Although portable and water efficient, sorbent cartridges were expensive. Single pass dialysis technology triumphed. Other concerns signalled the apparent end of the sorbent era: reported aluminium release from early cartridges containing aluminium hydroxide, acetate exposure and the potential for cartridge saturation with ammonia ‘spill-over’. A conventional single pass dialysis

system (Fig. 1) needs a power source, a water source, Gefitinib solubility dmso a proportioning system, a water treatment plant (both a multilayered pre-filtration system and, then, reverse osmosis) and an effluent drain. Water circuit sterilization is also required after each treatment run and regular decalcification of the internalized water and dialysate circuits of the machine is essential. In comparison, a sorbent system (Fig. 2) needs only a power source. Sorbent technology is free of a water source, needs no water filtration or reverse osmosis water treatment equipment and does not need an effluent drain. Importantly, as its dialysate circuitry is all self-contained and disposable, it also needs no internal fluid-exposed circuitry and, as such,

requires little or no regular maintenance or cleaning. Equipment decalcification and circuit sterilization are not required beyond, of www.selleckchem.com/products/yap-tead-inhibitor-1-peptide-17.html course, the inescapable pre-use sterilization of the blood lines and dialyser. The key to sorbent technology is the capacity for the used (effluent) dialysate – previously drained to waste in single pass systems – to pass through an disposable absorbent ‘cartridge’ and emerge, cleaned and purified, for representation to the dialyser. This markedly reduces the required total volume of dialysate. An initial 6 L of tap, bottled, bore or tank water added to a dialysate reservoir, next the pre-dialysis, intra-dialysis and post-dialysis weight of which allows calculation of the progressive and ultimate ultrafiltration

volume. Before commencing dialysis, this initial 6 L volume is cartridge-circulated. This permits progressive pre-dialysis sterilization and decontamination by a dialyser-excluded circuit. After this short ‘clean and prime phase’, the dialyser is circuit-included and dialysis begins. The ‘effluent’ dialysate in a sorbent system is identical to that which exits the used dialysate port of a standard single pass system. In a single pass system, the effluent dialysate is drained to waste. By contrast, in a sorbent system the effluent dialysate is presented to the sorbent cartridge where it is passed through several contiguous layers. Although described in depth by Ash,15 a summary of the basic process is as follows: The first layer consists of activated charcoal, a material with an exceptionally high surface area. A single gram has a surface area of approximately 500 m2 and is highly microporous. It absorbs any dialysed heavy metals, oxidants, chloramines, creatinine, uric acid, a variety of middle molecules – including B2 microglobulin – and other organic substances.

2A). Localization of pro-IL-16 in both the cytoplasm and nucleus was confirmed by confocal laser scanning microscopy; pro-IL-16 was present in both the cytoplasmic and nuclear compartments of B cells (Fig. 2B-b). In addition, a substantial amount of pro-IL-16 co-localized with MHC class II molecules on the cell surface (Fig. 2B-d). These results suggest that pro-IL-16 is associated with MHC class II molecules MEK inhibitor either directly or indirectly in resting B cells and that translocation of pro-IL-16 into the nucleus is increased by negative signalling through MHC class II molecules. The increase in nuclear translocation

of pro-IL-16 after negative signalling suggested that pro-IL-16 may exert a negative effect on resting B cell activation. To directly test the role of pro-IL-16 in the suppression of resting B cell activation, we transfected pro-IL-16 cDNA into cells and determined the effect of pro-IL-16 overexpression on resting B cell activation (Fig. 3). After selection of positive Y-27632 molecular weight transfectants after a 2-week culture in selection medium, the expression of the transfected pro-IL-16 gene was confirmed through RT-PCR (data not shown) and Western blot analysis (Fig. 3B). Then, levels of cell proliferation and NF-κB activation were compared between the pro-IL-16 and vector control transfectants (Fig. 3A).

The proliferation of cells transfected with pro-IL-16 gene was significantly suppressed

(about 40%, P < 0.001) compared to that of vector control transfectant cells that grew normally (Fig. 3A). When we assessed the effect of pro-IL-16 gene transfection on activation of NF-κB subfamilies by Western blot analysis, we found that the translocation of NF-κB1 (p50), NF-κB2 (p52) and c-Rel of NF-κB subfamilies Ceramide glucosyltransferase into the nucleus, and the levels of these subfamilies in nuclear extracts were reduced by pro-IL-16 gene transfection (Fig. 3B). LPS treatment did not change the suppressive effect of pro-IL-16 on nuclear translocation of the p50, p52 and c-Rel NF-κB subfamilies (Fig. 3B). The finding that activation of NF-κB subfamilies (p50, p52 and c-Rel) is influenced by pro-IL-16 is consistent with our previous observations that MHC class II-mediated negative signalling in resting B cell activation is closely associated with the activation of p50, p52 and c-Rel NF-κB subfamilies [16, 17]. Collectively, these results suggest that B cell proliferation induced by NF-κB activation is significantly impaired by the overexpression of pro-IL-16. To confirm the negative role of pro-IL-16 in resting B cell proliferation, siRNA for pro-IL-16 was introduced into 38B9 cells as described in the materials and methods section. Initially, knock-down of target pro-IL-16 gene expression by siRNA transfection was confirmed at 40 h after transfection through Western blot analysis and RT-PCR (Fig. 4A).

A sample of the supernatant was added to SYTOX green nucleic acid stain (1 µM) in a black 96-well plate to quantify NET-DNA fragments by fluorometry selleck products (Twinkle LB970, Berthold Technologies,

Harpenden, UK; excitation 485 nm, emission 525 nm) and recorded as arbitrary fluorescent units (AFU). Neutrophils (1 × 105) suspended in 500 µl RPMI-1640 were seeded into BSA-coated 24-well plates and allowed to settle for 30 min at 37°C, prior to stimulation for 3 h at 37°C [2] and staining of NET-DNA using 1 µM SYTOX green. NETs and cells were observed at room temperature under a fluorescence microscope (Nikon Eclipse TE300, Kingston upon Thames, UK) using a × 20 objective and images captured by digital camera (Nikon CoolPix 450, Kingston upon Thames, UK). The InnoZyme myeloperoxidase activity kit was Selleck ICG-001 used according to the manufacturers’ instructions to examine the effect of 3-AT (1 mM) on the activity of purified human MPO (100 ng/ml). ROS generation was quantified

by enhanced chemiluminescence assay [19]. Neutrophils (1 × 105) suspended in PBS supplemented with glucose (10 mM), MgCl2 (1·5 mM) and CaCl2 (1·35 mM) were seeded into a BSA-coated 96-well plate with luminol (450 µM) to detect total ROS, isoluminol (900 µM) plus horseradish peroxidase (7.5 units/ml) to detect extracellular ROS or lucigenin (50 µg/ml) to detect superoxide. Cells were allowed to settle for 30 min at 37°C prior to stimulation. ROS generation was recorded as the peak relative light units (RLU) per second recorded by microplate luminometer (Berthold LB96v) over Fenbendazole the 2·5-h incubation period, as reported

previously [19]. Sodium hypochlorite was diluted and the concentration of hypochlorite ions (OCl–) estimated by optical density at 292 nm of pH 12·0 solutions using an extinction coefficient of 350 M/cm [23]. The final pH when used in experiments was approximately the same as the pKa for HOCl (7·5), thus it was assumed that 50% existed as HOCl and 50% existed as OCl–. S. aureus (NCTC 6571) was grown aerobically at 37°C on tryptone soya agar and inoculated into tryptone soya broth. Bacteria were isolated from broth culture by centrifugation, washed three times in sterile PBS and heat-treated at 100°C for 10 min. Opsonization was performed as described previously [24] and stored as a 1·2 × 109 cells/ml suspension at −80°C. Data were analysed using Excel 2007 (Microsoft). Each in vitro experiment was performed at least four times using independent neutrophil donors, and each experiment was performed in quadruplicate. Comparison between groups was made using two-tailed paired t-test where P-values of less than 0·05 were considered significant. It has been reported previously that NADPH oxidase-dependent generation of ROS, and specifically H2O2, is required for NET release [3].

Results: XG-102 or HBO alone reduced the total infarct area by 43% and 63%, respectively. The combination diminished total infarct area by 78%, improved the neurological function and reduced brain oedema.

Co-application of HBO and XG-102 also significantly reduced the cleavage of PARP, by 96% and 91% in cortical penumbra and ischaemic core, respectively. Moreover, cotreatment significantly attenuated the number of cells labelled with transferase-mediated Raf kinase assay biotinylated UTP nick end labelling and phosphorylated c-Jun. Conclusion: Our study demonstrates that HBO reinforces the efficiency of neuroprotective drugs such as XG-102 and vice versa. Both treatments, physical HBO and pharmacological XG-102, are already in phase I/II studies and promising strategies for clinical use. “
“G. R. Campbell, A. Reeve, I. Ziabreva, T. M. Polvikoski, R. W. Taylor, R. Reynolds, D. M. Turnbull and

D. J. Mahad (2013) Neuropathology and Applied Neurobiology39, 377–389 Mitochondrial DNA deletions and depletion within paraspinal muscles Aims: Although mitochondrial abnormalities have been reported within paraspinal muscles in patients with axial weakness and neuromuscular disease as well as with ageing, the basis of respiratory deficiency in paraspinal muscles is not known. This study aimed to determine the extent and basis of respiratory deficiency in paraspinal muscles from cases undergoing surgery for degenerative spinal disease and post mortem cases without a history of spinal disease, where age-related histopathological changes were previously reported. Methods: Cervical and lumbar paraspinal muscles HM781-36B supplier were obtained peri-operatively from 13 patients and from six post mortem control cases (age range 18–82 years) without a neurological disease. Sequential COX/SDH (mitochondrial respiratory chain complex IV/complex II) histochemistry was performed to identify respiratory-deficient muscle fibres (lacking complex IV with intact complex II activity). Real-time polymerase chain reaction, long-range polymerase chain reaction and sequencing were used to identify and characterize mitochondrial DNA (mtDNA) deletions and determine

mtDNA copy number status. Mitochondrial respiratory chain complex subunits were detected by immunohistochemistry. Results: The density of respiratory-deficient Non-specific serine/threonine protein kinase fibres increased with age. On average, 3.96% of fibres in paraspinal muscles were respiratory-deficient (range 0–10.26). Respiratory deficiency in 36.8% of paraspinal muscle fibres was due to clonally expanded mtDNA deletions. MtDNA depletion accounted for further 13.5% of respiratory deficiency. The profile of immunohistochemically detected subunits of complexes was similar in respiratory-deficient fibres with and without mtDNA deletions or mtDNA depletion. Conclusions: Paraspinal muscles appeared to be particularly susceptible to age-related mitochondrial respiratory chain defects.

An alteration in the Treg cell population might correspond

to the diminishment of the tumour mass in patients with cancer and could therefore be a useful marker of the intensity of the selective suppression of the host immune system and also of the degree of radicalism of a procedure. Certainly, it is well known that in order for anti-cancer therapy to succeed the proper immune response against cancer cells must be restored. Furthermore, monitoring the level of selective immune system suppression during cancer therapy might yield information that would support a decision to supplement standard therapy by immunotherapy or to increase the degree of radicalism of the applied therapy. Method of study  We examined the Treg cell populations in the peripheral blood of a group of patients treated surgically for ovarian cancer. In each patient, find more the peripheral blood samples were collected both prior to and 1 day after the surgical procedure, and then again 5 days after the procedure. The presence of regulatory T cells in the samples was analyzed by means of flow cytometry. Results  In our study, the percentages of FOXP3+ cells in the subpopulation of CD4+ T lymphocytes found in the peripheral blood of the patients before the surgical intervention were statistically

significantly higher than those observed in the peripheral blood of these same patients after the surgical procedure. Conclusion  It would seem that the alteration in the Treg cell Venetoclax chemical structure subpopulation could be a key factor in determining the status of the tumour microenvironment. Most likely, it could provide information about whether the proper level of anti-cancer immune response could be restored. The possibility of restoring the immune response may directly correspond to the degree of radicalism of the surgical intervention. “
“Like many other complex human disorders of unknown aetiology, autoimmune-mediated type 1 diabetes may Astemizole ultimately be controlled via a therapeutic approach that combines multiple agents, each with differing modes of action. The numerous advantages of such a strategy include the ability to minimize toxicities

and realize synergies to enhance and prolong efficacy. The recognition that combinations might offer far-reaching benefits, at a time when few single agents have yet proved themselves in well-powered trials, represents a significant challenge to our ability to conceive and implement rational treatment designs. As a first step in this process, the Immune Tolerance Network, in collaboration with the Juvenile Diabetes Research Foundation, convened a Type 1 Diabetes Combination Therapy Assessment Group, the recommendations of which are discussed in this Perspective paper. Type 1 diabetes (T1D), one of the most common autoimmune diseases, results from the progressive destruction of insulin-producing pancreatic β cells by CD4+ and CD8+ T cells.

This study involves minimal to no risk to patients. All patient records would be anonymised. As all clinical specimens would be collected from samples that were drawn for standard clinical indications, no extra blood will be drawn. Since the study is not designed to assess for genetic risks, patient DNA will not be extracted. None “
“Many relapses and deaths resulting from disseminated histoplasmosis (DH) in acquired immunodeficiency syndrome (AIDS) patients have been observed in an endemic area in north-eastern Brazil. The objective of this study was to evaluate the risk factors associated with selleck the clinical outcomes

of DH/AIDS coinfection in patients from the state of Ceará, Brazil. A retrospective cohort of AIDS patients, after their hospital discharge due to first DH episode in the period 2002–2008, was followed until December 31, 2010, to investigate the factors associated with relapse and mortality. A total of 145 patients were evaluated in the study. Thirty patients (23.3%) relapsed and the overall mortality

was 30.2%. The following variables were significantly (P < 0.05) associated with relapse and overall mortality (univariate analysis): non-adherence to highly active antiretroviral therapy (HAART), irregular use of an antifungal, non-recovery of the CD4+ count and having AIDS before DH; histoplasmosis relapse was also significantly associated with mortality. In the multivariate analysis, non-adherence to HAART was the independent risk factor that was associated with both relapse (Adj OR = 6.28) Selleckchem Quizartinib and overall mortality (Adj OR = 8.03); efavirenz usage was discovered to be significant only for the overall mortality rate (Adj OR = 4.50). Adherence

Etomidate to HAART was the most important variable that influenced the outcomes in this specific population. “
“The Cryptococcus neoformans/C. gattii species complex members are the main agents of systemic cryptococcosis. This disease is believed to be acquired from the environment via fungal cell inhalation. Often, isolates recovered from environmental and clinical sources have proven to be genotypically similar. We assessed the occurrence of C. neoformans and C. gattii in environmental substrates collected in a Portuguese region. Twenty-eight isolates were identified as C. neoformans – five from decaying Eucalyptus leaves and 23 from domestic pigeon droppings. The isolates were genotyped using a URA5-RFLP approach. The C. neoformans VNIV (53.6%, n = 15) and VNI (32.1%, n = 9) genotypes were abundantly present among environmental isolates. The hybrid VNIII (14.3%, n = 4) genotype was underrepresented and the VNII was not found. Cryptococcus gattii was also not found although some isolates yielded a positive canavanine–glycine–bromothymol blue test. “
“Black yeast-like fungi are rarely reported from superficial infections.

As indicated in Figure 5, splenocytes from naive mice contained a consistently low overall copy

number of MHC II RNA up to the age of 3 weeks. From week 4 on, MHC II copy numbers continuously increased through week 8. A similar scenario occurred in Epigenetics Compound Library mice immunized with MOG p35–55, although the upregulation of MHC II appeared to be more abrupt between week 5 and 6. We applied the same technique to evaluate upregulation of MHC II within the CNS. Here, the copy numbers also increased in an age-dependent manner in immunized mice, although upregulation of MHC II appeared to occur at a later age, suggesting that this overall increase in copy numbers within the CNS may primarily relate to infiltration of peripheral immune cells starting to express MHC II. In order to induce EAE, T cells require MHC II-restricted activation twice, first in the periphery followed by their reactivation within the CNS [5]. The data presented

in Peripheral and CNS MHC class II expression increases with age indicated that besides peripheral APC function, MHC II-restricted reactivation of T cells within the CNS may be similarly impaired in young mice. To elucidate this possibility we transferred readily primed encephalitogenic T cells from adult mice into 2-week-old recipients, an induction regimen, which bypasses peripheral APC function. As demonstrated in Table 2, encephalitogenic T cells induced EAE in 8-week-old recipients, but failed to do so in 2-week-old mice. In conjunction with the lower CNS MHC II mRNA expression presented FK506 cell line in oxyclozanide Figure 5, this finding suggests that in young mice both peripheral as well as CNS APCs are incapable of sufficiently activating or reactivating autoreactive T cells, respectively. In an approach to formally proof that protection of young mice from EAE refers to the observed alterations and immaturity within the innate immune cell compartment, we adoptively transferred splenic myeloid APCs and B cells from 8-week-old mice into 2-week-old

recipients at the time point of immunization and 2 days thereafter. Prior to transfer, CD3+ T cells were removed by MACS separation. As indicated in Table 3, adoptive transfer of adult APCs into 2-week-old mice restored susceptibility to actively induced EAE in three out of three independent experiments. When recipient mice were evaluated for splenic T-cell responses to the immunogen, recipients of adult APCs showed an increased proliferation of myelin-reactive T cells (Supporting Information Fig. 2), indicating that donor adult APCs restored the ability of young mice to generate an encephalitogenic T-cell response. Collectively, these data highlight the conclusion that the age-related increase in susceptibility to CNS autoimmune disease may be determined by a paralleling maturation of the predominant APC phenotype.

Our center participated in a randomized, multi-center trial comparing sotrastaurin and the calcineurin inhibitor neoral in de novo renal transplant recipients [15]. We conducted an ex vivo study on patient samples (stage 1 phase) to investigate the frequency and function of FoxP3+CD4+CD25high T cells. We also performed in vitro functional studies on samples of blood bank volunteers to study the different effects of sotrastaurin on T effector and regulatory cells. Twenty-one patients were randomized to receive either sotrastaurin 300 mg twice daily (n = 14) or neoral [starting dose 4 mg/kg/day, aimed trough levels 100–200 ng/ml (month 1), 75–150 ng/ml (months 2–3), 50–100 ng/ml (months 4–5) and 25–50 ng/ml

(months 6–12), n = 7] 1 day after living (un)related de novo kidney transplantation. This cohort involved Autophagy inhibitors all (adult) patients in our center participating in an open-label, multi-centre, randomized Phase II trial [15] (trial number CAEB071A2206, stage 1) (Table 1). Both regimens included steroids, basiliximab [anti-CD25 monoclonal antibody (mAb)] and the mTOR-inhibitor everolimus [starting dose 1·5 mg twice daily, aimed trough levels 4–8 ng/ml)]. Patient blood Opaganib mouse samples were collected pre-, 2, 3 and 6 months after transplantation. Blood sampling was approved by the local ethical committee on human research. All patients

gave written informed consent (Medical Ethic Committee number MEC-2007-219). Donor age in years median (range) Type of transplantation LR : LUR HLA mismatch mean ± s.e.m. A: 0·79 (0·15) B: 1·0 (0·21) DR: 1·07 (0·22) A: 0·71 (0·36) B: 0·57 (0·20) DR: 1·0 (0·22) Peripheral blood mononuclear cells (PBMC) from patient heparinized blood samples were isolated by density gradient using Ficoll-Paque (density gradient 1077 g/ml).

After isolation the PBMC samples were frozen in 10% dimethylsulphoxide (DMSO) (Merck, Schuchardt, Enzalutamide chemical structure Germany) and stored at −140°C until analysis. PBMC from healthy blood bank donors were also isolated and served as control. Neoral infusion (SandImmune®; Novartis Pharma, Switzerland) and sotrastaurin (Novartis Pharma) powder were dissolved in RPMI-1640 (Gibco BRL, Paisley, UK) and DMSO, respectively, and stored at −80°C until use. On the day of the experiment, stock solutions were dissolved in RPMI-1640. Defrosted PBMC were resuspended in cold magnetic-activated cell sorting (MACS) buffer according to the manufacturer’s protocol (Miltenyi Biotec, Bergisch Gladbach, Germany) and supplemented with 7 μl CD25-microbeads (directed against epitope A of the CD25 molecule; Miltenyi Biotec)/107 PBMCs to isolate the CD25high T cells. After 15 min at 4°C, the cells were washed with MACS buffer and resuspended in 1 ml MACS buffer. Subsequently, the POSSEL-D protocol was performed on the autoMACS (Miltenyi Biotec). The CD4+CD25high population was defined as cells with high CD25 expression with a slightly lower CD4 expression.

Results. Fourteen free latissimus dorsi muscle flaps were performed in 11 children with a mean age of 13 ± 4 years. The injuries

were caused by traffic accidents, lawnmower accidents, and a crush trauma. Thirteen (92.8%) flaps needed surgical LY294002 in vitro revision. Three complete flap losses and 1 partial flap loss were registered. Conclusions. Free latissimus dorsi muscle flaps seem to be a useful technique for lower extremity salvage after severe injury, but there is a relevant flap failure risk in children. © 2010 Wiley-Liss, Inc. Microsurgery 30:537–540, 2010. “
“Proficient microsurgical skills are considered essential in plastic and reconstructive surgery. Specialized courses offer trainees opportunity to improve their technical skills. Trainee aptitude may play an important role in the ability of a

trainee to acquire proficient skills as individuals have differing fundamental abilities. We delivered an intensive 5-day microsurgical training course. We objectively assessed the impact of the course on microsurgical selleck kinase inhibitor skill acquisition and whether aptitudes as assessed with psychometric tests were related to surgical performance. Sixteen surgical trainees (male = 10 and female = 6) participated in the courses. Trainees’ visual spatial, perceptual, and psychomotor aptitudes were assessed on day 1 of the course. The trainees’ performance of an end-to-end arterial anastomosis was assessed on days 2 and 5. Surgical performance was assessed with objective structured assessment of technical skills(OSATS) and time to complete the task. The trainees showed a significant improvement in OSATS scores from days 2 to 5 (P < 0.001) and the time taken to complete the anastomosis (P < 0.001). Aptitude scores correlated strongly with objectively assessed microsurgical skill performance for male trainees but not for females. We demonstrated that participating in a microsurgical training course results in significant improvement in objectively assessed microvascular surgical skills. The degree of skills improvement was strongly correlated with psychomotor

aptitude assessments scores for male trainees. © 2012 Wiley Periodicals, Inc. “
“Medical leech therapy (MLT) with Hirudo medicinalis is well established as a treatment ifenprodil for venous congestion of tissue flaps, grafts, and replants. Unfortunately, this treatment is associated with surgical site infections with bacterial species, most commonly Aeromonas hydrophila, which is an obligate symbiot of H. medicinalis. For this reason, prophylactic antibiotics are recommended in the setting of MLT. After culturing Aeromonashydrophila resistant to ciprofloxacin from a tissue specimen from a patient with a failed replant of three digits post-MLT, we performed environmental surveillance cultures and antibiotic susceptibility testing on water collected from leech tanks.

PMMTM exposure reduced overall vasodilation in coronary arterioles compared with sham-treated animals; however, individual doses of Spermine NONOate were not significantly (p = 0.053 at 10 nm dose) different between exposure groups (max% 58 ± 7 sham, 46 ± 6 PMMTM, Figure 5A). Furthermore, endothelium-independent arteriolar dilation was different following PMMTM exposure in mesenteric arteries

beginning at the 10 nm (max% 70 ± 8 sham, 44 ± 8 PMMTM Figure 5A). Myogenic responsiveness of coronary arterioles was not different between sham and PMMTM-exposed Selleck DAPT animals (Figure 5B). However, at 105 mmHg arterioles from PMMTM-exposed rats displayed a significantly greater myogenic Inhibitor Library research buy response to the highest transmural pressure (Figure 5B). This probably suggests an enhanced vascular smooth muscle cell contractile responsiveness to transmural pressure; however, the biological relevance of this effect is unclear at present. To determine the responsiveness of coronary and mesenteric arterioles to α-adrenergic stimulation, PE was performed. Neither coronary nor mesenteric arterioles showed any difference in reactivity to PE. Figure 6 depicts the maximal arteriolar constriction induced by PE in sham or PMMTM-exposed rats. This is the first study to demonstrate systemic microvascular effects of pulmonary exposure to particles

collected near active MTM sites. Furthermore, this study demonstrates that pulmonary PMMTM exposure results in acute microvascular dysfunction that (1) can be characterized across disparate vascular beds, (2) may be mediated through aberrant NO signaling, and (3) may also result from sympathetic nerve influences. The particle composition reported in Figure 1D is consistent with a predominantly crustal particle sample. MTM sites are active areas of blasting, crushing, and grinding of materials that can blanket the surrounding areas Mannose-binding protein-associated serine protease with PM. In addition to mineralogical materials, engine exhaust emissions, likely off-road diesel, are

normally thought to contribute to the overall PM burden. Indeed, particle characterization from opencast mines suggests a mix of natural and exhaust emissions with the mass dominated by geological PM [23]. However, based on our results of a high OC measurement with null amounts of EC, the overall composition would suggest a particulate largely composed of mineralogical dust and coal dust [4]. Preliminary particle monitoring from these sites suggests that, by total number, ultrafine to 0.2 μm PM dominate the air sample (data not shown). This suggests that the bulk of the particles, by number, are anthropogenic in origin [46]. However, based on mass measurement (Figure 1D), the predominant particle composition is likely crustal.