Histologic evidence indicates southern Africa as the origin of the amphibian chytrid fungus.

This paper reports the results of a "cost-of-illness" study of low back pain (LBP) in Australian adults. It estimates the direct cost of LBP in 2001 to be AU dollars 1.02 billion. Approximately 71% of this amount is for treatment by chiropractors, general practitioners, massage therapists, physiotherapists and acupuncturists. However, the direct costs are minor compared to the indirect costs of AU dollars 8.15 billion giving a total cost of AU dollars 9.17 billion. LBP in Australian adults represents a massive health problem with a significant economic burden. This burden is so great that it has compelling and urgent ramifications for health policy, planning and research. This study identifies that research should concentrate on both direct but particularly the indirect costs including cost-effective management regimes that encourage an early return to duties.

AimsThis randomized controlled trial (RCT) evaluated whether a process with single combined testing of copeptin and troponin at admission in patients with low-to-intermediate risk and suspected acute coronary syndrome (ACS) does not lead to a higher proportion of major adverse cardiac events (MACE) than the current standard process (non-inferiority design).Methods and resultsA total of 902 patients were randomly assigned to either standard care or the copeptin group where patients with negative troponin and copeptin values at admission were eligible for discharge after final clinical assessment. The proportion of MACE (death, survived sudden cardiac death, acute myocardial infarction (AMI), re-hospitalization for ACS, acute unplanned percutaneous coronary intervention, coronary artery bypass grafting, or documented life threatening arrhythmias) was assessed after 30 days. Intention to treat analysis showed a MACE proportion of 5.17% [95% confidence intervals (CI) 3.30–7.65%; 23/445] in the standard group and 5.19% (95% CI 3.32–7.69%; 23/443) in the copeptin group. In the per protocol analysis, the MACE proportion was 5.34% (95% CI 3.38–7.97%) in the standard group, and 3.01% (95% CI 1.51–5.33%) in the copeptin group. These results were also corroborated by sensitivity analyses. In the copeptin group, discharged copeptin negative patients had an event rate of 0.6% (2/362).ConclusionAfter clinical work-up and single combined testing of troponin and copeptin to rule-out AMI, early discharge of low- to intermediate risk patients with suspected ACS seems to be safe and has the potential to shorten length of stay in the ED. However, our results need to be confirmed in larger clinical trials or registries, before a clinical directive can be propagated.

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In the early 1990s stream-associated amphibian populations in tropical upland North Queensland experienced severe declines resulting in extinction of three species, local elimination of four species, marked reductions in one species and apparently no declines in other species, Chytridiomycosis, a disease due to the amphibian chytrid fungus, Batrachochylrium dendrobatidis, was the likely cause of this epidemic. We conducted a monitoring study for chytridiomycosis in four species of frogs in North Queensland from October 1998 to October 2002 by collecting specimens in the field and using histology of removed digits to diagnose chytridiomycosis. Chytridiomycosis was diagnosed in 112 (7,1%) of the 1 578 specimens and prevalence was significantly associated with season and altitude, with higher prevalences in winter and above 300 metres altitude. A multivariate model adjusting for potential confounding effects arising from the sampling process demonstrated a significant decline in the time trend of prevalence of chytridiomycosis. The study supports the hypothesis that B. dendrobatidis becomes endemic after the initial epidemic wave. Since the surviving species of stream-associated frog, Litoria genimaculata, has increased to pre-decline numbers, the decline in prevalence of chytridiomycosis is evidence of a changed pathogen-host relationship. The reasons for this change are speculative but could be due to an increase in innate host resistance in response to selection pressure by B. dendrobatidis or to lower rainfall associated with an EI Nino effect. These findings justify management strategies that assist susceptible amphibian species to survive an initial epidemic wave of chytridiomycosis.

This study suggests that plasma D-dimer can play a role in the diagnosis and prognosis of AAA.

The topic of interference of pacemakers by mobile phones has evoked a surprisingly strong interest, not only in pacemaker patients, but also in the public opinion. The latter is the more surprising, as in the past, the problem of interference has scarcely found the attention that it deserves in the interest of the patient. It was the intention of our investigation to test as many pacemaker models as possible to determine whether incompatibility with mobile phones of different modes may exist, using an in vitro measuring setup. We had access to 231 different models of 20 manufacturers. During the measurements, a pulse generator together with a suitable lead was situated in a 0.9 g/L saline solution, and the antenna of a mobile phone was positioned as close as possible. If the pulse generator was disturbed, the antenna was elevated until interference ceased. The gap in which interference occurred was defined as "maximum interference distance." All three nets existing in Germany, the C-net (450 MHz, analogue), the D-net (900 MHz, digital pulsed), and the E-net (1,800 MHz, digital pulsed) were tested in succession. Out of 231 pulse generator models, 103 pieces corresponding to 44.6% were influenced either by C- or D-net, if both results were totaled. However, this view is misleading as no patient will use C- and D-net phones simultaneously. Separated into C- or D-net interference, the result is 30.7% for C or 34.2% for D, respectively, of all models tested. The susceptible models represent 18.6% or 27% of today's living patients, respectively. All models were resistant to the E-net. With respect to D-net phones, all pacemakers of six manufacturers proved to be unaffected. Eleven other manufacturers possessed affected and unaffected models as well. A C-net phone only prolonged up to five pacemaker periods within 10 seconds during dialing without substantial impairment to the patient. Bipolar pacemakers are as susceptible as unipolar ones. The following advice for patients and physicians can be derived from our investigations: though 27% of all patients may have problems with D-net phones (not C- or E-net), the application should generally not be questioned. On the contrary, patients with susceptible devices should be advised that a distance of 20 cm is sufficient to guarantee integrity of the pacemaker with respect to hand held phones. Portables, on the other hand, should have a distance of about 0.5 m. Pacemaker patients really suffering from mobile phones are very rare unless the phone is just positioned in the pocket over the pulse generator. The contralateral pocket or the belt position guarantees, in 99% of all patients, undisturbed operation of the pacemaker. A risk analysis reveals that the portion of patients really suffering from mobile phones is about 1 out of 100,000. Nevertheless, it would be desirable in the future if implanting physicians would use only pacemakers with immunity against mobile phones as guaranteed by the manufacturers.