bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diacetylplatinum(II) and ‐platinum(IV) Complexes Bearing κ2‐ and κ3‐Coordinated Tris(pyrazolyl)methane Ligands: Investigations on the Synthesis, Fluxionality, and Reactivity in Relation to the Substitution Pattern of the Ligands
Authors: Bette Martin , Schmidt Jürgen , Steinborn Dirk 
Published: March 2013

AbstractReactions of the dinuclear platina‐β‐diketone [Pt2{(COMe)2H}2(μ‐Cl)2] (1) with HC(pz)3 and HC(3,5‐Me2pz)3 (pz = pyrazol‐1‐yl; 3,5‐Me2pz = 3,5‐dimethylpyrazol‐1‐yl) afforded cationic, thermally labile diacetyl(hydrido)platinum(IV) complexes [Pt(COMe)2H{(pz)3CH}]Cl (3a) and [Pt(COMe)2H{(3,5‐Me2pz)3CH}]Cl (3b) with κ3‐coordinated tris(pyrazolyl)methane ligands, which were found to react with NaOH or NEt3 to yield neutral diacetylplatinum(II) complexes with κ2‐coordinated tris(pyrazolyl)methane ligands {[Pt(COMe)2{(pz)3CH}] (4a); [Pt(COMe)2{(3,5‐Me2pz)3CH}] (4b)}. In 4a/b, a molecular rearrangement (decoordination of a pyrazolyl ring and coordination of the originally pendant one) has been found that has been investigated by variable‐temperature 1H NMR spectroscopic measurements (coalescence method) as well as by DFT calculations. Diacetylplatinum(II) complexes 4 were found to react in oxidative addition reactions with ROTf (R = H, Me; OTf = trifluoromethanesulfonate) and methyl iodide to yield cationic diacetylplatinum(IV) complexes of the type [Pt(COMe)2R{(pz)3CH}]X (R/X = H/OTf, 5a; Me/OTf, 6a; Me/I, 7a) and [Pt(COMe)2R{(3,5‐Me2pz)3CH}]X [R/X = H/OTf (5b), Me/OTf (6b), Me/I (7b)] with κ3‐bonded tris(pyrazolyl)methane ligands. Treatment of 4b with alkynyliodine(III) reagents of the type [IPh(C≡CR)]X (R/X = SiMe3/OTf, Ph/OTf, tBu/OTos, iPr/OTos; OTos = p‐toluenesulfonate) led to the formation of cationic diacetyl(alkynyl)platinum(IV) complexes [Pt(COMe)2(C≡CR){(3,5‐Me2pz)3CH}]X [R/X = SiMe3/OTf (8a), Ph/OTf (8b), tBu/OTos (8c), iPr/OTos (8d)]. The identities of all platinum complexes were unambiguously proven by high‐resolution mass spectrometric investigations, by NMR (1H, 13C, 195Pt) and IR spectroscopy, as well as by single‐crystal X‐ray diffraction analyses (4a, 4b, 7a, 8a/d). The constitution of the thermally labile complexes 3a/b has been confirmed by low‐temperature (–80 °C) NMR (1H, 13C) spectroscopic measurements. The electronic and steric influence of the additional methyl groups in HC(3,5‐Me2pz)3 on reactivity, stability, and properties of the investigated compounds will be discussed.
Evaluation of fundamental period of low‐rise and mid‐rise reinforced concrete buildings
Authors: Hatzigeorgiou George D. , Kanapitsas George 
Published: March 2013

SUMMARYFundamental period of vibration appears to be one of the most critical parameter for the seismic design of buildings because this period strongly affects the magnitude of seismic forces. In this paper, an empirical formula for estimating the fundamental period of reinforced concrete structures is recommended, on the basis of the vibration analysis of 20 different real building configurations. These structures have already been constructed in Greece, and they are analyzed by using in detail 3‐D finite element models and modal eigenvalue analysis. These models take into account the presence of external and internal infill walls, which are usually ignored as nonstructural elements. This neglect leads to unreliable evaluation of period because the infill walls' contribution to the lateral stiffness and therefore to the fundamental period of vibration is also ignored. Furthermore, taking into account that the flexibility of soil elongates the fundamental period, the soil–structure interaction effect is also considered. To achieve a unique, simple, and effective empirical expression for the fundamental period of vibration, a comprehensive nonlinear regression analysis is applied for the datasets of buildings under consideration. This empirical expression is also compared with the similar expressions from the pertinent literature. Copyright © 2013 John Wiley & Sons, Ltd.
Low prevalence of metabolic syndrome and its prediction in Japanese inpatients with schizophrenia
Authors: Suzuki Yutaro , Sugai Takuro , Fukui Naoki , Watanabe Junzo , Ono Shin , Tsuneyama Nobuto , Saito Mami , Someya Toshiyuki 
Published: March 2013

ObjectivesThere have so far been few papers studying the metabolic syndrome (MetS) prevalence rate in Japanese patients with schizophrenia. We studied the MetS prevalence rate in Japanese controls and inpatients with schizophrenia and compared the prediction factors for the occurrence of MetS.MethodsThe subjects were 319 inpatients with schizophrenia and 154 controls. The predictive utilities of body mass index (BMI) and the individual components of MetS for MetS diagnosis were evaluated.ResultsThe prevalence of MetS did not differ between schizophrenia and control subjects. Subjects with schizophrenia showed higher prevalences of the MetS criteria for high‐density lipoprotein cholesterol (HDL) (p < 0.001) and waist circumference (WC) (p < 0.001). In subjects with schizophrenia, the predictive power was found to be highest for HDL, followed by WC, BMI, triglyceride, diastolic blood pressure (BP), systolic BP and fasting plasma glucose. However, in control subjects, the predictive power was found to be highest for triglyceride, followed by WC, systolic BP, BMI, HDL, diastolic BP and fasting plasma glucose. HDL was the component most predictive of MetS in subjects with schizophrenia treated with antipsychotics.ConclusionBecause, in normal clinical practice, it is difficult to obtain temporal measurements for all of the MetS criteria, measurement of HDL may be useful for predicting the MetS. Copyright © 2013 John Wiley & Sons, Ltd.
Acylated ghrelin: A potential marker for fibromyalgia?
Authors: Homann D. , Louzada F.M. , Góes S.M. , Roizenblatt S. , Lopes A.L. , de Oliveira Á.R. , Leite N. 
Published: March 2013

AbstractBackgroundFibromyalgia is characterized by chronic widespread pain and sleep disturbances. Overweight and obesity, which lead to metabolic changes, are additional comorbidities that are rarely explored, although they are highly prevalent in patients with fibromyalgia.MethodsWe compared the plasma levels of leptin and acylated ghrelin in 17 women with fibromyalgia (patients) and 16 healthy women (controls) with similar age, anthropometric measurements and levels of physical activity. We also investigated the relationships between these two neuropeptides and sleep and various pain characteristics in patients with fibromyalgia. Anthropometric measurements were recorded, and physical activity levels were assessed using a questionnaire. Pain intensity was measured using visual analogue scales (weekly general and mean pain scores). Sleep was assessed using an accelerometry technique.ResultsCompared to the control group, the patient group had increased leptin levels (patients: 22.4 ± 10.6 vs. controls: 13.3 ± 17.9 ng/mL; p < 0.01) and decreased acylated ghrelin levels (patients: 126.7 ± 47.8 vs. controls: 183.3 ± 102.2 pg/mL; p = 0.048). The leptin level was not significantly correlated with any of the variables. Acylated ghrelin level was inversely correlated with the weekly mean pain score (r = −0.67, p < 0.01) and the weekly general pain score (r = −0.67, p < 0.01). Multiple regression analysis revealed that the variations in acylated ghrelin levels accounted for 35% of the weekly general pain and 29% of the weekly mean pain variability.ConclusionsThese findings indicate that the decreased acylated ghrelin levels in women with fibromyalgia are related to pain intensity.
Book Reviews
Authors: PROCITA LEONARD 
Published: March 2013

Book reviewed in this article:Psychopharmacology: A Generation of Progress. M. A. Lipton, A. DiMascio, and K. F. Killam, editors.Medication Guide for Patient Counseling. D. L. Smith.Quantitative Aspects of Allosteric Mechaisms. (Molecular Biology, Biochemistry and Biophysics, Vol. 28). A. Levitski.
Sulindac Kinetics and Effects on Renal Function and Prostaglandin Excretion in Renal Insufficiency
Authors: Klassen David K. , Stout Robert L. , Spilman Patricia S. , Whelton Andrew 
Published: March 2013

The purpose of this study was to evaluate the pharmacokinetics of sulindac, a purported “renal sparing” nonsteroidal anti‐inflammatory drug, and its effects on renal function and prostaglandin excretion in patients with reduced glomerular filtration rate.Twelve female patients (glomerular filtration rate 37 ± 4 mL/min) were treated with sulindac 200 mg bid for 11 days. Urinary PGE2, 6‐keto‐PGF1α and serum thromboxane (TxB2) generation were measured by radioimmunoassay (BIA) following extraction on C‐18 columns. Glomerular filtration rate and effective renal plasma flow were measured by 99TC‐DPTA and 131I‐para‐aminohippuric acid clearance. In six patients serum and urine levels of sulindac and its metabolites were measured by high‐pressure liquid chromatography (HPhC).Sulindac was rapidly absorbed and converted to sulindac sulfide with peak levels 2 hours after a single dose, but steady state levels were not reached prior to drug discontinuation. Sulindac sulfide AUC (0–5 hours μg min/mL) progressively increased from 382 to 3,030 on day 11. It did not appear in the urine. Baseline urinary PGE2 and 6‐keto‐PGF1α excretion were 23.8 ± 5.6 and 18.9 ± 2.7 ng/hr respectively and were reduced by 68% and 47% by day 4 of therapy. TxB2 generation fell by 34% after one dose and by 67% by day 11. There was a significant increase in serum creatinine from 1.88 ± 0.13 mg/dl before treatment to 2.16 ± 0.15 mg/dL (P <.05) after eleven days. There was a significant (P < .001) decrease in effective renal plasma flow, 184.9 ± 16.3 mh/min before therapy vs 164.1 ± 17.0 mh/min on day 11 of therapy. Glomerular filtration rate (GFR) was significantly reduced following 4 days of therapy (P < .05: day 1 vs day 4) but by day 11 had returned to baseline.We concluded that in this population the active sulindac sulfide metabolite accumulates systemically and can significantly inhibit renal prostaglandin metabolism as well as peripheral TxB2 generation and may effect renal function.
Bronchial and Cardiovascular Effects of Ocular Topical B‐antagonists in Asthmatic Subjects: Comparison of Timolol, Carteolol, and Metipranolol
Authors: Jeunne C. L. Le , Hugues F. C. , Dufier J. L. , Munera Y. , Bringer L. 
Published: March 2013

B antagonists eye drops are most effective for the treatment of chronic open angle glaucoma. By this way of administration they have a very good systemic bioavailability.Bronchial, and cardiovascular effects of three of these topicals: timolol, carteolol and metipranolol have been evaluated in three parallel groups of asthmatic patients. The three topics induce bronchoconstriction without significant difference between them, and lower heart rate (sometimes very intensely) whatever the B antagonist studied.From these data, it is recommended to practitioners to follow carefully the rules of administration of B blockers, even in eye drops.
Pharmacokinetics of Continuous Intravenous Infusion of Methadone in the Early Post‐Burn Period
Authors: Denson Donald D. , Concilus Robert R. , Warden Glenn , Raj P. Prithvi 
Published: March 2013

The pharmacokinetics of methadone were studied in 14 patients with acute, severe burns and receiving an intravenous infusion of methadone to control their pain. Serum methadone concentrations were measured by gas chromatography on 5 mL arterial blood samples obtained at 0.5, 1.0, 1.5, 2.0, 3.0, 4.0, 5.0 and 24 hours after the start of infusion. Albumin and Alpha‐1‐Acid glycoprotein (AAG) were measured by radial immunodiffusion. Serum methadone concentration‐time data were fit with the appropriate sum of exponentials equation using iterative nonlinear regression analysis.All serum methadone concentration‐time data were best described by a monoexponential equation. Estimates of Vd (180 ± 62 L) were not significantly different from those predicted for Vc from body weight using literature values (156 ± 41). Estimates of Vd were, however, significantly lower than those predicted for Vz using literature values (282 ± 74) (P < 0.001). in addition, CL values (53.0 ± 19.3 L/h) were significantly higher than those predicted from body weight using literature values (9.2 ± 2.3 L/h) (P < 0.001). These changes resulted in estimates of the elimination half‐life for methadone of 2.6 ± 1.1 h. Methadone protein binding was independent of both albumin and AAG concentration. Multiple regression demonstrated that the significant predictors of CL in the early post burn injury period were serum albumin, days post injury and age. The coefficient of determination (r2) for this model was 0.8190.In summary, methadone CL is markedly elevated while the Vc is essentially unchanged during the early post burn injury period. These changes suggest that normal loading doses but increased maintenance doses of methadone should be used during this period to provide prolonged analgesia.
The Relationship Between Metoprolol Plasma Concentration and Beta1‐Blockade in Healthy Subjects: A Study on Conventional Metoprolol and Metoprolol CR/ZOK Formulations
Authors: Abrahamsson Bertil , Lücker Peter , Olofsson Bertil , Regårdh Carl‐Gunnar , Sandberg Anders , Wieselgren Ingrid , Bergstrand Robert 
Published: March 2013

Four studies using different daily doses (100 mg, 200 mg, 300 mg and 400 mg) have examined the bioequivalence of the once daily formulation metoprolol CR/ZOK and conventional metoprolol tablets (CT). These studies showed metoprolol CR/ZOK to have a similar beta1‐blocking activity to metoprolol CT but that the bioavailability of the new formulation was lower. This paper presents the analysis of data from all four studies, looking at the relationship between plasma concentrations and beta1‐blockade measured as reduction of exercise induced tachycardia.The log linear pharmacodynamic model was used for each of the four doses to compare the two formulations. Mean slopes and intercepts in the linear regression analysis of log plasma concentration of metoprolol versus beta1‐blockade did not differ significantly between CR/ZOK and CT in any of the four studies. After having shown lack of influence of the absorption rate on the plasma concentration—effect relationship, data for CR/ZOK and CT formulations from the 200 mg study were pooled for each individual subject and fitted to an Emaxmodel. The maximal β1‐blocking effect (Emax) was 28% (95% confidence interval: 25–31%) and the plasma concentration for obtaining 50% ofEmax(C50) was 105 nmol/L (95% confidence interval: 74–135 nmol/L). The plasma concentration‐effect data from the 100 mg, 300 mg and 400 mg studies were reasonably well within the 95% prediction interval based on the 200 mg study, which showed the validity of the obtained relationship. The hyperbolic concentration‐beta1‐blocking effect relationship, as described by the Emax‐model explains why a similar or even increased effect is obtained over a dosing interval for metoprolol CR/ZOK compared with metoprolol CT, in spite of the reduced bioavailability of the CR/ZOK formulation.
Tolerability and Well‐Being with Metoprolol in a Controlled Release (CR/ZOK) Formulation: A Review Article
Authors: Dimenäs Elof , Dahlöf Carl 
Published: March 2013

Extensive research and clinical usage of metoprolol have shown the compound to be safe and well tolerated if the contraindications are taken into consideration. However, as with other beta‐blockers, unwanted effects may occur during treatment. Although usually mild, these side effects may be of considerable clinical importance, especially since once initiated, therapy is often life‐long.Results of previous studies have indicated that some of these symptoms are associated with high plasma concentrations of the drug. Theoretically, side effects may thus be reduced by administration of metoprolol in a controlled‐release formulation (CR/ZOK) which yields relatively low plasma concentrations over approximately 24 hours.Using clinically relevant doses, metoprolol CR/ZOK affects beta2‐adrenoceptor‐mediated functions (e.g., broncho‐dilatation in asthmatics) less than tablets do. In addition, less leg fatigue during exercise has been reported. The clinical studies published so far indicate that metoprolol CR/ZOK is as well tolerated as or better tolerated than, conventional metoprolol tablets. Furthermore, metoprolol CR/ZOK is tolerated equally or better than atenolol in terms of CNS‐related symptoms.
Reassessment of Benefit—Risk Ratio and Treatment Algorithms for Antiarrhythmic Drug Therapy After the Cardiac Arrhythmia Suppression Trial
Authors: Anderson Jeffrey L. 
Published: March 2013

The Cardiac Arrhythmia Suppression Trial (CAST) has led to serious reconsideration of both the benefit—risk ratio of antiarrhythmic drug therapy and the appropriate therapeutic approach to various cardiac arrhythmias. Class IC drugs, such as encainide and flecainide, should not be used to treat asymptomatic postinfarction arrhythmias. Furthermore, because the CAST raises serious questions about the concept of treating asymptomatic but “potentially malignant” (prognostically important) arrhythmias guided by ambulatory monitoring, the prophylactic use of any of the antiarrhythmic agents (except beta blockers) must be considered inappropriate and potentially harmful until otherwise established by specific clinical trials.For prophylaxis of malignant ventricular arrhythmias (sustained ventricular tachycardia or ventricular fibrillation), treatment may still begin with standard agents in classes IA, IB, or both, preferably guided by electrophysiologic testing alone or in combination with noninvasive testing. Class IC therapy may be most useful in those patients in this group who do not have such high‐risk characteristics for proarrhythmia as a history of multiple myocardial infarctions (MIs), congestive heart failure, or low ejection fraction. Amiodarone is moderately effective for treating these arrhythmias but is reserved as second‐ or third‐line therapy because of its potential organ toxicity. Sotalol, a beta blocker with class III activity, is often effective and relatively well tolerated in these patients and may become a preferred drug when approved.For symptomatic but nonmalignant ventricular arrhythmias, a more conservative approach is more appropriate than in the past, with therapy reversed for those with debilitating symptoms. An initial trial of beta blockade is often appropriate before class I agents are considered. Class IC therapy should be avoided in patients with a history of MI (especially recent or multiple MIs), and probably in other patients with symptomatic coronary artery disease (e.g., angina, heart failure). The CAST emphasizes the need for further experimental and clinical trials and the development of new agents based on a better understanding of the overall benefit—risk ratio. As this occurs, treatment algorithms will continue to evolve.
BOOK REVIEWS
Authors: Maggio Beth 
Published: March 2013

Book reviewed in this article:Handbook of Psychiatric Drug Therapy, Second EditionLithium and the Blood (Karger) Vincent S. Gallicchio, EditorTriglycerides: Their Role in Diabetes and Atherosclerosis (Atherosclerosis Reviews, Vol. 22). Antonio M. Gotto, Jr., and Rodolfo Paoletti, EditorsHandbook of Therapy in Liver and Kidney Disease (Little, Brown and Company), Robert W. Schrier, MD, and John G. Gambertoglio, Pharm, D, Editors
Book Reviews
Authors: Maggio Beth 
Published: March 2013

Book reviewed in this article:β‐Adrenoceptors: Molecular Biology, Biochemistry and Pharmacology Ruffolo RR Jr., Editor.β‐Adrenoceptors: Molecular Biology, Biochemistry and Pharmacology Ruffolo RR Jr., Editor.Advances in Drug Therapy of Gastroesophageal Reflux Disease Scarpignato C, Editor.Immunological and Pharmacological Aspects of Atopic and Contact Eczema Czernielewski JM, Editor.Bacterial Meningitis Schönfeld H and Helvig H, Editors.Atrial Fibrillation: Mechanisms and Management Falk RH and Podrid PJ, Editors.USAN and the USP Dictionary of Drug Names United States Pharmacopeial Convention, Inc.
BOOK REVIEWS
Authors: Maggio Beth 
Published: March 2013

Book reviewed in this article:Kidney, Proteins and Drugs Bianchi C, Bocci V, Carone FA, and Rabkin R, Editors.Pain Versus Man (Advances in Pain Research and Therapy, Vol. 20) Sicuteri F, Vecchiet L, Terenius L, and Maggi CA, Editors; Nicoloci M and Alessandri M, Associate Editors.The Biology of Nicotine Lippiello PM, Collins AC, Gray JA, and Robinson JH, Editors.Cardiovascular Drugs and the Management of Heart Disease, 2nd Edition Ewy GA and Bressler R, Editors.Clinical Immunotoxicology Newcombe DS, Editor‐in‐Chief, Rose NR and Bloom JC, Editors.
Book Reviews
Authors: Maggio Beth 
Published: March 2013

Book reviewed in this article:Patient Recruitment in Clinical Trials Spilker B, Cramer J.Ophthalmic Toxicology Target Organ Toxicology Series, Chiou G, Editor.Cardiovascular Toxicology, Second Edition Target Organ Toxicology Series, Acosta D, Editor.Toxicology of the Kidney, Second Edition Target Organ Toxicology Series, Hook J, Goldstein R, Editors.
BOOK REVIEWS
Authors: Maggio Beth 
Published: March 2013

Book reviewed in this article:Neurotherapeutics: Emerging Strategies. LM Pullan, J Patel, Editors.Oral Cephalosporins. RC Moellering, Jr., Editor.Quality of Life and Pharmacoeconomics in Clinical Trials, Second Edition. B Spilker, Editor.The Peroxisome: A Vital Organelle. C Masters, D Crane, Editors.Pharmaceutical Powder Compaction Technology. G Alderborn, C Nystrom, Editors.
AMR‐Me inhibits PI3K/Akt signaling in hormone‐dependent MCF‐7 breast cancer cells and inactivates NF‐κB in hormone‐independent MDA‐MB‐231 cells
Authors: Rabi Thangaiyan , Huwiler Andrea , Zangemeister‐Wittke Uwe 
Published: March 2013

AbstractAMR‐Me, a C‐28 methylester derivative of triterpenoid compound Amooranin isolated from Amoora rohituka stem bark and the plant has been reported to possess multitude of medicinal properties. Our previous studies have shown that AMR‐Me can induce apoptosis through mitochondrial apoptotic and MAPK signaling pathways by regulating the expression of apoptosis related genes in human breast cancer MCF‐7 cells. However, the molecular mechanism of AMR‐Me induced apoptotic cell death remains unclear. Our results showed that AMR‐Me dose‐dependently inhibited the proliferation of MCF‐7 and MDA‐MB‐231 cells under serum‐free conditions supplemented with 1 nM estrogen (E2) with an IC50 value of 0.15 µM, 0.45 µM, respectively. AMR‐Me had minimal effects on human normal breast epithelial MCF‐10A + ras and MCF‐10A cells with IC50 value of 6 and 6.5 µM, respectively. AMR‐Me downregulated PI3K p85, Akt1, and p‐Akt in an ERα‐independent manner in MCF‐7 cells and no change in expression levels of PI3K p85 and Akt were observed in MDA‐MB‐231 cells treated under similar conditions. The PI3K inhibitor LY294002 suppressed Akt activation similar to AMR‐Me and potentiated AMR‐Me induced apoptosis in MCF‐7 cells. EMSA revealed that AMR‐Me inhibited nuclear factor‐kappaB (NF‐κB) DNA binding activity in MDA‐MB‐231 cells in a time‐dependent manner and abrogated EGF induced NF‐κB activation. From these studies we conclude that AMR‐Me decreased ERα expression and effectively inhibited Akt phosphorylation in MCF‐7 cells and inactivate constitutive nuclear NF‐κB and its regulated proteins in MDA‐MB‐231 cells. Due to this multifactorial effect in hormone‐dependent and independent breast cancer cells AMR‐Me deserves attention for use in breast cancer prevention and therapy. © 2013 Wiley Periodicals, Inc.