21 research outputs found

    On the reactivity of zinc hydroxide acetate dihydrate in ethanol

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    Zinc hydroxide acetate dihydrate, Zn5(OH)8(CH 3CO2)2·2H2O, reacts in ethanol at room temperature to yield a mixture of zinc oxide and anhydrous zinc acetate. The process is driven by dehydration of the starting salt. Dehydration of Zn5(OH)8(CH3CO2) 2·2H2O also occurs when it is heated in air, but the product obtained in that case depends on the heating rate, environment and temperature. For example, when it is kept in a sealed silica capillary at 100 °C, Zn5(OH)8(CH3CO2) 2·1.5H2O is formed after 15 min, whereas treatment in the range 90-100°C in an open environment results in the formation of anhydrous zinc hydroxide acetate. Heating of any of these products further causes their decomposition to Zn(CH3CO2)2 and ZnO. The coordination bonding mode of the acetate groups in the anhydrous layered zinc hydroxide acetate prepared by reaction with ethanol was studied by using solid-state NMR spectroscopy. The presence of chelating, unidentate and bidentate bridging modes for the carbonyl carbon atom was revealed, but there was no evidence for the inclusion of ethanol in the resultant structure. Therefore, the reaction in ethanol offers a convenient strategy to prepare anhydrous zinc hydroxide acetate and/or zinc oxide, because it avoids the sensitivity of the thermally induced dehydroxlation process to time, temperature and environment. Decomposition of zinc hydroxide acetate dihydrate in ethanol can be exploited to generate ZnO nanoparticles at room temperature. The mechanism involves the removal of waters of hydration and the formation of Zn5(OH)8(CH3CO2)2 followed by the generation of Zn(CH3CO)2 and ZnO. Copyright © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim

    Screen-detected vs clinical breast cancer: the advantage in the relative risk of lymph node metastases decreases with increasing tumour size

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    Screen-detected (SD) breast cancers are smaller and biologically more indolent than clinically presenting cancers. An often debated question is: if left undiagnosed during their preclinical phase, would they become more aggressive or would they only increase in size? This study considered a registry-based series (1988–1999) of 3329 unifocal, pT1a-pT3 breast cancer cases aged 50–70 years, of which 994 were SD cases and 2335 clinical cases. The rationale was that (1) the average risk of lymph node involvement (N+) is lower for SD cases, (2) nodal status is the product of biological aggressiveness and chronological age of the disease, (3) for any breast cancer, tumour size is an indicator of chronological age, and (4) for SD cases, tumour size is specifically an indicator of the duration of the preclinical phase, that is, an inverse indicator of lead time. The hypothesis was that the relative protection of SD cases from the risk of N+ and, thus, their relative biological indolence decrease with increasing tumour size. The odds ratio (OR) estimate of the risk of N+ was obtained from a multiple logistic regression model that included terms for detection modality, tumour size category, patient age, histological type, and number of lymph nodes recovered. A term for the detection modality-by-tumour size category interaction was entered, and the OR for the main effect of detection by screening vs clinical diagnosis was calculated. This increased linearly from 0.05 (95% confidence interval: 0.01–0.39) in the 2–7 mm size category to 0.95 (0.64–1.40) in the 18–22 mm category. This trend is compatible with the view that biological aggressiveness of breast cancer increases during the preclinical phase

    Eosinophils in glioblastoma biology

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    Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults. The development of this malignant glial lesion involves a multi-faceted process that results in a loss of genetic or epigenetic gene control, un-regulated cell growth, and immune tolerance. Of interest, atopic diseases are characterized by a lack of immune tolerance and are inversely associated with glioma risk. One cell type that is an established effector cell in the pathobiology of atopic disease is the eosinophil. In response to various stimuli, the eosinophil is able to produce cytotoxic granules, neuromediators, and pro-inflammatory cytokines as well as pro-fibrotic and angiogenic factors involved in pathogen clearance and tissue remodeling and repair. These various biological properties reveal that the eosinophil is a key immunoregulatory cell capable of influencing the activity of both innate and adaptive immune responses. Of central importance to this report is the observation that eosinophil migration to the brain occurs in response to traumatic brain injury and following certain immunotherapeutic treatments for GBM. Although eosinophils have been identified in various central nervous system pathologies, and are known to operate in wound/repair and tumorstatic models, the potential roles of eosinophils in GBM development and the tumor immunological response are only beginning to be recognized and are therefore the subject of the present review

    25th Annual Computational Neuroscience Meeting: CNS-2016

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    Abstracts of the 25th Annual Computational Neuroscience Meeting: CNS-2016 Seogwipo City, Jeju-do, South Korea. 2–7 July 201

    Zinc hydroxide sulphate and its transformation to crystalline zinc oxide

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    The thermal transformation of zinc hydroxide sulphate hydrate to zinc oxide has been examined using synchrotron X-ray diffraction, thermogravimetric analysis, scanning electron microscopy, and surface area measurements. By collecting X-ray diffraction data in situ, we found that the dehydration of zinc hydroxide sulphate pentahydrate proceeded in discrete steps to form anhydrous zinc hydroxide sulphate. This compound then decomposed to a mixture of zinc oxide and a compound tentatively identified as Zn3(OH) 2(SO4)2 at ∼235 °C. At ∼360 °C, the final dehydroxylation occurred with the formation of zinc oxy-sulphate, Zn3O(SO4)2, which then decomposed to ZnO at about ∼800 °C. Interruption of the dehydration process can be used to synthesize the intermediate compounds. © 2013 The Royal Society of Chemistry

    Zinc oxide particles: Synthesis, properties and applications

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    Zinc oxide powder has traditionally been used as a white pigment and as an additive to rubber. While it has largely been displaced as a pigment in paints, its usage in rubber remains very important. However, the myriad of other practical uses of ZnO are sometimes overlooked, and reviews in the recent scientific literature tend to emphasize high technology applications that do not yet have any commercial reality. Similarly, while some of the low-volume processes used to manufacture ZnO nanostructures have been well covered in the literature, there has been far less reported on the tonnage chemical engineering processes by which most ZnO is actually made. The multiplicity of processes by which ZnO can be produced is a potential source of confusion, however, the process used has a large influence on the properties of the oxide, and hence on its suitability for various applications. Here we provide a contemporary review and analysis of the manufacture of ZnO, and its properties, applications, and future prospects. © 2012 Elsevier B.V

    Formation of zinc hydroxide nitrate by H<sup>+</sup>-catalyzed dissolution-precipitation

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    The formation of zinc hydroxide nitrate, Zn5(OH) 8(NO3)2·2H2O, by reaction between zinc oxide and aqueous zinc nitrate solution was examined. Scanning electron microscopy, X-ray diffraction and thermogravimetric analysis were used to analyze the conversion of nanoscale ZnO particles into much larger crystals of the hydroxide nitrate. The rate of the reaction displayed sigmoidal behavior with the maximum conversion rate at ca. 75 min. The reaction stoichiometry involves a 1:1 ZnO/Zn(NO3)2 molar ratio. The data indicate that an amorphous zinc-containing intermediate phase is formed during the transition, and that the zinc hydroxide nitrate crystals nucleate and grow from this phase. The crystals of zinc hydroxide nitrate are several μm in size, but are formed from zinc oxide crystals of only a few hundred nanometers in size, indicating that mass transfer in the aqueous phase plays an important role. We propose that H+-catalyzed dissolution/precipitation is the key process in the mechanism of the reaction. The zinc hydroxide nitrate is stable to about 110°C, but decomposes above that temperature to a series of less hydrated phases, with associated loss of mass, until zinc oxide is formed at about 190°C. The solubility product, Ksp, of Zn 5(OH)8(NO3)2·2H2O in water was measured by two independent techniques and found to be in the range of 7.4-8.5 × 10-11. Copyright © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim

    On the thermal decomposition of zinc hydroxidenitrate, Zn5(OH)8(NO3)2⋅2H2O

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    © 2020 Elsevier Inc. The layered basic hydroxide Zn5(OH)8(NO3)2⋅2H2O can be thermally decomposed to ZnO via a series of intermediary compounds. Application of in situ X-ray diffraction to dry powder samples reveals three reactions: formation of anhydrous Zn5(OH)8(NO3)2, then de-hydroxylation to Zn3(OH)4(NO3)2 and, finally, decomposition of the latter to ZnO. In contrast, thermal analysis and mass spectroscopy of the evolved volatiles suggests that four reactions take place. Whereas de-hydroxylation reactions only produce H2O, there is also a distinctive pulse of NOx and O2 at the end of the sequence of reactions. The evidence points to the formation of an intermediate, poorly crystalline phase with a stoichiometry of [Zn(OH)2-x]⋅[NO3]x (1 ​< ​x ​< ​2) during the final stages of the reaction sequence. Isothermal calcination of Zn5(OH)8(NO3)2⋅2H2O at 120 ​°C showed that the anhydrous Zn5(OH)8(NO3)2 compound is unstable, rehydrating very rapidly on cooling or decomposing within 6 or 7 ​h at 120 ​°C to Zn3(OH)4(NO3)2 (at a rate of 1.33 ​× ​10-4 s-1). Zn3(OH)4(NO3)2 itself decomposes slowly to ZnO at 120 ​°C, but the process is slower (5.33 ​× ​10-6 s-1) and there was still considerable Zn3(OH)4(NO3)2 present even after 140 ​h. The mixtures of Zn3(OH)4(NO3)2 and ZnO prepared by calcination are unstable under ambient conditions and react with moisture to reform Zn5(OH)8(NO3)2⋅2H2O

    Management of post-LASIK dry eye: a multicenter randomized comparison of a new multi-ingredient artificial tear to carboxymethylcellulose

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    Avi Wallerstein,1,2 W Bruce Jackson,3 Jeffrey Chambers,4 Amir M Moezzi,5 Hugh Lin,6 Peter A Simmons6 1Department of Ophthalmology, McGill University, Montreal, QC, Canada; 2LASIK MD, Montreal, QC, Canada; 3University of Ottawa Eye Institute of the Ottawa Hospital, Ottawa, ON, Canada; 4Kelowna Eye Care Center, Kelowna, BC, Canada; 5Centre for Ocular Research &amp; Education (CORE, formerly Centre for Contact Lens Research), School of Optometry&nbsp;&amp; Vision Science, University of Waterloo, Waterloo, ON, Canada; 6Allergan Clinical Research, Allergan plc, Irvine, CA, USA Purpose: To compare the efficacy and safety of a preservative-free, multi-ingredient formulation of carboxymethylcellulose 0.5%, hyaluronic acid 0.1%, and organic osmolytes (CMC-HA), to preservative-free carboxymethylcellulose 0.5% (CMC) in the management of postoperative signs and symptoms of dry eye following laser-assisted in situ keratomileusis (LASIK). Methods: This was a double-masked, randomized, parallel-group study conducted in 14 clinical centers in Canada and Australia. Subjects with no more than mild dry eye instilled CMC-HA or CMC for 90 days post-LASIK. Ocular Surface Disease Index&copy; (OSDI; primary efficacy measure), corneal staining, tear break-up time (TBUT), Schirmer&rsquo;s test, acceptability/tolerability surveys, and visual acuity were assessed at screening and days 2, 10, 30, 60, and 90 post-surgery. Safety analyses included all enrolled. Results: A total of 148 subjects (CMC-HA, n=75; CMC, n=73) were enrolled and assigned to receive treatment, and 126 subjects completed the study without any protocol violations. Post-LASIK, dry eye signs/symptoms peaked at 10 days. OSDI scores for both groups returned to normal with no differences between treatment groups at day 90 (P=0.775). Corneal staining, Schirmer&rsquo;s test, TBUT, and survey results were comparable. Higher mean improvements in uncorrected visual acuity were observed in the CMC-HA group at all study visits, reaching statistical significance at day 30 (P=0.013). Both treatments were well tolerated. Conclusion: CMC-HA-containing artificial tears relieved post-LASIK ocular dryness as well as CMC alone, and demonstrated incremental benefit in uncorrected vision, with a favorable safety profile. Results support use of CMC-HA eye drops to reduce signs and symptoms of ocular dryness post-LASIK. Keywords: LASIK, dry eye, artificial tears, carboxymethylcellulose, hyaluronic acid, ocular surface diseas

    The Relationship Between Cpap Usage And Corneal Thickness

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    The purpose of this study was to determine whether there is a correlation between CPAP usage and corneal thickness in patients with sleep disordered breathing. Full-night polysomnography (PSG) recordings were collected. Ten patients had undergone PSG recordings with continuous positive airway pressure (CPAP), and seven patients had undergone PSG recordings without CPAP. We measured corneal thickness by ultrasonic pachymeter before sleep and ten minutes after waking. We also measured visual acuity with a routine ophthalmologic eye chart before and after sleep. We asked patients to fill out a post-sleep questionnaire to get their subjective opinions. In the without-CPAP group, corneal thickness increased significantly during sleep in both eyes (left, p = 0.0025; right, p0.05 for both left and right cornea). There was no significant difference in visual acuity tests (p>0.05 for both left and right eye) between the two groups. According to our results, there is a significant increase in corneal thickness in the without-CPAP group. Our data show that a low percentage of Rapid Eye Movement (REM) sleep may cause an increase in corneal thickness, which can indicate poor corneal oxygenation. In fact, many sleep-disordered breathing (SDB) patients have low REM. Since a contact lens may cause low corneal oxygenation, SDB patients with contact lenses should be monitored carefully for their corneal thickness.PubMedWoSScopu
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