Hyperglycemia is associated with a reduced number of endothelial progenitor cells (EPCs) that impairs vascular function. Circulating EPCs play important roles in postnatal neovasculogenesis and the prevention of ischemic injury. Frequent consumption of fish oil (FO) that is abundant with eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA) is reportedly associated with an alleviation of diabetic complications and a lowered incidence of cardiovascular disease. The aim of this study was to examine whether N-3 polyunsaturated fatty acids such as EPA and DHA would reverse the high glucose-mediated dysfunction of EPCs in vitro and thereby prevent the ischemic injury that occurs under the hyperglycemic conditions in Type 2 diabetes (T2D) db−/− mice. The results demonstrate that EPA and DHA alleviate high glucose-mediated impairment of tubular formation in EPCs through a rescue of neovasculogenic capability. The molecular mechanisms underlying the effects of EPA and DHA include the activation of the extracellular signal-regulated kinase 1/2, Akt/endothelial nitric oxide synthase (eNOS) and AMP-activated kinase (AMPK) signaling cascades as well as the phosphorylation of the downstream FOXO3a protein in EPCs. Moreover, EPA and DHA up-regulate the expression of c-kit, erythroid 2-related factor and heme oxygenase-1 proteins. Daily consumption of FO at dosages of 4% and 6% (wt/wt) significantly increased the level of bone marrow-derived and circulating EPCs, induced a recovery of blood flow and prevented ischemic injuries in a T2D db−/− mouse model. The effects of FO consumption were exerted the activation of Akt/eNOS and AMPK signaling cascades without any effect on the plasma VEGF level in vivo.

Background and Objective: This study is a systemic review of coronally positioned flap, coronally positioned flap + chemical root surface conditioning, or coronally positioned flap + enamel matrix derivative (EMD) for the treatment of Miller class I and II gingival recession.Material and Methods: All studies available through the Medline database by the end of October 2005 were used. Each study provided mean clinical attachment level, keratinized tissue, probing pocket depth, gingival recession depth and root coverage percentage before and after treatment with coronally positioned flap alone, coronally positioned flap + chemical root surface conditioning , or coronally positioned flap + EMD. Effectiveness was evaluated by comparing the weighted mean average in gingival recession depth, probing pocket depth, clinical attachment level, keratinized tissue and root coverage percentage achieved with the three treatments.Results: Seven studies for the coronally positioned flap + EMD group, four studies for the coronally positioned flap + chemical root surface conditioning group, and seven studies for the coronally positioned flap group were retrieved for this weighted mean analysis. The results of clinical attachment level, gingival recession depth, and root coverage percentage in the coronally positioned flap + EMD group were statistically significantly better than the changes in the coronally positioned flap and coronally positioned flap + chemical root surface conditioning group at 6 and 12 mo (p < 0.001). There was no significant difference at the 6-mo comparison among clinical attachment level, keratinized tissue, probing pocket depth, and gingival recession depth, except in the root coverage percentage for coronally positioned flap and coronally positioned flap + chemical root surface conditioning groups.Conclusion: The results suggest that root coverage by the coronally positioned flap and coronally positioned flap + chemical root surface conditioning procedures were unpredictable but became more predictable when the coronally positioned flap procedure was improved by the modification of adding EMD.

The relationship between radiographic measures of severity of osteoarthritis (OA) and changes in gene expression in joints are not well characterised. In this study, the expression of 11 candidate genes was characterised by quantitative reverse transcriptase polymerase chain reaction in normal and OA cartilage and bone from the elbows of dogs with fragmented coronoid disease. The levels of expression of type I collagen α2 chain (COL1A2), type III collagen α1 chain (COL3A1), lumican (LUM), matrix metalloproteinase-2 (MMP2), -9 (MMP9) and -13 (MMP13) genes were increased and the expression of tissue inhibitor of metalloproteinase-2 (TIMP2) and cathepsin D (CTSD) genes were decreased in OA cartilage relative to normal cartilage. All differences correlated with radiographic measures of severity of OA. Levels of expression of COL1A2, MMP2, MMP9, MMP13 and TIMP1 were increased, whereas expression of TIMP2 was decreased in OA bone relative to normal bone. Cartilage gene expression may be correlated with the radiographic severity of OA.

To examine the possibility that interleukin-9 (IL-9) may be involved in oncogenesis and the proliferation of adult T-cell leukemia (ATL) cells, we examined the expression of IL-9 mRNA and growth response to IL-9 in five human T-lymphotropic virus type-I (HTLV-I) infected T-cell lines and in primary leukemia cells in peripheral blood from eight patients with ATL (four acute ATL and four chronic). Four out of five cell lines expressed IL-9 mRNA not correlated with Tax expression. Primary ATL cells from all patients also expressed IL-9 mRNA not correlated with the clinical forms. Recombinant IL-9 showed growth enhancing activity in only one out of five cell lines and one out of eight patients' primary leukemic cells. These results suggest the infrequent involvement of IL-9 in the proliferation of ATL cells, both primary tumor cells and HTLV-I infected T-cell lines.

Restenosis may develop in response to cytokine activation and smooth muscle cell proliferation. Ginkgo biloba extract (EGb) has been used to treat cardiovascular and cerebrovascular diseases. In the present study, the effects of EGb on the growth of cultured vascular smooth muscle cells (VSMC), as well as on the expression of interleukin-1beta (IL-1beta) and the intimal response in balloon-injured arteries of cholesterol-fed rabbits, were investigated. Using bromodeoxyuridine incorporation as an index of cell proliferation, EGb was found to inhibit serum-induced mitogenesis of cultured rat aorta VSMC in a dose-dependent manner. In vivo, EGb and probucol ( positive control) reduced the atheroma area in thoracic aortas of male New Zealand white rabbits fed a 2% cholesterol diet for 6 weeks with balloon denudation of the abdominal aorta being performed at the end of the third week. Intimal hyperplasia, expressed as the intimal/medial area ratio, in the abdominal aortas was significantly inhibited in the both the EGb group (0.61 +/- 0.06) and the probucol group (0.55 +/- 0.03) compared to the C group (0.87 +/- 0.02). In the balloon-injured abdominal aorta, both EGb and probucol significantly reduced IL-1beta mRNA and protein expression and the percentage of proliferating cells. The inhibitory effects of EGb on the intimal response might be attributed to its antioxidant capacity. EGb may have therapeutic potential for the prevention of restenosis after angioplasty.

Apoptosis has been suggested to participate in stabilizing cell number in restenosis. Salvia miltiorrhiza (SM) Bunge which is a Chinese herb widely used for the treatment of cardiovascular disorders contains a potent antioxidant, Salvianolic acid B. To determine whether the antioxidant affects vascular apoptosis, the present study examined the frequency of apoptotic cell death in atherosclerotic plaques and in restenotic lesions of cholesterol-fed rabbits. New Zealand White rabbits were treated with a normal diet (normal), a 2% cholesterol diet (HC), a 2% cholesterol diet and endothelial denudation (HC-ED), a 2% cholesterol diet with 5% water-soluble extract of SM (4.8 g/Kg B.W./day) and endothelial denudation (HC-ED-SM), or with a 2% cholesterol diet containing probucol (0.6 g/kg B.W./day) and endothelial denudation (HC-ED-probucol). Apoptosis and associated cell types were examined in serial paraffin sections by in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and immunohistochemistry. The expression of p53, an apoptosis-related protein, was also examined. Apoptosis was mainly detected in the neointima of the three groups with endothelial denudation. The percentage of apoptotic cells in SM-treated group (68.5+/-5.9%) was significantly higher than that of normal (0%), HC (1.9+/-1.2%), HC-ED (46.1+/-5.4%), and probucol-treated (32.8+/-3.9%) groups. The SM treatment markedly reduced the thickness of the neointima which was mainly composed of smooth muscle cells with few macrophages. In accordance with the apoptotic cell counts, positive immunoreactivity for p53 was observed in restenotic lesions from HC-ED, SM-treated and probucol-treated groups but not in the intima of the other two groups. These results suggest that the treatment with salvianolic acid B-rich fraction of SM induces apoptosis in neointima which in turn may help prevent the neointimal thickening.

The term "syndrome X" is now widely used to specify a group of patients with anginal chest pain, ischemia-like electrocardiogram, normal coronary angiograms, and no evidence of coronary spasm. Though chest pain and exercise-induced myocardial ischemia may both be present in patients with syndrome X and those with coronary artery disease, the underlying pathogenesis of these two disease entities is different. In patients with syndrome X, the causes of angina and myocardial ischemia are multifarious while coronary angiograms are normal. Coronary microvascular function has been shown to be impaired in these patients. However, the presentation of myocardial ischemia may be varied and even subclinical, suggesting dynamic characteristics and regional distribution of coronary microvascular insufficiency in them. Recently, there is increasing evidence that chest pain may develop without detectable myocardial ischemia and has been attributed to abnormal pain perception in at least some of the patients. Thus, there is a heterogeneous group of patients with syndrome X. The rational patient management should be related to individual clinical presentation and depend upon the proper identification of the underlying mechanisms of anginal chest pain or myocardial ischemia or both in these patients.