2010 Canadian Cardiovascular Society/Canadian Society of Echocardiography Guidelines for Training and Maintenance of Competency in Adult Echocardiography

Guidelines for the provision of echocardiography in Canada were jointly developed and published by the Canadian Cardiovascular Society and the Canadian Society of Echocardiography in 2005. Since their publication, recognition of the importance of echocardiography to patient care has increased, along with the use of focused, point-of-care echocardiography by physicians of diverse clinical backgrounds and variable training. New guidelines for physician training and maintenance of competence in adult echocardiography were required to ensure that physicians providing either focused, point-of-care echocardiography or comprehensive echocardiography are appropriately trained and proficient in their use of echocardiography. In addition, revision of the guidelines was required to address technological advances and the desire to standardize echocardiography training across the country to facilitate the national recognition of a phy sician's expertise in echocardiography. This paper summarizes the new Guidelines for Physician Training and Maintenance of Competency in Adult Echocardiography, which are considerably more comprehensive than earlier guidelines and address many important issues not previously covered. These guidelines provide a blueprint for physician training despite different clinical backgrounds and help standardize physician training and training programs across the country. Adherence to the guidelines will ensure that physicians providing echocardiography have acquired sufficient expertise required for their specific practice. The document will also provide a framework for other national societies to standardize their training programs in echocardiography and will provide a benchmark by which competency in adult echocardiography may be measured.     

Activation of ERK and Akt Signaling in Focal Cerebral Ischemia: Modulation by TGF-α and Involvement of NMDA Receptor

Cerebral ischemia activates ERK and Akt pathways. We studied whether these activations were affected by treatment with the protective growth factor transforming growth factor-α (TGF-α), and whether they were mediated through N-methyl -aspartate (NMDA) receptors. The middle cerebral artery was occluded in rats and signaling was studied 1 h later. Noncompetitive NMDA receptor antagonist MK-801 was injected i.p. before the occlusion, whereas in other rats TGF-α was given intraventricularly before and after occlusion. Ischemia caused ERK phosphorylation in the nucleus, localized in the endothelium and neurons. Phosphorylation of ERK was prevented by TGF-α, but it was enhanced in the nucleus and cytoplasm by MK-801. Also, MK-801 but not TGF-α increased p-Akt. Results suggest that preventing ERK activation is related to the protective effect of TGF-α, whereas the protective effect of MK-801 is associated with activation of pro-survival Akt. While results support that NMDA receptor signaling precludes Akt activation, we did not find evidence to support that it underlies ischemia-induced ERK phosphorylation. This study illustrates that neuroprotection results from a fine balance between death and survival signaling pathways.     

Association of herpesviruses in the aqueous humor of patients with serpiginous choroiditis: a polymerase chain reaction-based study

Purpose: To determine the presence of herpesvirus DNA in the aqueous humor (AH) of patients with serpiginous choroiditis using polymerase chain reaction (PCR). Methods: AH from nine patients previously diagnosed with serpiginous choroiditis were investigated for herpes simplex virus (HSV), varicella zoster virus (VZV), and cytomegalovirus (CMV) by conventional virological methods and PCR. The PCR-positive DNA was gel-purified, extracted, and sequenced using a dye-based Applied Biosystems procedure. The sequences were processed through the National Cancer Institute’s BLAST inquiry for species identification. Results: Culture and cytological examination of AH from all nine patients were negative for HSV,VZV, and CMV. Five were positive for VZV, one was positive for HSV, and three were wholly negative using PCR. Subsequent DNA sequencing of the positive samples authenticated the presence of VZV and HSV DNA in the respective patients. Conclusion: VZV and HSV DNA were detected in a subset of patients with serpiginous choroiditis, suggesting that these viruses may function in the pathogenesis of this disease.     

Protonectin (1-6): A novel chemotactic peptide from the venom of the social wasp Agelaia pallipes pallipes

Peptides constitute the largest group of Hymenoptera venom toxins; some of them interact with GPCR, being involved with the activation of different types of leukocytes, smooth muscle contraction and neurotoxicity. Most of these toxins vary from dodecapeptides to tetradecapeptides, amidated at their C-teminal amino acid residue. The venoms of social wasps can also contains some tetra-, penta-, hexa- and hepta-peptides, but just a few of them have been structurally and functionally characterized up to now. Protonectin (ILGTILGLLKGL-NH₂) is a polyfunctional peptide, presenting mast cell degranulation, release of lactate dehydrogenase (LDH) from mast cells, antibiosis against Gram-positive and Gram-negative bacteria and chemotaxis for polymorphonucleated leukocytes (PMNL), while Protonectin (1-6) (ILGTIL-NH₂) only presents chemotaxis for PMNL. However, the mixture of Protonectin (1-6) with Protonectin in the molar ratio of 1:1 seems to potentiate the biological activities dependent of the membrane perturbation caused by Protonectin, as observed in the increasing of the activities of mast cell degranulation, LDH releasing from mast cells, and antibiosis. Despite both peptides are able to induce PMNL chemotaxis, the mixture of them presents a reduced activity in comparison to the individual peptides. Apparently, when mixed both peptides seems to form a supra-molecular structure, which interact with the receptors responsible for PMNL chemotaxis, disturbing their individual docking with these receptors. In addition to this, a comparison of the sequences of both peptides suggests that the sequence ILGTIL is conserved, suggesting that it must constitute a linear motif for the structural recognition by the specific receptor which induces leukocytes migration.     

Trajectories of social isolation in adult survivors of childhood cancer

Purpose

Long-term childhood cancer survivors may be at increased risk for poor social outcomes as a result of their cancer treatment, as well as physical and psychological health problems. Yet, important challenges, namely social isolation, are not well understood. Moreover, survivors' perspectives of social isolation as well as the ways in which this might evolve through young adulthood have yet to be investigated. The purpose of this research was to describe the trajectories of social isolation experienced by adult survivors of a childhood cancer.

Methods

Data from 30 in-depth interviews with survivors (9 to 38 years after diagnosis, currently 22 to 43 years of age, 60 % women) were analyzed using qualitative, constant comparative methods.

Results

Experiences of social isolation evolved over time as survivors grew through childhood, adolescence and young adulthood. Eleven survivors never experienced social isolation after their cancer treatment, nor to the present day. Social isolation among 19 survivors followed one of three trajectories; (1) diminishing social isolation: it got somewhat better, (2) persistent social isolation: it never got better or (3) delayed social isolation: it hit me later on.

Conclusions

Knowledge of when social isolation begins and how it evolves over time for different survivors is an important consideration for the development of interventions that prevent or mitigate this challenge.

Implications for Cancer Survivors

Assessing and addressing social outcomes, including isolation, might promote comprehensive long-term follow-up care for childhood cancer survivors.     

m-Trifluoromethyl diphenyl diselenide attenuates glutaric acid-induced seizures and oxidative stress in rat pups: involvement of the γ-aminobutyric acidergic system

Glutaric acidemia type I (GA-I) is an inherited metabolic disease characterized by accumulation of glutaric acid (GA) and seizures. The intrastriatal GA administration in rats has been used as an animal model to mimic seizures presented by glutaric acidemic patients. m-Trifluoromethyl diphenyl diselenide, (m-CF(3) -C(6) H(4) Se)(2) , is an organoselenium compound that protects against seizures induced by pentylenetetrazole in mice. Thus, the aim of this study was to investigate whether (m-CF(3) -C(6) H(4) Se)(2) is effective against GA-induced seizures and oxidative stress in rat pups 21 days of age. Our findings demonstrate that (m-CF(3) -C(6) H(4) Se)(2) preadministration (50 mg/kg; p.o.) protected against the reduction in latency and the increased duration of GA (1.3 μmol/right striatum)-induced seizures in rat pups. In addition, (m-CF(3) -C(6) H(4) Se)(2) protected against the increase in reactive species generation and the reduction in antioxidant defenses glutathione peroxidase and glutathione S-transferase activities induced by GA. By contrast, no change in glutathione reductase or catalase activities was found. In addition, (m-CF(3) -C(6) H(4) Se)(2) was effective in protecting against inhibition of Na(+) ,K(+) -ATPase activity caused by GA in striatum of rat pups. This study showed for the first time that GA administration caused an increase in [(3) H]GABA uptake from striatum slices of rat pups and that (m-CF(3) -C(6) H(4) Se)(2) preadministration protected against this increase. A positive correlation between duration of seizures and [(3) H]GABA uptake levels was demonstrated. The results indicate that (m-CF(3) -C(6) H(4) Se)(2) protected against GA-induced seizures. Moreover, these findings suggest that the protection against oxidative stress, the inhibition of Na(+) ,K(+) -ATPase activity, and the increase in [(3) H]GABA uptake are possible mechanisms for the potential anticonvulsant action of (m-CF(3) -C(6) H(4) Se)(2).