The design,synthesis and catalytic performance of vanadium-incorporated mesoporous silica with 3D mesoporous structure for propene epoxidation

V-containing mesoporous silica with 3D structure was prepared by a hydrothermal procedure using NH₄VO₃ as the vanadium precursor and with varied reaction mixture pH values (pH = 3 and pH = 5). The combined use of DR UV-vis and H₂-TPR techniques confirmed the successful incorporation of vanadium into the structure of the mesoporous silica material. The number of acid sites, evidenced by ammonia TPD, strongly correlates with the vanadium content. Propene oxidation with N₂O revealed the noticeable activity of the synthesised vanadium-containing mesoporous materials in epoxidation reactions. The activity of the synthesized vanadosilicates is compared with the performance of vanadium-supported catalysts (on mesoporous silica of 3D structures) prepared by wet-impregnation method. On the basis of TOF analysis indicating the activity of particular vanadium ions, it was evidenced that although the presence of isolated V species is crucial in propene epoxidation, the availability of the active species is of paramount importance for proper vanadium utilization.

Novel promising vanadium catalysts based on mesoporous silica of 3D structure, namely KIT-6, SBA-12, and MCF, for the direct propene epoxidation with N₂O.     

Hyporesponsiveness to Erythropoietin Therapy in Hemodialyzed Patients: Potential Role of Prohepcidin,Hepcidin, and Inflammation

Hepcidin is the key regulator of iron metabolism. Iron supplementation is often introduced in dialyzed patients to replete or to maintain iron stores, particularly in patients treated with erythropoietic-stimulating agents. The present study was aimed to assess possible relation between hepcidin and erythropoietin therapy, with particular attention being paid to erythropoietin-hyporesponsiveness in hemodialyzed patients. Prohepcidin and hepcidin were studied using commercially available kits from DRG Instruments GmbH, Germany (ELISA method) and Bachem, UK (RIA method). TNFα and IL-6 were studied using kits from and R&D (Abington, UK), and hsCRP was studied using kits from American Diagnostica, USA. Hyporesponsive patients to erythropoietin therapy had significantly lower serum albumin, cholesterol, LDL, hemoglobin, hematocrit, and residual renal function, and significantly higher serum ferritin, hsCRP, IL-6, TNFα, and erythropoietin dose. The difference in serum prohepcidin and hepcidin did not reach statistical significance; however, there was a tendency toward higher values of both prohepcidin and hepcidin in hyporesponsive patients. In conclusion, though hyporesponsiveness to erythropoietin therapy occur in dialyzed patients, it is mainly associated with subclinical inflammation than with hepcidin excess. Further studies are needed to develop a reliable and reproducible assay to elucidate the potential contribution of hepcidin to hyporesponsiveness during erythropoietin therapy.     

Exercise training after coronary angioplasty improves cardiorespiratory function

Aim. The aim of this prospective randomized study was to evaluate the impact of long-term aerobic exercise training on respiratory function, left ventricular systolic function and remodeling in patients with coronary heart disease and ischemic heart failure after successful angioplasty. Design. Patients (n=185) have undergone Doppler echocardiography and ergospirometry. Ninety-five patients practiced 6 month-term aerobic exercise training, less by 10% to their anaerobic threshold. Ninety patients were studied as controls. They were given only drug treatment without training. Measurements were repeated after 6 and 12 months. Results. Training group patients after 6 months showed significant (p<0.05) improvement in exercise capacity, oxygen consumption and ventilating equivalents. The Doppler echocardiographic findings revealed significant (p<0.05) improvement in ejection fraction, left ventricular and atria morphometric data. Improved ergospirometric and echocardiographic data were established after 12 months, too. Conclusions. Long-term aerobic exercise training is an effective and workable measure improving respiratory efficiency, left ventricular systolic function, attenuating negative remodeling and stopping further progression in patients with coronary heart disease and chronic heart failure after successful angioplasty.     

Platelet Inhibition by Abciximab Bolus-Only Administration and Oral ADP Receptor Antagonist Loading in Acute Coronary Syndrome Patients: The Blocking and Bridging Strategy

Introduction

Current guidelines still recommend the bolus and infusion administration of glycoprotein IIbIIIa inhibitors in patients with high-risk acute coronary syndrome undergoing percutaneous coronary intervention. We sought to evaluate the extent of platelet inhibition by a blocking and bridging strategy with intracoronary abciximab bolus-only administration and oral loading of adenosine diphosphate receptor antagonists.

Patients and methods

Fifty-six consecutive high-risk acute coronary syndrome patients with bolus-only abciximab administration (0.25 mg/kg i.c.) and loading with 600 mg clopidogrel (55%) or 60 mg prasugrel (45%) were included in this study. Platelet aggregation induced by thrombin receptor-activating peptide and adenosine diphosphate was measured by multiple electrode aggregometry up to 7 days.

Results

Thrombin receptor-activating peptide induced platelet aggregation was significantly suppressed for a minimum of 48 h (45 ± 17 U) and returned to a normal range (> 84 U) after 6 days (90 ± 26 U; p < 0.001). Co-medication with prasugrel significantly reduced adenosine diphosphate-induced (p = 0.002) and thrombin receptor-activating peptide-induced (p = 0.02) platelet aggregation compared with clopidogrel throughout the observation period. No stent thrombosis or repeat myocardial infarction occurred at 30-day follow-up.

Conclusions

Immediate blocking of platelet aggregation in high-risk acute coronary syndrome patients by intracoronary abciximab bolus-only administration and bridging to prolonged inhibition via oral blockade of ADP receptors effectively inhibited overall platelet reactivity for at least 48 h, questioning the value of continuous abciximab infusion. Co-medication with prasugrel vs. clopidogrel synergistically augmented platelet inhibition.     

Obstructive sleep apnea and heart rate asymmetry microstructure during sleep

Purpose

Heart rate decelerations and accelerations have unequal input to heart rate variability (HRV) and patterns created by consecutive cardiac cycles—this phenomenon is known as heart rate asymmetry (HRA). The analysis of monotonic runs of heart rate decelerations and accelerations provides a detailed insight into the HRA microstructure and thus of HRV.

Aim

To evaluate the relation between the severity of obstructive sleep apnea (OSA) and the HRA microstructure during sleep.

Methods

Seventy-eight patients with suspected OSA underwent overnight polysomnography. The 300-min ECGs from the polysomnography were selected and analyzed. The HRA microstructure was quantified by measuring (1) the contribution of monotonic runs of decelerations or accelerations of different lengths to the number of all sinus beats, and (2) the length of the longest deceleration and acceleration runs.

Results

There were 19 patients with no/mild OSA (Apnea/Hypopnea Index (AHI) 5.1 ± 2.5/h), 18 with moderate OSA (AHI 21.8 ± 4.0/h) and 41 with severe OSA (AHI 42.8 ± 17.4/h). Patients with severe OSA had significantly reduced deceleration and acceleration runs of length 1 compared to the moderate OSA group, and compared to patients with no/mild OSA they had an increased number of longer runs (from 5 to 10 for accelerations and from 5 to 8 for decelerations; p < 0.05 for all comparisons). The longest acceleration runs were significantly longer in severe OSA group (p < 0.05) than in subjects with no/mild OSA.

Conclusions

HRA microstructure is related with OSA severity. An increased number of longer deceleration and acceleration runs is more common in severe OSA patients.     

Pain among the oldest old in community and institutional settings

The relationship between pain and increasing age was investigated using data from two different care settings collected on a province-wide basis in Ontario. Home care clients (HC) and complex continuing care patients (CCC) are assessed using the Resident Assessment Instrument-Home Care and Resident Assessment Instrument 2.0 instruments, respectively, as part of normal clinical practice. For this study, the sample was restricted to those aged 65 years and older and totaled 193,158 individuals. Centenarians (those 100 years of age or older) made up 0.41% (n=788) of the sample. Pain was assessed according to a previously validated pain scale embedded in both assessments that uses items on frequency and intensity. Based on 5-year age groups beginning at 65, the mean reported pain score was lower with each increment in age for men and women. Multiple logistic regression models were constructed and the odds ratios for pain in both HC and CCC groups decreased consistently in higher age groups after adjusting for disease diagnoses, cognition, functional status and health indicators. A model that included categories of analgesic medications coded based on the WHO pain ladder showed the relationship persisted after controlling for analgesia. In clinical settings, the oldest old appear to have lower levels of pain compared with the young old after adjusting for a variety of potential confounding variables.     

The complement system in primary Sjögren’s syndrome: the expression of certain cascade and regulatory proteins in labial salivary glands – observational study

IntroductionThe complement cascade and regulatory proteins are involved in the pathogenesis of the Sjögren’s syndrome and other autoimmune diseases. The complement activation via the alternative pathway was recognized as a major pathogenic mechanism in autoimmune conditions. The aim of this study was to assess expression of complement cascade components and regulatory proteins in minor salivary glands in patients with primary Sjögren’s syndrome (pSS).Materials and methodsThe expression of C1q and C5b-9 – membrane attack complex and regulatory proteins such as: membrane cofactor protein (MCP), decay-accelerating factor (DAF) and protectin were examined using immunochemistry method in specimens from biopsy of minor salivary glands in pSS patients. The biopsy material was obtained from 20 pSS patients, 5 patients with non-specific sialadenitis and from 5 patients with suspicion of dryness syndrome without sialadenitis confirmation.ResultsNone of the examined samples showed the expression of C1q or the effector C5b-9. Membrane cofactor protein expression was lower in pSS group than in both non-specific sialadenitis and noninflamed salivary glands. The inflammatory cells in pSS samples partially expressed MCP. There were differences in the sites and intensity of membrane protectin expression exclusively on the luminal surfaces in pSS; on the luminal and, partially, antiluminal surface in non-specific inflammation, and on the entire cell surface in unaffected salivary glands. There were no DAF expression in salivary gland tissue in biopsy specimens in all studied subjects.ConclusionsThe study demonstrated the absence of complement-cascade proteins (C1q, MAC) in the salivary glands of pSS patients, which may indicated a lack of local complement activation via the classical pathway and the observed gland tissue damage being due to a mechanism other than MAC-induced cytolysis. The differences in the expression of complement regulatory proteins between pSS, non-specific sialadenitis, and normal salivary glands may indicate that alternative functions of these regulatory proteins may be of greater significance in pSS. Low MCP expression in pSS in comparison with non-specific sialadenitis and normal salivary glands, may suggest altered modulation of cell-mediated immunity in pSS. The differences in the location and intensity of protectin (CD59) expression indicates a possibility of reducing the proinflammatory effect of protectin in pSS.