Behavior of FRP wrapped concrete cylinders

In this research, increases in strength, stiffness and ductility due to external wrapping of Carbon Fiber Reinforced Polymer (CFRP) sheets on plain and steel reinforced concrete cylinders were studied. The research focused on behavior of plain and wrapped concrete cylinders with respect to parameters such as: (1) concrete compressive strength (fc\u27); (2) fiber orientation of CFRP wrap (0°, 45° and +/-45°); (3) cylinder size (3 x 6 , 4 x 8 , 6 x 12 ); (4) number of CFRP wraps (1, 3, 6); (5) wrapping height and location (top and bottom, middle); (6) degree of fabric wetting; and (7) degree of bonding fabric onto concrete. The mechanical properties evaluated include confinement related increase in axial strength/stiffness, energy absorption (deformability factor), and failure modes. The experimental results were correlated to analytical models consisting of terms representing lateral confining/radial pressure generated by the wrap in hoop direction.;The mechanical properties were compared to those of non-wrapped specimens. An increase in strength of 1.5--3 times and hoop strain of 10--20 times was noticed. The increase in axial strength of 3 x 6 concrete cylinder per layer of wrap for 1, 3 and 6 layer wrapped cylinder was 29%, 43.7% and 33.93%, respectively. Cylinders completely bonded with wrap showed 1.52 times increase in strength whereas cylinders with 31.8% and 21.2% bond showed 1.48 times and 1.23 times increase in strength, respectively. Thus the small delaminations or discontinuities in bonding that may be caused during hand or machine wrapping of column specimens are not critical and do not affect the confinement related strength increase. Deformability factor or energy absorption of specimen wrapped with 3 wraps of 0° fiber direction showed 12 times increase and specimens with +/-45° wrap showed 9 times increase compared to non-wrapped specimens.;Aging of wrapped and non-wrapped cylinders with and without internal steel reinforcement and carbon strip specimens was studied by subjecting them to elevated temperature (175°F) and freeze-thaw (-20°F to 120°F) condition. Wrapped cylinders showed a maximum decrease in strength of 12% in elevated temperature aging and 5% in freeze thaw aging. Further Aging is underway for both conditions.;Non-destructive infrared thermography tests were done to study the interfacial bond between concrete and wrap. Thermograms were recorded to identify the presence of localized delaminations in the wrapped specimens. Infrared thermography was also used to examine delamination size increase in aged specimens, and no detectable growth was observed with thermography

Aneurysmal bone cyst in proximal phalanx treated without bone grafting

Aneurysmal bone cyst involving the hand are a rare occurrence especially in the proximal phalanx. We report a case of 5 years old female child with proximal phalanx aneurysmal bone cyst treated without bone grafting. Magnetic resonance imaging may show fluid filled spaces but definite diagnosis can only be obtained histologically. It is a benign lesion still it can involve growth plate hence intervention is necessary. The treatment includes curettage with or without bone grafting

Aneurysmal bone cyst of medial end of clavicle: a rare case report

Aneurysmal bone cyst is a benign, but locally aggressive benign tumor. The clavicle being a rare site of tumors and very few cases of aneurysmal bone cyst of clavicle have been reported in literature. Due to its rarity of location of its presentation we hereby report a rare case of aneurysmal bone cyst of medial end of clavicle in a 20-year-old female which was treated by wide local resection and reconstruction

Synthesis and metal complexation of chiral 3-mono-or 3, 3-bis-allyl-2-hydroxypyrrolopyrazine-1, 4-diones

A novel synthesis of chiral cyclic hydroxamic acids (4, 6, 8 and 10) related to cyclodipeptides is described. The crucial reduction of the nitro group of the N-nitroacetyl derivatives of (S)-α-amino acid esters is brought about by zinc-aq. ammonium chloride. The FeIII and CuII complexes of one such cyclic hydroxamic acid 10a have been prepared and their DNAse activity investigated

Thioltransferase (glutaredoxin) mediates recovery of motor neurons from excitotoxic mitochondrial injury

Mitochondrial dysfunction involving electron transport components is implicated in the pathogenesis of several neurodegenerative disorders and is a critical event in excitotoxicity. Excitatory amino acid L-β-N-oxalylamino-L-alanine (L-BOAA), causes progressive corticospinal neurodegeneration in humans. In mice, L-BOAA triggers glutathione loss and protein thiol oxidation that disrupts mitochondrial complex I selectively in motor cortex and lumbosacral cord, the regions affected in humans. We examined the factors regulating postinjury recovery of complex I in CNS regions after a single dose of L-BOAA. The expression of thioltransferase (glutaredoxin), a protein disulfide oxidoreductase regulated through AP1 transcription factor was upregulated within 30 min of L-BOAA administration, providing the first evidence for functional regulation of thioltransferase during restoration of mitochondrial function. Regeneration of complex I activity in motor cortex was concurrent with increase in thioltransferase protein and activity, 1 hr after the excitotoxic insult. Pretreatment with α-lipoic acid, a thiol delivery agent that protects motor neurons from L-BOAA-mediated toxicity prevented the upregulation of thioltransferase and AP1 activation, presumably by maintaining thiol homeostasis. Downregulation of thioltransferase using antisense oligonucleotides prevented the recovery of complex I in motor cortex and exacerbated the mitochondrial dysfunction in lumbosacral cord, providing support for the critical role for thioltransferase in maintenance of mitochondrial function in the CNS

Thioltransferase (glutaredoxin) mediates recovery of motor neurons from excitotoxic mitochondrial injury

Mitochondrial dysfunction involving electron transport components is implicated in the pathogenesis of several neurodegenerative disorders and is a critical event in excitotoxicity. Excitatory amino acid L-␤-N-oxalylamino-L-alanine (L-BOAA), causes progressive corticospinal neurodegeneration in humans. In mice, L-BOAA triggers glutathione loss and protein thiol oxidation that disrupts mitochondrial complex I selectively in motor cortex and lumbosacral cord, the regions affected in humans. We examined the factors regulating postinjury recovery of complex I in CNS regions after a single dose of L-BOAA. The expression of thioltransferase (glutaredoxin), a protein disulfide oxidoreductase regulated through AP1 transcription factor was upregulated within 30 min of L-BOAA administration, providing the first evidence for functional regulation of thioltransferase during restoration of mitochondrial function. Regeneration of complex I activity in motor cortex was concurrent with increase in thioltransferase protein and activity, 1 hr after the excitotoxic insult. Pretreatment with ␣-lipoic acid, a thiol delivery agent that protects motor neurons from L-BOAA-mediated toxicity prevented the upregulation of thioltransferase and AP1 activation, presumably by maintaining thiol homeostasis. Downregulation of thioltransferase using antisense oligonucleotides prevented the recovery of complex I in motor cortex and exacerbated the mitochondrial dysfunction in lumbosacral cord, providing support for the critical role for thioltransferase in maintenance of mitochondrial function in the CNS

Investigation of Laurus Tamala leaves extract as an environmentally acceptable corrosion inhibitor for soft steel in 1M HCl: Electrochemical, DFT, and surface characterization techniques

Laurus Tamala leaves extract (LTLE) has been employed as a soft steel corrosion inhibitor in a 1M Hydrochloric acid media. Chemical (weight loss) and electrochemical investigations were carried out to assess the corrosion rate and percentage inhibition efficiency of the extract. The electrochemical polarization results have demonstrated that plant leaves extract functions as a mixed type inhibitor. The stability of the inhibitor is tested at elevated temperatures by weight loss method. The corrosion inhibition mechanism is interpreted through adsorption mechanism, and the LTLE components has obeyed the Langmuir adsorption isotherm for soft steel. The interaction of the components of the extract is assessed through FT-IR technique. The surface morphology, roughness and hydrophobicity in presence and absence of the extract have been characterized through SEM, AFM and water contact angle techniques respectively. The highest inhibitory efficiency is 96.21% for 24 h as recorded by weight loss method. Additionally, the DFT computations has revealed the inhibitor’s adsorption through electron donor-acceptor interactions

Is there a positive effect of participation on a clinical trial for patients with advanced non-small cell lung cancer?

Background: There is general belief that patients who enrolled on a clinical trial have better outcomes compared to those who are treated outside of a trial. We analyzed if there was a \u2032trial effect\u2032 for patients with advanced non-small cell lung cancer (NSCLC) treated with chemotherapy. Materials and methods: A retrospective analysis of cohorts of patients with advanced NSCLC who received chemotherapy inside and outside of a clinical trial were analyzed for response rates (RR), progression free survival (PFS), overall survival (OS), 1 and 2 year survival. Results: There were 194 patients who received chemotherapy of which, 54 were on a clinical trial and 140 outside of it. For the whole group, the RR, median PFS, OS, one and two-year survivals were 35.4%, six months (range, 2-70), seven months (range, 2-72), 29.8% and 9.7% respectively. The differences in RR and PFS of patients who were treated inside and outside of a clinical trial were not significant (P=0.6164, 0.0881). The differences in median OS and one-year survivals between the groups were significant (P=0.0052, 0.022). For the whole group, patients who received II line chemotherapy had better OS (P\ua30.0001). More patients in the trial group received II line chemotherapy (P=0.0004).The difference in the median OS between the groups continued to be significant even after patients who received II line chemotherapy were censored (P=0.0437). Conclusion: Patients with advanced NSCLC who were treated inside of a clinical trial had better OS compared to those who were treated outside of it

Intraplaque haemorrhages as the trigger of plaque vulnerability

Atherothrombosis remains one of the main causes of morbidity and mortality in the western countries. Human atherothrombotic disease begins early in life in relation to circulating lipid retention in the inner vascular wall. Risk factors enhance the progression towards clinical expression: dyslipidaemia, diabetes, smoking, hypertension, ageing, etc. The evolution from the initial lipid retention in the arterial wall to clinical events is a continuum of increasingly complex biological processes. Current strategies to fight the consequences of atherothrombosis are orientated either towards the promotion of a healthy life style1 and preventive treatment of risk factors, or towards late interventional strategies.2 Despite this therapeutic arsenal, the incidence of clinical events remains dramatically high,3 dependent, at least in part, on the increasing frequency of type 2 diabetes and ageing. But some medical treatments, focusing only on prevention of the metabolic risk, have failed to reduce cardiovascular mortality, thus illustrating that our understanding of the pathophysiology of human atherothrombosis leading to clinical events remain incomplete. New paradigms are now emerging which may give rise to novel experimental strategies to improve therapeutic efficacy and prediction of disease progression. Recent studies strengthen the concept that the intraplaque neovascularization and bleeding (Figure 1, upper panel) are events that could play a major role in plaque progression and leucocyte infiltration, and may also serve as a measure of risk for the development of future events. The recent advances in our understanding of IntraPlaque Hemorrhage as a critical event in triggering acute clinical events have important implications for clinical research and possibly future clinical practice. Figure 1Macroscopic view and schematic representation of the detrimental consequences of intraplaque haemorrhages on plaque biology and stability

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes