Miracle-dz/UniFAR-FTUs huggingface dataset:
Directional MEWMA Schemes for Multistage Process Monitoring and Diagnosis

Statistical process control, monitoring, and diagnosis of a multistage process remain challenging problems in both the manufacturing and service industries. This paper proposes a directional multivariate exponentially weighted moving average (directional MEWMA) scheme integrating the EWMA scheme with the generalized likelihood ratio test (GLRT) scheme that can incorporate directional information based on the multistage state-space model and effectively monitor the process mean shift. The proposed directional MEWMA scheme not only provides a statistical process control (SPC) solution that incorporates both interstage and intrastage correlations but also resolves the confounding issue in monitoring and diagnosis due to the cumulative effects from stage to stage. In addition, a systematic diagnostic approach is provided to isolate and identify an out-of-control stage and to locate its change point. Our simulation results show that the proposed monitoring and diagnostic scheme consistently outperforms almost all existing approaches to multistage processes. A sensitivity analysis and discussion on performance indicators for multistage process monitoring are also presented.
Seismic Response of Single Piles and Pile Groups

This paper presents a comprehensive set of dimensionless graphs that could be readily utilized in practical applications. A comparative study of these graphs leads to interesting conclusions that may contribute towards an improved appreciation of the nature of seismic pile-soil-pile interaction. The graphs should be of practical value in determining the 'effective' seismic input motion at the base of structures, if the free-field motion is known. The discussion of the study results focuses on elucidating the role of the key parameters, and aims at developing engineering insight into kinematic soil-pile and pile-pile interactions during earthquakes.
Multiple initiation sites of DNA replication flanking the origin region of Xdv genome

Early replicative intermediates of Xdv plasmid were prepared by an in vitro replication system in the presence of 2',3'-dideoxycytidine 5'-triphosphate, an inhibitor of DNA chain elongation. Short-chain DNAs produced from regions near the replication origin were purified from the intermediates. A fraction of the DNAs was covalently linked to primer RNA. The transition sites from primer RNA to DNA synthesis were mapped along the nucleotide sequence of the genome, by eliminating the RNA by alkaline hydrolysis and labeling the freshly exposed 5' ends of DNA with 12p. The transition sites were found to be located on both sides of the ori region, which includes four 19-base-pair repeats where one of the X specific initiator proteins, 0, binds. No transition arose within the oni region. The transition sites are multiple on both sides of the on region and are clustered in one of the two strands in such a way that DNA syntheses from the two sides converge. The frequency of the "leftward" DNA synthesis is several times higher than that of "rightward" synthesis, re-flecting the asymmetric bidirectional replication of Xdv DNA.
Neural Antecedents of Emotional Disorders: An fMRI Study of Subsyndromal Emotional Symptoms in Adolescent Girls

Background— Emotional symptoms (ES) emerge forme fruste in adolescence, prior to manifesting as fully-fledged emotional disorders (ED). Studies indicate that subsyndromal ES precede the onset of ED. We hypothesised that adolescents showing subsyndromal ES will show perturbations in the emotion regulatory fronto-limbic network (FLN) during emotion-processing. Methods— Fifty-eight female adolescents underwent functional magnetic resonance imaging (fMRI) whilst viewing an image-based emotion-processing task. Within this sample 33 (56.9%) displayed emotional symptoms and 25 (43.1%) did not. Clinical measures including assessments of mood and anxiety were administered and participants were allocated to one of two groups based on the presence (ES+) or absence (ES−) of subsyndromal ES. Group comparisons were used to identify differential patterns of neural engagement and their relationship to clinical variables. Results— Groups displayed emotion-specific differences in FLN activity with increased frontal activity in ES+ girls during positive emotion-processing and decreased frontal and limbic activity during negative emotion-processing. Trait anxiety was the strongest clinical predictor of group membership neural activity during negative emotion-processing. In addition, between the groups the hippocampus displayed a pattern of reverse coupling with the amygdala and insula that was also significantly correlated with trait anxiety. Conclusions— There is divergence in the pattern of FLN neural processing in adolescent females determined by emotional symptoms. Future research is needed to corroborate these findings and to underline their implications longitudinally.
Di(cid:128)erential response to chloroethylclonidine in blood vessels of normotensive and spontaneously hypertensive rats: role of a 1D - and a 1A -adrenoceptors in contraction

1 The e(cid:128)ects of chloroethylclonidine on a 1 -adrenoceptor-mediated contraction in endothelium- denuded caudal arteries and aorta from normotensive Wistar and Wistar Kyoto (WKY), and from spontaneously hypertensive (SHR) rats were evaluated. 2 Chloroethylclonidine elicited concentration-dependent contractions. Maximal contraction was similar in caudal arteries among strains ( & 40% of noradrenaline e(cid:128)ect). However, chloroethylclonidine elicited a higher contraction in aorta from SHR than from normotensive rats. In Wistar aorta chloroethylclonidine produced the smallest contractile response. 3 In SHR aorta, BMY 7378 and 5-methylurapidil blocked chloroethylclonidine-elicited contraction, while (+)-cyclazocine did not inhibit it; while in caudal arteries, 5-methylurapidil blocked chloroethylclonidine action; the other antagonists had no e(cid:128)ect. 4 In chloroethylclonidine-treated aorta noradrenaline elicited biphasic contraction-response curves, indicating a high a(cid:129)nity (pD 2 , 8.5–7.5) chloroethylclonidine-sensitive component and a low a(cid:129)nity (pD 2 , 6.3–5.2) chloroethylclonidine-insensitive component. The high a(cid:129)nity component was blocked by chloroethylclonidine; while in caudal arteries noradrenaline elicited monophasic contraction-response curves with pD 2 values (6.5– 5.7) similar to the low a(cid:129)nity component in aorta. 5 Chloroethylclonidine inhibition of noradrenaline response was greater in aorta than in caudal arteries. Chloroethylclonidine increased the EC 50 values of noradrenaline & 1000 fold in aorta and & 10 fold in caudal arteries. 6 In SHR aorta BMY 7378 protected a 1D -adrenoceptors and in caudal arteries 5-methylurapidil protected a 1A -adrenoceptors from chloroethylclonidine alkylation, allowing noradrenaline to elicit contraction. 7 These results show marked strain-dependent di(cid:128)erences in the ability of chloroethylclonidine to contract aorta; moreover, chloroethylclonidine stimulates a 1D -adrenoceptors in aorta and a 1A adrenoceptors in caudal arteries. The higher contraction observed in aorta from SHR and WKY suggests an augmented number of a 1D -adrenoceptors in these strains. British Journal of Pharmacology (2000) 129, 653 –660
Allogeneic transplants, Fas-signaling, and dysregulation of hepcidin

Hepatic iron overload is common in patients undergoing hematopoietic cell transplantation. We showed previously in a murine model that transplantation of allogeneic T cells induced iron deposition and down-regulation of hepcidin (Hamp) in hepatocytes. We hypothesized that hepatic injury was related to disrupted iron homeostasis triggered by the interaction of Fas-ligand, expressed on activated T cells, with Fas on hepatocytes. In the current study, we determined the effects of modified expression of the Flice inhibitory protein (FLIP long [FLIPL]), which interferes with Fas signaling, on the impact of Fas-initiated signals on the expression of IL-6 and Stat3 and their down-stream target, Hamp. To exclude a possible contribution by other pathways, we used agonistic anti-Fas antibodies (rather than allogeneic T cells) to trigger Fas signaling. Inhibition of FLIPL by RNA interference resulted, as expected, in enhanced hepatocyte apoptosis in response to Fas signals, but also in decreased levels of IL-6, Stat3 and Hamp. In contrast, overexpression of FLIPL protected hepatocytes against agonistic anti-Fas antibody-mediated apoptosis, and increased the levels of IL-6 and Stat3, thereby maintaining the expression of Hamp in an NF- κ B-dependent fashion. In vivo over-expression of FLIPL in the liver via hydrodynamic transfection, similarly, interfered with Fas-initiated apoptosis and prevented down-regulation of IL-6, Stat3 and Hamp. These data indicate that Fas-dependent signals alter the regulation of iron homeostasis and suggest that signals initiated by Fas may contribute to peri-transplant iron accumulation.
African Swine Fever 1. Antiserum Production

These studies report on the production of African swine fever antiserum for use in serological tests. The first attempt to obtain anti- serum was made by inoculating ASF virus infected pig blood into the lactiferous sinus of lactating bovines. This failed to result in the development of detectable antibody, but re- sulted in propagation of the virus over a 14 to 21 day period. In the second attempt use was made of a tissue culture - attenuated virus to produce re- sistance in normal pigs. Clinical response to inoculation with the attenuated virus was limited to a one day increase of temperature. These pigs were subsequently orally exposed to virulent ASF virus and later challenged by intramuscular injection. The sera were sub- jected to testing by the modified direct com-plement-fixation test and the agar gel double- diffusion technique in order to follow the development of antibodies. Some sera were also conjugated with fluorescein isothiocyanate and used for the detection of viral antigen by the fluorescent antibody technique. It was found that with the atte- nuated brought about the development of low antibody levels in the pigs. This antibody level did not increase following oral exposure. One pig following challenge underwent a series of ascending temperature peaks, coinciding with increased complement- fixing titres. RESUME
STX, a novel membrane estrogen receptor ligand, protects against A β toxicity

Because STX is a selective ligand for membrane estrogen receptors, it may be able to confer the beneficial effects of estrogen without eliciting the deleterious side effects associated with activation of the nuclear estrogen receptors. This study evaluates the neuroprotective properties of STX in the context of amyloid- β (A β ) exposure. MC65 and SH-SY5Y neuroblastoma cell lines, as well as primary hippocampal neurons from wild type (WT) and Tg2576 mice, were used to investigate the ability of STX to attenuate cell death, mitochondrial dysfunction, dendritic simplification, and synaptic loss induced by A β . STX prevented A β -induced cell death in both neuroblastoma cell lines; it also normalized the decrease in ATP and mitochondrial gene expression caused by A β in these cells. Notably, STX also increased ATP content and mitochondrial gene expression in control neuroblastoma cells (in the absence of A β ). Likewise in primary neurons, STX increased ATP levels and mitochondrial gene expression in both genotypes. In addition, STX treatment enhanced dendritic arborization and spine densities in WT neurons and prevented the diminished outgrowth of dendrites caused by A β exposure in Tg2576 neurons. These data suggest that STX can act as an effective neuroprotective agent in the context of A β toxicity, improving mitochondrial function as well as dendritic growth and synaptic differentiation. In addition, since STX also improved these endpoints in the absence of A β , this compound may have broader therapeutic value beyond
Influences of surfactant on the breakup of a fluid jet in viscous surrounding

INFLUENCE OF SURFACTANT ON THE BREAKUP OF A FLUID JET IN VISCOUS SURROUNDING by Muhammad Irfan Hameed The effect of insoluble surfactant on the breakup of a fluid jet surrounded by another viscous fluid at low Reynolds number is studied both theoretically and experimentally. Equations governing the evolution of the interface and surfactant concentration are derived using a long wavelength approximation for the case of an inviscid jet and a slightly viscous jet surrounded by a more viscous fluid. These one dimensional partial differential equations governing the evolution of the slender jet are solved numerically for given initial interfacial perturbations and surfactant concentration. It is found that the presence of insoluble surfactant at the interface retards the pinch-off. The influence of surface diffusion of surfactant on the jet deformation is studied by varying surface Peclet number. It is found that greater diffusion of surfactant causes the jet to pinch faster. To check the predictions of our model, we performed experiments both for clean interface and as well as in presence of surfactants. The experimental results support the prediction of the theoretical model that the presence of surfactant slows down the pinch-off process. Results of the long wavelength model are also compared against the numerical simulations of the full problem. The solution of the full problem shows similar behavior to the simplified long wavelength model. INFLUENCE OF SURFACTANT ON THE BREAKUP OF A FLUID JET IN VISCOUS SURROUNDING by Muhammad Irfan Hameed A Dissertation Submitted to the Faculty of New Jersey Institute of Technology and Rutgers, The State University of New Jersey — Newark in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy in Mathematical Sciences Department of Mathematical Sciences, NJIT Department of Mathematics and Computer Science, Rutgers-Newark
The Regulated Expression of miRNAs in Normal and Polycythemia Vera Erythropoiesis

Objective— Polycythemia vera (PV) is a myeloproliferative disorder, arising from the acquired mutation(s) of a hematopoietic stem cell. The JAK2 V617F somatic mutation is found in most PV patients; however, it is not the disease-initiating mutation. Since microRNAs (miRNAs) play a regulatory role in hematopoiesis, we studied miRNA expressions in PV and normal erythropoiesis. Methods— The peripheral blood mononuclear cells were cultured in a three-phase liquid system resulting in synchronized expansion of erythroid progenitors. Using gene expression profiling by CombiMatrix MicroRNArray , we searched for PV specific changes at day1, 14 and 21. Twelve miRNA candidates were then reevaluated by quantitative RealTime PCR in a larger number of samples obtained from progenitors at the same stage of differentiation. Results— A significant difference of miR-150 expression was found in PV. In normal erythropoiesis, three expression patterns of miRNAs were observed: progressive down-regulation of miR-150, miR-155, miR-221, miR-222 ; up-regulation of miR-451 , miR-16 at late stages of erythropoiesis; and biphasic regulation of miR-339, miR-378 . The miR-451 appears to be erythroid specific. Conclusions— We identified the miRNAs with regulated expression in erythropoiesis; one appeared to be PV specific. Their miRNA expression levels define early, intermediate, and late stages of erythroid differentiation. The validity of our findings was confirmed in non-expanded peripheral blood cells.
Short Communication CNS Elevation of Vascular and Not Mucosal Addressin Cell Adhesion Molecules in Patients with Multiple Sclerosis

The mucosal addressin cell adhesion molecule (MAdCAM) and vascular cell adhesion molecule (VCAM) appear to play roles in the recruitment of leukocytes to specialized endothelium lining the gastrointestinal tract. The purpose of this study was to clarify the role of MAdCAM and VCAM in the central nervous system by comparing protein expression in patients with multiple sclerosis (MS) and control subjects by immunohistochemistry. Specific antibodies to human VCAM and MAdCAM were used to confirm expression in control and MS nervous system specimens by immunohistochemistry. VCAM immunoreactivity was detected in endothelial cells, perivascular tissue, and in some cases, leukocytes within the meninges, gray, and white matter, of both controls and MS patients. VCAM immunoreactivity was maximal in a patient with acute active plaques, but of lower intensity and reduced distribution in controls and those with chronic active or inactive MS plaques. In contrast, MAdCAM immunoreactivity could not be detected in brain tissue from unaffected or MS patients. Taken together, these data support a role of VCAM, but not MAdCAM in the development of MS. (Am J Pathol 2010, 176:556–562; DOI: 10.2353/ajpath.2010.090437) that interfere with normal leukocyte trafficking as alternative mechanisms to conventional immunosuppressive agents for
x 2 3 Long-chain polyunsaturated fatty acid intake and 12-y incidence of neovascular age-related macular degeneration and central geographic atrophy: AREDS report 30, a prospective cohort study from the Age-Related Eye Disease Study 1–4

Background: x 2 3 (n 2 3) Long-chain polyunsaturated fatty acids (LCPUFAs) affect processes implicated in vascular and neural retinal pathogenesis and thus may inﬂuence the risk of developing age-related macular degeneration (AMD). Objective: We investigated whether x 2 3 LCPUFA intake was associated with a reduced likelihood of developing central geographic atrophy (CGA) and neovascular (NV) AMD. Design: We undertook a nested cohort study within a multicenter phase 3 clinical trial, the Age-Related Eye Disease Study (AREDS), to study progression to advanced AMD in 1837 persons at moderate-to-high risk of this condition. The AREDS was designed to assess the clinical course, prognosis, risk factors, and nutrient-based treatments of AMD and ran from November 1992 to December 2005. We obtained baseline data on x 2 3 LCPUFA intake with a validated food-frequency questionnaire. Trained fundus graders ascertained AMD status from annual stereoscopic color photographs by using standardized methods at a single reading center across a 12-y pe-riod. We applied multivariable repeated-measures logistic regression with the incorporation of generalized estimating equation methods, because this permitted determination of progression to outcome at each visit. Results: Participants who reported the highest x 2 3 LCPUFA intake (median: 0.11% of total energy intake) were 30% less likely than their peers to develop CGA and NVAMD. The respective odds ratios were 0.65 (95% CI: 0.45, 0.92; P (cid:1) 0.02) and 0.68 (95% CI: 0.49, 0.94; P (cid:1) 0.02). Conclusions: The 12-y incidence of CGA and NV AMD in participants at moderate-to-high risk of these outcomes was lowest for those reporting the highest consumption of x 2 3 LCPUFAs. If these results are generalizable, they may guide the development of low-cost and easily implemented preventive interventions for progression to advanced AMD. This trial was registered at clinicaltrials.gov as NCT00594672. Am 2009;90:1601–7.
cAMP levels within Mycobacterium tuberculosis and M. bovis BCG increase upon infection of macrophages

Adenosine 3',5'-cyclic monophosphate (cAMP)-mediated signal transduction is common in both prokaryotes and eukaryotes, and several bacterial pathogens modulate cAMP signaling pathways with their mammalian hosts during infection. In this study, cAMP levels associated with M. tuberculosis and M. bovis BCG were measured during macrophage infection. cAMP levels within both bacteria increased approximately 50-fold during infection of J774.16 macrophages, relative to the cAMP levels within bacteria incubated in tissue culture media alone. cAMP levels also increased within the macrophage cytoplasm upon uptake of live, but not dead, mycobacteria. The presence of albumin in the absence of oleic acid significantly decreased cAMP secretion and production by both M. tuberculosis and M. bovis BCG. These results suggest that cAMP signaling plays a role in the interaction of TB-complex mycobacteria with macrophages during infection, and that albumin may be a physiological indicator differentiating host environments during infection.
Stromal Cell-Derived Factor-1 b Potentiates Bone Morphogenetic Protein-2-Stimulated Osteoinduction of Genetically Engineered Bone Marrow-Derived Mesenchymal Stem Cells In Vitro

Skeletal injuries are among the most prevalent clinical problems and bone marrow-derived mesenchymal stem/ stromal cells (BMSCs) have successfully been used for the treatment thereof. Stromal cell-derived factor-1 (SDF-1; CXCL12) is a member of the CXC chemokine family with multiple splice variants. The two most abundant variants, SDF-1 a and SDF-1 b , share identical amino acid sequences, except for four additional amino acids at the C-terminus of SDF-1 b , which may mediate surface stabilization via glycosaminoglycans and protect SDF-1 b from proteolytic cleavage, rendering it twice as potent as SDF-1 a . Increasing evidence suggests that SDF-1 is involved in bone formation through regulation of recruitment, engraftment, proliferation, and differentiation of stem/progenitor cells. The underlying molecular mechanisms, however, have not yet been fully elucidated. In this study, we tested the hypothesis that SDF-1 b can potentiate bone morphogenetic protein-2 (BMP-2)-stimu-lated osteogenic differentiation and chemotaxis of BMSCs in vitro . Utilizing retrovirus-mediated gene transfer to generate novel Tet-Off-SDF-1 b BMSCs, we found that conditional SDF-1 b expression is tightly regulated by doxycycline in a dose-dependent and temporal fashion, leading to signiﬁcantly increased SDF-1 b mRNA and protein levels. In addition, SDF-1 b was found to enhance BMP-2-stimulated mineralization, mRNA and protein expression of key osteogenic markers, and regulate BMP-2 signal transduction via extracellular signal-regulated kinases 1/2 (Erk1/2) phosphorylation in genetically engineered BMSCs in vitro . We also showed that SDF-1 b promotes the migratory response of CXC chemokine receptor 4 (CXCR4)-expressing BMSCs in vitro. Taken together, these data support that SDF-1 b can play an important role in BMP-2-stimulated osteogenic differentiation of BMSCs and may exert its biological activity in both an autocrine and paracrine fashion. the exact mechanisms have not yet been elucidated. Our studies reveal the speciﬁc contribution of SDF-1 b to the regulation of BMP-2 signaling in vitro . Future studies aim to investigate the detailed kinase-mediated temporal activation mechanisms and elucidate the identity of the molecular players involved in regulating this cross talk between the SDF-1- and BMP-2-mediated signal transduction pathways.
Measurement of dependence of backscatter coefficient from cylinders on frequency and diameter using focused transducers – with applications in trabecular bone

A theory for the elastic scattering response from a cylinder insonified by a plane wave was previously derived by Faran. In the present paper, the empirical relationship between Faran’s theory and measurements of backscatter coefficient from cylindrical targets using focused transducers is investigated. Experimental measurements of dependence of backscatter coefficient on frequency and diameter for nylon wires are reported. It is found that, under certain conditions (including weak, incoherent scattering), backscatter coefficient measurements from collections of cylindrical scatterers may be meaningfully compared with Faran’s model predictions. At low frequencies, the theory and experimental measurements exhibit similar dependences on frequency and diameter, provided that the scatterers are not too densely packed. At higher frequencies, the fine structure of Faran’s predictions becomes difficult to reproduce experimentally with a focused transducer. Implications regarding applications to characterization of trabecular bone are discussed.