Efeitos da terapia periodontal na função endotelial e na expressão de marcadores inflamatórios sistêmicos

A periodontite é uma doença infecciosa, crônica e altamente prevalente causando uma resposta inflamatória. A infecção e a inflamação são consideradas a base etiológica para o desenvolvimento da aterosclerose. Recentes estudos indicam que a periodontite severa pode influenciar o aumento de marcadores inflamatórios e de disfunção endotelial associados com o aumento de risco da doença coronariana e o acidente vascular cerebral. Embora alguns estudos tenham sugerido esta associação, os reais efeitos do tratamento da doença periodontal sobre a rede complexa de marcadores envolvidos na aterosclerose são pouco conhecidos. O objetivo deste estudo foi avaliar o efeito da terapia periodontal nos biomarcadores inflamatórios (TNF-α, fibrinogênio, PCRus, INFγ, IL-1β, IL-6 e IL-10), perfil lipídico (CT, HDL, LDL, TG, oxLDL e anti-oxLDL) e função endotelial (IMT) das artérias carótidas. Um total de trinta e dois indivíduos saudáveis sistemicamente e afetados pela periodontite severa (16 mulheres, 16 homens; 51,87 anos de idade), incluindo 17 sujeitos para o grupo teste e 15 sujeitos para o grupo controle foram recrutados para o estudo. A ultrassonografia das artérias carótidas e os níveis séricos inflamatórios foram avaliados no início, 40 e 100 dias após o tratamento periodontal não-cirúrgico, comparando tempo e grupos. O tratamento periodontal resultou em significante redução dos parâmetros da doença periodontal. O grupo que recebeu tratamento mostrou decréscimos significativos de oxLDL (P<0.0001), anti-oxLDL (P<0,0001), TNF-α (P<0,0001), fibrinogênio (P=0,008), INFγ (P<0,0001), IL-1β (P<0,0001), IL-6 (P<0,0001), IMT (P=0,006) e significante aumento de IL-10 (P<0,0001) após 100 dias do tratamento periodontal comparando com grupo controle. Entretanto, os resultados não foram significativos para PCRu (P=0,109), colesterol total (P=0,438), HDL (P=0,119), LDL (P=0,425) e triglicerídeos (P=0,939). Com base nestes resultados, o tratamento da periodontite pode melhorar o perfil inflamatório e a função endotelial, sendo uma importante ferramenta adicional para a prevenção das doenças cardiovasculares.

A型、D型人格影响冠心病预后的心理生理机制

Coronary heart disease （CHD）is a common cardiovascular disease in the elderly, is also a typical psychosomatic disease. Personality factors are very important in many psychological factors impacting on the prognosis of patients with CHD. The most influential personality factors to CHD are Type A and Type D personality. The previous research has shown that although Type A personality increased the prevalence of CHD, it cannot predict the development and prognosis after diagnosis. In contradict, Type D personality can predict prognosis. There is still no clinic-based or theory-based answer to the question: Why Type A personality cannot predict the outcome while Type D personality could predict the prognosis independently. The current research conducted a systematic investigation to the above question, which included one comparison study between CHD patients and control group, and four studies on reaction experiment and answered the question: why Type A personality cannot predict whereas Type D personality could effectively predict prognosis of CHD. The findings of the current research were: Type A and Type D personality influence CHD prognosis through different psychological mechanisms: both dimensions of Type D personality have direct influence on social support, whereas neither dimensions of Type A personality related to social support, directly of indirectly. Negative affection component of Type D personality significantly related to anxiety and depression, Social repression significantly related to anxiety but not depression. Both dimensions of Type A personality significantly related to anxiety but not depression. Neither under rest or diaphragmatic breathing conditions, Type A personality had no significant influence on vestibular autonomic reaction among healthy young males. Neither Type A nor Type D personality had significant influence on vestibular autonomic reaction among old CHD patients under rest condition. Type D personality predicted lower sympathetic excitation under rest condition, and lower cardiac vagal tone under diaphragmatic breathing condition among healthy young males. When actively reacted to stimuli (math calculation) under rest condition, Type A personality increased sympathetic excitation among healthy young males. When actively reacted to stimuli (math calculation) under diaphragmatic breathing condition, Type A personality increased cardiac vagal tone among the same group of subjects. When actively reacted to stimuli under neither condition, Type D personality showed no significant influence on vestibular autonomic reaction among young males. When passively reacted to stimuli under neither condition, Type A personality showed no significant influence on vestibular autonomic reaction among young males. When passively stimulated followed rest, Type D personality increased sympathetic excitation and decreased cardiac vagal tone among young males. When passively stimulated followed diaphragmatic breathing, Typed showed no significant influence on vestibular autonomic reaction among young males. The above results indicated that Type A and Type D personalities had different psychological mechanisms to the outcome of CHD treatment: neither dimensions of Type A personality had direct or indirect effects on social support; both dimensions of Type D personality had direct and indirect effects on social support. Negative affection component of Type D personality significantly related to anxiety and depression, Social repression significantly related to anxiety but not depression. Both dimensions of Type A personality significantly related to anxiety but not depression. Social support positively related to the outcome after CHD treatment. The biological mechanisms of Type A and Type B personality to CHD prognosis differed in the following ways: Type A personality increased sympathetic excitation when actively stimulated, but had no influence when passively stimulated among young male subjects. When passively stimulated after rest, Type D personality predicted high sympathetic excitation and low cardiac vagal tone among young males, but not vestibular autonomic reaction among young males. Key words: Type A personality, Type D personality, Coronary Heart Disease (CHD), Prognosis, Psychobiological Mechanisms

A型行为核心特征与血管紧张素转换酶基因型相关性研究

In order to study the role of inherited factors and Type A Behavior Pattern (TABP) in the development of CHD, the present study chose the angiotensin I-converting enzyme (ACE) gene as the target gene, and investigated the associations of TABP, the polymorphism of ACE gene with susceptibility to development of CHD in the healthy population and CHD patients from Northern China. 1. Correlation Analysis Between TABP and serum level of ACE in Chinese healthy individuals TABP and serum of ACE were determined in 137 Chinese healthy individuals. The results showed that there was a significant correlation between the scores of CH in TABP invertory and the serum level of ACE. 2 The distribution charicteristics of ACE gene polymorphism frequencies and association with serum level of ACE in Chinese healthy individuals population The polymorphism of ACE gene and serum of ACE were determined in 137 Chinese healthy individuals. The results showed that: the ethnic differences in I/D polymorphism of ACE gene are obvious; deletion polymorphism of the ACE gene is associated with serum ACE level. 3. The relationship between insertion/deletion polymorphism of ACE gene and CHD in a Chinese population I/D polymorphism in intron 16 of the ACE gene was determined by polymerase chain reaction(PCR) in a study of 109 patients with CHD. The results showed: The frequencies of DD genotype(0.39) and D allele(0.63) were higher among the CHD group than among the control subjects(0.12 and 0.42 respectively, P < 0.01). Furthermore, MI and multivessel disease was more strongly associated with (P < 0.01). It is indicated that D allele and DD gentype of ACE might be an important risk factor for CHD, especially for MI or multivessel disease in Chinese population. 4. Correlation Analysis Between Type A Behavior Pattern and the Polymorphism of ACE Gene The polymorphism of ACE gene and type A behavior pattern (TABP) survey were determined in 291 Chinese healthy individuals. The result showed that the higher frequency of rare D allele of an insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene was found in type A behavior individuals compared with type B behavior individuals in 291 healthy individuals; there was a significant correlation between the scores of CH in TABP invertory and DD genotype of the ACE gene. It is suggested that the behavioral attributes of competitiveness, achievement striving, hostility, being irritated easily and impatience may be associated with heredity. 5. Correlation Analysis Between Angiotensin I-Converting Enzyme Gene Polymorphism, Type A Behavior Pattern and Coronary Heart Disease in Chinese The polymorphism of ACE gene and type A behavior pattern (TABP) survey were determined in 109 patients with CHD. The results showed the development of coronary heart disease(CHD) is influenced mainly by the behavioral attributes of competitiveness, achievement striving, hostility, being irritated easily and impatience; the deletion polymorphism of ACE gene may be play a important role in the process of it. 6. Correlation Analysis Between Type A Behavior Pattern Core Components and the Polymorphism of ACE Gene The polymorphism of ACE gene and type A behavior pattern (TABP) survey were determined in1306 Chinese healthy individuals. The results showed that there was a significant correlation between the scores of CH in TABP invertory and DD genotype of the ACE gene. Furthermore, the behavioral attributes of hostility, being irritated easily and impatience may be associated with heredity. At the end of this research, in terms of theory, the research approaches of TABP and the factors influenced the relationship between TABP and CHD were explored and discussed. Furthermore, several new opinions were put forward.

Trade-offs between cancer and other diseases: do they exist and influence longevity?

Relationships between aging, disease risks, and longevity are not yet well understood. For example, joint increases in cancer risk and total survival observed in many human populations and some experimental aging studies may be linked to a trade-off between cancer and aging as well as to the trade-off(s) between cancer and other diseases, and their relative impact is not clear. While the former trade-off (between cancer and aging) received broad attention in aging research, the latter one lacks respective studies, although its understanding is important for developing optimal strategies of increasing both longevity and healthy life span. In this paper, we explore the possibility of trade-offs between risks of cancer and selected major disorders. First, we review current literature suggesting that the trade-offs between cancer and other diseases may exist and be linked to the differential intensity of apoptosis. Then we select relevant disorders for the analysis (acute coronary heart disease [ACHD], stroke, asthma, and Alzheimer disease [AD]) and calculate the risk of cancer among individuals with each of these disorders, and vice versa, using the Framingham Study (5209 individuals) and the National Long Term Care Survey (NLTCS) (38,214 individuals) data. We found a reduction in cancer risk among old (80+) men with stroke and in risk of ACHD among men (50+) with cancer in the Framingham Study. We also found an increase in ACHD and stroke among individuals with cancer, and a reduction in cancer risk among women with AD in the NLTCS. The manifestation of trade-offs between risks of cancer and other diseases thus depended on sex, age, and study population. We discuss factors modulating the potential trade-offs between major disorders in populations, e.g., disease treatments. Further study is needed to clarify possible impact of such trade-offs on longevity.

Health status of an elderly population in Sharpeville, South Africa

The objective of this cross-sectional study was a comprehensive nutrition and health assessment to provide a basis for future intervention strategies for an elderly population attending a day-care centre. Socio-demographic, health and 24-hour recall dietary intake questionnaires were administered and anthropometric and biochemical measurements taken. The results indicate that the majority of respondents had an income of between R501 and R1 000 (South African rand) per month and most of them reported an occasional lack of funds to meet basic household needs, confirming the presence of food insecurity. Daily dietary intakes (mean [+ or -] Standard Deviation [SD]) of the women were 5 395 [+ or -] 2 946 kJ energy, 47 [+ or -] 27 g protein, 28 [+ or -] 21 g fat and 196 [+ or -] 123 g carbohydrates compared to 8 641 [+ or -] 3 799 kJ, 86 [+ or -] 48 g, 49 [+ or -] 32 g and 301 [+ or -] 139 g of the men, respectively. The majority (83.6%) of the women were overweight (body mass index [BMI] [greater than or equal to] 25) or obese (BMI [greater than or equal to] 30) whilst 78% had a mid-upper arm circumference (MUAC) of [greater than or equal to] 21.7 cm. Mean intakes of micronutrients were low in comparison to reference standards and serum zinc levels were suboptimal. Obesity, hypertension and raised total serum cholesterol levels indicated an increased risk for coronary heart disease. It can be concluded that a low income, household food insecurity and risk factors associated with malnutrition and non-communicable diseases were prevalent in this elderly population. OPSOMMING Die doelwit van hierdie dwarssnitstudie was ‘n omvattende bepaling van voeding- en gesondheidstatus om as basis te dien vir toekomstige intervensiestrategieë vir ’n groep bejaardes wat ’n dagsentrum besoek. Sosiodemografiese, gesondheid- en 24-uur herroep-dieetinname vraelyste is voltooi en antropometriese en biochemiese metings is geneem. Die resultate het bevestig dat die meerderheid respondente ‘n maandelikse inkomste van tussen R501 en R1 000 (Suid-Afrikaanse rand) gehad het. Die meeste het ‘n geldtekort vir basiese huishoudelike behoeftes gerapporteer wat dui op huishoudelike voedselinsekuriteit. Daaglikse dieetinnames (gemiddeld±standaardafwyking [SA]) van die vroue was onderskeidelik 5 395±2 946 kJ energie, 47±27 g proteïen, 28±21 g vet en 196±123 g koolhidrate in vergelyking met 8 641±3 799 kJ, 86±48 g, 49±32 g en 301±139 g vir die mans. Die meerderheid (83.6%) van die vroue was oorgewig (liggaamsmassa-indeks [LMI] >25) of vetsugtig (LMI > 30) en 78% het ’n middel-bo-armomtrek (MUAC) van > 21.7 cm gehad. Gemiddelde mikronutriëntinnames was laag in vergelyking met die verwysingstandaarde en serumsink was suboptimaal. Vetsug, hipertensie en verhoogde totale serumcholesterolvlakke het op ‘n verhoogde risiko van kardiovaskulêre siekte gedui. Die resultate het dus bewys dat lae inkomste, huishoudelike voedselinsekuriteit en die risikofaktore wat met wanvoeding en leefstylsiektes geassosieer word, teenwoordig was.

THE ROLE OF LIPOPROTEIN(a)/APOLIPOPROTEIN(a) IN ENDOTHELIAL DYSFUNCTION: MECHANISTIC STUDIES IN VASCULAR ENDOTHELIUM

Multiple lines of evidence suggest that elevated plasma lipoprotein(a) (Lp(a)) concentrations are a significant risk factor for the development of a number of vascular diseases including coronary heart disease and stroke. Lp(a) consists of a low-density lipoprotein (LDL)-like moiety and an unique glycoprotein, apolipoprotein(a) (apo(a)), that is covalently attached to the apolipoproteinB-100 (apoB-100) component of LDL by a single disulfide bond. Many studies have suggested a role for Lp(a) in the process of endothelial dysfunction. Indeed, Lp(a) has been shown to increase both the expression of adhesion molecules on endothelial cells (EC), as well as monocyte and leukocyte chemotactic activity in these cells. We have previously demonstrated that Lp(a), through its apo(a) moiety, increases actomyosin-driven EC contraction which, as a consequence, increases EC permeability. In this thesis, we have demonstrated a role for the strong lysine-binding site in the kringle IV type 10 domain of apo(a) in increasing EC permeability, which occurs through a Rho/Rho kinase-dependent pathway. We have further validated these findings using mouse mesenteric arteries in a pressure myograph system. We also have dissected another major signaling pathway initiated by apo(a) that involves in a disruption of adherens junctions in EC. In this pathway, apo(a)/Lp(a) activates the PI3K/Akt/GSK3β-dependent pathway to facilitate nuclear translocation of beta-catenin. In the nucleus beta-catenin induced the expression of cyclooxygenase-2 (COX-2) and the secretion of prostaglandin E2 (PGE2) from the EC. Finally, we have presented data to suggest a novel inflammatory role for apo(a) in which it induces the activation of nuclear factor-kappaB through promotion of the dissociation of IkappaB from the inactive cytoplasmic complex; this allows the nuclear translocation of NFkappaB with attendant effects on the transcription of pro-inflammatory genes. Taken together, our findings may facilitate the development of new drug targets for mitigating the harmful effects of Lp(a) on vascular EC which corresponds to an early step in the process of atherogenesis.

Analysis of Lipoprotein(a) Catabolism

Elevated plasma concentrations of lipoprotein(a) [Lp(a)] have been identified as an independent risk factor for vascular diseases including coronary heart disease and stroke. In the current study, we have examined the binding and degradation of recombinant forms of apolipoprotein(a) [r-apo(a)], the unique kringle-containing moiety of Lp(a), using a cultured cell model. We found that the incubation of human hepatoma (HepG2) cells with an iodinated 17 kringle-containing (17K) recombinant form of apo(a) resulted in a two-component binding system characterized by a high affinity (Kd = 12 nM), low capacity binding site, and a low affinity (Kd = 249 nM), high capacity binding site. We subsequently determined that the high affinity binding site on HepG2 cells corresponds to the LDL receptor. In the HepG2 cell model, association of apo(a) with the LDL receptor was shown to be dependent on the formation of Lp(a) particles from endogenous LDL. Using an apo(a) mutant incapable of binding to the high affinity site through its inability to form Lp(a) particles (17KΔLBS7,8), we further demonstrated that the LDL receptor does not participate in Lp(a) catabolism. The low affinity binding component observed on HepG2 cells, familial hypercholesterolemia (FH) fibroblasts and human embryonic kidney (HEK) 293 cells may correspond to a member(s) of the plasminogen receptor family, as binding to this site(s) was decreased by the addition of the lysine analogue epsilon-aminocaproic acid. The lysine-dependent nature of the low affinity binding site was further confirmed in HepG2 binding studies utilizing r-apo(a) species with impaired lysine binding ability. We observed a reduction maximum binding capacity for 17K r-apo(a) variants lacking the strong lysine binding site (LBS) in kringle IV type 10 (17KΔAsp) and the very weak LBS in kringle V (17KΔV). Degradation of Lp(a)/apo(a) was found to be mediated exclusively by the low affinity component on both HepG2 cells and FH fibroblasts. Fluorescence confocal microscopy, using the 17K r-apo(a) variant fused to green fluorescent protein, further confirmed that degradation by the low affinity component on HepG2 cells does not proceed by the activity of cellular lysosomes. Taken together, these data suggest a potentially significant route for Lp(a)/apo(a) clearance in vivo.

APOLIPROTEIN(A)-INDUCED APOPTOSIS IN VASCULAR ENDOTHELIAL CELLS

Elevated plasma concentrations of lipoprotein(a) (Lp(a)) are a risk factor for a variety of atherosclerotic disorders including coronary heart disease. In the current study, the investigators report that incubation of cultured human umbilical vein endothelial cells (HUVECs) with high concentrations of apolipoprotein(a)(apo(a)/Lp(a)) induces apoptosis and endothelial dysfunction in a dose dependent manner. Apo(a), the component of Lp(a) mediates these effects by inducing externalization of Annexin V, DNA condensation and fragmentation which are the hallmarks of death by apoptosis. The pathway of apo(a)-induced apoptosis is associated with overexpression of Bax, caspase-9, p53 phosphorylation, decreased in Bcl-2 expression and activation of caspase-3. Taken together, the data suggest that elevated concentration of apo(a) induces apoptosis in endothelial cells probably by activating the intrinsic pathway. The data also showed that apo(a) induces increased expression of the growth arrest protein (Gas1), which has been known to induce apoptosis and growth arrest in vitro. In addition the data showed that elevated apo(a)/Lp(a) attenuates endothelial nitric oxide (eNOS) activity and endothelin-1 (ET-1) in a dose and time-dependent manner, particularly with small apo(a) isoforms. In summary, the authors proposed a new signaling pathway by which apo(a)/Lp(a) induce apoptosis and this finding could help explain how apo(a)/Lp(a) mediate atherosclerosis related diseases.

Qutting and restarting smoking: cohort study of patients with angina in primary care

Objective To examine variations in self-reported smoking habit among a cohort of individuals with chronic coronary heart disease over a five year period. Design Cross-sectional cohort; interviews at baseline, 2 years and 5 years. Setting Primary care. Participants A cross-sectional sample of 688 patients previously diagnosed as having angina, identified from 18 general practices in the Greater Belfast Area; a cohort of 487 were followed for five years. Outcome measures Changes in self-reported smoking habits; breath carbon monoxide measurement. Results Initially 92 of the 487 participants (19%) reported smoking, 34 (27%) subsequently reported non-smoking. Of the 395 self-reported non-smokers at baseline, 21 (5%) subsequently reported smoking. The prevalence of self-reported smoking amongst the cohort was 19% and 15% at two and five years respectively. However, changes in reported smoking habits indicating periods of abstinence and resumption were reported by 55/487 (11%) participants. Of the 21 non-smokers who changed their report, 20 had smoked previously, five reported having stopped for less than one year but nine for more than five years. Of the initial sample twice as many smokers as non-smokers had died by 2 years (10% v 5%; p

LDL particle size in habitual exercisers, lean sedentary men and abdominally obese sedentary men

Habitual exercisers enjoy considerable protection from coronary heart disease (CHD). Often, however, only modest differences in traditional CHD risk factors are apparent between habitual exercisers and their sedentary counterparts. For this reason, there is increasing interest in novel predictors of CHD, such as a preponderance of small, dense low-density lipoprotein (LDL) particles. Polyacrylamide gel electrophoresis was used to separate lipoprotein subfractions in 32 lean exercisers, 36 lean sedentary men and 21 obese sedentary men aged 30-45 years. Well-validated equations were used to determine LDL concentration and peak particle diameter. Waist girth was used to identify lean (<100 cm) and obese ( >= 100cm) individuals. LDL concentration was lower in lean exercisers than in lean sedentary men (2.64 +/- 0.44 vs. 3.76 +/- 0.79 mmol.l(-1), p <0.001), suggesting that habitual exercise influences this risk factor. In contrast, there were no significant differences in LDL peak particle diameter between lean exercisers, lean sedentary men and obese sedentary men (27.92 +/- 0.67, 28.09 +/- 0.62 and 27.77 +/- 0.77 nm, respectively). In multiple linear regression analysis, triglyceride concentration was the only significant predictor of LDL PPD. These data suggest that habitual exercise influences LDL concentration but does not influence LDL particle size in men aged 30-45 years.

BELFAST centenarians: A Case of Optimal Cardiovascular Risk?

Introduction: Centenarians are reservoirs of genetic and environmental information to successful ageing and local centenarian groups may help us to understand some of the factors that contribute to longevity. The current centenarian cohort in Belfast survived the 1970s epidemic of death from coronary heart disease in Northern Ireland, where cardiovascular mortality was almost highest in the world. These centenarians provided an opportunity to assess biological and genetic factors important in cardiovascular risk and ageing. Methods: Thirty-five (27 female, 8 male) centenarians, participants of the Belfast Elderly Longitudinal Free-living Ageing STudy (BELFAST), were community-living and of good cognition at enrolment. Results: Centenarians showed median Body Mass Index (BMI) at 25.7, systolic blood pressure 140mmHg and diastolic blood pressure 90mmHg, and fasting glucose of 5.54 mmol/l with no sex-related difference. Lipoproteins showed median cholesterol 5.3, High Density Lipoprotein (HDL) 1.10 and Low Density Lipoprotein (LDL) 3.47umol/l respectively. Centenarian smokers showed no different blood pressure or lipid measurements compared with non-smokers. Malondialdehyde, a measure of lipid peroxidation, was low at 1.19 umol/l, and measures of antioxidant status were varied. Male centenarians did not carry any of the vascular risk genotypes studied-ApoE4 for Apolipoprotein E (ApoE), DD for Angiotensinogen Converting Enzyme (ACE) and tt for 5,10-methylenetetrahydrofolate reductase (MTFHR), though this was not true for female centenarians.. Conclusions: This small local study shows that Belfast centenarians carry a reasonably favourable risk profile, except for age, with respect to cardiovascular disease. There is also some evidence that vascular risk factors and genotypes may be tolerated differently between the male and female centenarians. Maintaining a favourable cardiovascular risk profile seems likely to improve the chance of becoming a centenarian, especially for males.

Effect of phytoestrogen and antioxidant supplementation on oxidative DNA damage assessed using the comet assay

Antioxidant species may act in vivo to decrease oxidative damage to DNA, protein and lipids thus reducing the risk of coronary heart disease and cancer. Phytoestrogens are plant compounds which are a major component of traditional Asian diets and which may be protective against certain hormone-dependent cancers (breast and prostate) and against coronary heart disease. They may also be able to function as antioxidants, scavenging potentially harmful free radicals. In this study, the effects of the isoflavonoids (a class of phytoestrogen) genistein and equol on hydrogen peroxide-mediated DNA damage in human lymphocytes were determined using alkaline single-cell gel electrophoresis (the comet assay). Treatment with hydrogen peroxide significantly increased the levels of DNA strand breaks. Pre-treatment of the cells with both genistein and equol offered protection against this damage at concentrations within the physiological range. This protection was greater than that offered by addition of the known antioxidant vitamins ascorbic acid and alpha -tocopherol, or the compounds 17 beta -oestradiol and Tamoxifen which have similar structures to isoflavonoids and are known to have weak antioxidant properties. These findings are consistent with the hypothesis that phytoestrogens can, under certain conditions, function as antioxidants and protect against oxidatively-induced DNA damage. (C) 2001 Elsevier Science B.V. All rights reserved.

In vitro isoflavone supplementation reduces hydrogen peroxide-induced DNA damage in sperm

Isoflavones are plant compounds, proposed to have health benefits in a variety of human diseases, including coronary heart disease and endocrine-responsive cancers. Their physiological effects include possible antioxidant activity, therefore suggesting a role for isoflavones in the prevention of male infertility. The aim of this study was to test the antioxidant effects of the isoflavones genistein and equol on sperm DNA integrity, assessed in vitro after hydrogen peroxide-mediated damage, using the cornet assay. Pre-treatment with genistein or equol at doses of 0.01-100 mumol/l significantly protected sperm DNA against oxidative damage. Both ascorbic acid (10-600 mumol/l) and alpha-tocopherol (1-100 mumol/l) also protected. Compared with ascorbic acid and alpha-tocopherol, added at physiological concentrations, genistein was the most potent antioxidant, followed by equol, ascorbic acid, and alpha-tocopherol. Genistein and equol added in combination were more protective than when added singly. Based on these preliminary data, which are similar to those observed previously in lymphocytes, these compounds may have a role to play in antioxidant protection against male infertility.

Therapeutic revascularisation of ischaemic tissue. The opportunities and challenges for therapy using vascular stem/ progenitor cells

Ischaemia-related diseases such as peripheral artery disease and coronary heart disease constitute a major issue in medicine as they affect millions of individuals each year and represent a considerable economic burden to healthcare systems. If the underlying ischaemia is not sufficiently resolved it can lead to tissue damage, with subsequent cell death. Treating such diseases remains difficult and several strategies have been used to stimulate the growth of blood vessels and promote regeneration of ischaemic tissues, such as the use of recombinant proteins and gene therapy. Although these approaches remain promising, they have limitations and results from clinical trials using these methods have had limited success. Recently, there has been growing interest in the therapeutic potential of using a cell-based approach to treat vasodegenerative disorders. In vascular medicine, various stem cells and adult progenitors have been highlighted as having a vasoreparative role in ischaemic tissues. This review will examine the clinical potential of several stem and progenitor cells that may be utilised to regenerate defunct or damaged vasculature and restore blood flow to the ischaemic tissue. In particular, we focus on the therapeutic potential of endothelial progenitor cells as an exciting new option for the treatment of ischaemic diseases. © 2012 BioMed Central Ltd

Cigarette smoking and random serum cholesterol levels in a Northern Ireland general practice population of 18- to 20-year-old students and non-students

Coronary heart disease is the commonest cause of death in Northern Ireland, but few data exist on the incidence of risk factors in young adult students and non-students.