Chamaedorea (xatÉ) in the Greater Maya Mountains and the chiquibul forest reserve, Belize: An economic assessment of a non-timber forest product

Of the twelve species ofChamaedorea palm recorded for Belize, three are of international economic value because their cut leaves (xaté) are traded in the floricultural industry. Traditionally, Belize has not harvested xaté, the industry being based in Mexico and Guatemala. However, a decline in wild xaté stocks in these countries means Guatemalan leaf harvesters now illegally harvest xaté in Belize. To assess the local abundance of the BelizeanChamaedorea resource, its economic value, and the extent to which it has been illegally harvested, 209 plots measuring 20 meters (m) by 20 m were established in the Greater Maya Mountains (GMM) in western Belize, which includes the Chiquibul Forest Reserve (CFR). We estimate that 37.8 million leaves with a value of U.S. 0.3 million to xateros have been extracted from the CFR. The standing export value is calculated as U.S.0.3 million to xateros have been extracted from the CFR. The standing export value is calculated as U.S. 1.8 million for the CFR and U.S. $5 million for the GMM.     

Tolerability and efficacy of single dose albendazole,diethylcarbamazine citrate (DEC) or co-administration of albendazole with DEC in the clearance of <Emphasis Type="Italic">Wuchereria bancrofti</Emphasis>in asymptomatic microfilaraemic volunteers in Pondicherry,South India: a hospital-based study

Background  

The tolerability and efficacy of single dose albendazole (400 mg), diethylcarbamazine citrate (DEC) (6 mg/kg bodyweight) or co-administration of albendazole (400 mg) + DEC (6 mg/kg bodyweight) was studied in 54 asymptomatic Wuchereria bancrofti microfilaraemic volunteers in a double blind hospital-based clinical study.     

The effect of sub-lethal ammonia exposure on fed and unfed rainbow trout: the role of glutamine in regulation of ammonia

Many species of fishes have evolved mechanisms for coping with ammonia caused by either high ammonia environments or an inability to excrete nitrogenous wastes. Rainbow trout (Oncorhynchus mykiss), have not been known to have such a mechanism. The present study investigated whether rainbow trout can use amino acid synthesis and storage to cope with ammonia. Experiments were performed on fed and unfed rainbow trout under both control and elevated ammonia conditions (0 and 10 mgN/l (total ammonia nitrogen), pH 7.2). The results indicate that both feeding and ammonia exposure increased plasma ammonia significantly 6 h postprandial and post ammonia exposure. After 48 h the fed/ammonia exposed fish had plasma ammonia levels that were not significantly different than the fed/control fish. Plasma ammonia was reduced by more than 50%, attributable to ammonia being converted to glutamine in brain, liver and muscle tissue. Feeding alone also increased glutamine levels in brain tissue. Activity of glutamine synthetase in brain and liver was increased corresponding to an increase in glutamine concentrations when fish were exposed to ammonia. This is the first report showing that rainbow trout can detoxify endogenous and exogenous ammonia.     

Increased 30-day and 1-year mortality rates and lower coronary revascularisation rates following acute myocardial infarction in patients with autoimmune rheumatic disease

IntroductionIt is now well-recognised that patients with autoimmune rheumatic disease (AIRD) have a predisposition to cardiovascular disease that results in increased morbidity and mortality. Following myocardial infarction (MI), patients with rheumatoid arthritis have been shown to have an increased case fatality rate; however, this has not been demonstrated in other forms of AIRD. The aim of this study was to compare case fatality rates following a first MI in patients with AIRD versus the general population. The secondary aim was to compare revascularisation treatment following MI in patients with AIRD versus the general population.MethodsA retrospective cohort study using two population-based linked databases was undertaken. Cases of first MI from July 2001 to June 2007 were identified based on International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, Australian Modification, codes. Thirty-day and one-year mortality rates were calculated (all-cause and cardiovascular causes of death). Logistic regression models were fitted to calculate the odds of mortality by AIRD status with adjustment for relevant characteristics.ResultsThere were 79,390 individuals with a first MI, of whom 1,409 (1.8%) had AIRD. After adjusting for relevant covariates, the odds ratio (OR) for 30-day cardiovascular mortality in patients with AIRD was 1.44 (95% confidence interval (CI): 1.25 to 1.66), and the OR for 12-month cardiovascular mortality was 1.71 (95% CI: 1.51 to 1.94). The 90-day adjusted odds of percutaneous transluminal coronary angioplasty and coronary artery bypass graft were significantly lower in the AIRD group compared with controls (OR: 0.81, 95% CI: 0.70 to 0.94, and OR: 0.52, 95% CI: 0.39 to 0.69, respectively).ConclusionsWe identified a higher risk-adjusted mortality rate for the majority of patients with AIRD at 30 days and 12 months after first MI. We also identified lower post-MI revascularisation rates in the AIRD group, suggesting there may be current gaps in cardiovascular treatment for patients with AIRD.

Electronic supplementary material

The online version of this article (doi:10.1186/s13075-015-0552-2) contains supplementary material, which is available to authorized users.     

Synthesis of quinolinate from D-aspartate in the mammalian liver-Escherichia coli quinolinate synthetase system.

Two proteins (A and B) from $\text{Escherichia coli}$ are required for the synthesis of the NAD precursor quinolinate from aspartate and dihydroxyacetone phosphate. Mammalian liver contains a FAD linked protein which replaces $\text{E. coli}$ B protein for quinolinate synthesis. D-aspartic acid but not L-aspartic acid is a substrate for quinolinic acid synthesis in a system composed of the B protein replacing activity of mammalian liver and $\text{E. coli}$ A protein. In contrast the $\text{E. coli}$ B protein-$\text{E. coli}$ A protein quinolinate synthetase system requires L-aspartic acid as substrate. The previous report that L-aspartate was a substrate in the liver-$\text{E. coli}$ system was due to contamination of commercially available [¹⁴C]L-aspartate with [¹⁴C]D-aspartate. These and other observations suggest that liver B protein is D-aspartate oxidase and $\text{E. coli}$ B protein is L-aspartate oxidase.     

Characterization of rat liver nuclear proteins which recognize the cAMP responsive element.

1. The data herein reveal the existence of cAMP-responsive element (CRE)-binding factors (CRF) in the nuclear extracts from cAMP-treated rat liver. 2. DNAase I and DMS footprinting analysis showed that the CRFs protected the CRE (-77 to -92) in the phosphoenolpyruvate carboxykinase (PEPCK) promoter and the TGACGTCA motif in a consensus oligodeoxynucleotide based on the sequence of the CRE's of 6 cAMP-regulated genes (C32mer). 3. Competition assays indicate that the CRF(s) is a CGTCA-specific, ATF/CREB-like factor(s). 4. Southwestern (SW) blot analysis detected 2 apparent CRFs which have molecular weights of about 30 and 32 kDa, respectively. 5. Based on the comparison of the size and binding specificity of the CRFs with the CREBs reported to date, the CRFs appear to be novel CRE-binding nuclear factors.     

Regulation of interleukin‐1β by interferon‐γ is species specific,limited by suppressor of cytokine signalling 1 and influences interleukin‐17 production

Reports describing the effect of interferon‐γ (IFNγ) on interleukin‐1β (IL‐1β) production are conflicting. We resolve this controversy by showing that IFNγ potentiates IL‐1β release from human cells, but transiently inhibits the production of IL‐1β from mouse cells. Release from this inhibition is dependent on suppressor of cytokine signalling 1. IL‐1β and Th17 cells are pathogenic in mouse models for autoimmune disease, which use Mycobacterium tuberculosis (MTB), in which IFNγ and IFNβ are anti‐inflammatory. We observed that these cytokines suppress IL‐1β production in response to MTB, resulting in a reduced number of IL‐17‐producing cells. In human cells, IFNγ increased IL‐1β production, and this might explain why IFNγ is detrimental for multiple sclerosis. In mice, IFNγ decreased IL‐1β and subsequently IL‐17, indicating that the adaptive immune response can provide a systemic, but transient, signal to limit inflammation.