262 research outputs found
(2,2âČ-Bipyridine-Îș2 N,NâČ)chlorido[4âČ-(2,5-dimethoxyÂphenÂyl)-2,2âČ:6âČ,2âČâČ-terpyridine-Îș3 N,NâČ,NâČâČ]ruthenium(II) hexaÂfluoridoÂphosphate acetonitrile monosolvate
In the title compound, [RuCl(C10H8N2)(C23H19N3O2)]PF6·CH3CN, the ligand environment about the RuII atom is distorted octaÂhedral, with the substituted terpyridyl ligand coordinated in a meridional fashion, the bipyridyl ligand coordinated in a cis fashion and the Cl atom trans to one of the bipyridyl N atoms. The RuâN distances are in the range 2.036â
(2)â2.084â
(2)â
Ă
with the exception of the central RuâN bond from the terpyridyl ligand, which is shorter [1.9503â
(19)â
Ă
], as expected. The pendant dimethoxyÂphenyl substituent is not coplanar with the terpyridyl unit; the dihedral angle between the central pyridyl ring and the benzene ring is 46.72â
(11)°. The anion is disordered equally over two positions around an FâPâF bond axis
AquaÂ[2-(2-pyridÂyl)-1,8-naphthyridine-Îș2 N 1,N 2](2,2âČ:6âČ,2âČâČ-terpyridine-Îș3 N,NâČ,NâČâČ)ruthenium(II) bisÂ(hexaÂfluoridoÂphosphate) acetone sesquisolvate
The asymmetric unit of the title compound, [Ru(C13H9N3)(C15H11N3)(H2O)](PF6)2·1.5C3H6O, consists of two crystallographically independent RuII complexes. Each complex is approximately octaÂhedral with the RuII atom bound by an N,NâČ-coordinated 2-(2-pyridÂyl)-1,8-naphthyridine (pynp) ligand, a meridional 2,2âČ:6âČ,2âČâČ-terpyridine (tpy) ligand and one aqua ligand. The tpy ligand is coordinated in a planar tridentate fashion with the central N atom closest to the RuII atom. The aqua ligand is trans to the pyridine N atom of pynp. The long RuâO distances [2.150â
(5) and 2.138â
(5)â
Ă
] are typical for aqua ligands in polypyridyl ruthenium complexes. In the crystal, both intraÂmolecular OâHâŻN and interÂmolecular OâHâŻO hydrogen bonds are observed
Gold nanoparticles electrodeposited on glassy carbon using cyclic voltammetry: Application to Hg(II) trace analysis
The electrochemical determination of Hg(II) at trace level using gold nanoparticlesâmodified glassy carbon (AuNPsâGC) electrodes is described. Starting from HAuCl4 in NaNO3, gold nanoparticles (AuNPs) were deposited onto Glassy Carbon (GC) electrodes using Cyclic Voltammetry (CV). Different deposits were obtained by varying the global charge consumed during the whole electroreduction step, depending on the number of cyclic potential scans (N). AuNPs were characterized as a function of the charge using both CV in H2SO4 and Field Emission Gun Scanning Electron Microscopy (FEG-SEM). The AuNPsâGC electrodes were then applied to determine low Hg(II) concentrations using Square Wave Anodic Stripping Voltammetry (SWASV). The AuNPsâGC electrodes provided significantly improved performances in Hg(II) determination compared to unmodified GC and bare Au electrodes. It was shown that the physico-chemical properties of the deposits are correlated to the performances of the AuNPsâGC electrode with respect to Hg(II) assay. The best results were obtained for four electrodeposition cyclic scans, where small-sized particles (36 ± 13 nm) with high density (73 particles ÎŒm-ÂČ) were obtained. Under these conditions, a linearity range from 0.64 to 4.00 nM and a limit of detection of 0.42 nM were obtained
The Frequency of Nonmotor Symptoms among Advanced Parkinson Patients May Depend on Instrument Used for Assessment
Background. Nonmotor symptoms (NMS) of Parkinson's disease (PD) may be more debilitating than motor symptoms. The purpose of this study was to determine the frequency and corecognition of NMS among our advanced PD cohort (patients considered for deep brain stimulation (DBS)) and caregivers.
Methods. NMS-Questionnaire (NMS-Q), a self-administered screening questionnaire, and NMS Assessment-Scale (NMS-S), a clinician-administered scale, were administered to PD patients and caregivers. Results. We enrolled 33 PD patients (23 males, 10 females) and caregivers. The most frequent NMS among patients using NMS-Q were gastrointestinal (87.9%), sleep (84.9%), and urinary (72.7%), while the most frequent symptoms using NMS-S were sleep (90.9%), gastrointestinal (75.8%), and mood (75.8%). Patient/caregiver scoring correlations for NMS-Q and NMS-S were 0.670 (P < 0.0001) and 0.527 (P = 0.0016), respectively. Conclusion The frequency of NMS among advanced PD patients and correlation between patients and caregivers varied with the instrument used. The overall correlation between patient and caregiver was greater with NMS-Q than NMS-S
Effect of Deep Brain Stimulation on Parkinson's Nonmotor Symptoms following Unilateral DBS: A Pilot Study
Parkinson's disease (PD) management has traditionally focused largely on motor symptoms. Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and globus pallidus internus (GPi) are effective treatments for motor symptoms. Nonmotor symptoms (NMSs) may also profoundly affect the quality of life. The purpose of this pilot study was to evaluate NMS changes pre- and post-DBS utilizing two recently developed questionnaires. Methods. NMS-Q (questionnaire) and NMS-S (scale) were administered to PD patients before/after unilateral DBS (STN/GPi targets). Results. Ten PD patients (9 STN implants, 1 GPi implant) were included. The three most frequent NMS symptoms identified utilizing NMS-Q in pre-surgical patients were gastrointestinal (100%), sleep (100%), and urinary (90%). NMS sleep subscore significantly decreased (â1.6 points ± 1.8, P = 0.03). The three most frequent NMS symptoms identified in pre-surgical patients using NMS-S were gastrointestinal (90%), mood (80%), and cardiovascular (80%). The largest mean decrease of NMS scores was seen in miscellaneous symptoms (pain, anosmia, weight change, and sweating) (â7 points ± 8.7), and cardiovascular/falls (â1.9, P = 0.02). Conclusion. Non-motor symptoms improved on two separate questionnaires following unilateral DBS for PD. Future studies are needed to confirm these findings and determine their clinical significance as well as to examine the strengths/weaknesses of each questionnaire/scale
Sitagliptin and Carotid Atherosclerosis in Type 2 Diabetes
Background
Experimental studies have suggested that dipeptidyl peptidase-4 (DPP-4) inhibitors provide cardiovascular protective effects. We performed a randomized study to evaluate the effects of sitagliptin added on to the conventional therapy compared with conventional therapy alone (diet, exercise, and/or drugs, except for incretin-related agents) on the intima-media thickness (IMT) of the carotid artery, a surrogate marker for the evaluation of atherosclerotic cardiovascular disease, in people with type 2 diabetes mellitus (T2DM).
Methods and Findings
We used a multicenter PROBE (prospective, randomized, open label, blinded endpoint) design. Individuals aged â„30 y with T2DM (6.2% †HbA1c < 9.4%) were randomly allocated to receive either sitagliptin (25 to 100 mg/d) or conventional therapy. Carotid ultrasound was performed at participating medical centers, and all parameters were measured in a core laboratory. Of the 463 enrolled participants with T2DM, 442 were included in the primary analysis (sitagliptin group, 222; conventional therapy group, 220). Estimated mean (± standard error) common carotid artery IMT at 24 mo of follow-up in the sitagliptin and conventional therapy groups was 0.827 ± 0.007 mm and 0.837 ± 0.007 mm, respectively, with a mean difference of â0.009 mm (97.2% CI â0.028 to 0.011, p = 0.309). HbA1c level at 24 mo was significantly lower with sitagliptin than with conventional therapy (6.56% ± 0.05% versus 6.72%± 0.05%, p = 0.008; group mean difference â0.159, 95% CI â0.278 to â0.041). Episodes of serious hypoglycemia were recorded only in the conventional therapy group, and the rate of other adverse events was not different between the two groups. As it was not a placebo-controlled trial and carotid IMT was measured as a surrogate marker of atherosclerosis, there were some limitations of interpretation.
Conclusions
In the PROLOGUE study, there was no evidence that treatment with sitagliptin had an additional effect on the progression of carotid IMT in participants with T2DM beyond that
achieved with conventional treatment
Long-term effect of sitagliptin on endothelial function in type 2 diabetes: a sub-analysis of the PROLOGUE study
Sustained proliferation in cancer: mechanisms and novel therapeutic targets
Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression
Quantitative analysis of lung elastic fibers in idiopathic pleuroparenchymal fibroelastosis (IPPFE): comparison of clinical, radiological, and pathological findings with those of idiopathic pulmonary fibrosis (IPF)
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