The continuous combustion of glycerol in a fluidised bed

It is difficult to burn a liquid fuel inside a fluidised bed. For the first time, liquid glycerol has been burned, when continuously injected into the bottom of an electrically heated bed of alumina particles (sieved to 355 – 425 μm), fluidised by air. The temperature in the bed was held at 700, 800 or 900oC; usually (U/Umf) was 2.5. The bed’s depth was varied, as also were (U/Umf) and the ratio of fuel to air supplied to the bed. Measurements were made of the concentrations of CH4, O2, CO and CO2, and also of the temperature, in the freeboard well above the bed. On entering the bed, the liquid glycerol, rapidly formed bubbles of vapour, which quickly decomposed thermally, yielding mostly CO and H2. These gases then mixed with the other gases in the bed. It appears that the diffusive H2 mainly burns between the fluidised particles. With the bed at 700 – 900oC, no CO was detected far downstream of the bed, provided the equivalence ratio, θ, was below 0.7, i.e. with more than 43 % excess air. Under these fuel-lean conditions, all the carbon in the glycerol was oxidised to CO2. However, in a more fuel-rich situation, with θ > 0.7, CO was detected well above the bed, particularly with a deeper bed, at a lower temperature and operating more fuel-rich. Thus, with the bed at 900oC, CO was mostly oxidised inside the bed, but occasionally some CO burned on top of the bed. When a fuel-rich bed was below 850oC, not all the CO burned in the bed. Achieving complete combustion inside a fluidised bed is partly a problem of mixing the products of glycerol’s thermal decomposition with the fluidising air, which on entry exists mainly in bubbles. Consequently, increasing (U/Umf) promoted both mixing and combustion in a bed. In addition, in-bed combustion requires the bed to be sufficiently deep, hotter than 850oC and θ to be less than a critical value. The effects of other variables are discussed

Power output, cadence, and torque are similar between the forward standing and traditional sprint cycling positions

Purpose: Compare power output, cadence, and torque in the seated, standing, and forward standing cycling sprint positions. Methods: On three separated occasions (ie, one for each position), 11 recreational male road cyclists performed a 14 seconds sprint before and directly after a high-intensity lead-up. Power output, cadence, and torque were measured during each sprint. Results: No significant differences in peak and mean power output were observed between the forward standing (1125.5 ± 48.5 W and 896.0 ± 32.7 W, respectively) and either the seated or standing positions (1042.5 ± 46.8 W and 856.5 ± 29.4 W; 1175.4 ± 44.9 W and 927.5 ± 28.9 W, respectively). Power output was higher in the standing, compared with the seated position. No difference was observed in cadence between positions. At the start of the sprint before the lead-up, peak torque was higher in the standing position vs the forward standing position; and peak torque occurred later in the pedal revolution for both the forward standing and standing positions when compared with the seated position. At the start of the sprint after the lead-up, peak torque occurred later in the forward standing position when compared with both the seated and standing position. At the end of the sprint, no difference in torque was found between the forward standing and standing position either before or after the lead-up. Conclusion: Sprinting in the forward standing sprint position does not impair power output, cadence, and torque when compared with the seated and standing sprint positions

The impact of HIV infection on tuberculosis transmission in a country with low tuberculosis incidence: a national retrospective study using molecular epidemiology

Background: HIV is known to increase the likelihood of reactivation of latent tuberculosis to active TB disease; however, its impact on tuberculosis infectiousness and consequent transmission is unclear, particularly in lowincidence settings. Methods: National surveillance data from England, Wales and Northern Ireland on tuberculosis cases in adults from 2010 to 2014, strain typed using 24-locus mycobacterial-interspersed-repetitive-units–variable-number-tandem-repeats was used retrospectively to identify clusters of tuberculosis cases, subdivided into ‘first’ and ‘subsequent’ cases. Firstly, we used zero-inflated Poisson regression models to examine the association between HIV status and the number of subsequent clustered cases (a surrogate for tuberculosis infectiousness) in a strain type cluster. Secondly, we used logistic regression to examine the association between HIV status and the likelihood of being a subsequent case in a cluster (a surrogate for recent acquisition of tuberculosis infection) compared to the first case or a non-clustered case (a surrogate for reactivation of latent infection). Results: We included 18,864 strain-typed cases, 2238 were the first cases of clusters and 8471 were subsequent cases. Seven hundred and fifty-nine (4%) were HIV-positive. Outcome 1: HIV-positive pulmonary tuberculosis cases who were the first in a cluster had fewer subsequent cases associated with them (mean 0.6, multivariable incidence rate ratio [IRR] 0.75 [0.65–0.86]) than those HIV-negative (mean 1.1). Extra-pulmonary tuberculosis (EPTB) cases with HIV were less likely to be the first case in a cluster compared to HIVnegative EPTB cases. EPTB cases who were the first case had a higher mean number of subsequent cases (mean 2.5, IRR (3.62 [3.12–4.19]) than those HIV-negative (mean 0.6). Outcome 2: tuberculosis cases with HIV co-infection were less likely to be a subsequent case in a cluster (odds ratio 0.82 [0.69–0.98]), compared to being the first or a non-clustered case. Conclusions: Outcome 1: pulmonary tuberculosis-HIV patients were less infectious than those without HIV. EPTB patients with HIV who were the first case in a cluster had a higher number of subsequent cases and thus may be markers of other undetected cases, discoverable by contact investigations. Outcome 2: tuberculosis in HIV-positive individuals was more likely due to reactivation than recent infection, compared to those who were HIV-negative

The impact of HIV infection on tuberculosis transmission in a country with low tuberculosis incidence:A national retrospective study using molecular epidemiology

BACKGROUND: HIV is known to increase the likelihood of reactivation of latent tuberculosis to active TB disease; however, its impact on tuberculosis infectiousness and consequent transmission is unclear, particularly in low-incidence settings. METHODS: National surveillance data from England, Wales and Northern Ireland on tuberculosis cases in adults from 2010 to 2014, strain typed using 24-locus mycobacterial-interspersed-repetitive-units-variable-number-tandem-repeats was used retrospectively to identify clusters of tuberculosis cases, subdivided into 'first' and 'subsequent' cases. Firstly, we used zero-inflated Poisson regression models to examine the association between HIV status and the number of subsequent clustered cases (a surrogate for tuberculosis infectiousness) in a strain type cluster. Secondly, we used logistic regression to examine the association between HIV status and the likelihood of being a subsequent case in a cluster (a surrogate for recent acquisition of tuberculosis infection) compared to the first case or a non-clustered case (a surrogate for reactivation of latent infection). RESULTS: We included 18,864 strain-typed cases, 2238 were the first cases of clusters and 8471 were subsequent cases. Seven hundred and fifty-nine (4%) were HIV-positive. Outcome 1: HIV-positive pulmonary tuberculosis cases who were the first in a cluster had fewer subsequent cases associated with them (mean 0.6, multivariable incidence rate ratio [IRR] 0.75 [0.65-0.86]) than those HIV-negative (mean 1.1). Extra-pulmonary tuberculosis (EPTB) cases with HIV were less likely to be the first case in a cluster compared to HIV-negative EPTB cases. EPTB cases who were the first case had a higher mean number of subsequent cases (mean 2.5, IRR (3.62 [3.12-4.19]) than those HIV-negative (mean 0.6). Outcome 2: tuberculosis cases with HIV co-infection were less likely to be a subsequent case in a cluster (odds ratio 0.82 [0.69-0.98]), compared to being the first or a non-clustered case. CONCLUSIONS: Outcome 1: pulmonary tuberculosis-HIV patients were less infectious than those without HIV. EPTB patients with HIV who were the first case in a cluster had a higher number of subsequent cases and thus may be markers of other undetected cases, discoverable by contact investigations. Outcome 2: tuberculosis in HIV-positive individuals was more likely due to reactivation than recent infection, compared to those who were HIV-negative

Spectrum of Clinical Signs and Genetic Characterization of Gelatinous Drop-Like Corneal Dystrophy in a Colombian Family

PURPOSE: To describe the clinical signs of gelatinous drop-like corneal dystrophy (GDLD) in a consanguineous Colombian family and determine the underlying genetic cause. METHODS: We performed ocular examination of available family members and bidirectionally Sanger sequenced the GDLD-associated gene, TACSTD2. In one individual, the presence of subepithelial amyloid was confirmed with biopsy. RESULTS: The parents were consanguineous and 5 of their 10 children had GDLD. Typical mulberry subepithelial deposits with subepithelial vascularization were present in 3 individuals; 2 individuals only had mild polymorphic anterior stromal opacity. We identified a homozygous TACSTD2 missense mutation, c.551A>G, p.(Tyr184Cys), in the affected family members. Both parents were heterozygous for the mutation, and unaffected siblings were either heterozygous or homozygous wild-type for this allele. In the Colombian population, this mutation has a minor allele frequency of 0.53%. CONCLUSION: The clinical presentation of GDLD in this family was variable and does not solely support an age-dependent progression of the phenotype, suggesting that environmental or other genetic factors can modify phenotypic expression. The relatively high prevalence of this mutation in the Colombian population suggests that other individuals may have undiagnosed subclinical disease

Genotype-Phenotype Correlation for TGFBI Corneal Dystrophies Identifies p.(G623D) as a Novel Cause of Epithelial Basement Membrane Dystrophy.

Purpose: The majority of anterior corneal dystrophies are caused by dominant mutations in TGFBI (transforming growth factor β-induced) collectively known as the epithelial-stromal TGFBI dystrophies. Most cases of epithelial basement membrane dystrophy (EBMD) are thought to result from a degenerative (nongenetic) process; however, a minority of cases are associated with specific TGFBI mutations. We evaluated the spectrum of TGFBI mutations and associated phenotypes in a United Kingdom cohort with typical epithelial-stromal TGFBI dystrophies and an EBMD cohort. Methods: We recruited 68 probands with a clinical diagnosis of epithelial-stromal TGFBI dystrophy and 23 probands with bilateral EBMD. DNA was extracted from peripheral leukocytes, and TGFBI was bi-directly Sanger sequenced. Results: Nine TGFBI mutations were identified. The most common occurred at the mutation hot-spot residues R124 and R555 in 61 probands; these individuals had a genotype-phenotype correlation consistent with prior reports. Four probands with lattice corneal dystrophy carried a mutation in exon 14: p.(A620D), p.(V625D), and p.(H626R). We identified a p.(G623D) mutation in five probands, including two probands from the EBMD cohort. These subjects typically had an onset of severe recurrent corneal epithelial erosion in the fourth decade with mild diffuse or geographic subepithelial corneal opacities and only small anterior stromal lattice structures in older individuals. Symptoms of painful epithelial erosion improved markedly following phototherapeutic keratectomy. Conclusions: There was a strong correlation between genotype and phenotype for the majority of TGFBI mutations. In this cohort, the p.(G623D) mutation caused a greater proportion of TGFBI-associated disease than anticipated, associated with variable phenotypes including individuals diagnosed with EBMD

Plankton community respiration and bacterial metabolism in a North Atlantic Shelf Sea during spring bloom development (April 2015)

Spring phytoplankton blooms are important events in Shelf Sea pelagic systems as the increase in carbon production results in increased food availability for higher trophic levels and the export of carbon to deeper waters and the sea-floor. It is usually accepted that the increase in phytoplankton abundance and production is followed by an increase in plankton respiration. However, this expectation is derived from field studies with a low temporal sampling resolution (5–15 days). In this study we have measured the time course of plankton abundance, gross primary production, plankton community respiration, respiration of the plankton size classes (> 0.8 μm and 0.2–0.8 μm) and bacterial production at ≤5 day intervals during April 2015 in order to examine the phasing of plankton autotrophic and heterotrophic processes. Euphotic depth-integrated plankton community respiration increased five-fold (from 22 ± 4 mmol O2m−2 d−1 on 4th April to 119 ± 4 mmol O2m−2 d−1 on 15th April) at the same time as gross primary production also increased five-fold, (from 114 ± 5 to 613 ± 28 mmol Cm−2 d−1). Bacterial production began to increase during the development of the bloom, but did not reach its maximum until 5 days after the peak in primary production and plankton respiration. The increase in plankton community respiration was driven by an increase in the respiration attributable to the> 0.8 μm size fraction of the plankton community (which would include phytoplankton, microzooplankton and particle attached bacteria). Euphotic depth-integrated respiration of the 0.2–0.8 μm size fraction (predominantly free living bacteria) decreased and then remained relatively constant (16 ± 3 – 11 ± 1 mmol O2m−2 d−1) between the first day of sampling (4th April) and the days following the peak in chlorophyll-a (20th and 25th April). Recent locally synthesized organic carbon was more than sufficient to fulfil the bacterial carbon requirement in the euphotic zone during this productive period. Changes in bacterial growth efficiencies (BGE, the ratio of bacterial production to bacterial carbon demand) were driven by changes in bacterial production rates increasing from<30 ± 14% on 4th April to 51 ± 11% on 25th of April. This study therefore shows a concurrent rather than a phased increase in primary production and community respiration attributable to cells>0.8 μm during the development of the spring bloom, followed 5 days later by a peak in bacterial production. In addition, the size fractionated respiration rates and high growth efficiencies suggest that free living bacteria are not the major producers of CO2 before, during and a few days after this shelf sea spring phytoplankton bloom

The influence of soil communities on the temperature sensitivity of soil respiration

Soil respiration represents a major carbon flux between terrestrial ecosystems and the atmosphere, and is expected to accelerate under climate warming. Despite its importance in climate change forecasts, however, our understanding of the effects of temperature on soil respiration (RS) is incomplete. Using a metabolic ecology approach we link soil biota metabolism, community composition and heterotrophic activity, to predict RS rates across five biomes. We find that accounting for the ecological mechanisms underpinning decomposition processes predicts climatological RS variations observed in an independent dataset (n = 312). The importance of community composition is evident because without it RS is substantially underestimated. With increasing temperature, we predict a latitudinal increase in RS temperature sensitivity, with Q10 values ranging between 2.33 ±0.01 in tropical forests to 2.72 ±0.03 in tundra. This global trend has been widely observed, but has not previously been linked to soil communities