Knowledge of the CSF pathways holds implications for our ability to understand, prognose, and even treat diseases related to CSF circulation and so is a matter of considerable relevance to neuroradiology and neurology.

Background Mortality in patients with HIV infection is increasingly due to comorbid medical conditions. Research on how adherence to medications for comorbidities relates to antiretroviral (ARV) medication adherence and how interrelations between illness perceptions and medication beliefs about HIV and comorbidities affect medication adherence is needed to inform adherence interventions. Methods HIV-infected adults with hypertension (n=151) or chronic kidney disease (CKD; n=41) were recruited from ambulatory practices at an academic medical center. Illness perceptions and medication beliefs about HIV and hypertension or CKD were assessed and adherence to one ARV medication and one medication for either hypertension or CKD was electronically monitored for ten weeks. Results Rates of taking, dosing, and timing adherence to ARV medication did not differ from adherence to medication for hypertension or CKD, with the exception that patients were more adherent to the timing of their ARV (78%) than to the timing of their anti-hypertensive (68%;p=0.01]. Patients viewed HIV as better understood, more chronic, having more negative consequences, and eliciting more emotions, compared to hypertension. Patients viewed ARVs as more necessary than medication for hypertension or CKD. Having a realistic view of the efficacy of ARVs (r=−0.20;p<0.05) and a high level of perceived HIV understanding (r=0.21;p<0.05) correlated with better ARV adherence. Conclusions HIV patients showed similar rates of adherence to ARVs as to medications for comorbidities, despite perceiving HIV as more threatening and ARVs as more important. This can be used in adapting existing interventions for ARV adherence to encompass adherence to medications for comorbid conditions.

Introduction: Doxorubicin (DOX) is an anthracycline that is used for a wide range of malignant conditions. However its off-target effect causes cardiotoxicity. Dexrazoxane (DEX) is the only clinically approved cardioprotective agent against anthracycline toxicity. Its activity has been attributed to its iron-chelating effects. The aim of this project was to assess the protective effect of DEX against DOXinduced toxicity in an HL-1 cardiomyocyte model, and to investigate an early stage marker involved in cellular damage by DOX. Methods: HL-1 cardiomyocytes were cultured for the purpose of bioactivity studies. The half maximal inhibitory concentration (IC-50) of DOX was established. Then the ability of DEX to recover damaged cells was assessed using measures of cell viability. A variety of DEX concentrations with HL-1 s were studied in vitro. Finally, an early stage marker involved in cellular damage by DOX was examined. An assay kit was used for the study of dsDNA breaks through the detection of γ-H2AX -a phosphorylated histone historically proven as a highly specific and sensitive molecular marker for dsDNA damage detection. Results: The IC-50 of DOX was 3 μM. When DEX was combined, there was an additional toxic effect on HL-1 s. The inhibitory effect of DEX on cell viability ceased at 10 μM. The γ-H2AX assay showed decreased dsDNA breaks in cells treated with DEX compared with those treated with DOX alone. The dsDNA breaks were increased in cells treated with DOX alone compared with control (cells alone) (P < 0.05), and dsDNA breaks were increased in cells treated with DOX alone versus those treated with combined DOX and DEX (P < 0.05). Discussion: DEX was found to abolish the DNA damage signal γ-H2AX caused by DOX in HL-1 s as demonstrated in the γ-H2AX assay, suggesting an alternative mechanism of cardioprotective action of DEX.

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