primary marine productivity. This approach brings nutrient-rich deep water to the surface and alters the physical characteristics of water and thus the distribution of the nutrient over an effective period. Various water physical characteristics may affect chlorophyll a concentration, a key indicator for assessing primary marine productivity. Therefore, it is important to study the correlation between chlorophyll a concentration and various water physical characteristics in the artificial upwelling, which has never been examined in literature. In this paper, several water quality parameters, which have potential correlation with chlorophyll a concentration, are selected and multiple linear regression (MLR) and multivariate quadratic regression (MQR) are employed to test the correlation. Then, two novel neural network approaches, i.e., genetic-algorithm-based neural network (GA-NN) and particle-swarm-optimization-based neural network (PSO-NN) are proposed to model the correlation, which are further compared with regular backpropagation neural network (BP-NN), MLR, and MQR. The experimental data are collected from Qiandao Lake, China. The modeling results show that chlorophyll a concentration has a strong correlation with salinity, temperature, dissolved oxygen (DO), and pH in the process of artificial upwelling, and GA-NN and PSO-NN can provide reliable prediction of the correlation.
Socioeconomic Factors, Nutrition, and Food Choices: An Analysis of the Salad Dressing Market

Most studies utilize consumer surveys or experimental data to investigate the relationship between socioeconomic variables and food choices. The author examines actual purchase behavior (supermarket scanner data) in the natural shopping environment. The author focuses on whether the propensity to purchase high-fat unlabeled products within a product category varies across supermarkets with different demographic profiles. The results show differences in this propensity across demographic groups, even after accounting for price and sale promotions. The findings are consistent with consumer survey and experimental design research on the relationship between demographic characteristics and the processing of nutrition information.
Extracellular Heat Shock Proteins in Cell Signaling and Immunity

Abstract: Extracellular stress proteins including heat shock proteins (Hsps) and glucose‐regulated proteins (Grps) are emerging as important mediators of intercellular signaling and transport. Release of such proteins from cells is triggered by physical trauma and behavioral stress as well as exposure to immunological “danger signals. ” Stress protein release occurs both through physiological secretion mechanisms and during cell death by necrosis. After release into the extracellular fluid, Hsp or Grp may then bind to the surfaces of adjacent cells and initiate signal transduction cascades as well as the transport of cargo molecules, such as antigenic peptides. In addition, Hsp60 and Hsp70 are able to enter the bloodstream and may possess the ability to act at distant sites in the body. Many of the effects of extracellular stress proteins are mediated through cell‐surface receptors. Such receptors include toll‐ like receptors (TLRs) 2 and 4, CD40, CD91, CCR5, and members of the scavenger receptor family, such as LOX‐1 and SREC‐1. The possession of a wide range of receptors for the Hsp and Grp family permits binding to a diverse range of cells and the performance of complex multicellular functions particularly in immune cells and neurons.
Late renal dysfunction in adult survivors of bone marrow transplantation

Until recently long‐term renal toxicity has not been considered a major late complication of bone marrow transplantation (BMT). Late renal dysfunction has been described in a pediatric population status post‐BMT which was attributable to the radiation in the preparatory regimen. A thorough review of adults with this type of late renal dysfunction has not previously been described. Fourteen of 103 evaluable adult patients undergoing allogeneic (96) or autologous (7) bone marrow transplantation, predominantly for leukemia and lymphomas, at the Medical College of Wisconsin (Milwaukee, WI) have had a syndrome of renal insufficiency characterized by increased serum creatinine, decreased glomerular filtration rate, anemia, and hypertension. This syndrome developed at a median of 9 months (range, 4.5 to 26 months) posttransplantation in the absence of specific identifiable causes. The cumulative probability of having this renal dysfunction is 20% at 1 year. Renal biopsies performed on seven of these cases showed the endothelium widely separated from the basement membrane, extreme thickening of the glomerular basement membrane, and microthrombi. Previous chemotherapy, antibiotics, and antifungals as well as cyclosporin may add to and possibly potentiate a primary chemoradiation marrow transplant renal injury, but this clinical syndrome is most analogous to clinical and experimental models of radiation nephritis. This late marrow transplant‐associated nephritis should be recognized as a potentially limiting factor in the use of some intensive chemoradiation conditioning regimens used for BMT. Some selective attenuation of the radiation to the kidneys may decrease the incidence of this renal dysfunction.
The vertebral venous plexuses: The internal veins are muscular and external veins have valves

The internal and external vertebral venous plexuses (VVP) extend the length of the vertebral column. Authoritative sources state that these veins are devoid of valves, permitting bidirectional blood flow and facilitating the hematogenous spread of malignant tumors that have venous connections with these plexuses. The aim of this investigation was to identify morphologic features that might influence blood flow in the VVP. The VVP of 12 adult cadavers (seven female, mean age 79.5 years) were examined by macro‐ and micro‐dissection and representative veins removed for histology and immunohistochemistry (smooth muscle antibody staining). A total of 26, mostly bicuspid, valves were identified in 19 of 56 veins (34%) from the external VVP, all orientated to promote blood flow towards the internal VVP. The internal VVP was characterized by four main longitudinal channels with transverse interconnections; the maximum caliber of the longitudinal anterior internal VVP veins was significantly greater than their posterior counterparts (P < 0.001). The luminal architecture of the internal VVP veins was striking, consisting of numerous bridging trabeculae (cords, thin membranes and thick bridges) predominantly within the longitudinal venous channels. Trabeculae were composed of collagen and smooth muscle and also contained numerous small arteries and nerve fibers. A similar internal venous trabecular meshwork is known to exist within the dural venous sinuses of the skull. It may serve to prevent venous overdistension or collapse, to regulate the direction and velocity of venous blood flow, or is possibly involved in thermoregulation or other homeostatic processes. Clin. Anat. 25:609–618, 2012. © 2011 Wiley Periodicals, Inc.
PDLIM2 Inhibits T Helper 17 Cell Development and Granulomatous Inflammation Through Degradation of STAT3

An E3 ubiquitin ligase inhibits the development of inflammatory T cells involved in autoimmune diseases. LIMiting Inflammation by T Cells Although much is known about the development of T helper 17 (TH17) cells, a proinflammatory T cell type that is important for the immune response to pathogens, comparatively little is known about how these cells are inhibited to prevent chronic inflammation and autoimmune diseases. Tanaka et al. have identified the E3 ubiquitin ligase PDLIM2 as an endogenous inhibitor of TH17 development by targeting the essential transcription factor STAT3 (signal transducer and activator of transcription 3) for destruction. Mice lacking PDLIM2 had worse inflammatory disease than did control mice, suggesting that PDLIM2 might be a therapeutic target to prevent TH17 cell–mediated inflammatory diseases. Granuloma formation is an important host defense mechanism against intracellular bacteria; however, uncontrolled granulomatous inflammation is pathologic. T helper 17 (TH17) cells are thought to have a pathogenic role in autoimmune and inflammatory diseases, including in granulomas. Here, we report that the PDZ-LIM domain protein PDLIM2 inhibited TH17 cell development and granulomatous responses by acting as a nuclear ubiquitin E3 ligase that targeted signal transducer and activator of transcription 3 (STAT3), a transcription factor critical for the commitment of naïve CD4+ T cells to the TH17 lineage. PDLIM2 promoted the polyubiquitination and proteasomal degradation of STAT3, thereby disrupting STAT3-mediated gene activation. Deficiency in PDLIM2 resulted in the accumulation of STAT3 in the nucleus, enhanced the extent of TH17 cell differentiation, and exacerbated granuloma formation. This study delineates an essential role for PDLIM2 in inhibiting TH17 cell–mediated inflammatory responses by suppressing STAT3 signaling and provides a potential therapeutic target for the treatment of autoimmune diseases.
Canonical WNT signaling promotes mammary placode development and is essential for initiation of mammary gland morphogenesis

Mammary glands, like other skin appendages such as hair follicles and teeth, develop from the surface epithelium and underlying mesenchyme; however, the molecular controls of embryonic mammary development are largely unknown. We find that activation of the canonical WNT/β-catenin signaling pathway in the embryonic mouse mammary region coincides with initiation of mammary morphogenesis, and that WNT pathway activity subsequently localizes to mammary placodes and buds. Several Wnt genes are broadly expressed in the surface epithelium at the time of mammary initiation, and expression of additional Wnt and WNT pathway genes localizes to the mammary lines and placodes as they develop. Embryos cultured in medium containing WNT3A or the WNT pathway activator lithium chloride (LiCl) display accelerated formation of expanded placodes, and LiCl induces the formation of ectopic placode-like structures that show elevated expression of the placode marker Wnt10b. Conversely, expression of the secreted WNT inhibitor Dickkopf 1 in transgenic embryo surface epithelium in vivo completely blocks mammary placode formation and prevents localized expression of all mammary placode markers tested. These data indicate that WNT signaling promotes placode development and is required for initiation of mammary gland morphogenesis. WNT signals play similar roles in hair follicle formation and thus may be broadly required for induction of skin appendage morphogenesis.
Dividend Capture Returns: Anomaly or Risk Premium? Evidence from the Equity Options Markets

In the run-up to the ex-dividend day a measure based on option implied dividends predicts ex-day abnormal stock returns. These expected ex-dividend day returns increase on stocks where it is less worthwhile to capture the dividend, stocks that are less liquid, stocks with high idiosyncratic risk, and stocks that have experienced a build up in selling pressure. The evidence from the options markets suggests the positive abnormal ex-day returns, net of transactions costs, achieved by institutions skilled in trading are a risk premium for their role in providing liquidity to non-informational stock traders.
Immunohistochemical Study of Cell Proliferation, Bcl-2, p53, and Caspase-3 Expression on Preneoplastic Changes Induced by Cadmium and Zinc Chloride in the Ventral Rat Prostate

This work was directed to evaluate immunoexpression of markers for apoptosis, resistance to apoptosis, and cell proliferation, as well as estimates of nuclear size in ventral prostate of rats treated with cadmium chloride and cadmium + zinc chloride because a possible protective effect of zinc has been postulated. The following variables were studied: volume fraction (VF) of Bcl-2 immunostaining, percentage of cells immunoreactive to proliferating cell nuclear antigen (LIPCNA) and p53 (LIp53), numerical density of caspase-3 immunoreactive cells (NV caspase-3), and estimates of volume-weighted mean nuclear volume (υV). The LIPCNA and VF of Bcl-2 were significantly increased in the treated animals. The dysplasias (independent of their origin) showed a significant increase of the LIp53, NV caspase-3, and υV in comparison with normal acini from treated and control animals. It can be concluded that cell proliferation is enhanced in long-term cadmium-exposed rats, and exposure to zinc combined with cadmium had no effect on any of the variables studied when comparing with normal acini. The increase of nuclear υV could indicate a more aggressive behavior for pretumoral lesions.
BMI1–UBR5 axis regulates transcriptional repression at damaged chromatin

Significance The BMI1-containing Polycomb Repressive Complex is an important gene silencer during development, stem cell maintenance, and cancer progression. BMI1 is also involved in DNA damage response, but its downstream mechanism is unclear. Here we identified UBR5 as a downstream factor whose chromatin recruitment is regulated by BMI1. We showed that BMI1 and UBR5 repress the RNA polymerase II (Pol II) elongation and nascent RNA synthesis at UV-induced DNA lesions. UBR5 associates with and regulates the abundance of the histone chaperon complex FACT at damaged chromatin and regulates elongation of Pol II at the lesions. Thus, our studies identify a pathway that regulates the damage-induced transcriptional repression that is governed by BMI1. BMI1 is a component of the Polycomb Repressive Complex 1 (PRC1), which plays a key role in maintaining epigenetic silencing during development. BMI1 also participates in gene silencing during DNA damage response, but the precise downstream function of BMI1 in gene silencing is unclear. Here we identified the UBR5 E3 ligase as a downstream factor of BMI1. We found that UBR5 forms damage-inducible nuclear foci in a manner dependent on the PRC1 components BMI1, RNF1 (RING1a), and RNF2 (RING1b). Whereas transcription is repressed at UV-induced lesions on chromatin, depletion of the PRC1 members or UBR5 alone derepressed transcription elongation at these sites, suggesting that UBR5 functions in a linear pathway with PRC1 in inducing gene silencing at lesions. Mass spectrometry (MS) analysis revealed that UBR5 associates with BMI1 as well as FACT components SPT16 and SSRP1. We found that UBR5 localizes to the UV-induced lesions along with SPT16. We show that UBR5 ubiquitinates SPT16, and depletion of UBR5 or BMI1 leads to an enlargement of SPT16 foci size at UV lesions, suggesting that UBR5 and BMI1 repress SPT16 enrichment at the damaged sites. Consistently, depletion of the FACT components effectively reversed the transcriptional derepression incurred in the UBR5 and BMI1 KO cells. Finally, UBR5 and BMI1 KO cells are hypersensitive to UV, which supports the notion that faulty RNA synthesis at damaged sites is harmful to the cell fitness. Altogether, these results suggest that BMI1 and UBR5 repress the polymerase II (Pol II)-mediated transcription at damaged sites, by negatively regulating the FACT-dependent Pol II elongation.