Process intensification for post combustion CO₂ capture with chemical absorption: a critical review

The concentration of CO₂ in the atmosphere is increasing rapidly. CO₂ emissions may have an impact on global climate change. Effective CO₂ emission abatement strategies such as carbon capture and storage (CCS) are required to combat this trend. Compared with pre-combustion carbon capture and oxy-fuel carbon capture approaches, post-combustion CO₂ capture (PCC) using solvent process is one of the most mature carbon capture technologies. There are two main barriers for the PCC process using solvent to be commercially deployed: (a) high capital cost; (b) high thermal efficiency penalty due to solvent regeneration. Applying process intensification (PI) technology into PCC with solvent process has the potential to significantly reduce capital costs compared with conventional technology using packed columns. This paper intends to evaluate different PI technologies for their suitability in PCC process. The study shows that rotating packed bed (RPB) absorber/stripper has attracted much interest due to its high mass transfer capability. Currently experimental studies on CO₂ capture using RPB are based on standalone absorber or stripper. Therefore a schematic process flow diagram of intensified PCC process is proposed so as to motivate other researches for possible optimal design, operation and control. To intensify heat transfer in reboiler, spinning disc technology is recommended. To replace cross heat exchanger in conventional PCC (with packed column) process, printed circuit heat exchanger will be preferred. Solvent selection for conventional PCC process has been studied extensively. However, it needs more studies for solvent selection in intensified PCC process. The authors also predicted research challenges in intensified PCC process and potential new breakthrough from different aspects

Th1 type lymphocyte reactivity to metals in patients with total hip arthroplasty

<p>Abstract</p> <p>Background</p> <p>All prostheses with metallic components release metal debris that can potentially activate the immune system. However, implant-related metal hyper-reactivity has not been well characterized. In this study, we hypothesized that adaptive immunity reaction(s), particularly T-helper type 1 (Th1) responses, will be dominant in any metal-reactivity responses of patients with total joint replacements (TJAs). We tested this hypothesis by evaluating lymphocyte reactivity to metal "ions" in subjects with and without total hip replacements, using proliferation assays and cytokine analysis.</p> <p>Methods</p> <p>Lymphocytes from young healthy individuals without an implant or a history of metal allergy (Group 1: n = 8) were used to assess lymphocyte responses to metal challenge agents. In addition, individuals (Group 2: n = 15) with well functioning total hip arthroplasties (average Harris Hip Score = 91, average time in-situ 158 months) were studied. Age matched controls with no implants were also used for comparison (Group 3, n = 8, 4 male, 4 female average age 70, range 49–80). Group 1 subjects' lymphocyte proliferation response to Aluminum⁺³, Cobalt⁺², Chromium⁺³, Copper⁺², Iron⁺³, Molybdenum⁺⁵, Manganeese⁺², Nickel⁺², Vanadium⁺³and Sodium⁺²chloride solutions at a variety of concentrations (0.0, 0.05, 0.1, 0.5, 1.0 and 10.0 mM) was studied to establish toxicity thresholds. Mononuclear cells from Group 2 and 3 subjects were challenged with 0.1 mM CrCl₃, 0.1 mM NiCl₂, 0.1 mM CoCl₂and approx. 0.001 mM titanium and the reactions measured with proliferation assays and cytokine analysis to determine T-cell subtype prominence.</p> <p>Results</p> <p>Primary lymphocytes from patients with well functioning total hip replacements demonstrated a higher incidence and greater magnitude of reactivity to chromium than young healthy controls (p < 0.03). Of the 15 metal ion-challenged subjects with well functioning total hip arthroplasties, 7 demonstrated a proliferative response to Chromium, Nickel, Cobalt and/or Titanium (as defined by a statistically significant >2 fold stimulation index response, p < 0.05) and were designated as metal-reactive. Metals such as Cobalt, Copper, Manganese, and Vanadium were toxic at concentrations as low as 0.5 mM while other metals, such as Aluminum, Chromium, Iron, Molybdenum, and Nickel, became toxic at much higher concentrations (>10 mM). The differential secretion of signature T-cell subsets' cytokines (Th1 and Th2 lymphocytes releasing IFN-gamma and IL-4, respectively) between those total hip arthroplasty subjects which demonstrated metal-reactivity and those that did not, indicated a Th1 type (IFN-gamma) pro-inflammatory response.</p> <p>Conclusion</p> <p>Elevated proliferation and production of IFN-gamma to metals in hip arthroplasty subjects' lymphocytes indicates that a Th1 (vs. Th2) type response is likely associated with any metal induced reactivity. The involvement of an elevated and specific lymphocyte response suggests an <it>adaptive </it>(macrophage recruiting) immunity response to metallic implant debris rather than an <it>innate </it>(nonspecific) immune response.</p

Enhanced photodynamic destruction of a transplantable fibrosarcoma using photochemical internalisation of gelonin

Photochemical internalisation (PCI) is a technique for releasing biologically active macromolecules from endocytic vesicles by light activation of a photosensitiser localised in the same vesicles of targeted cells. This study investigated the PCI of the toxin gelonin as a way of enhancing the effect of photodynamic therapy (PDT) on a human malignant fibrous histiocytoma transplanted into nude mice using the photosensitiser disulphonated aluminium phthalocyanine (AlPcS2a). Pharmacokinetic studies after intraperitoneal administration showed that the serum level of AlPcS2a fitted a biexponential model (half-lives of 1.8 and 26.7 h). The tumour concentration was roughly constant up to 48 h, although fluorescence microscopy showed that the drug location was initially mainly vascular, but became intracellular by 48 h. To compare PDT with PCI, 48 h after intraperitoneal injection of 10 mg kg−1 AlPcS2a, and 6 h after direct intratumour injection of 50 μg gelonin (PCI) or a similar volume of phosphate-buffered saline (PDT controls), tumour-bearing animals were exposed to red light (150 J cm−2). Complete response was observed for more than 100 days in 50% of the PCI tumours but only 10% of the PDT tumours (P<0.01). In tumours examined histologically 4 days after light delivery, the depth of necrosis was 3–4 mm after PDT, but 7 mm after PCI. The deeper effect after PCI demonstrates that the light fluence needed to kill tumour is less than with PDT. We conclude that PCI with gelonin can markedly enhance the effect of PDT on this type of tumour and may have a role clinically as an adjunct to surgery to control localised disease

The effect of radio-adaptive doses on HT29 and GM637 cells

<p>Abstract</p> <p>Background</p> <p>The shape of the dose-response curve at low doses differs from the linear quadratic model. The effect of a radio-adaptive response is the centre of many studies and well known inspite that the clinical applications are still rarely considered.</p> <p>Methods</p> <p>We studied the effect of a low-dose pre-irradiation (0.03 Gy – 0.1 Gy) alone or followed by a 2.0 Gy challenging dose 4 h later on the survival of the HT29 cell line (human colorectal cancer cells) and on the GM637 cell line (human fibroblasts).</p> <p>Results</p> <p>0.03 Gy given alone did not have a significant effect on both cell lines, the other low doses alone significantly reduced the cell survival. Applied 4 h before the 2.0 Gy fraction, 0.03 Gy led to a significant induced radioresistance in GM637 cells, but not in HT29 cells, and 0.05 Gy led to a significant hyperradiosensitivity in HT29 cells, but not in GM637 cells.</p> <p>Conclusion</p> <p>A pre-irradiation with 0.03 Gy can protect normal fibroblasts, but not colorectal cancer cells, from damage induced by an irradiation of 2.0 Gy and the application of 0.05 Gy prior to the 2.0 Gy fraction can enhance the cell killing of colorectal cancer cells while not additionally damaging normal fibroblasts. If these findings prove to be true in vivo as well this may optimize the balance between local tumour control and injury to normal tissue in modern radiotherapy.</p

In vivo quantification of photosensitizer fluorescence in the skin-fold observation chamber using dual-wavelength excitation and NIR imaging

A major challenge in biomedical optics is the accurate quantification of in vivo fluorescence images. Fluorescence imaging is often used to determine the pharmacokinetics of photosensitizers used for photodynamic therapy. Often, however, this type of imaging does not take into account differences in and changes to tissue volume and optical properties of the tissue under interrogation. To address this problem, a ratiometric quantification method was developed and applied to monitor photosensitizer meso-tetra (hydroxyphenyl) chlorin (mTHPC) pharmacokinetics in the rat skin-fold observation chamber. The method employs a combination of dual-wavelength excitation and dualwavelength detection. Excitation and detection wavelengths were selected in the NIR region. One excitation wavelength was chosen to be at the Q band of mTHPC, whereas the second excitation wavelength was close to its absorption minimum. Two fluorescence emission bands were used; one at the secondary fluorescence maximum of mTHPC centered on 720 nm, and one in a region of tissue autofluorescence. The first excitation wavelength was used to excite the mTHPC and autofluorescence and the second to excite only autofluorescence, so that this could be subtracted. Subsequently, the autofluorescence-corrected mTHPC image was divided by the autofluorescence signal to correct for variations in tissue optical properties. This correction algorithm in principle results in a linear relation between the corrected fluorescence and photosensitizer concentration. The limitations of the presented method and comparison with previously published and validated techniques are discussed

The combined effects of extracts containing carotenoids and vitamins E and C on growth and pigmentation of cultured human melanocytes

The combined effects of extracts containing carotenoids and vitamins E and C on growth and pigmentation of cultured human melanocytes. Smit N, Vicanova J, Cramers P, Vrolijk H, Pavel S. Department of Clinical Chemistry, Leiden University Medical Centre, Leiden, The Netherlands. [email protected] In the present study, we investigated the effects of tomato extract (TE) containing lycopene and palm fruit extract (PE) rich in carotenoids on the growth and pigmentation of melanocyte cultures of Caucasian origin. The extracts were tested at different concentrations and in combination with vitamins E and C. Melanocytes with basic and increased (tyrosine-induced) pigmentation were treated in short-term and long-term experiments. Prevention of UVA-induced DNA damage was studied by using the comet assay. Melanocytes with stimulated melanin production showed reduced growth. Incubation of the cells with TE/PE (20/4 microg/ml) in combination with 35 microM vitamin E and 100 microM vitamin C (COMB 20/4) reduced this growth inhibition, especially in the long-term cultures. Increased production of melanin pigment was obtained when the cells were treated with 2.5 x and 10 x higher concentrations of the TE/PE and the same concentration of vitamins E and C (COMB 50/10 and 200/40). Reduced DNA damage was found after UVA irradiation in cells preincubated with COMB 50/10. The results indicate that the presence of carotenoids from TE and PE in combination with vitamins E and C may influence growth and pigmentation in melanocyte monocultures. Depending on the concentration of the carotenoid mixtures, their presence may provide some protection against the melanogenic intermediates and/or exogenous DNA damage. 2004 S. Karger AG, Base

Determination of acidic catecholamine metabolites in plasma and cerebrospinal fluid using gas chromatography-negative-ion mass spectrometry Citation for published version (APA): DETERMINATION OF ACIDIC CATECHOLAMINE METABOLITES IN PLASMA AND CEREBROSPINAL

. (1986). Determination of acidic catecholamine metabolites in plasma and cerebrospinal fluid using gas chromatography-negative-ion mass spectrometry. Journal of Chromatography. Biomedical Applications, 382(1), 19-30. DOI: 10.1016/S0378-4347(00)83501-X DOI: 10.1016/S0378-4347(00)83501-X Document status and date: Published: 01/01/1986 Document Version: Publisher&apos;s PDF, also known as Version of Record (includes final page, issue and volume numbers) Please check the document version of this publication: • A submitted manuscript is the version of the article upon submission and before peer-review. There can be important differences between the submitted version and the official published version of record. People interested in the research are advised to contact the author for the final version of the publication, or visit the DOI to the publisher&apos;s website. • The final author version and the galley proof are versions of the publication after peer review. • The final published version features the final layout of the paper including the volume, issue and page numbers. Link to publication General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal. If the publication is distributed under the terms of Article 25fa of the Dutch Copyright Act, indicated by the &quot;Taverne&quot; license above, please follow below link for the End User Agreement: SUMMARY A method for the assay of acidic catecholamine metabolites in biological fluids using capillary gas chromatography-electron-capture negative-ion mass spectrometry is described. The method combmes acetylatlon of phenolic hydroxy groups in buffered aqueous solution followed by pentafluorobenzyl ester formation and acetylation of aliphatic hydroxy groups under anhydrous conditions. The resulting per-O-acetyl carboxypentafluorobenzyl esters provided excellent negative-ion mass spectra with intense and diagnostic anions. The sensitivity of the analysis using electron-capture negative-ion mass spectrometry exceeds that using electron-impact mass spectrometry by two to three orders of magnitude. Analysis of acidic catecholamine metabolites in human lumbar cerebrospinal fluid and plasma were performed with good precision (a=~ &lt; 5%) at the low nanomoles per litre level. 0378