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Background: Arboviruses are an emerging group of viruses that are causing increasing health concerns globally, including in Europe. Clinical presentation usually consists of a nonspecific febrile illness that may be accompanied by rash, arthralgia and arthritis, with or without neurological or haemorrhagic syndromes. The range of differential diagnoses of other infectious and noninfectious aetiologies is broad, presenting a challenge for physicians. While knowledge of the geographical distribution of pathogens and the current epidemiological situation, incubation periods, exposure risk factors and vaccination history can help guide the diagnostic approach, the nonspecific and variable clinical presentation can delay final diagnosis., Aims and Sources: This narrative review aims to summarize the main clinical and laboratory-based findings of the three most common imported arboviruses in Europe. Evidence is extracted from published literature and clinical expertise of European arbovirus experts., Content: We present three cases that highlight similarities and differences between some of the most common travel-related arboviruses imported to Europe. These include a patient with chikungunya virus infection presenting in Greece, a case of dengue fever in Turkey and a travel-related case of Zika virus infection in Romania., Implications: Early diagnosis of travel-imported cases is important to reduce the risk of localized outbreaks of tropical arboviruses such as dengue and chikungunya and the risk of local transmission from body fluids or vertical transmission. Given the global relevance of arboviruses and the continuous risk of (re)emerging arbovirus events, clinicians should be aware of the clinical syndromes of arbovirus fevers and the potential pitfalls in diagnosis., (Copyright © 2018. Published by Elsevier Ltd.)

Background: The frequency in which HIV and AIDS and mental health problems co-exist, and the complex bi-directional relationship between them, highlights the need for effective care models combining services for HIV and mental health. Here, we present a systematic review that synthesizes the literature on interventions and approaches integrating these services., Methods: This review was part of a larger systematic review on integration of services for HIV and non-communicable diseases. Eligible studies included those that described or evaluated an intervention or approach aimed at integrating HIV and mental health care. We searched multiple databases from inception until October 2015, independently screened articles identified for inclusion, conducted data extraction, and assessed evaluative papers for risk of bias., Results: Forty-five articles were eligible for this review. We identified three models of integration at the meso and micro levels: single-facility integration, multi-facility integration, and integrated care coordinated by a non-physician case manager. Single-site integration enhances multidisciplinary coordination and reduces access barriers for patients. However, the practicality and cost-effectiveness of providing a full continuum of specialized care on-site for patients with complex needs is arguable. Integration based on a collaborative network of specialized agencies may serve those with multiple co-morbidities but fragmented and poorly coordinated care can pose barriers. Integrated care coordinated by a single case manager can enable continuity of care for patients but requires appropriate training and support for case managers. Involving patients as key actors in facilitating integration within their own treatment plan is a promising approach., Conclusion: This review identified much diversity in integration models combining HIV and mental health services, which are shown to have potential in yielding positive patient and service delivery outcomes when implemented within appropriate contexts. Our review revealed a lack of research in low- and middle- income countries, and was limited to most studies being descriptive. Overall, studies that seek to evaluate and compare integration models in terms of long-term outcomes and cost-effectiveness are needed, particularly at the health system level and in regions with high HIV and AIDS burden., (© The Author 2017. Published by Oxford University Press in association with The London School of Hygiene and Tropical Medicine.)

Background: The incentivization of UK primary care through the Quality and Outcomes Framework (QOF) has released an unprecedented supply of data that in theory could aid health equity audit and reduce health inequalities. The current system allows for 'exception reporting' whereby patients can be excluded from calculation of payment for reasons such as failure to attend review. We speculated that such exclusions could be linked to socioeconomic deprivation., Methods: We assessed 'exception reporting' rates for 15 diabetes indicators using 2004/05 QOF data for 49 general practitioner (GP) practices in Brighton and Hove and related it to a deprivation ranking for each practice., Results: The standardized diabetes prevalence was 26% higher (P < 0.001) in the highest compared to the lowest quintile of deprivation. Correlations between 'exception reporting' and deprivation were seen for 10 of the 15 diabetes indicators (r = 0.20-0.41, P < 0.05). Practices with a more deprived patient population were more likely to report 'exceptions' for QOF indicators, although there was no such relationship with the achievement of QOF targets., Conclusions: Strategies to reduce health inequalities need to take into account that high levels of exception reporting, particularly in practices with deprived populations, may be disguising unmet need in those populations.

It has been proposed that low activities of antioxidant enzymes in pancreatic beta cells may increase their susceptibility to autoimmune attack. We have therefore used the spontaneously diabetic BB/S rat model of type 1 diabetes to compare islet catalase and superoxide dismutase activities in diabetes-prone and diabetes-resistant animals. In parallel studies, we employed the RINm5F beta cell line as a model system (previously validated) to investigate whether regulation of antioxidant enzyme activity by inflammatory mediators (cytokines, nitric oxide) occurs at the gene or protein expression level. Diabetes-prone rat islets had high insulin content at the age used (58-65 days) but showed increased amounts of DNA damage when subjected to cytokine or hydrogen peroxide treatments. There was clear evidence of oxidative damage in freshly isolated rat islets from diabetes-prone animals and significantly lower catalase and superoxide dismutase activities than in islets from age-matched diabetes-resistant BB/S and control Wistar rats. The mRNA expression of antioxidant enzymes in islets from diabetes-prone and diabetes-resistant BB/S rats and in RINm5F cells, treated with a combination of cytokines or a nitric oxide donor, DETA-NO, was analysed semi-quantitatively by real time PCR. The mRNA expression of catalase was lower, whereas MnSOD expression was higher, in diabetes-prone compared to diabetes-resistant BB/S rat islets, suggesting regulation at the level of gene expression as well as of the activities of these enzymes in diabetes. The protein expression of catalase, CuZnSOD and MnSOD was assessed by Western blotting and found to be unchanged in DETA-NO treated cells. Protein expression of MnSOD was increased by cytokines in RINm5F cells whereas the expression of CuZnSOD was slightly decreased and the level of catalase protein was unchanged. We conclude that there are some changes, mostly upregulation, in protein expression but no decreases in the mRNA expression of catalase, CuZnSOD or MnSOD enzymes in beta cells treated with either cytokines or DETA-NO. The lower antioxidant enzyme activities observed in islets from diabetes-prone BB/S rats could be a factor in the development of disease and in susceptibility to DNA damage in vitro and could reflect islet alterations prior to immune attack or inherent differences in the islets of diabetes-prone animals, but are not likely to result from cytokine or nitric oxide exposure in vivo at that stage.

Pancreatic beta-cells have low activities of the antioxidant enzyme catalase. Nitric oxide interacts with the haem group of catalase inhibiting its activity. We have studied the activity of catalase in beta-cells under conditions mimicking prediabetes and in which nitric oxide is generated from cytokine treatment in vitro. We also studied whether there is regulation of catalase enzyme activity by nitric oxide at the protein or gene expression level. RINm5F insulin-producing cells, treated for 24 h with cytokines, showed increased medium nitrite production (17+/-2.2 vs 0.3+/-0.2 pmol/ micro g protein) and significantly decreased cellular catalase activity (42.4+/-4.5%) compared with control cells. A similar reduction was seen in catalase-overexpressing RIN-CAT cells and in rat or human pancreatic islets of Langerhans. Catalase activity was also suppressed by the long-acting nitric oxide donor diethylenetriamine/nitric oxide adduct (Deta-NO) and this inhibition was reversible. The inhibition of catalase activity by cytokines in RINm5F cells was significantly reversed by the addition of the nitric oxide synthase 2 (NOS2) inhibitors nitro monomethylarginine or N-(3-(aminomethyl)benzyl)acetamidine (1400W). Protein expression was found to be unchanged in cytokine- or Deta-NO-treated RINm5F cells, while mRNA expression was marginally increased. We have shown that inhibition of catalase activity by cytokines is nitric oxide dependent and propose that this inhibition may confer increased susceptibility to cytokine- or nitric oxide-induced cell killing.