Mounting evidence implicates the disease chytridiomycosis, caused by the fungus Batrachochytrium dendrobatidis, in global amphibian declines and extinctions. While the virulence of this disease has been clearly demonstrated, there is, as yet, no mechanistic explanation for how B. dendrobatidis kills amphibians. To investigate the pathology of chytridiomycosis, blood samples were collected from uninfected, aclinically infected and clinically diseased amphibians and analyzed for a wide range of biochemical and hematological parameters. Here, we show that green tree frogs Litoria caerulea with severe chytridiomycosis had reduced plasma osmolality, sodium, potassium, magnesium and chloride concentrations. Stable plasma albumin, hematocrit and urea levels indicated that hydration status was unaffected, signifying depletion of electrolytes from circulation rather than dilution due to increased water uptake. We suggest that B. dendrobatidis kills amphibians by disrupting normal epidermal functioning, leading to osmotic imbalance through loss of electrolytes. Determining how B. dendrobatidis kills amphibians is fundamental to understanding the hostpathogen relationship and thus the population declines attributed to B. dendrobatidis. Understanding the mechanisms of mortality may also explain interspecific variation in susceptibility to chytridiomycosis. KEY WORDS:Amphibian declines · Chytridiomycosis · Batrachochytrium dendrobatidis · Pathogenesis · Mortality · Osmoregulation Resale or republication not permitted without written consent of the publisherDis Aquat Org 77: [113][114][115][116][117][118] 2007 Amphibian skin is well studied due to its unique functions (Deyrup 1964, Heatwole & Barthalmus 1994, Jorgensen 1997. The integument is a site of regulated transport for water, ions (electrolytes) and respiratory gases (Deyrup 1964, Heatwole & Barthalmus 1994, Jorgensen 1997. Permeability of frog skin varies over the body surface of an individual and also among species (Deyrup 1964, Heatwole & Barthalmus 1994. In some species osmotic permeability is greatest in an area of ventral integument commonly referred to as the pelvic patch (Czopek 1965, Baldwin 1974, Word & Hillman 2005, where there is dense cutaneous vasculature (Czopek 1965). Concomitantly, Batrachochytrium dendrobatidis occurs more commonly and at higher density in the ventral integument of infected frogs (Berger et al. 2005b, Puschendorf & Bolaños 2006. B. dendrobatidis grows within the keratinized cells of the superficial epidermis and causes irregular skin sloughing, hyperplasia and hyperkeratosis (Berger et al. 1998, 2005b, 2007. Other pathological changes including cytoplasmic degeneration and vacuolation in scattered cells have been observed by light and electron microscopy, but these changes are not usually severe (Berger et al. 2007). Thus, it is unclear how a superficial skin infection kills frogs.The aim of this research was to investigate pathogenesis in amphibians with chytridiomycosis. We evaluated changes in physiological parameters...

This study investigated the effects of cold water immersion on recovery from anaerobic cycling. Seventeen (13 male, 4 female) active subjects underwent a crossover, randomised design involving two testing sessions 2 - 6 d apart. Testing involved two 30-s maximal cycling efforts separated by a one-hour recovery period of 10-min cycling warm-down followed by either passive rest or 15-min cold water immersion (13 - 14 degrees C) with passive rest. Peak power, total work and postexercise blood lactate were significantly reduced following cold water immersion compared to the first exercise test and the control condition. These variables did not differ significantly between the control tests. Peak exercise heart rate was significantly lower after cold water immersion compared to the control. Time to peak power, rating of perceived exertion, and blood pH were not affected by cold water immersion compared to the control. Core temperature rose significantly (0.3 degrees C) during ice bath immersion but a similar increase also occurred in the control condition. Therefore, cold water immersion caused a significant decrease in sprint cycling performance with one-hour recovery between tests.

Nephrin is a 180 KD trans-membrane protein expressed in glomerular podocytes. It was first identified in children with congenital nephrotic syndrome of the Finnish type (NPHS1). Nephrin forms an integral part of podocytes, which—together with endothelial cells and the basement—form the glomerular filtration barrier. Podocytopathies result in the detection of nephrin in the urine. We reviewed the literature to determine if urine nephrin measurements could become useful as a biomarker to detect early podocyte injury. Our search identified a total of 19 studies that have been published to date. The most common clinical conditions for which urine nephrin analyses were carried out included diabetic nephropathy, glomerulonephritis and pre-eclampsia. Nephrin measurement was carried out using commercially available ELISA kits, the messenger ribonucleic acid real-time polymerase chain Reaction, or electrophoresis. Nephrinuria showed positive correlation with proteinuria and severity of podocyte injury. In two studies, the level of nephrinuria declined in conjunction with clinical improvement in the patient following immunosuppressive treatment. Currently, there is no published data on the value of measuring urinary nephrin in pediatric patients.

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A new nondepolarizing, normokalemic adenosine-lidocaine arrest solution in Krebs-Henseleit buffer with 10-mmol/L glucose was versatile at both 4 degrees C and 28 degrees C to 30 degrees C relative to Celsior, and the addition of 1-mmol/L pyruvate significantly improved cardiac output at warmer arrest temperatures. This new arrest paradigm may be useful in the harvest, storage, and implantation of donor hearts.

Retinopathy of prematurity (ROP), a vasoproliferative disorder exclusive to premature infants is an important cause of childhood blindness. The number of premature infants surviving with this condition is expected to increase globally. Animal models of oxygen-induced retinopathy studies have shown vascular endothelial growth factor (VEGF) to be a key player in the pathogenesis of ROP. This has led to increased use of VEGF antagonist as an alternative treatment for ROP. The purpose of this systematic review is to determine the association between VEGF and ROP in human newborn. The literature review identified 12 studies to date which fulfilled the search criteria. Investigators used cord blood, serum, plasma and tissue samples to investigate the association between ROP and VEGF. Studies that measured VEGF in cord blood found mixed results, with low VEGF (at birth) associated with ROP in one study and no difference noted in two others. Mixed results were also seen in studies determining VEGF in postnatal venous samples. Four studies showed no difference in VEGF level between premature infants with and without ROP, one study showed an increased VEGF level in premature infants with ROP and another study found serum VEGF to be low in premature infants with ROP. The most recent study demonstrated an initial increase in serum VEGF followed by a decline at the time of treatment. These contradictory results indicate that we are yet to fully understand the role of VEGF in human premature infants and question the rationale of treating ROP with anti-VEGF. Anti-VEGF therapy results in systemic effect on serum VEGF levels for up to 2 months and this could have an effect on neurodevelopmental outcome. The effect of this on other developing organs is currently unknown. More studies are required to determine the mechanistic relationships between systemic VEGF and ROP in premature infants.

The persistent rise in global incidence of type 2 diabetes (T2D) continues to have significant public health and economic implications. The availability of relevant animal models of T2D is critical to elucidating the complexity of the pathogenic mechanisms underlying this disease and the implications this has on susceptibility to T2D complications. Whilst many high-fat diet-induced rodent models of obesity and diabetes exist, growing appreciation of the contribution of high glycaemic index diets on the development of hyperglycaemia and insulin resistance highlight the requirement for animal models that more closely represent global dietary patterns reflective of modern society. To that end, we sought to develop and validate a murine model of T2D based on consumption of an energy-dense diet containing moderate levels of fat and a high glycaemic index to better reflect the aetiopathogenesis of T2D. Male C57BL/6 mice were fed an energy-dense (ED) diet and the development of pathological features used in the clinical diagnosis of T2D was assessed over a 30-week period. Compared with control mice, 87% of mice fed an ED diet developed pathognomonic signs of T2D including glucose intolerance, hyperglycaemia, glycosylated haemoglobin (HbA1c) and glycosuria within 30 weeks. Furthermore, dyslipidaemia, chronic inflammation, alterations in circulating leucocytes and renal impairment were also evident in ED diet-fed mice compared with mice receiving standard rodent chow. Longitudinal profiling of metabolic and biochemical parameters provide support of an aetiologically and clinically relevant model of T2D that will serve as a valuable tool for mechanistic and therapeutic studies investigating the pathogenic complications of T2D.

Rewarming the rat heart after cold static storage in polarizing adenosine-lidocaine arrest solution resulted in significantly higher aortic flow, coronary flow, and cardiac output compared with that seen after Krebs-Henseleit or Celsior rewarming. Rewarming cold Celsior hearts with adenosine-lidocaine solution reduced stunning. Adenosine-lidocaine cardioplegia might offer a new reperfusion strategy after cold static storage.