No abstract

The chromosome numbers of four Chinese Begonia species were counted for the first time as follows: 2n = 22 in B. rubropunctata, 2n = 18 in B. purpureofolia, 2n = 44 in B. pedatifida, and 2n = 22 in B. villifolia. The first two species had relatively large chromosomes with early condensed chromatin in the distal and interstitial or proximal regions, whereas the last two had small chromosomes with early condensed chromatin in the proximal regions. Although they have been reduced in the literature to synonyms of B. pedatifida and B. villifolia, respectively, B. rubropunctata and B. purpureofolia should be treated as distinct species because of the differences in chromosome numbers and other chromosome features.

Background: Hyperlipidaemia causes kidney damage over the long term. We investigated the effect of the administration of endothelial progenitor cells (EPCs) on the progression of kidney damage in a mouse model of hyperlipidaemia. Methods: Apolipoprotein E-knockout (ApoE −/−) mice were treated with a high-cholesterol diet after spleen resection. Twenty-four weeks later, the mice were divided into two groups and intravenously injected with PBS or EPCs. Six weeks later, the recruitment of EPCs to the kidney was monitored by immunofluorescence. The lipid, endothelial cell, and collagen contents in the kidney were evaluated by specific immunostaining. The protein expression levels of transforming growth factor-β (TGF-β), Smad2/3, and phospho-Smad3 (p-smad3) were detected by western blot analysis. Results: ApoE −/− mice treated with a high-fat diet demonstrated glomerular lipid deposition, enlargement of the glomerular mesangial matrix, endothelial cell enlargement accompanied by vacuolar degeneration and an area of interstitial collagen in the kidney. Six weeks after EPC treatment, only a few EPCs were detected in the kidney tissues of ApoE −/− mice, mainly in the kidney interstitial area. No significant differences in TGF-β, p-smad3 or smad2/3 expression were found between the PBS group and the EPC treatment group (TGF-β expression, PBS group: 1.06 ± 0.09, EPC treatment group: 1.09 ± 0.17, P = 0.787; p-smad3/smad2/3 expression: PBS group: 1.11 ± 0.41, EPC treatment group: 1.05 ± 0.33, P = 0.861). Conclusions: Our findings demonstrate that hyperlipidaemia causes basement membrane thickening, glomerulosclerosis and the vascular degeneration of endothelial cells. The long-term administration of EPCs substantially has limited effect in the progression of kidney damage in a mouse model of hyperlipidaemia.