The only significant adverse effect of obesity on renal transplant outcomes was an increase in wound complications, which were generally of minor consequence. Provided that adequate care is taken to avoid transplanting patients with significant cardiovascular disease, obese recipients can achieve excellent long-term patient and graft survivals that are on par with their nonobese counterparts. Denying patients access to renal transplantation on the basis of obesity per se does not appear to be justified.

These results support the role of binge drinking in reduced impulse control and decision-making deficits. The findings indicate that high-binge drinkers demonstrate impairments on an impulse control task similar to that observed in dependent samples and this may be a factor in understanding the negative behavioral consequences associated with excessive alcohol use.

No abstract

OBJECTIVE To report the use of a novel donor source as a further option to increase the number of patients who might be able to receive a renal transplant. PATIENTS AND METHODS Between May 1996 and July 2007, 43 kidneys were transplanted using kidneys obtained from patients with small (<3 cm diameter) incidentally detected tumours. After bench surgery to excise the tumour, they were all successfully transplanted into patients who were elderly or had significant comorbidities. RESULTS Apart from four patients who died from unrelated illnesses, all grafts continued to function with a median and mean follow‐up of 25 and 32 months. The follow‐up, which included 3‐monthly renal ultrasonography and chest X‐rays, showed only one case of tumour recurrence, which occurred 9 years after transplantation; the patient remains stable under observation after 18 months. CONCLUSIONS From our experience we consider that where nephrectomy is used for small, localized, incidentally detected renal tumours, the kidney should be considered for transplantation into carefully selected patients. Such patients with numerous medical comorbidities might benefit from renal transplantation, but not survive the waiting period if they are dependent on a deceased donor graft. Paradoxically the use of these marginal kidneys has the potential to increase the quality and length of life of these patients, despite the apparent contradiction of an intuitive principle of organ transplantation and immunosuppression.

In 2016, the Transplantation Society of Australia and New Zealand, with the support of the Australian Government Organ and Tissue authority, commissioned a literature review on the topic of infectious disease transmission from deceased donors to recipients of solid organ transplants. The purpose of this review was to synthesize evidence on transmission risks, diagnostic test characteristics, and recipient management to inform best-practice clinical guidelines. The final review, presented as a special supplement in Transplantation Direct, collates case reports of transmission events and other peer-reviewed literature, and summarizes current (as of June 2017) international guidelines on donor screening and recipient management. Of particular interest at the time of writing was how to maximize utilization of donors at increased risk for transmission of human immunodeficiency virus, hepatitis C virus, and hepatitis B virus, given the recent developments, including the availability of direct-acting antivirals for hepatitis C virus and improvements in donor screening technologies. The review also covers emerging risks associated with recent epidemics (eg, Zika virus) and the risk of transmission of nonendemic pathogens related to donor travel history or country of origin. Lastly, the implications for recipient consent of expanded utilization of donors at increased risk of blood-borne viral disease transmission are considered.

Canine T cell lymphoma has previously been found to be a poor prognostic indicator compared with its B cell counterpart. The cyclophosphamide, doxorubicin, vincristine, and prednisolone protocol is widely accepted as a first line treatment for canine lymphoma. There have been several studies investigating alternative protocols for T cell lymphoma. This study investigated the use of a modified lomustine, vincristine, procarbazine and prednisolone protocol as a first line treatment in 35 dogs with T Cell lymphoma. Median progression free survival (PFS) time for all 35 dogs was 431 days with a 6-month, 1-year, 2-year, and 3-year PFS of 69%, 54%, 29%, and 12%. Median survival time (MST) was 507 days. Twenty-nine dogs attained a complete response and had a median PFS time of 509 days. Thirty dogs experienced adverse events during the protocol, with 73% of these being grade 1 or 2. This protocol has shown increased median PFS time and MST compared with previous studies and suggests its use as a first line chemotherapy protocol against canine T cell lymphoma.

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Cutaneous squamous cell carcinomas (CSCC) are a common malignancy of keratinocytes that arise in sites of the skin exposed to excessive UV radiation. In the present study, we show that human SCC cell lines, preneoplastic solar keratoses (SK), and CSCC are associated with perturbations in glutathione peroxidase (GPX) activity and peroxide levels. Specifically, we found that two of three SKs and four of five CSCCs, in vivo, were associated with decreased GPX activity and all SKs and CSCCs were associated with an elevated peroxide burden. Given the association of decreased GPX activity with CSCC, we examined the basis for the GPX deficiency in the CSCCs. Our data indicated that GPX was inactivated by a posttranslational mechanism and that GPX could be inactivated by increases in intracellular peroxide levels. We next tested whether the decreased peroxidase activity coupled with an elevated peroxidative burden might contribute to CSCC formation in vivo. This was tested in Gpx1 À/À and Gpx2 À/À mice exposed to solar-simulated UV radiation. These studies showed that Gpx2 deficiency predisposed mice to UV-induced CSCC formation. These results suggest that inactivation of GPX2 in human skin may be an early event in UV-induced SCC formation. [Cancer Res 2007;67(10):4751-8]