BackgroundAfrican Americans have higher rates of cardiovascular disease (CVD) mortality than other ethnic groups. Young adults are prime targets for intervention strategies to prevent and reduce disease risk. The study purpose was to determine the level of knowledge of lifestyle risk factors for CVD among young African American adults in Phoenix. The results will be used to guide the development of CVD outreach programs targeted to this population. The Health Belief Model was used as a conceptual framework.MethodsA convenience sample of 172 African American men and women aged 18-26 years completed a questionnaire adapted from the American Heart Association national surveys. Descriptive statistics were compared by age, gender, education level, and health status variables including BMI, smoking status, and physical activity.ResultsSome aspects of heart-disease were well known among young adult African Americans. Knowledge of certain other important risk factors (menopause) and preventive behaviors (eating fewer animal products), however, was more variable and inconsistent among the respondents. Differences in knowledge of individual variables was greater by education level than by gender overall. Predictors of a summary CVD knowledge score included higher education, female gender, and high self-efficacy (adjusted R2 = 0.158, p < .001). Predictors of self-efficacy in changing CVD risk were higher education and perceived low risk of CVD (adjusted R2 = 0.064, p < .001), but these characteristics explained only 6% of the variance.ConclusionsEvaluation of baseline knowledge of CVD is essential before designing and implementing health promotion programs. Existing strengths and weaknesses in knowledge can guide tailoring of programs to be more effective. Further research would help to identify the range of other characteristics that determine knowledge and risk perception.

School of Veterinary and Biomedical Sciences, James Cook University, Townsville, Australia Amphibian populations suffer massive mortalities from infection with frog virus 3 (FV3, genus Ranavirus, family Iridoviridae), a pathogen also involved in mortalities of fish and reptiles. Experimental oral infection with FV3 in captive-raised adult wood frogs, Rana sylvatica (Lithobates sylvaticus), was performed as the first step in establishing a native North American animal model of ranaviral disease to study pathogenesis and host response. Oral dosing was successful; LD 50 was 10 2.93 (2.42-3.44) p.f.u. for frogs averaging 35 mm in length. Onset of clinical signs occurred 6-14 days post-infection (p.i.) (median 11 days p.i.) and time to death was 10-14 days p.i. (median 12 days p.i.). Each tenfold increase in virus dose increased the odds of dying by 23-fold and accelerated onset of clinical signs and death by approximately 15 %. Ranavirus DNA was demonstrated in skin and liver of all frogs that died or were euthanized because of severe clinical signs. Shedding of virus occurred in faeces (7-10 days p.i.; 3-4.5 days before death) and skin sheds (10 days p.i.; 0-1.5 days before death) of some frogs dead from infection. Most common lesions were dermal erosion and haemorrhages; haematopoietic necrosis in bone marrow, kidney, spleen and liver; and necrosis in renal glomeruli, tongue, gastrointestinal tract and urinary bladder mucosa. Presence of ranavirus in lesions was confirmed by immunohistochemistry. Intracytoplasmic inclusion bodies (probably viral) were present in the bone marrow and the epithelia of the oral cavity, gastrointestinal tract, renal tubules and urinary bladder. Our work describes a ranavirus-wood frog model and provides estimates that can be incorporated into ranavirus disease ecology models.

Wood frogs ( Rana sylvatica) are highly susceptible to infection with Frog virus 3 (FV3, Ranavirus, Iridoviridae), a cause of mass mortality in wild populations. To elucidate the pathogenesis of FV3 infection in wood frogs, 40 wild-caught adults were acclimated to captivity, inoculated orally with a fatal dose of 10 pfu/frog, and euthanized at 0.25, 0.5, 1, 2, 4, 9, and 14 days postinfection (dpi). Mild lesions occurred sporadically in the skin (petechiae) and bone marrow (necrosis) during the first 2 dpi. Severe lesions occurred 1 to 2 weeks postinfection and consisted of necrosis of medullary and extramedullary hematopoietic tissue, lymphoid tissue in spleen and throughout the body, and epithelium of skin, mucosae, and renal tubules. Viral DNA was first detected (polymerase chain reaction) in liver at 4 dpi; by dpi 9 and 14, all viscera tested (liver, kidney, and spleen), skin, and feces were positive. Immunohistochemistry (IHC) first detected viral antigen in small areas devoid of histologic lesions in the oral mucosa, lung, and colon at 4 dpi; by 9 and 14 dpi, IHC labeling of viral antigen associated with necrosis was found in multiple tissues. Based on IHC staining intensity and lesion severity, the skin, oral, and gastrointestinal epithelium and renal tubular epithelium were important sites of viral replication and shedding, suggesting that direct contact (skin) and fecal-oral contamination are effective routes of transmission and that skin tissue, oral, and cloacal swabs may be appropriate antemortem diagnostic samples in late stages of disease (>1 week postinfection) but poor samples to detect infection in clinically healthy frogs.

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Feline oral squamous cell carcinoma (OSCC) is a highly invasive form of cancer in cats. In human OSCC, cluster of differentiation 147 (CD147) contributes to inflammation and tumor invasiveness. CD147 is a potential therapeutic target, but the expression of CD147 in feline OSCC has not been examined. Immunohistochemistry was used to determine if cyclooxygenase 2 (COX-2) and CD147 expression in feline OSCC biopsies was coordinated. Tumor cells were more likely to express COX-2 (22/43 cases or 51%) compared to stroma (8/43 or 19%) and adjacent oral epithelium (9/31 cases or 29%) (p < 0.05). CD147 was also more likely to occur in tumor cells compared to stroma and adjacent mucosa, with 21/43 (49%) of cases having >50% tumor cells with mild or moderate CD147 expression, compared to 9/28 (32%) in adjacent epithelium and only 5/43 (12%) in adjacent stroma (p < 0.05). In feline OSCC cell lines (SCCF1, SCCF2, and SCCF3), CD147 gene expression was more consistently expressed compared to COX-2, which was 60-fold higher in SCCF2 cells compared to SCCF1 cells (p < 0.05). CD147 expression did not correlate with COX-2 expression and prostaglandin E2 (PGE2) secretion, indicating that they may be independently regulated. CD147 potentially represents a novel therapeutic target for the treatment of feline OSCC and further study of CD147 is warranted.