Market Discounts for Sinks: A Concept for Restricting Forest Contributions in Accounting for Emission Reductions?

Forests are capable of the best and the worst when greenhouse gases are at stake. Their controversial contribution for helping developed countries to reach their emission reduction targets is largely responsible for the November 2000 failure of the Kyoto Protocol being enforced in the near future. Regarding the unit price of emission credits for fossil fuels, future transactions for carbon offsets associated with land use change and forestry projects may well reveal market discounts due to risks and uncertainties related to their evaluation and management. The author proposes to apply these market discounts for assessing "at intergovernmental level" the the 'contributive' value of forestry activities eligible for meeting countries' emission reduction targets. This proposal is preceded by an outline of the position of the forestry projects within the Kyoto treaty, as well as by an outlook on the establishment of a market for carbon offsets. Indications are given for correcting emission reductions and removal assessments by adjustments that are required when assuming that the true contributive value of one CO2-e ton to be retained may vary (1) according to the uncertainty degree associated to evaluations and (2) that this degree is closely related to project features and origins. Fixing consensual rules for consideration and quantification of uncertainties associated with carbon uptakes and removal evaluations, including market appraisals as a last resort, has the potential of moving international negotiations from divergences in the eligibility of activities towards verification and penalty, in short to policing the Protocol. The chances for the treaty to be effective and successful would then be enhanced

Paediatric and adolescent athletes in Switzerland: age-adapted proposals for pre-participation cardiovascular evaluation

High-level sports competition is popular among Swiss youth. Even though preparticipation evaluation for competitive athletes is widespread, screening strategies for diseases responsible for sudden death during sport are highly variable. Hence, we sought to develop age-specific preparticipation cardiovascular evaluation (PPCE) proposals for Swiss paediatric and adolescent athletes (under 18 years of age). We recommend that all athletes practising in a squad with a training load of at least 6 hours per week should undergo PPCE based on medical history and physical examination from the age of 12 years on. Prior to 12 years, individual judgement of athletic performance is required. We suggest the inclusion of a standard 12-lead electrocardiogram (ECG) evaluation for all post-pubertal athletes (or older than 15 years) with analysis in accordance with the International Criteria for ECG Interpretation in Athletes. Echocardiography should not be a first-line screening tool but rather serve for the investigation of abnormalities detected by the above strategies. We recommend regular follow-up examinations, even for those having normal history, physical examination and ECG findings. Athletes with an abnormal history (including family history), physical examination and/or ECG should be further investigated and pathological findings discussed with a paediatric cardiologist. Importantly, the recommendations provided in this document are not intended for use among patients with congenital heart disease who require individualised care according to current guidelines

Diagnostic yield and cost analysis of electrocardiographic screening in Swiss paediatric athletes

OBJECTIVES Athletes performing sports on high level are at increased risk for sudden cardiac death. This includes paediatric athletes, even though data on screening strategies in this age group remain scarce. This study aimed to assess electrocardiogram interpretation criteria in paediatric athletes and to evaluate the cost of screening. METHODS National, multicentre, retrospective, observational study on 891 athletes of paediatric age (<18 years) evaluated by history, physical examination and 12-lead electrocardiogram. The primary outcome measure was abnormal electrocardiogram findings according to the International Recommendations for Electrographic Interpretation in Athletes. The secondary outcome measure was cost of screening. RESULTS 19 athletes (2.1%) presented abnormal electrocardiogram findings requiring further investigations, mainly abnormal T-wave inversion. These 19 athletes were predominantly males, performing endurance sports with a mean volume of 10 weekly hours for a mean duration of 6 years of training. Further investigations did not identify any relevant pathology. All athletes were cleared for competition with regular follow-up. Total costs of the screening were 108,860 USD (122 USD per athlete). CONCLUSIONS Our study using the International Recommendations for Electrographic Interpretation in Athletes identified a low count of abnormal findings in paediatric athletes, yet raising substantially the cost of screening. Hence, the utility of electrocardiogram-inclusive screening of paediatric athletes remains to be elucidated by longitudinal data

Tropheryma whipplei tricuspid endocarditis: a case report and review of the literature

INTRODUCTION: The main clinical manifestations of Whipple's disease are weight loss, arthropathy, diarrhea and abdominal pain. Cardiac involvement is frequently described. However, endocarditis is rare and is not usually the initial presentation of the disease. To the best of our knowledge, this is the first reported case of a patient with Tropheryma whipplei tricuspid endocarditis without any other valve involved and not presenting signs of arthralgia and abdominal involvement. CASE PRESENTATION: We report a case of a 50-year-old Caucasian man with tricuspid endocarditis caused by Tropheryma whipplei, showing signs of severe shock and an absence of other more classic clinical signs of Whipple's disease, such as arthralgia, abdominal pain and diarrhea. Tropheryma whipplei was documented by polymerase chain reaction of the blood and pleural fluid. The infection was treated with a combined treatment of doxycycline, hydroxychloroquine and sulfamethoxazole-trimethoprim for one year. CONCLUSION: Tropheryma whipplei infectious endocarditis should always be considered when facing a blood-culture negative endocarditis particularly in right-sided valves. Although not standardized yet, treatment of Tropheryma whipplei endocarditis should probably include a bactericidal antibiotic (such as doxycycline) and should be given over a prolonged period of time (a minimum of one year)

A short purification process for quantitative isolation of PrP(Sc) from naturally occurring and experimental transmissible spongiform encephalopathies

BACKGROUND: Transmissible spongiform encephalopathies (TSEs) are neurodegenerative diseases affecting both humans and animals. They are associated with post-translational conversion of the normal cellular prion protein (PrP(C)) into a heat- and protease-resistant abnormal isoform (PrP(Sc)). Detection of PrP(Sc) in individuals is widely utilized for the diagnosis of prion diseases. METHODS: TSE brain tissue samples have been processed in order to quantitatively isolate PrP(Sc). The protocol includes an initial homogenization, digestion with proteinase K and salt precipitation. RESULTS: Here we show that over 97 percent of the PrP(Sc) present can be precipitated from infected brain material using this simple salting-out procedure for proteins. No chemically harsh conditions are used during the process in order to conserve the native quality of the isolated protein. CONCLUSION: The resulting PrP(Sc)-enriched preparation should provide a suitable substrate for analyzing the structure of the prion agent and for scavenging for other molecules with which it may associate. In comparison with most methods that exist today, the one described in this study is rapid, cost-effective and does not demand expensive laboratory equipment

Argonaute2 Suppresses Drosophila Fragile X Expression Preventing Neurogenesis and Oogenesis Defects

Fragile X Syndrome is caused by the silencing of the Fragile X Mental Retardation gene (FMR1). Regulating dosage of FMR1 levels is critical for proper development and function of the nervous system and germ line, but the pathways responsible for maintaining normal expression levels are less clearly defined. Loss of Drosophila Fragile X protein (dFMR1) causes several behavioral and developmental defects in the fly, many of which are analogous to those seen in Fragile X patients. Over-expression of dFMR1 also causes specific neuronal and behavioral abnormalities. We have found that Argonaute2 (Ago2), the core component of the small interfering RNA (siRNA) pathway, regulates dfmr1 expression. Previously, the relationship between dFMR1 and Ago2 was defined by their physical interaction and co-regulation of downstream targets. We have found that Ago2 and dFMR1 are also connected through a regulatory relationship. Ago2 mediated repression of dFMR1 prevents axon growth and branching defects of the Drosophila neuromuscular junction (NMJ). Consequently, the neurogenesis defects in larvae mutant for both dfmr1 and Ago2 mirror those in dfmr1 null mutants. The Ago2 null phenotype at the NMJ is rescued in animals carrying an Ago2 genomic rescue construct. However, animals carrying a mutant Ago2 allele that produces Ago2 with significantly reduced endoribonuclease catalytic activity are normal with respect to the NMJ phenotypes examined. dFMR1 regulation by Ago2 is also observed in the germ line causing a multiple oocyte in a single egg chamber mutant phenotype. We have identified Ago2 as a regulator of dfmr1 expression and have clarified an important developmental role for Ago2 in the nervous system and germ line that requires dfmr1 function

Ligand Binding and Hydration in Protein Misfolding: Insights from Studies of Prion and p53 Tumor Suppressor Proteins†

Protein misfolding has been implicated in a large number of diseases termed protein- folding disorders (PFDs), which include Alzheimer’s disease, Parkinson’s disease, transmissible spongiform encephalopathies, familial amyloid polyneuropathy, Huntington’s disease, and type II diabetes. In these diseases, large quantities of incorrectly folded proteins undergo aggregation, destroying brain cells and other tissues