Introduction. Ethanol is a commonly used fixative. Fixation of the inner layers of the tissue depends on the ability of the fixative to diffuse into the tissue. It is unknown whether the concentration of ethanol affects its penetration into tissues. This study aimed to compare the penetration rates of 50% and 100% ethanol into bovine heart and liver tissues. Materials and methods. The penetration distance and tissue shrinkage or expansion were measured by analysing the digital images of the heart and liver tissues before and after immersion in ethanol at 20°C for 2, 6, 24 or 30 hours. The penetration coefficients were calculated as the slope of the regression line using the linear regression function between the penetration distance and square root of fixation time. Differences in tissue shrinkage or expansion and penetration distance at various time points between the two concentrations of ethanol were analysed using a mixed design ANOVA followed by Bonferroni's post-hoc test. Results. The penetration distance of 100% ethanol was significantly greater in both heart and liver tissues compared with that of 50% ethanol (n = 4, p < 0.05 for both). 100% ethanol shrank immersed liver tissue significantly more than 50% ethanol (p = 0.002), but the shrinkage of the heart tissue caused by two concentrations of ethanol did not significantly differ (p = 0.054). The greater penetration distance of 100% over 50% ethanol remained unchanged after normalising the penetration distance to the individual tissue's shrinkage (n = 4, p < 0.001). The mean penetration coefficient of 100% ethanol was significantly greater than 50% ethanol in the heart tissue (0.906 vs. 0.442, p = 0.003) and in the liver tissue (0.988 vs. 0.622, p = 0.028). Conclusions. It was proven that in two types of tissue that substantially differ in histological structures, 100% ethanol penetrated tissue significantly faster than 50% ethanol.

The Australian blueberry industry is worth over $300 million, but there is limited information on factors influencing their chemical composition, particularly their ripeness and harvest stage. This pilot study investigated changes in total monomeric anthocyanin content (TMAC; measured using the pH-differential method) and total antioxidant capacity (TAC; measured with the cupric reducing antioxidant capacity assay) of four Australian highbush blueberry cultivars (Denise, Blue Rose, Brigitta and Bluecrop) at four time points and three maturity stages (unripe, moderately ripe and fully ripe). The TAC of most cultivars decreased by 8–18% during ripening, although that of the Blue Rose cultivar increased markedly. However, the TAC of ripe fruit from this cultivar also fluctuated markedly throughout the harvest season (between 1168–2171 mg Trolox equivalents 100 g−1). The TMAC increased sharply between the medium-ripe and fully ripe maturity stages, with the Blue Rose cultivar showing the highest TMAC values (211 mg 100 g−1, compared to 107–143 mg 100 g−1 for the remaining varieties). The TMAC of ripe fruit from this cultivar also rose steadily throughout the harvest season, in contrast to most other cultivars where the TMAC fell slightly over time. These results indicate that the levels of health-benefitting compounds in Australian-grown highbush blueberries may depend not only on the cultivar, but also upon the time of harvest.

Periodontal disease is an inflammatory condition around the teeth which affects 20-50% of the worldwide population. In periodontal disease, the bacterial plaque destroys the epithelium of the periodontal pocket and breaks the barrier that separates the tissue and the circulation, allowing oral bacteria and their endotoxins and exotoxins to enter the bloodstream. This can cause health problems, such as atherosclerosis. Aggregatibacter actinomycetemcomitans (Aa) is commonly found in patients with periodontitis and the number of Aa is associated with atherosclerotic lesion size in humans. This review focuses on Aa and atherosclerosis with an emphasis on the interaction of Aa with cell types involved in atherosclerosis formation.

Methanol, ethanol and formalin are commonly used as fixatives to preserve biological tissues from decay in the preparation of histological sections. Fixation of the inner layers of the tissue depends on the ability of the fixative to diffuse into the tissue. It is unknown whether methanol penetrates tissues at similar rates to other fixatives. This study aimed to compare the penetration rates of methanol, ethanol and formalin into bovine heart and liver tissues. The penetration distance and tissue shrinkage or expansion were measured by analysing the digital images of tissue before and after immersion in different fixatives for 1, 2, 6 or 10 h. Data were analysed using two-way ANOVA, followed by Bonferroni’s post-hoc test. The penetration distance of methanol was significantly greater in both heart and liver tissues compared with that of ethanol (N=4, P<0.001). Methanol or ethanol immersion led to similar shrinkage of both tissues (P>0.05). The penetration rate of formalin was similar to that of ethanol in both tissues however it was significantly slower than methanol (N=4, P<0.005 in the heart; P<0.001 in the liver). The mean penetration coefficients of methanol, formalin and ethanol in the heart tissue were 2.609, 1.994 and 1.801, respectively, and 3.012, 2.153 and 2.113, respectively, in the liver tissue. The penetration coefficient of methanol was significantly greater than that of ethanol or formalin in both tissues (P<0.001 for each comparison). In conclusion, methanol penetrates tissue significantly faster than ethanol and formalin.

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Objectives: Moxonidine is believed to decrease blood pressure via inhibiting sympathetic activity in the brain and consequently decreasing vascular tone. However, whether direct peripheral mechanisms are involved in this process is unknown. This study aimed to investigate possible peripheral mechanisms of moxonidine in lowering blood pressure. Methods: Two groups (N = 10 in each group) of apolipoprotein E-deficient mice were used. These animals were treated with or without moxonidine (18 mg/kg body weight per day) via drinking water throughout the experiment. Three days after the initiation of moxonidine treatment, hypertension was induced by subcutaneous infusion of angiotensin II (1 μg/kg body weight per min) for 28 days. Blood pressure was measured by the tail cuff method. Size and area of kidney tubules and glomeruli were analyzed by morphometric analysis. Gene expression was assessed by quantitative PCR. Results: Moxonidine treatment significantly decreased blood pressure (P<0.05). It did not change the size or area of either kidney tubules or glomeruli (P>0.05), nor the renal expression of inflammatory markers. Both types of moxonidine receptors (imidazoline 1 and alpha-2 adrenergic receptors) were found to be expressed in the kidney, and their gene expression was not altered by moxonidine treatment. However, moxonidine treatment significantly increased the expression of prostaglandin EP3 receptor (P<0.05). Increased prostaglandin EP3 receptor has been reported to be associated with promoting diuresis and natriuresis and thus decreasing blood pressure. Summary: The results indicate that moxonidine may lower blood pressure partially through an unrecognized non-central pathway by upregulating prostaglandin EP3 receptor in the kidney in mice.