Miracle-dz/UniFAR-FTUs huggingface dataset:
A Strictly Contractive Peaceman-Rachford Splitting Method with Logarithmic-Quadratic Proximal Regularization for Convex Programming

Recently, a strictly contractive Peaceman-Rachford splitting method (PRSM) was proposed for a separable convex minimization model whose variables are subject to some linear constraints and two additional generic constraints. In general, the strictly contractive PRSM requires to solve two constrained minimization subproblems at each iteration. In this paper, we consider the case where the additional constraints on variables are positive orthants and apply the well-developed logarithmic-quadratic proximal (LQP) regularization to regularize the subproblems of the strictly contractive PRSM. A new algorithm in combination with the strictly contractive PRSM and the LQP regularization is thus proposed. The new algorithm only needs to solve two unconstrained subproblems at each iteration. An inexact version allowing the unconstrained subproblems to be solved approximately subject to certain inexactness criterion is also studied. We prove the global convergence and establish a worst-case convergence rate measured .
Effects of vaginal cylinder position on dose distribution in patients with endometrial carcinoma in treatment of vaginal cuff brachytherapy

Purpose To investigate the impact of different cylinder positions on dosimetry of critical structures in patients with endometrial carcinoma undergoing three-dimensional image-based vaginal cuff brachytherapy (VCB). Material and methods We delivered VCB at a dose of 4 Gy to a depth of 5 mm in the vaginal cuff of 15 patients using three different cylinder positions (neutral [N], parallel [P], and angled [A]) according to the longitudinal axis of the patient. We analyzed the dose-volume distribution and volumetric variability of the rectum and bladder. We converted the total doses to equivalent doses in 2 Gy (EQD2) using a linear-quadratic model (a/b = 3 Gy). Results The mean rectum volume for the N, P, and A positions was 68.2 ± 22.7 cc, 79.3 ± 33.7 cc, and 74.2 ± 29.6 cc, respectively. The mean rectum volume for the P position was significantly larger than that for the N position (p = 0.03). Relative to the N position, the A position resulted in a lower total EQD2 in the highest irradiated 2 cc (D2cc; p = 0.001), 1 cc (D1cc; p = 0.004), and 0.1 cc (D0.1cc; p = 0.047) of the rectum. Similarly, the P position resulted in a lower EQD2 in the D2cc (p = 0.018) and D1cc (p = 0.024) of the rectum relative to the N position. In the bladder, the P position resulted in a higher EQD2 in the D2cc relative to the N position (p = 0.02). There was no dosimetric difference between the P and A positions in either the rectum or the bladder. Conclusions Vaginal cuff brachytherapy in the P and A positions is significantly superior to that in the N position in terms of rectum dosimetry. The bladder dose in the N position is considerably lower than that in the other positions.
Fluoroquinolone resistance in staphylococci: new challenges.

Staphylococci show only marginal susceptibility to the newer fluoroquinolones. Minimum inhibitory concentrations (MICs) for susceptible strains usually range from 0.25 to 2.0 mg/l. As a single mutational event involving the gyrase target or permeability diminishes fluoroquinolone susceptibility fourfold on average, such a mutation in staphylococci would lead to a clinical level of resistance. Therefore, it is not surprising that in some institutions, the use of fluoroquinolones has been quickly followed by greatly increased prevalence of fluoroquinolone-resistant staphylococci. The greatest increase in resistance has been seen among methicillin-resistant staphylococci although increased prevalence of resistance among Staphylococcus saprophyticus and other methicillin-susceptible staphylococci has also been reported. Clinical isolates of staphylococci recovered since the introduction of the fluoroquinolones fall into three fluoroquinolone susceptibility groups: susceptible (MIC < 0.5 mg/l), moderately resistant (MIC 0.5 to 4 mg/l) and highly resistant (MIC > 4 mg/l). The first group represents wild type strains while the second and third groups represent single- and multiple-step mutants, respectively. To prevent increasing prevalence of isolates in the second and third groups, it would be prudent to avoid use of quinolones whenever possible. However, when it is necessary, a fluoroquinolone, which achieves serum/tissue levels eight times the MIC of the infecting strain, should be used.
The Colonial History of Wye Plantation, the Lloyd Family, and their Slaves on Maryland's Eastern Shore: Family, Property, and Power

PAGE The history of the Lloyd family at Wye Plantation in Talbot County, Maryland, from the 1650s to the early 1770s refines and complicates the dominant historical narrative of the rise of a native-born Protestant planter elite in colonial Chesapeake scholarship. First, the Lloyds were a wealthy and politically prominent Protestant family that benefited from close ties to Catholics up to the end of the colonial period. Second, in contrast to traditional histories of the colonial Chesapeake that emphasize the raising and marketing of tobacco, Wye Plantation's history attests to the importance of grain and livestock farming on a commercial scale, in addition to tobacco production, on the upper Eastern Shore since the seventeenth century. This study examines the strategies of the Lloyd family to build their wealth and influence in Maryland in the context of the colony's political, economic, and social development. In the seventeenth and early eighteenth centuries, the Lloyds forged kinship ties to Maryland's Catholic gentry, to Quakers, and to the Bennetts of Virginia and Maryland. With these connections, the plantation's trade with London and the West Indies expanded. In the mideighteenth century, Edward Lloyd Ill used his status as a trusted client within Lord Baltimore's patronage network to develop Wye Plantation as a locus of power. Upon his death in 1770, his son moved aggressively to preserve assets that would be the basis of his own independence. This dissertation uses an interdisciplinary approach to document Wye Plantation's history. Sources include probate records, government proceedings, the Lloyd Papers and the Calvert Papers at the Maryland Historical Society, the Cadwalader Collection at the Historical Society of Pennsylvania, and portraits by Charles Willson Peale. While plantation ownership remained the basis of social and political authority in the colony, each generation of the Lloyd family made use of the home plantation in contextspecific ways. This thesis examines change in the uses of a Chesapeake plantation, and the meanings attached to plantation ownership, from the point of view of each generation of the Lloyd family during the colonial period. TABLE OF CONTENTS Page Acknowledgments n List of Figures IV Introduction 1 Chapter I. The Origins of Wye Plantation: An Investment in Colonial Trade 20 Chapter II. Fashioning a Role among Maryland's Protestant Elite: 60 Edward Lloyd II of Wye Plantation at the Turn of the Eighteenth Century Chapter III. Power Play: Wye Plantation under Edward Lloyd III, 1730-1770 135 Chapter IV. "Uneasiness and Confusion" at Wye Plantation: The Division of 186 Edward Lloyd III's Estate in 1770 Conclusion 235 Figures 244 Appendix A. Lloyd Family Genealogy 266 Appendix B. The Lloyd House at Wye Plantation, 1770, based on Inventories 268 Bibliography 276 Vita 295
Myopathies related to systemic sclerosis: a case–control study of associated clinical and immunological features

Objective: Little is known about systemic sclerosis (SSc)-related myopathy. We aimed to compare the clinical and immunological features of SSc patients with or without associated myopathy. Methods: Forty SSc patients with myopathy, defined by myalgia or muscle weakness associated with creatine kinase (CK) more than five times the upper limit range or myopathic electromyography (EMG) or abnormal myopathology, were identified from the records of four French hospital centres. For each patient, we selected two SSc controls matched for cutaneous SSc form, sex, age at SSc onset, and disease duration. We performed a case–control study testing clinical and immunological SSc-related features for association with myopathy by conditional logistic regression. Results: Muscle and SSc features of patients with myopathy did not differ significantly among the four centres of origin. Only four (10%) patients with SSc-associated myopathy had anti-polymyositis-scleroderma (PM-Scl) antibodies. Case–control univariate analysis revealed that reduced forced vital capacity (FVC) [odds ratio (OR) 3.0, 95% confidence interval (CI) 1.3–34.9], heart involvement, defined as clinical congestive heart failure, left ventricular ejection fraction (LVEF) < 60%, arrhythmia or conductive abnormalities (OR 2.9, 95% CI 1.3–6.5), and scleroderma renal crisis (OR 3.0, 95% CI 1.3–34.9) were significantly more frequent in patients with myopathy than in controls. Two autoantibodies were more frequent in patients with myopathy: anti-PM-Scl (OR 5.0, 95% CI 1.1–23.9) and anti-RNP (OR 6.9, 95% CI 1.1–64.4). Multivariate analysis retained two variables associated positively with myopathy [reduced FVC (OR 3.1, 95% CI 1.3–9.8) and heart involvement (OR 2.5, 95% CI 1.1–7.1)], while anti-centromere antibodies were associated negatively (OR 0.11, 95% CI 0.03–0.53). Conclusion: Heart monitoring of SSc patients with myopathy should be undertaken regularly because of the association of myocardial and skeletal myopathies in such patients.
Genetic and Biochemical Analysis of the Functional Domains of Yeast tRNA Ligase*

Yeast tRNA ligase (Trl1) converts cleaved tRNA half-molecules into spliced tRNAs containing a 2′-PO4, 3′-5′ phosphodiester at the splice junction. Trl1 performs three reactions: (i) the 2′,3′-cyclic phosphate of the proximal fragment is hydrolyzed to a 3′-OH, 2′-PO4 by a cyclic phosphodiesterase (CPD); (ii) the 5′-OH of the distal fragment is phosphorylated by an NTP-dependent polynucleotide kinase; and (iii) the 3′-OH, 2′-PO4, and 5′-PO4 ends are sealed by an ATP-dependent RNA ligase. Trl1 consists of an N-terminal adenylyltransferase domain that resembles T4 RNA ligase 1, a central domain that resembles T4 polynucleotide kinase, and a C-terminal CPD domain that resembles the 2H phosphotransferase enzyme superfamily. Here we show that all three domains are essential in vivo, although they need not be linked in the same polypeptide. We identify five amino acids in the adenylyltransferase domain (Lys114, Glu266, Gly267, Lys284, and Lys286) that are essential for Trl1 activity and are located within motifs I (114KANG117), IV (266EGFVI270), and V (282FFKIK286) that comprise the active sites of DNA ligases, RNA capping enzymes, and T4 RNA ligases 1 and 2. Mutations K404A and T405A in the P-loop (401GXGKT405) of the central kinase-like domain had no effect on Trl1 function in vivo. The K404A and T405A mutations eliminated ATP-dependent kinase activity but preserved GTP-dependent kinase activity. A double alanine mutant in the P-loop was lethal in vivo and abolished GTP-dependent kinase activity. These results suggest that GTP is the physiological substrate and that the Trl1 kinase has a single NTP binding site of which the P-loop is a component. Two other mutations in the central domain were lethal in vivo and either abolished (D425A) or severely reduced (R511A) GTP-dependent RNA kinase activity in vitro. Mutations of the signature histidines of the CPD domain were either lethal (H777A) or conferred a ts growth phenotype (H673A).
Solving the Continuous Berth Allocation and Specific Quay Crane Assignment Problems with Quay Crane Coverage Range

This work solves an integrated model of the continuous berth allocation and specific quay crane QC assignment problem with QC coverage range. Based on the analysis of vessel berth position and QC coverage range, a nonlinear mixed-integer programming model is developed. A novel heuristic method based on spatiotemporal conflict analysis is applied to derive a high-quality berth-QCs plan. The initial pessimistic priorities of vessels are employed to reflect the preferences of vessels for terminal resources. The proposed cluster of vessels focuses on spatiotemporal conflicts among vessels. Coordinated assignments of resources for the clustered vessels are realized via the branch-and-bound method. The QC feasibility check identifies infeasibility of QCs-to-vessel assignment. Several experiments are conducted to validate the effectiveness of the proposed method. Numerical results demonstrate that high-quality berth-QCs plans can be obtained within an acceptable time. Further, the influence of coverage range of QC is discussed in detail.
Role of Thiocyanate, Bromide and Hypobromous Acid in Hydrogen Peroxide-induced Apoptosis

We have previously reported that H2O2-induced apoptosis in HL-60 human leukemia cells takes place in the presence of chloride, requires myeloperoxidase (MPO), and occurs through oxidative reactions involving hypochlorous acid and chloramines. We now report that when chloride is replaced by the pseudohalide thiocyanate, there is little or no H2O2-induced apoptosis. Furthermore, thiocyanate inhibits H2O2-induced apoptosis when chloride is present at physiological concentrations, and this occurs at thiocyanate concentrations that are present in human serum and saliva. In contrast, bromide can substitute for chloride in H2O2-induced apoptosis, but results in a lower percent of the cells induced into apoptosis. Hypobromous acid is likely a short-lived intermediate in this H2O2/MPO/bromide apoptosis, and reagent hypobromous acid and bromamines induce apoptosis in HL-60 cells. We conclude that the physiologic concentrations of thiocyanate found in human plasma could modulate the cytototoxicity of H2O2 and its resulting highly toxic MPO-generated hypochlorous acid by competing with chloride for MPO. Furthermore, the oxidative products of the reaction of thiocyanate with MPO are relatively innocuous for human leukemic cells in culture. In contrast, bromide can support H2O2/MPO/halide apoptosis, but is less potent than chloride and it has no effect in the presence of physiological levels of chloride.
Protective effects of LM22A-4 on injured spinal cord nerves.

OBJECTIVE The goal of this study was to elucidate the protection by and potential mechanisms of LM22A-4, a specific agonist of tyrosine kinase receptor B, against spinal cord injury (SCI). METHODS Spinal cord trauma was induced by the application of vascular clips to the dura of mice via a four-level T7-T11 laminectomy. Thirty minutes after the injury, an abdominal injection of LM22A-4 (at dosages of 10 mg/kg and 15 mg/kg) or an equal volume of solvent was provided. Twenty-four hours after SCI, a Western blot was performed to examine the expression of p-TrkB, p-Akt, p-ERK, cleaved-caspase-3, and Bcl-2; a TUNEL assay and Nissl staining were performed to study apoptosis and the survival of neurons. In addition, another batch of mice was allowed to live for 14 days after the SCI treatment, during which the LM22A-4 was provided at the same time each day and the neurological function was assessed. RESULTS Spinal cord injury in mice resulted in severe trauma characterized by tissue damage and apoptosis. Treatment of the mice with LM22A-4 (10 mg/kg) significantly reduced the degree of tissue injury (histological score) and apoptosis (TUNEL staining and caspase-3 and Bcl-2 expression) compared with vehicle treated group (P < 0.05). In a separate set of experiments, chronic treatment with LM22A-4 also significantly ameliorated the recovery of limb function (P < 0.05). CONCLUSION This study provides an experimental evidence that LM22A-4 reduces the development of tissue injury associated with spinal cord trauma, and activation of the activity of TrkB may represent a novel approach for the therapy of spinal cord trauma.
Preparation and Characterization of Mucoadhesive Microcapsules of Gliclazide with Natural Gums

Gliclazide is an oral hypoglycemic agent used in management of non-insulin dependent diabetes mellitus. Among people who are suffering from long term disorders, the major were categorized under diabetes so, a dosage form is needed to provide continuous therapy with high margin of safety & such dosage form can be achieved by microencapsulation. Gliclazide microspheres with sodium alginate (coat material, gum kondagogu, gum guar and xanthan gum (mucoadhesive agents) were prepared by orifice-ionic gelation and emulsification ionic gelation techniques varying concentrations (1:0.25, 1:0.5, 1:0.75 and 1:1). Formulations were then evaluated for surface morphology, particle shape, Carr’s index, microencapsulation efficiency, drug release, mucoadhesion studies. Compatibility studies were performed by FTIR, DSC, and XRD techniques and no interactions were found between drug and excepients used. The microspheres were found spherical and free flowing with emulsion ionic gelation technique with a size range 400-600μm. % drug content and encapsulation efficiency found in the range of 55%-68% and, 86.23%-94.46% respectively. All microspheres showed good mucoadhesive property in in-vitro wash of test. In vitro drug release studies showed that the guar gum has more potentiality to retard the drug release compared to other gums and concentrations. Drug release from the microspheres was found slow following zero order release kinetics with non-fickian release mechanism stating release depended on the coat: core ratio and the method employed. The concentration of 1:1 of SA: GG (EMG 4) found suitable for preparing the controlled release formulation of gliclazide stating emulsification gelation technique is the best among followed. Key words : Gliclazide; Natural gums; orifice ionic gelation technique; emulsification ionic gelation technique DOI: http://dx.doi. org/10.3329/sjps.v4i1. 8865 SJPS 2011; 4(1): 38-48
Regulated Interaction of Protein Kinase Cδ with the Heterogeneous Nuclear Ribonucleoprotein K Protein*

The heterogeneous nuclear ribonucleoprotein (hnRNP) K protein recruits a diversity of molecular partners that are involved in signal transduction, transcription, RNA processing, and translation. K protein is phosphorylated in vivo andin vitro by inducible kinase(s) and contains several potential sites for protein kinase C (PKC) phosphorylation. In this study we show that K protein is phosphorylated in vitro by PKCδ and by other PKCs. Deletion analysis and site-directed mutagenesis revealed that Ser302 is a major K protein site phosphorylated by PKCδ in vitro. This residue is located in the middle of a short amino acid fragment that divides the two clusters of SH3-binding domains. Mutation of Ser302decreased the level of phosphorylation of exogenously expressed K protein in phorbol 12-myristate 13-acetate-treated COS cells, suggesting that Ser302 is also a site for PKC-mediated phosphorylation in vivo. In vitro, PKCδ binds K protein via the highly interactive KI domain, an interaction that is blocked by poly(C) RNA. Mutation of Ser302 did not alter the K protein-PKCδ interaction in vitro, suggesting that phosphorylation of this residue alone is not sufficient to alter this interaction. Instead, binding of PKCδ to K protein in vitro and in vivo was greatly increased by K protein phosphorylation on tyrosine residues. The ability of PKCδ to bind and phosphorylate K protein may serve not only to alter the activity of K protein itself, but K protein may also bridge PKCδ to other K protein molecular partners and thus facilitate molecular cross-talk. The regulated nature of the PKCδ-K protein interaction may serve to meet cellular needs at sites of active transcription, RNA processing and translation in response to changing extracellular environment.
Finite Subgroups of Morava Stabilizer Groups

Introduction The purpose of this paper is to present results from Higher realK-theories and topological automorphic forms by M. Behrens and M.J. Hopkins, and to indicate a direction in which these results may be extended in future work. The first section of this paper introduces basic algebraic geometry constructs which we hope to apply to the problem addressed by Behrens and Hopkins. In the second section we motivate the problem addressed by Behrens and Hopkins, and we summarize their results. We conclude with a short section indicating the direction in which we hope to extend these results.
5-amino-4-imidazolecarboxamide riboside confers strong tolerance to glucose starvation in a 5'-AMP-activated protein kinase-dependent fashion.

Acadesine, 5-amino-4-imidazolecarboxamide riboside (AICAR), has been claimed to protect the heart, lung, and small intestine against ischemic damage. The biochemical mechanisms of this effect of AICAR are not yet fully understood. To understand the mechanism, we examined the effect of AICAR on glucose starvation, since cellular responses to ischemia could be regarded as a protective response to an insufficient blood supply, cells might display adaptive reactions not only to oxygen deficiency but to nutrient deficiency. AICAR was found to confer strong tolerance to glucose starvation. By using antisense RNA expression vector for alpha subunit of 5'-AMP-activated protein kinase, the effect of AICAR was found to be dependent on 5'-AMP-activated protein kinase containing the alpha2 subunit. The AICAR effect was also dependent on the presence of amino acids, indicating an energy source switch from glucose to amino acids.
Pilot study of minocycline for the prevention of paclitaxel-associated neuropathy: ACCRU RU221408I.

220 Background: Paclitaxel is associated with both an acute pain syndrome (P-APS) and chronic chemotherapy-induced peripheral neuropathy (CIPN). Preliminary animal data suggest that minocycline may be effective for the prevention of chemotherapy-induced neurotoxicity. The purpose of this pilot study was to investigate the efficacy of minocycline for the prevention of CIPN and P-APS. METHODS Patients with breast cancer were enrolled prior to initiating neoadjuvant or adjuvant weekly paclitaxel for 12 weeks. They were randomized to receive minocycline 200mg on day 1 followed by 100mg twice daily or a placebo, with the same dosing schedule. Patients completed (1) an acute pain syndrome questionnaire daily during chemotherapy, and (2) the EORTC QLQ-CIPN20 questionnaire at baseline, prior to each dose of paclitaxel, and monthly for 6 months post treatment. The primary goal was to obtain pilot data regarding the possible effect of minocycline on the prevention of paclitaxel-induced CIPN and P-APS, to determine if conducting a larger phase III placebo-controlled trial was indicated. Scores obtained from patient questionnaires were converted to a 0-100 scale, where higher scores = better quality of life. RESULTS Forty-seven patients were randomized, 45 of which were evaluable, with a mean age of 55. There were no remarkable differences noted between the two groups for the overall sensory score of the EORTC-CIPN 20 or its individual sub-questions, which evaluated tingling, numbness, or shooting burning pain in hands and feet. However, there was a significant difference in the daily average AUC pain score attributed to P-APS, favoring minocycline (median 96.0 vs 84.3; p = 0.02). Correspondingly, patients receiving minocycline used less opioid pain medications for control of P-APS (0% vs 23%, P = 0.05). Not only were no increased toxicities reported with minocycline, but there was an apparent improvement in fatigue (median AUC 76.7 vs 59.0; P = 0.02). CONCLUSIONS Based on the results of this pilot study, minocycline did not appear to be beneficial for the prevention of CIPN, but did look promising for reducing P-APS. Further study of this effect may be warranted. CLINICAL TRIAL INFORMATION NCT02297412.