Distinct patterns in the diurnal and seasonal variability in four components of soil respiration in a temperate forest under free-air CO₂ enrichment

Soil respiration (RS) is a major flux in the global carbon (C) cycle. Responses of RS to changing environmental conditions may exert a strong control on the residence time of C in terrestrial ecosystems and in turn influence the atmospheric concentration of greenhouse gases. Soil respiration consists of several components oxidizing soil C from different pools, age and chemistry. The mechanisms underlying the temporal variability of RS components are poorly understood. In this study, we used the long-term whole-ecosystem 13C tracer at the Duke Forest Free Air CO2 Enrichment site to separate forest RS into its autotrophic (RR) and heterotrophic components (RH). The contribution of RH to RS was further partitioned into litter decomposition (RL), and decomposition of soil organic matter (RSOM) of two age classes – up to 8 yr old and SOM older than 8 yr. Soil respiration was generally dominated by RSOM during the growing season (44% of daytime RS), especially at night. The contribution of heterotrophic respiration (RSOM and RL) to RS was not constant, indicating that the seasonal variability in RR alone cannot explain seasonal variation in RS. Although there was no diurnal variability in RS, there were significant compensatory differences in the contribution of individual RS components to daytime and nighttime rates. The average contribution of RSOM to RS was greater at night (54%) than during the day (44%). The average contribution of RR to total RS was ~30% during the day and ~34% during the night. In contrast, RL constituted 26% of RS during the day and only 12% at night. About 95% of the decomposition of soil C older than 8 yr (Rpre-tr) originated from RSOM and showed more pronounced and consistent diurnal variability than any other RS component; nighttime rates were on average 29% higher than daytime rates. In contrast, the decomposition of more recent, post-treatment C (Rpre-tr) did not vary diurnally. None of the diurnal variations in components of RH could be explained by only temperature and moisture variations. Our results indicate that the variation observed in the components of RS is the result of complex interaction between dominant biotic controls (e.g. plant activity, mineralization kinetics, competition for substrates) over abiotic controls (temperature, moisture). The interactions and controls among roots and other soil organisms that utilize C of different chemistry, accessibility and ages, results in the overall soil CO2 efflux. Therefore understanding the controls on the components of RS is necessary to elucidate the influence of ecosystem respiration on atmospheric C-pools at different time scales

Exfoliation and pigmentary glaucoma – overlap syndrome

Introduction: Concomitant signs, characteristic for both pigmentary dispersion syndrome (PDS) and exfoliation syndrome (XFS) can cause sudden IOP spike, and lead to optic nerve damage progression and associated visual field (VF) loss. This development often remains undetected. Purpose: To describe the characteristic signs of XFS and pigmentary glaucoma (PG), and to discuss the specific management of overlap syndrome. Methods: A retrospective analysis of 40 consecutive patients diagnosed with overlap syndrome for a period of 18 months and follow up period of 9 to 18 months. Accumulation of abnormal material on lens capsule and pupil, iris transillumination defects, Krukenberg’s spindle, trabecular pigmentation, increased IOP and more difficult control of IOP are main features. Treatment: topical medications, laser peripheral iridotomy (LPI), and surgical - trabeculectomy (TE) or ExPress implant. Results: Most patients had typical signs of PDS and XFS, with XFS predominating over PDS. Patients with overlap syndrome were 50-65 years of age. Glaucoma progression was registered in all overlapping forms. In 25 (62%) patients we achieved good pressure lowering effect with medication and LPI. At lack of IOP control 15 patients underwent surgery - TE (9) and ExPress implantation (6). In 3 patients with TE additional needling with 5-FU was necessary. In 2 patients with ExPress transient posterior pole edema was registered. As a result of our treatment approach, no progression of glaucoma damage was observed. Visual impairment was due to late referral with very high levels of IOP and advanced VF defects. Conclusion: Awareness of sequential appearance and overlap of those two forms of glaucoma is of decisive importance for appropriate management. The alarming signs of unexcpected loss of IOP control, rapid progression of glaucomatous optic nerve changes and VF loss indicate of need for more aggressive treatment

Surfactant Protein A Forms Extensive Lattice-Like Structures on 1,2-Dipalmitoylphosphatidylcholine/Rough-Lipopolysaccharide- Mixed Monolayers

Due to the inhalation of airborne particles containing bacterial lipopolysaccharide (LPS), these molecules might incorporate into the 1,2-dipalmitoylphosphatidylcholine (DPPC)-rich monolayer and interact with surfactant protein A (SP-A), the major surfactant protein component involved in host defense. In this study, epifluorescence microscopy combined with a surface balance was used to examine the interaction of SP-A with mixed monolayers of DPPC/rough LPS (Re-LPS). Binary monolayers of Re-LPS plus DPPC showed negative deviations from ideal behavior of the mean areas in the films consistent with partial miscibility and attractive interaction between the lipids. This interaction resulted in rearrangement and reduction of the size of DPPC-rich solid domains in DPPC/Re-LPS monolayers. The adsorption of SP-A to these monolayers caused expansion in the lipid molecular areas. SP-A interacted strongly with Re-LPS and promoted the formation of DPPC-rich solid domains. Fluorescently labeled Texas red-SP-A accumulated at the fluid-solid boundary regions and formed networks of interconnected filaments in the fluid phase of DPPC/Re-LPS monolayers in a Ca2+-independent manner. These lattice-like structures were also observed when TR-SP-A interacted with lipid A monolayers. These novel results deepen our understanding of the specific interaction of SP-A with the lipid A moiety of bacterial LPS

Enzyme-assisted extraction of carotenoids from Bulgarian tomato peels

Enzyme-assisted extraction of carotenoids from tomato peels of the Bulgarian cultivar “Stela”, one of the most widely used cultivars by the canning industry, was examined in this study. The carotenoid content in raw tomato peels was established by HPLC analysis. A two-step protocol was followed: the tomato peels were first treated with enzymes and then extracted by the use of acetone as a solvent for 30 min at 20±1 °C and solid/liquid ratio of 1:30. The total carotenoid, lycopene, and β-carotene extraction yields were increased by the use of pectinase, cellulase, endo-xylanase, and proteinase enzymes in comparison with the non-enzyme-treated samples. The increase in the extraction yield was affected by the enzymes used, the enzyme concentration, the pretreatment time and temperature. Maximum total carotenoid (55.15 mg/100 g d.w.), β-carotene (35.85 mg/100 g d.w.), and lycopene (15.44 mg/100 g d.w.) extraction yields were obtained in peels pretreated with mixed cellulase (100 U g−1) and endo-xylanase (400 U g−1) for 4 h at 50 °C. Carotenoid recovery by mixed cellulolytic and hemi-cellulolytic enzyme pretreatment of tomato peels is a good approach, which can be used for waste utilization

The association between older age and receipt of care and outcomes in patients with acute coronary syndromes

Peer reviewedPostprin

The association between prior statin usage and long-term outcomes after critical care admission

Background: Statins may have immunomodulatory effects that benefit critically ill patients. Therefore we retrospectively examined the association between survival and the prescription of statins prior to admission to an intensive care unit (ICU), or high dependency unit (HDU), as a result of major elective surgery, or as an emergency with a presumed diagnosis of sepsis. Methods: We retrospectively studied critical care patients (ICU or HDU) from a tertiary referral UK teaching hospital. Nottingham University Hospitals has over 2200 beds, of which 39 are critical care beds. Over a five-year period (2000–2005) 414 patients were identified with a presumed diagnosis of sepsis, and 672 patients were identified with a planned ICU/HDU admission following elective major surgery. Patients prescribed statins prior to hospital admission were compared with those who were not. Demographics, past medical history, drug history, and Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were examined. Univariate and multivariate analyses were applied using the primary endpoint of survival at five years after admission. Results: Patients prescribed statins prior to critical care admission were, on average, older, with higher initial APACHE II scores and more pre-existing comorbidities. Statins were almost invariably stopped following admission to critical care. Statin usage was not associated with significantly altered survival during hospital admission, or at five years, for either patients with sepsis (9% v 15%, P=0.121; 73% v 84%, P=0.503 respectively), or post-operative patients (55% v 58%, P=0.762; 57% v 63%, P=0.390). Conclusions: Prior statin usage was not associated with improved or worsening outcomes in patients admitted to critical care after elective surgical cases or with a presumed diagnosis of sepsis

Multicentre prospective validation of a urinary peptidome-based classifier for the diagnosis of type 2 diabetic nephropathy

Background Diabetic nephropathy (DN) is one of the major late complications of diabetes. Treatment aimed at slowing down the progression of DN is available but methods for early and definitive detection of DN progression are currently lacking. The ‘Proteomic prediction and Renin angiotensin aldosterone system Inhibition prevention Of early diabetic nephRopathy In TYpe 2 diabetic patients with normoalbuminuria trial' (PRIORITY) aims to evaluate the early detection of DN in patients with type 2 diabetes (T2D) using a urinary proteome-based classifier (CKD273). Methods In this ancillary study of the recently initiated PRIORITY trial we aimed to validate for the first time the CKD273 classifier in a multicentre (9 different institutions providing samples from 165 T2D patients) prospective setting. In addition we also investigated the influence of sample containers, age and gender on the CKD273 classifier. Results We observed a high consistency of the CKD273 classification scores across the different centres with areas under the curves ranging from 0.95 to 1.00. The classifier was independent of age (range tested 16-89 years) and gender. Furthermore, the use of different urine storage containers did not affect the classification scores. Analysis of the distribution of the individual peptides of the classifier over the nine different centres showed that fragments of blood-derived and extracellular matrix proteins were the most consistently found. Conclusion We provide for the first time validation of this urinary proteome-based classifier in a multicentre prospective setting and show the suitability of the CKD273 classifier to be used in the PRIORITY tria

NLP is a novel transcription regulator involved in VSG expression site control in Trypanosoma brucei

Trypanosoma brucei mono-allelically expresses one of approximately 1500 variant surface glycoprotein (VSG) genes while multiplying in the mammalian bloodstream. The active VSG is transcribed by RNA polymerase I in one of approximately 15 telomeric VSG expression sites (ESs). T. brucei is unusual in controlling gene expression predominantly post-transcriptionally, and how ESs are mono-allelically controlled remains a mystery. Here we identify a novel transcription regulator, which resembles a nucleoplasmin-like protein (NLP) with an AT-hook motif. NLP is key for ES control in bloodstream form T. brucei, as NLP knockdown results in 45- to 65-fold derepression of the silent VSG221 ES. NLP is also involved in repression of transcription in the inactive VSG Basic Copy arrays, minichromosomes and procyclin loci. NLP is shown to be enriched on the 177- and 50-bp simple sequence repeats, the non-transcribed regions around rDNA and procyclin, and both active and silent ESs. Blocking NLP synthesis leads to downregulation of the active ES, indicating that NLP plays a role in regulating appropriate levels of transcription of ESs in both their active and silent state. Discovery of the unusual transcription regulator NLP provides new insight into the factors that are critical for ES control

Disruption of PTH Receptor 1 in T Cells Protects against PTH-Induced Bone Loss

Hyperparathyroidism in humans and continuous parathyroid hormone (cPTH) treatment in mice cause bone loss by regulating the production of RANKL and OPG by stromal cells (SCs) and osteoblasts (OBs). Recently, it has been reported that T cells are required for cPTH to induce bone loss as the binding of the T cell costimulatory molecule CD40L to SC receptor CD40 augments SC sensitivity to cPTH. However it is unknown whether direct PTH stimulation of T cells is required for cPTH to induce bone loss, and whether T cells contribute to the bone catabolic activity of PTH with mechanisms other than induction of CD40 signaling in SCs.Here we show that silencing of PTH receptor 1 (PPR) in T cells blocks the bone loss and the osteoclastic expansion induced by cPTH, thus demonstrating that PPR signaling in T cells is central for PTH-induced reduction of bone mass. Mechanistic studies revealed that PTH activation of the T cell PPR stimulates T cell production of the osteoclastogenic cytokine tumor necrosis factor alpha (TNF). Attesting to the relevance of this effect, disruption of T cell TNF production prevents PTH-induced bone loss. We also show that a novel mechanism by which TNF mediates PTH induced osteoclast formation is upregulation of CD40 expression in SCs, which increases their RANKL/OPG production ratio.These findings demonstrate that PPR signaling in T cells plays an essential role in PTH induced bone loss by promoting T cell production of TNF. A previously unknown effect of TNF is to increase SC expression of CD40, which in turn increases SC osteoclastogenic activity by upregulating their RANKL/OPG production ratio. PPR-dependent stimulation of TNF production by T cells and the resulting TNF regulation of CD40 signaling in SCs are potential new therapeutic targets for the bone loss of hyperparathyroidism