The composition of the microbiota of the equine intestinal tract is complex. Determining whether the microbial composition of fecal samples is representative of proximal compartments of the digestive tract could greatly simplify future studies. The objectives of this study were to compare the microbial populations of the duodenum, ileum, cecum, colon and rectum (feces) within and between healthy horses, and to determine whether rectal  samples are representative of proximal segments of the gastrointestinal tract. Intestinal samples were collected from ten euthanized horses. 16S rRNA gene PCR-based TRFLP was used to investigate microbiota richness in various segments of the gastrointestinal tract, and dice similarity indices were calculated to compare the samples.Within horses large variations of microbial populations along the gastrointestinal tract were seen. The microbiota in rectal samples was only partially representative of other intestinal compartments. The highest similarity was obtained when feces were compared to the cecum. Large compartmental variations were also seen when microbial populations were compared between six horses with similar dietary and housing management.Rectal samples were not entirely representative of intestinal compartments in the small or large intestine. This should be taken into account when designing studies using fecal sampling to assess other intestinal compartments. Similarity between horses with similar dietary and husbandry management was also limited, suggesting that parts of the intestinal microbiota were unique to each animal in this study. The equine intestinal microbiota is complex and has an enormous impact on digestion, immune stimulation, pathogen protection and metabolism . StudiesAs the majority of microorganisms in the intestinal tract are not cultivable with standard methods ,16, moleThe objectives of this study were to assess the similarities of the microbial populations of the duodenum, ileum, cecum, colon and rectum (feces) within and between healthy horses using TRFLP.The legal and ethical requirements with regards to the humane treatment of animals described in the study were in accordance with the University of Guelph’s animal care guidelines. Between June and July 2009 intestinal contents were collected from ten horses euthanized for reasons unrelated to this study. Inclusion criteria were older than one year and euthanasia at our institution. Exclusion criteria were gastrointestinal or acute disease and current antibiotic administration. The horses originated from five farms; breeds included Standardbred, Thoroughbred, Welsh Pony and Bashkir Curly. Use and reason for euthanasia are described in Table Samples were collected from the duodenum, ileum, body of the cecum, pelvic flexure, and rectum via enterotomy within 4 h after euthanasia. Approximately 50 g of luminal intestinal content was collected with sterile forceps or a sterile spoon (depending on consistency of the ingesta). Samples were stored at −80°C until processed within 8 weeks of collection. The fecal sample was taken from the terminal part of the rectum.′GAACGCGAAGAACCTTAC3′ and the corresponding unlabeled primer 5′GGTGTGTACAAGACCC3′ were used for PCR analysis targeting the V6-V8 region of the 16S rRNA gene to amplify all bacteria and were adapted from a previous study in dogs ) where ‘a’ is the number of T-RF peaks unique for sample 1, ‘b’ is the number of T-RF peaks unique for sample 2, and ‘j’ is the number of common T-RF peaks . Thus, tSamples that produced no peaks on TRFLP were removed from analysis. The variation in patterns between different intestinal compartments within and between horses was calculated by pair-wise comparison of the Cs values of all samples. The means or mean ranges of both replicates are reported unless stated otherwise.To assess the differences between the six horses of the same breed under similar housing and dietary management and the remaining four horses the Student t-test or Mann Whitney test was performed for each compartment.Between 0–12 (mean: 5) T-RF peaks were generated per sample on TRFLP analysis. An example is shown in Figure Comparison of the T-RF peaks from the duodenum, ileum, cecum, colon and rectum within a horse demonstrated mean similarity indices from both replicates between all compartments ranging from 0.15-0.73, 0.31-0.71, 0.22-0.85, 0.13-0.88, 0.25-0.72, 0.26-0.90, 0.33-0.93, 0.20-0.74, 0–0.93, 0.27-0.89 for horses 1–10 respectively.The mean similarity index between duodenum and ileum was 0.44, duodenum and cecum 0.39, duodenum and colon 0.35, duodenum and feces 0.39, ileum and cecum 0.42, ileum and colon 0.42, ileum and feces 0.50, cecum and colon 0.58, cecum and feces 0.67 and colon and feces 0.49. The comparison between all compartment pairs from both replicates as well as both replicates combined (mean and ranges) are summarized in Table Rectal samples were most similar to cecal samples. Rectal samples had a mean similarity index of 0.39, 0.50, 0.67 and 0.49 when compared to the duodenum, ileum, cecum and colon, respectively Figure .p= 0.046) and cecal (p = 0.002) T-RF profiles were significantly different between the six similarly managed Bashkir Curly horses compared to the remaining 4 horses. The data for the jejunum showed a trend towards significance (p = 0.0587). The colonic and fecal T-RF profiles did not differ significantly between the two groups with p values of 0.1746 and 0.1348 respectively  are presented in Table This study identified limited similarities in richness (Cs 0.35-0.67) of the gastrointestinal microbial populations between the small intestine, large intestine and feces within individual horses. The microbial composition in fecal samples was only partially representative of the proximal gastrointestinal compartments with the closest similarity observed between fecal and cecal samples. There were also limited similarities in richness (Cs 0.44-0.74) when comparing the same intestinal segment between horses suggesting that substantial portions of the equine intestinal microbiota are unique to each animal.When comparing gastrointestinal compartments within a horse, the low similarity indices between compartment pairs indicated major differences in the richness of the microbiota along the gastrointestinal tract. This is consistent with results from a recent study by Dougal and co-workers (2012), who showed that that the microbial composition of the cecum is significantly different from the microbiota of the colon and feces. This is also consistent with results from other animal species; one study in cattle reported significant differences in the microbial community as ingesta travelled along the gastrointestinal tract . Likewiset al. (2007), who found that relative abundance of selected fecal bacterial populations, were similar but not consistently representative of cecal bacterial populations. In contrast to the above study, the method used in our study included all bacterial species and further strengthens the suggestion that fecal samples are not consistently representative of proximal compartments.Rectal samples only had limited similarity to other compartments (Cs 0.39-0.67). Overall the cecum had the highest similarity index to the rectum (Cs 0.67), which could be due to separation mechanisms or actual closer similarity. These data are in agreement with findings from Milinovich et al. (2012) investigated the microbial populations of the cecum, colon and feces of three healthy horses and five healthy ponies using TRFLP. Similar to our study, the authors found that the microbial populations of the cecum were significantly different from feces; however, in contrast to our study the microbial population of the colon and the cecum were not significantly different [et al. (2008) also found that the microbiota of the feces is representative of the distal colon; however, only certain bacterial species  where tested, therefore potentially biasing results. Schoster et al. (2012) investigated the presence of C. difficile in various intestinal compartments of horses and found that rectal samples were only positive in 63% of animals from which C. difficile could be isolated from one or more proximal compartments. The data from the present study lend further credence to concerns that the fecal microbiota is not representative of the entire gastrointestinal tract. It further supports the concerns raised about the accuracy of using fecal samples for investigation and interpretation of changes in the microbiota of proximal gastrointestinal compartments, which is commonly performed [Dougal ifferent . In theiet al. 012 inveserformed .The differences in microbiota along the gastrointestinal tract seen in our study have been observed in other studies in horses , as wellAlong the small intestine of the horse the secretion of sodium bicarbonate and bile neutralizes the hydrochloric acid from the stomach, thus favoring acid-tolerant bacteria by raising the pH of the ingesta to approximately 7.0 by the time it reaches the large intestine. Concurrently, an increase in the total amount of cultivable bacteria is seen . The ingSignificant differences in the T-RF profiles of the duodenum and cecum between the Bashkir Curly horses and the remaining horses were observed Figure . Thus, set al. (2010) investigated the fecal microbiota of 12 healthy horses using denaturing gradient gel electrophoresis (DGGE) and also assessed the influence of penicillin and anesthesia on the fecal microbiota. The authors demonstrated a very unique composition of the fecal microbiota for individual horses, with most of the variation attributable to the statistical effect of the individual horse, not anesthesia or penicillin administration. Willing et al. (2009) reported that consistency of the microbial composition of feces within an individual fed different diets was on average 73%, with a significant effect of horse on the diversity and stability of the gastrointestinal microbiota. Taken in relation to the results of these previous studies, our results support that the equine microbiota has a substantial portion unique to each animal. Such variability needs to be taken into account when comparing treatment effects between horses.Mean similarity indices for each compartment compared between animals were low suggesting substantial differences in the microbial richness between horses in all gastrointestinal compartments. This is consistent with data from other studies that found a high level of diversity between horses ,5,15. GrTRFLP allows for rapid assessment of complex bacterial communities, such as those present in the equine gastrointestinal system, and permit rapid comparison of the community richness; however, there are limitations. TRFLP cannot estimate bacterial community evenness or abundance, parameters necessary to evaluate bacterial diversity . Phylogeet al. (2012) assessing the microbiota of healthy horses and horses affected with acute colitis. Their study showed profound differences in the microbiome of diseased horses compared to healthy horses. Determining the specific composition of the gastrointestinal microbiota was not an objective of this study; therefore, TRFLP was deemed adequate.These recent advances in the field of metagenomics make this a more attractive option for future studies to conclusively determine the differing composition of the equine microbiota in different intestinal compartments. This technique has recently been used to characterize the fecal microbiota of two healthy horses, which showed that the equine microbiota is more diverse than the human microbiota, but less diverse than the gastrointestinal microbiota of cattle . MetagenComparable studies in other animals and humans have reported an average of 46–50 peaks per sample ,18. SimiThe primers for the amplification of the 16S rRNA gene for all bacteria were adapted from a previous study in dogs . The micThe sample size of 10 horses in our study was comparable to similar previous studies in horses ,15, and There was a large variation between the two technical replicates in some samples. This could potentially reflect the inherent bias of the methodology (biased PCR amplification) or insufficient restriction enzyme digestion; however, some variations between technical replicates can be expected.In conclusion this study showed that the microbial populations differ between gastrointestinal compartments of healthy horses. Fecal samples showed only moderate similarity to other gastrointestinal compartments and were most similar to the cecum. Similarity between the same compartments of different horses was low, further supporting that portions of the equine intestinal microbiota are unique to each animal.PCR: Polymerase chain reaction; T-RF: Terminally labeled restriction fragment; TRFLP: Terminal restriction fragment length polymorphismThe authors declare that they have no competing interests.AS was involved in study design, carried out sample collection, laboratory work and drafted the manuscript. JW conceived the study, took part in the study design and helped with laboratory analysis. LA participated in study design and interpretation of data. HS participated in study design and coordination, and helped revise the manuscript. All authors read and approved the final manuscript.


In the Bagnardi et al. (2001) meta-analysis, it was found that alcohol consumption increases the risk of stomach cancer (OR = 1.32 for heavy drinkers). However, it is unknown if drinking cessation reverses this alcohol-elevated risk.A systematic literature review was performed to provide the information for a meta-analysis where the dose-risk trend was estimated for years since drinking cessation and the risk of stomach cancer. A random effect generalised least squares model for trend estimation was used, employing study characteristics to control for heterogeneity.Nineteen observational studies were identified in the literature review, of which five studies quantified duration of cessation and risk of stomach cancer, giving a total of 1947 cancer cases. No significant effect of drinking cessation on the risk of stomach cancer could be found (OR = 0.99 CI: 0.97-1.02).This result should be interpreted with caution due to the limited number of studies in this area. Recent findings suggest a link between heavy drinking and stomach cancer, especially gastric noncardia, but not for moderate drinking. Since all but one of the included studies in this meta-analysis failed to control for consumption level, the current study could not test if the risk decline following drinking cessation differs between moderate and high consumers. Findiet al.  found a et al. -12. Basel. study , stomachl. study . More rel. study  stated tl. study  individuHowever, if stomach cancer, in any way, is caused by alcohol consumption, it is important for alcohol policy to have information on how fast, if at all, the increased risk from drinking falls after drinking cessation. This has implications for harm-reducing interventions as well as cost-effectiveness calculations . BesidesThe aim of this study was therefore to establish current knowledge regarding the effect of drinking cessation on the risk of stomach cancer. To this end, a meta-analysis was conducted based on relevant studies identified through a systematic literature review. This paper is structured as follows: First, the methods and materials are discussed, including the process by which studies were selected for the review and the data extraction process for the meta-analysis. This is then followed by the results of the meta-analysis, while the detailed results of the literature review are available as an Additional file http://www.prisma-statement.org).All studies were first identified through a systematic literature review. The purpose of the literature review was to both supply a complete collection of the available evidence for the meta-analysis of the trend in the relationship between time since drinking cessation and risk of gastric cancer without restrictions for study type and to give an indication of the quality and level of the current research. The process followed the PRISMA 2009 checklist  AND (“stomach cancer” OR “gastric cancer” OR “gastric adenocarcinomas”) AND (“cessation” OR “quit drinking” OR “ex drinker” OR “former drinker” OR “stop drinking” OR “stopping drinking” OR “abstainer” OR “abstinence” OR “consumption” OR “consumption level” OR “lifestyle” OR “habit” OR “protective”), searches were performed using the PUBMED database. These searches were supplemented by a review of papers cited in relevant articles. Studies were excluded for the following reasons: (1) the study was not published in English; (2) the study did not examine the risk of stomach cancer; or (3) the study did not investigate the risk of stomach cancer among former drinkers. Studies that investigated the relationship between alcohol consumption and the prognosis of already diseased individuals were not included. The results of the selection process are described by way of a flowchart , or did not provide sufficient information to allow this to be calculated, were excluded. Second, if a data set was used in more than one study, only one of the studies was included.et al. [A large amount of data was extracted from the identified studies, including but not limited to study type, sample size, gender, age distribution, risk estimates with confidence intervals, and adjustment variables  . We therThe effect measure of interest was the odds ratio (OR), although some studies reported the relative risk (RR). When the prevalence of a disease is small, the OR coincides with the RR .In order to find whether a common trend exists amongst the current literature for the effect of years since drinking cessation on risk of disease, meta-analysis in the form of a Generalised Least Squares model (GLS) was utilised . The appyit is the log of risk of stomach cancer for study i with cessation duration t. β1ti is the trend to be estimated of the change in cancer risk by alcohol cessation duration. z is an effect modifier, i.e. study characteristics that explain between-study heterogeneity (assuming no interaction between the trend and the effect modifiers). The effect modifiers can also influence the trend through interaction effects, such as β3tizi. Effect modifiers therefore estimate a different intercept (dummy) for those studies with a particular characteristic and/or a different slope (interaction term). The model goes through the origin by definition  = 0), so no intercept is estimated. In order to allow for a better fit by increasing the available information in the analysis, the data were first pooled [z). Fixed effects models assume that each included study estimated the same underlying effect [where t pooled . Variablg effect . The Q-tg effect , with thg effect . This as2-statistics, which is based on the Q-statistics above, adjusting for degrees of freedom [The trend estimation was followed by a meta-analysis comparing the highest cessation category (dose) with current drinkers, a type of analysis sometimes known as “highest vs. lowest”. This analysis was presented in a forest plot with weights based on the standard errors. Heterogeneity was assessed by the I freedom . All staNineteen observational studies that estimated the reduction in risk of stomach cancer following drinking cessation were identified. The detailed results of the literature review are available as an Additional file et al. [Inoue et al.  did quanet al. ,25-28, gA random effect linear model of the dose-risk relationship was estimated, see Models 1–4, Table 2-statistic). The random effect estimate showed about the same effect size as the fixed estimate, although a much larger confidence interval caused the estimate to be insignificant.Due to the inconclusive results from the trend meta-analysis estimations above, a so-called “high vs. low” estimation was performed in order to investigate if there was any association between drinking cessation and reduced risk of stomach cancer. Here, the longest drinking cessation group in each study was compared to current drinkers. The results are presented in the forest plot below Figure  and quesThe literature review reported several studies that estimated the risk of stomach cancer among former drinkers. All were observational studies with varying results, although more studies indicated an increase in risk for former drinkers compared to current drinkers than showed a reduction in risk. Individual studies also examined the independent effect of alcohol type on risk of stomach cancer  and the Smoking has traditionally been considered a risk factor for stomach cancer . ConnectThere is a concern that individuals who stop drinking do so for health-related reasons (or even suspicion of stomach cancer) . This mibefore cessation is expected to be higher than for current drinkers. The increase in risk after cessation may therefore be an artefact of poor matching of study groups. There is doubts about how well (some of) the included studies have matched their control and cases groups, although not enough information is available in order to test if any systematic differences exist that may explain why an increase in risk was observed for just quitters compared to current drinkers. In light of the findings in a recent meta-analysis that only heavy drinking is associated with stomach cancer [Prior studies have found “former drinker” categories often to be over-represented by former heavy drinkers and alcoholics . If thish cancer , the conUnderstanding the effect of drinking cessation on the risk of disease is important for many reasons. Several recent studies have estimated the societal cost of alcohol consumption ,35,36. SThis discussion and the results of the literature review and meta-analysis should be interpreted in relation to the discussion as to whether alcohol increases the risk of stomach cancer in the first place. As mentioned in the introduction, there is no consensus on the potential effect of alcohol, and many studies show different results although the latest meta-analysis finds an effect for heavy but not for moderate drinkers . The ratThe authors declare that they have no competing interests.JJ and U-GG designed the study. The literature review and data extraction were initially performed by JB and independently checked and updated by JJ. GH and JJ conducted the meta-analysis. All authors participated in interpretation of the results and the write-up and have approved the final version.The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2458/13/600/prepubLiterature review.[e review.-47.Click here for file


In conclusion, LFVC may be associated with ST-T abnormalities independent of metabolic abnormalities in asymptomatic adults, suggesting a plausible link between impaired pulmonary defects and cardiovascular diseases.Studies have shown that low forced vital capacity (LFVC) is associated with atherosclerosis. However, it is unclear whether LFVC is associated with resting electrocardiographic ST-T abnormalities, a common finding that is prognostic for cardiovascular events. Therefore, pulmonary functions, ST-T abnormalities defined with Minnesota Code, and cardiometabolic risk factors were examined in a cross-sectional study of 1,653 asymptomatic adults without past history of coronary heart diseases. The prevalence of diabetes, metabolic syndrome, and ST-T abnormalities significantly increased with decreasing percent of predicted forced vital capacity (%PFVC). ST-T abnormalities were observed in 73 subjects . Multiple logistic regression analysis showed that, compared with the highest quartile of %PFVC (≥99.7%), the lowest quartile of %PFVC (≤84.2%) was persistently associated with ST-T abnormalities even after further adjustment for diabetes or metabolic syndrome (odds ratio (95%CI): 2.44 (1.16–5.14) and 2.42 (1.15–5.10), resp.). Similar trends were observed when subjects were divided into quartiles according to percent of predicted forced expiratory volume in 1 second (FEV Accumulating evidence has shown that not only impaired obstructive pulmonary function but also low forced vital capacity (LFVC) and impaired restrictive pulmonary function are associated with increased risk of mortality, partially owing to cardiovascular disease , 2. SomeMeanwhile, ST depression, T-wave abnormalities, or both , particularly minor ST-T abnormalities, on the resting electrocardiogram are commonly observed in the general population without coronary heart disease –15. MajoIn the light of this evidence, we hypothesized that impaired pulmonary functions, especially LFVC, may be associated with ST-T abnormalities irrespective of cardiometabolic risk factors, diabetes, and MetS. So far, no large epidemiological studies have examined the associations between impaired lung functions and ST-T abnormalities in asymptomatic individuals without overt heart disease.Therefore, we examined lung functions, ST-T abnormalities that comprised major and minor ST-T abnormalities, cardiometabolic risk factors, diabetes, and MetS in a cross-sectional study of asymptomatic adults who underwent an annual checkup. Abnormal pulmonary function was evaluated by continuous pulmonary function variables including the percentage of predicted forced vital capacity (%PFVC).The current study represents a series of studies performed in collaboration with Josai University, Sakado, Japan, and Social Insurance Omiya General Hospital, Saitama, Japan, that were conducted to explore the causalities and mechanism in lifestyle-related diseases. The study design and protocol have been described elsewhere . The pron = 2,488) were randomly recruited from those who underwent complete medical checkups at their own will at the Health Care Center attached to Omiya General Hospital between April 2009 and March 2010. Most lived or worked close to the hospital . Individuals who required immediate treatment for suspected cancers, pneumothorax, or infectious pneumonia, including tuberculosis, were not included from the beginning. All recruited subjects, who were free from overt disability and hemiplegia, completed a questionnaire about their lifestyle characteristics. Exclusion criteria of subjects and a flow chart are shown in Asymptomatic healthy subjects . The diagnosis of MetS was based on the modified Third Report of the National Cholesterol Education Program Expert Panel/Adult Treatment Panel criteria  with the1), and ratio of forced expiratory volume in 1 second to observed forced vital capacity (FEV1/FVC) were calculated as in our previous report [1, and FEV1/FVC from data published by the Japanese Respiratory Society in 2001 [Pulmonary function tests were performed with a spirometry analyzer . The test was performed by trained technicians with the subject in a standing position. The %PFVC, percentage of predicted forced expiratory volume in 1 second . ST-T abnormalities were defined with the Minnesota Code [1, and FEV1/FVC. P values for continuous variables and categorical variables were determined with ANOVA and the χ2-test, respectively.Data are expressed as means ± SD or median/geometric mean (interquartile range). Subjects were divided into quartiles according to continuous pulmonary function variables: %PFVC, %PFEVP for trend) were calculated by treating quartile categories (Q1–Q4) as a continuous variable , and the same model analysis was conducted. In this study, hypertension (≥130/85 mmHg) was considered as a special confounder that substantially interferes with the associations because hypertension is likely to affect ST-T abnormalities and the decline of FVC [P < 0.05 were considered to be statistically significant.Multivariate logistic regression models were used to examine the associations between the lowest quartiles (Q1) of lung functions and ST-T abnormalities compared with the corresponding highest quartiles (Q4), controlling for clinical confounding factors including diabetes and MetS. This analysis yielded odds ratios (OR) and 95% confidential intervals (95% CI). Tests for linear trends  or MetS (Model 5) attenuated but did not remarkably alter the associations. In these conditions, diabetes and MetS were significantly associated with ST-T abnormalities (OR (95% CI), 2.18 (1.18–4.03), P = 0.01 and 2.20 (1.23–3.93), P = 0.008, resp.; data not shown).Multiple logistic analysis showed that compared with the highest quartile of %PFVC (≥99.7%) (Q1), the lowest quartile (≤84.2%) (Q4) was significantly associated with ST-T abnormalities . This as1. However, observed associations between lowest quartile of %PFEV1 and ST-T abnormalities were not significant after adjustment for diabetes or MetS. In contrast, no significant associations between lowest quartile of FEV1/FVC and ST-T abnormalities were observed in comparison with the highest quartile of FEV1/FVC, irrespective of adjustments for confounders.Likewise, similar trends were observed when subjects were divided into quartiles according to %PFEVP = 0.0003, data not shown) compared with the highest quartile, even after full adjustments for confounders in Model 3 of P = 0.02 and 2.58 (1.23–5.40), P = 0.01, resp., data not shown).Meanwhile, the lowest quartile of %PFVC was significantly associated with hypertension (≥130/85 mmHg) (OR (95%CI), 1.76 (1.30–2.38), 1, but not low FEV1/FVC, were significantly associated with ST-T abnormalities, which was attenuated by further adjustment for cardiometabolic risk factors, diabetes (presumably mostly type 2 diabetes in this study), or MetS, but remained significant. Notably, cardiometabolic risk factors included circulating CRP and waist circumference, surrogate markers of systemic inflammation, and amount of abdominal fat, respectively. Collectively, the current findings suggest that LFVC, which often reflects restrictive pulmonary function pattern, may be independently associated with ST-T abnormalities irrespective of clinical confounders, diabetes, and MetS, whereas obstructive pulmonary function defects are not.This study was conducted to investigate the relationship of impaired lung functions with resting electrocardiographic ST-T abnormalities in a cross-sectional analysis of asymptomatic adults without past history of heart disease. We found that LFVC and probably low FEVSo far, no clinical study has examined the relationship of LFVC with electrocardiographic abnormalities with the exception of a study by Sideris and Katsadoros . This stAccording to previous studies, LFVC and restrictive pulmonary defects have been associated with coronary artery calcification  and arteConsidering that LFVC was associated with ST-T abnormalities independently of cardiometabolic factors, circulating CRP, diabetes, and MetS, which are proatherosclerotic and proinflammatory , 10, sev1) are associated with low birth weight [Meanwhile, many studies in the past decade have shown that a predisposition for cardiovascular disease and impaired pulmonary functions (low vital capacity and low FEVh weight , 26, posh weight . LFVC anAlternatively, physicochemical factors might interfere with the associations. Of note, the American Heart Association recently updated its scientific statement to describe that exposure to particulate-matter air pollution contributes to cardiovascular morbidity and mortality . It highSeveral limitations should be mentioned. First, because of the nature of cross-sectional studies, causality remains unknown and must be elucidated in large prospective studies. Second, it was not possible to distinguish between major and minor ST-T abnormalities in this study because the electrocardiogram findings on individual checkup sheets in combinations of major and minor ST-T abnormalities were recorded together indistinguishably. However, most ST-T abnormalities were likely to be minor ST-T abnormalities because the prevalence of minor ST-T abnormalities is approximately 2-fold greater than that of major ST-T abnormalities in the Japanese population .Third, all subjects in this study were instructed by staff members trained in spirometry, and the subjects performed a few rehearsals. Nevertheless, it was not clear whether all subjects had acceptable results in the actual test, especially the elderly, regardless of cognitive status, physical performance, or education level. This is likely to result in potential bias of the outcomes.Finally, most subjects were healthy with good profiles in terms of various parameters, although a small portion of them had several critical conditions such as diabetes or history of stroke. Therefore, the current findings may not be applicable to other populations that have more cardiometabolic risk factors and ST-T abnormalities, where the observed associations, if any, might be dependent on hypertension, diabetes, or metabolic syndrome.LFVC may be associated with ST-T abnormalities independently of cardiometabolic risk factors, diabetes, and MetS in asymptomatic adults without overt heart disease. Our results suggest that there is a mechanism linking low vital capacity with common electrocardiographic abnormalities and that this mechanism is prognostic for increased risk for cardiovascular diseases, which needs to be confirmed in further larger studies.


To explore the relationship between the liver X receptor α gene (LXRα) rsl2221497 polymorphism and the susceptibility of coronary heart disease (CHD) and serum lipids and glucose levels.The single fluorescently labeled probes technique was used to detect the genotype of rsl2221497 in LXRα gene in 240 CHD patients and 250 healthy control subjects. The difference of genotype distribution between the two groups was analyzed using of Chi-square test. The serum lipids and glucose levels between the different genotypes were also compared.P <0.05), and the risk of CHD in carriers with A allele increased 0.88 times compared to that in G allele carriers . Logistic regression analysis showed that after adjusting for other confounding factors, A allele was an independent risk for CHD. However, there were no differences in serum lipids and glucose levels between each genotype.The risk of CHD in carriers with (AA + GA) genotype was 1.76 times as that in the GG genotype carriers (OR = 1.76, 95% CI: 1.18-2.87, The rsl2221497 polymorphism in LXRα gene was associated with susceptibility of CHD in Han population. Coronary heart disease (CHD) is a multifactorial disease resulting from the interaction between genetic factors and environmental factors-4. CurreThe present study has been performed with the approval of the ethics committee of General Hospital of the Air Force PLA and is in compliance with the Helsinki Declaration. The informed consents of the study were collected from all the candidate subjects.From August, 2009 to June, 2012, two hundred and forty hospitalized patients diagnosed as CHD in our hospital were enrolled as the case group, in which one hundred and ninety-one patients were male and forty-nine patients were female. The average age was 61.22 ± 10.22 years. CHD was diagnosed according to WHO issued ischemic heart disease diagnostic criteria in 1979. In the light of coronary angiography, ≥ 50% of stenosis of the main branches was defined as CHD.In control group, 250 healthy inpatients were selected during the same period in our hospital, 192 were male and 58 were female with mean age of 61.43 ± 11.21 years. The disease history, physical examination, laboratory tests , ECG and other preliminary tests were performed. The history of CHD, hypertension and diabetes were detected. All the subjects were Han Chinese people.The clinical data including past medical history, family disease history, smoking and drinking history, weight, height, blood pressure, body mass index (BMI) were collected in the present study.2 mL of 12 h-fasting venous blood was collected, and the triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), fasting blood glucose (FBG) and other biochemical parameters were detected using biochemical analyzer .100 uL of EDTA anti-coagulated blood was taken, and the blood genomic DNA was extracted from whole blood according to the protocol of DNA-extraction kit (Shanghai Shennengbocai company) and was dissolved in TE solution and stored at -20°C refrigerator.2 were purchased from Shanghai Shennengbocai company . Primer sequence was as follows: upstream primer: 5 '-GGCTTACTC CAA TAA TCC CCA CAC TT-3’, downstream primer: 5'-AAGGAAGAAGGCAGGTAATGATGAAGGAG-3' .Light Cycler gene amplification detector was utilized for PCR reaction. Taq DNA polymerase, 4 × dNTPs, 10 × Bufier buffer and MgClt test. Genotype and allele frequency distribution in the case group and the control group were calculated with direct counting method. Hardy-Weinberg equilibrium was performed using Chi-square test, genotype and allele frequencies distribution between the two groups were compared using chi-square test or Fisher's exact test. Multivariate Logistic regression model was used to analyze risk factors of CHD, the odds ratios (OR) and 95% confidence intervals (95% CI) were used to express the relative risk.Statistical analysis was performed using SPSSl3.0 . Continuous data were expressed as mean ± standard deviation (M ± SD). Difference between the two groups was compared by using of Three genotypes were detected in rsl2221497, namely as GG homozygote, AA homozygote, GA heterozygote.P > 0.05). However, there were significant difference between the two group in TG, TC, HDL-C, LDL-C, FBG  were not significantly different between the two groups (P > 0.05) indicating that the genotype frequency distribution reached the genetic equilibrium, the sample can represent the whole group. Genotype analysis showed that the CHD risk in AA + GA genotype carriers was1.76 times as that in GG genotype carriers . A allele frequency in CHD group was significantly higher than that in control group (P <0.01), and the odds ratio (OR) was 1.88 (95% CI:1.21-3.43), Table Genotypes in CHD and the control group were in line with Hardy-Weinberg equilibrium , Table P <0.05, 95% CI: 1.09 ~ 3.55) after adjustment of other confounders.In multivariate Logistic regression analysis, the CHD was taken as the dependent variable. The age, sex, BMI, TC, TG, LDL-C, HDL-C, FBG, A allele, smoking history, hypertension history, diabetes mellitus history were taken as independent variables in Logistic regression analysis. The results showed that HDL-C, TC, TG, history of hypertension, smoking history, age, BMI, A allele were independent risk factors for CHD, the OR for A allele was 1.85  which indicated that this locus had significantly increased risk for CHD. A recent study indicated that in the female population, LXR α polymorphism was significantly correlated with BMI and HDL-C concentration[Our studies suggested that in Chinese Han patients with CHD, the LXRα A allele frequency was significantly higher than that in the healthy population, A allele carries had 0.8 times increased risk of CHD (OR = 1.81). In the multivariate Logistic regression analysis, after the adjustment of age, sex, cholesterol, fasting glucose, hypertension, diabetes, smoking history and other confounding factors, A allele was still a risk factor of CHD independent of other traditional risk factors (ntration. In a Frntration. The dieThere were several limitations in our study. Firstly, the relative small sample size may reduce the statistics power and overestimate the OR value. Secondly, in the present study, we only investigated one SNP in LXRα gene. Although many previous studies suggested this SNP was associated risk factors of CHD, this SNP may not figure out the relationship between LXRα polymorphism and serum lipids and CHD risk. Finally, we only investigate this association in one case-control study, another independent case-control study for verification was not designed.In conclusion, this study first reported the association between genetic variation of LXR α gene and CHD in Han population. It provided some new clues to further understand the mechanism of the development of CHD and prevention. The study also confirmed from the genetic level that the lipid metabolism was the risk factor of CHD.The authors declared no competing interests exist.YFZ and ZXL carried out the molecular genetic studies and drafted the manuscript. YFZ and JZ carried out the genotyping. QX, JJL, and XYZ participated in the design of the study and performed the statistical analysis. YYL conceived of the study, and participated in its design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.


Lavender essential oil shows evidence of sedative properties in neurophysiological and animal studies but clinical trials of its effectiveness as a treatment of agitation in people with dementia have shown mixed results. Study methods have varied widely, however, making comparisons hazardous. To help remedy previous methodological shortcomings, we delivered high grade lavender oil in specified amounts to nursing home residents whose agitated behaviours were recorded objectively.64 nursing home residents with frequent physically agitated behaviours were entered into a randomized, single-blind cross-over trial of dermally-applied, neurophysiologically active, high purity 30% lavender oil versus an inactive control oil. A blinded observer counted the presence or absence of target behaviours and rated participants’ predominant affect during each minute for 30 minutes prior to exposure and for 60 minutes afterwards.Lavender oil did not prove superior to the control oil in reducing the frequency of physically agitated behaviours or in improving participants’ affect.Studies of essential oils are constrained by their variable formulations and uncertain pharmacokinetics and so optimal dosing and delivery regimens remain speculative. Notwithstanding this, topically delivered, high strength, pure lavender oil had no discernible effect on affect and behaviour in a well-defined clinical sample.12609000569202)Australian and New Zealand Clinical Trials Registry (ACTRN  Lavandula) is used as a relaxant in many aged care facilities. While evidence in support of its use is mixed, its potential for sedative and anticonvulsant activity is clear. After rapid absorption via skin or respiration [The fragrant oil extracted from lavender  participants demonstrate one or more behavioral symptom to a specified degree and frequency; (ii) treatments are deployed in time frames and settings when the behavioural symptom is most evident; (iii) behaviours are counted directly to limit the bias inherent in staff-completed rating scales; (iv) observers are blinded as much as possible, (v) and allowance is made for non-specific placebo effects . For stuOptimal dosing regimens and formulations have yet to be established . When laThe current study was designed to address these methodological issues by means of a single-blinded, randomised, controlled cross-over trial of high strength, certified pure lavender oil with proven neurophysiological activity. It was administered topically to nursing home residents with significant, persistent physically agitated behaviours that were counted by trained observers before and after application. Physically agitated behaviours were chosen in preference to physically aggressive and verbally agitated behaviours because of their higher frequency and greater ease of measurement. It was hypothesised that lavender would be associated with a significantly greater reduction in selected behaviours than a neutral control oil. Since lavender appears to act as a sedative, its calming effects on behaviour should be accompanied by an evident improvement in emotional well-being. Measures of positive and negative affect were therefore added as outcomes.Study participants were recruited from eight specialist psychogeriatric nursing homes and three private nursing homes in Melbourne, Australia, between 2009 and 2011. The following criteria were required for inclusion: (i) a rating by nursing staff of at least mild dementia on the Clinical Dementia Rating scale ; (ii) a The trial was approved by all relevant committees including the Monash University Human Research Ethics Committee. Written consent was obtained from the next of kin or legal guardians of all participants.Lavandula angustifolia) were submitted for electrophysiological analysis to the Department of Pharmacology and Toxicology, Otago University, New Zealand, using established methods [Four samples of 100% pure lavender oil  or absent (zero points) during each minute giving a maximum score of one point per minute of observation. Results were computed as mean counts over the three 30-minute observation periods. Inter-rater reliability was high with an average Kappa of 0.98 over five training sessions. This time-sampling method has been used successfully in our previous studies .Observers also used the Philadelphia Geriatric Center Affect Rating Scale to record the predominant type of affect  evident during every minute . The preOther measures included the Mini-Mental State Examination (MMSE) and the Cohen-Mansfield Agitation Inventory (CMAI) ,27. To iSample size was calculated with respect to the primary outcome measure of physically agitated behaviour for a two-sided hypothesis test with a Type I error rate of 0.05 and power set at 90%, based on data from an earlier repeated measures study of simulated family presence versus music therapy in a similar population and setting . In thatThe behaviour and affect scores were over-dispersed relative to Poisson expectations and were therefore modelled using random effects negative binomial regression, taking account of participants’ age, gender and dementia severity. The results of the analyses are shown as mean scores and incidence rate ratios for completed cases. Ratios over one signify an increase in a mean value, and ratios below one signify a decrease in that value, with respect to a reference condition. Ratios are displayed for treatment (lavender versus the control reference condition), time (post-exposure versus the pre-exposure reference condition) and treatment-time interaction.Figure Most participants were female (59%); very old ; markedly cognitively impaired , and physically agitated . The behaviours selected for observation (with numbers) included pacing (55), repetitive mannerisms (5), general restlessness (2), disrobing (1) and intrusiveness (1).For reasons of clarity, raw results are listed in Table Table Results were similar for affect ratings Table b. CountsNo dermatological or other possible or probable adverse effects were noted as a result of exposure to either the lavender or control oils.Counts of agitated behaviours were lower during exposure to lavender than to the control oil but this occurred before and after exposure. The observed differences were most probably due to chance. Counts of agitated behaviours also declined over the 90-minute observation period, irrespective of experimental condition, consistent with a spontaneous remission in symptom severity. Treatment was delivered at the time of day when agitated behaviours were expected to peak to maximise the chances of identifying any benefit. Since symptoms wax and wane over the 24-hour period, behaviours were likely to remit regardless of intervention, representing a simple regression to the mean rather than a genuine therapeutic effect.In devising the protocol, we had sought to avoid the methodological pitfalls identified in previous systematic reviews of treatments of the behavioural and psychological symptoms of dementia ,28. Partany improvement in behaviour or affect during exposure to lavender relative to the control oil based on a limited number of analyses of a very large number of data points.To ensure statistical power, we sought 77 subjects based on data from an earlier controlled trial of a psychosocial intervention using identical methods in a similar clinical sample. We succeeded in recruiting and retaining only 64 people, despite doubling the study period from one to two years. It seems very unlikely, however, that our negative results are due to inadequate power as there is no suggestion in the raw data of The most significant limitation to research of essential oils concerns product variability and the limited knowledge base of lavender’s pharmacological properties. There are very few studies of its absorption, metabolism and central nervous system availability in animals and healthy humans, let alone frail older people with dementia. Lavender appears to be well absorbed and to have sedative and anticonvulsant potential but information is otherwise limited with the result that dosing strategies are based largely on traditional practice. We settled on a topical dose of 1 ml 30% certified pure lavender oil applied to each forearm only because a higher strength was so viscous that application became impracticable. This was still much higher than the doses delivered by vapour in most previous studies. Future researchers should consider measuring plasma levels of linalool and linalyl acetate as a check on absorption.The current lack of information also makes it difficult to understand why two studies have returned positive results while five others, including the present one, have not. Without a consistent proprietary formulation and sound pharmacokinetic data, of the kind now reported routinely for new pharmaceutical products, there may be little value in further clinical trials.Studies of essential oils are constrained by their variable formulations and uncertain pharmacokinetics and so optimal dosing and delivery regimens remain speculative. Notwithstanding this, topically delivered, high strength, pure lavender oil had no discernible effect on affect and behaviour in a well-defined clinical sample.The authors do not have competing interests.All the authors participated in the preparation of the manuscript and have read and approved the final draft. DO’C conceptualised and designed the study; EvdP and BE conducted the study and analysed the results, and JT helped with statistical analysis. All authors have read and approved the manuscript.The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1472-6882/13/315/prepub


CD14 gene in subjects with chronic periodontitis.Periodontitis is a common disease that affects the periodontal tissue supporting the teeth. This disease is attributed to multiple risk factors, including diabetes, cigarette smoking, alcohol, pathogenic microorganisms, genetics and others. Human beta-defensin-1 (hBD-1) is a cationic antimicrobial peptide with cysteine-rich ß-sheets and broad-spectrum antimicrobial activity. CD14 is a protein involved in the detection of bacterial lipopolysaccharide (LPS) and has also been associated with periodontitis. This study investigates the single nucleotide polymorphic (SNP) region, -1654(V38I), of the human beta-defensin-1 (hBD-1) gene as well as the -159 region of the DEFB1 with the enzyme HincII. The polymorphic site 159TT of CD14 was digested with the enzyme AvaII. Enzyme-linked immunosorbent assay (ELISA) was performed on soluble samples to determine the protein expressions.Blood samples from periodontally healthy subjects and periodontitis patients were obtained. DNA was extracted from the blood and was used to perform restriction digest at the polymorphic G1654A site of DEFB1, respectively. The A allele frequency of the control group was 40%, while the patient blood group was 54%. The mean hBD-1 protein levels of the control and patient samples were 102.83 pg/mL and 252.09 pg/mL, respectively. The genotype distribution of CD14 in healthy subjects was 16% for C/C, 26% for T/T and 58% for C/T. The genotype frequencies of CD14 in periodontitis patients were 10% for C/C, 43% for T/T and 47% for C/T. The CD14 protein expression determined by ELISA showed a mean protein level of the control samples at 76.28ng/mL and the patient blood samples at 179.27ng/mL with a p value of 0.001.The control and patient groups expressed 35% and 38% 1654 A/A genotype of DEFB1 gene and the 159T/T genotype on the CD14 gene.Our study demonstrated that patients suffering from chronic periodontitis present more commonly with the 1654A/A genotype on the DEFB1 and CD14 gene, with the purpose of expanding knowledge for the future development in diagnostic markers or therapeutic interventions to combat this disease.This study purely investigated the association between periodontitis and one polymorphic site on both  Porphyromonas gingivalis  [Periodontitis is a chronic infectious disease involvingivalis) , geneticgivalis) , uncontrgivalis) , stress givalis) , impairegivalis) ,8, alcohgivalis) . Of the et al., 2007)[et al., 2007)[DEFB genes, are present in three main gene clusters located on chromosome 8p22-34 [In recent years, a number of genetic polymorphisms and their association with periodontal diseases have been studied, which il., 2007), IL-17 [l., 2007), matrix l., 2007). They col., 2007). These p 8p22-34 . Human ß 8p22-34 ,22. Alth 8p22-34 . hBD-2 e 8p22-34 .DEFB1) and hBD-3 (encoded by DEFB103) are constitutively expressed at low levels in the skin [DEFB4) is not expressed in normal skin but is highly expressed in inflammatory tissues. hBD-2 is absent or at low levels in normal epithelia. Serum hBD-2 levels in healthy individuals are very low (less than 1 ng per ml) [hBD-1 (encoded by the skin . hBD-1 i per ml) ; convers per ml) . The loc per ml)  and oral per ml) , gingiva per ml) , human a per ml) , nasolac per ml) , and ocu per ml) , as well per ml)  in respo per ml) .DEFB1 has been demonstrated to have a positive correlation with common diseases such as chronic obstructive pulmonary disease [Genetic polymorphisms of hBD-1 and their associations with periodontitis have been investigated at SNP sites -692 and -44, respectively . The con disease  and atop disease . HoweverCD14 is a 55-kDa glycosyl phosphatidylinositol-anchored glycoprotein expressed on the surface of white cells [CD14 exists in two forms: either anchored to a cell membrane by a glycosylphosphatidylinositol tail (mCD14), or in soluble form (sCD14). sCD14 is produced by enzymatically cleaved membrane CD14, mediated mainly by phospholipase C, and via secretion of CD14 [CD14 binds to LPS in the presence of lipopolysaccharide-binding protein. Subsequently, a series of reactions take place and eventually trigger intracellular signalling, causing the production of pro-inflammatory cytokines. Its concentration in serum has been found to increase in several clinical pathologies, such as periodontitis [CD14 promoter, where a C to T transition occurs [CD14-159 TT genotype with chronic periodontitis [te cells . As a LPte cells . CD14 ex of CD14 . Usuallydontitis , rheumatdontitis , systemidontitis  and tubedontitis . A SNP in occurs . Previoudontitis , myocarddontitis  and pulmdontitis .in vitro study in the reconstituted human gingival epithelium model shows that in addition to TLR2 and TLR4, CD14 may also be involved in the regulation of hBD-2 expression by P. gingivalis LPS [β-defensin inducers [Our recent alis LPS . Lipopolinducers .CD14 genetic polymorphisms with the severity of chronic periodontitis [CD14 polymorphisms and their serum levels with chronic periodontitis in Chinese subjects.Considering the association of dontitis , the pre108 systemically healthy, non-smoking Chinese adults  were randomly selected from the voluntary blood donors at Hong Kong Red Cross between September 2004 and March 2007. After the blood samples of these healthy volunteers were collected, they were scheduled for oral examinations at Keenlink Dental Clinic, Hong Kong, where they were determined to be clinically healthy or have gingivitis, without furcation involvement or generalized gingival recession. All subjects who were determined to be free of oral soft tissue abnormalities or severe dental caries were allocated to the control group.44 Chinese subjects  with moderate to advanced chronic periodontitis were recruited from West China Hospital of Stomatology, Sichuan University. The diagnosis of chronic periodontitis was made following the criteria defined by the American Academy of Periodontology in 1999 . The subThe sample size of this study was determined based on the reports of Machin and Lemeshow. In the report, the sample size was determined based on 0.05 level of significance for two arms to achieve 90% power ,48.The study protocols were approved by the Ethics Committee, Faculty of Medicine, The University of Hong Kong and Sichuan University, PRC. Informed consent was obtained from all subjects.Peripheral blood samples were collected by direct venipuncture from the arm vein of each subject: 20 ml in lithium heparin tubes and 10ml in clot blood tubes , respectively. The samples were certrifuged for 10 min at 1,500 rotations per minute (rpm), and serum and plasma was then collected for enzyme-linked immunosorbent assay (ELISA) analysis. The remaining cellular components were transferred to a 50 ml centrifuge tube with an addition of red blood cell lysis buffer up to 45 ml. The mixture in the tube was inverted several times and then centrifuged for 10 min at 1,500 rpm. The supernatants were discarded, and the remaining components were washed with 0.9% PBS used for DNA extraction.260. The extracted DNA was labelled and stored at -80°C until further analysis.Genomic DNA was extracted from each blood sample using the QIAamp DNA Blood Mini Kit . The DNA concentration was estimated by measurement of ODDEFB1 was amplified using the following primers: forward, 5’-CAAGCCATGAGTCTGAAGTGT-3’; and reverse, 5’-TCAACAGTGGAGGGCAATGT-3’ according to a previous study[2, and nuclease free water. All procedures were carried out in a sterile and stable environment to prevent external contamination. PCR was undertaken in a thermal cycler  with a mixture containing 20 units of nuclease-free water, 25 units of Master Mix, 0.5 units of each primer and 3 units of extracted DNA sample. The cycling conditions programmed were denaturation at 94°C for 5 min, followed by 30 cycles at 94°C for 30 sec, 30 sec at 56°C, extension at 72°C for 1 min, with a final extension at 72°C for 5 min. The products from the thermal cycling were stored at -80°C until restriction enzyme digestion [The 111 bp exon region consisting of the G1654A SNP region of ous study. A PCR kigestion .DEFB1 fragment generated from the PCR procedure was digested using HincII restriction enzyme . A 10 μl aliquot of the PCR product was mixed with 5 units of HincII, 10 μl of nuclease free water and 1 μl of restriction enzyme buffer. The entire mixture was incubated at 37°C for 2 hours. All digestion reagents were kept on ice before incubation.The 111 bp of The electrophoresis was performed with 5 μl of digestion product and 1μl of Ready-Load 1 Kb DNA Ladder  which were loaded onto a 4% agarose gel , and the gel was visualized with ethidium bromide .CD14 was performed following a previous protocol [CD14 gene promoter was amplified by a PCR fragment of about 500 base pairs of the following primers: forward, 5’-GTGCCAACAGATGAGGTTCAC-3’; and reverse, 5’-GCCTCTGACAGTTTATGTAATC-3’. PCR was performed with 250 ng DNA in Master Mix , 12.5 µl of each pairs of primers (15 pmol). The PCR conditions were denaturation at 94°C for 5 min, then 30 cycles at 94°C for 30 sec, 57°C for 30 sec, extension at 72°C for 1 min, and followed by a final extension at 72°C for 5 min. The products were stored at -80°C until restriction enzyme digestion. The PCR products was then digested by AvaII  at 37°C for 16 h and separated in a 2.5% agarose gel. The gel underwent electrophoresis at 100 volts, 100 milliAmperes for 30 min. Visualization was performed by means of a Dolphin-DOC ultraviolet illuminator .The analysis of -159 polymorphism of protocol . The CD1The supernatant of the blood samples were used for hBD-2 and CD14 assays , following the manufacturer’s instructions. 100 µl of serum samples were pipetted into a 96-well microplate for assay of hBD-2 and CD14, respectively. The microplates were incubated at 350 rpm for 2 hours and washed with washing buffer three times. The wells were then dried and 200 μL of substrate tetramethylbenizidine was added into each well for 20 min at room temperature. The plates were then read at 450 nm wavelength using Universal Microplate Reader . The levels of hBD-2 and CD14 were determined by comparison with the standard curve generated from the standards supplied by the manufacture. Each sample was analysed in triplicates. The levels of hBD-2 and CD14 were presented as pg/ml and ng/ml, respectively.DEFB1 and CD14 polymorphisms in the patient and control groups was compared by the Chi-square test. The relevant odds ratios between the groups were analyzed. The difference in serum levels of hBD-2 and CD14 between the groups were evaluated with an independent t-test. A p-value of 0.05 or less was regarded as statistically significant. Statistical analysis was performed using SPSS 15.0 for Windows .The detection frequency and genotype distribution of p<0.05) for the following clinical results: pocket depth (PD): 6.1 ± 2.7mm vs. 2.7 ± 1.2mm; Clinical Attachment Loss (CAL): 6.2 ± 2.9 mm vs. 0; percentage of sites with bleeding on probing (BOP): 78.2 ± 19.8% vs. 40.3 ± 9.5% and gingival recession: 38.9 ± 25.9% vs. 1 ± 1.2%. There was no significant difference found in the age and gender ratio between the groups.Table p < 0.05) compared to the healthy control group.The blood count of the control subjects and periodontitis patients are presented in Table DEFB1 and CD14 demonstrating where SNPs occur and restriction sites are shown in Figures DEFB1, homozygous G/G alleles were represented by a DNA band with a size of 111 bp, and the homozygous A/A alleles were represented by DNA bands with sizes 93 and 18 bp. Heterozygotes displayed a combination of both alleles .The DNA sequence of CD14 were represented by a DNA band with a size of 497 bp, and the homozygous T/T alleles were represented by DNA bands with sizes of 353 and 114 bp. Heterozygotes C/T displayed a combination of the alleles . Overall, significant difference was found in the distribution of DEFB1 and CD14 genotypes between the groups  than in the controls (59%) (p < 0.001). The subjects with the G allele are four-folded at lower risk for moderate to severe chronic periodontitis . The genotype of G/G was significantly lower in the patient group (20%) than the healthy controls (54%) (p < 0.001). Individuals with the G/G genotype are at approximately four times lower risk for moderate to severe periodontitis than people with A/A and G/A genotypes .Homozygous C/C alleles of CD14, the genotype of T/T was significantly higher in the patient group (43%) than the control group (26%) (p < 0.05). Individuals with the T/T genotype are at twice a greater risk to develop moderate to severe periodontitis than people with C/C and C/T genotypes .For p < 0.01)  , while no significant difference was found in the control subjects who presented with different CD14 genotypes  of hBD-2 than the patient group (252.09 pg/ml). The results suggest that subjects with the 1654AA genotype may tend to exhibit a higher serum level of hBD-2 in response to periodontal infection. Further investigations would be required to confirm this hypothesis.et al’s findings provide evidence for a significant association of the rare A allele of the DEFB1 variant with an increased risk for periodontal diseases [DEFB1 indicated that the G-A nucleotide transition could influence the putative binding site of its proteins [Schaefer diseases . This asdiseases . Their rproteins .CD14-159 C > T polymorphism, a SNP at position -159 in the promoter region of the gene encoding this pattern recognition receptor, is associated with elevated plasma/serum concentrations of soluble CD14, an increased risk for myocardial infarction and a decreased risk for allergies and asthma [The d asthma .CD14 along with TLR-4 and MD-2 detects bacterial LPS and causes the release of cytokines and antimicrobial peptides like hBDs. The present study extended to investigate CD14 gene polymorphisms along with antimicrobial peptide polymorphisms. In previous studies, it was proven that there would be increased soluble sCD14 levels in the saliva and serum of patients with periodontal infection [CD14 gene polymorphisms are considered as potential diagnostic markers for periodontitis. The results from this study established the detection frequency of CD14 T/T genotype in periodontitis patients (43%) to be significantly greater than periodontally healthy controls (26%). It is interesting to note the serum levels of CD14 in the periodontitis group was significantly higher than the levels in the controls. Similarly, periodontal patients with the same genotypes displayed higher levels of CD14 than their healthy subjects. Even within the periodontitis group, subjects with the T/T genotype exhibited higher levels of CD14 than subjects with C/C or C/T genotypes. The current findings on an increased detection frequency of T/T genotype in parallel with an increased serum level of CD14 protein is consistent with other studies on genetic polymorphisms of CD14 gene where the T/T genotype is also shown to be more frequent in severe periodontitis. The present study supports the notion that a T/T genotype at the -159 position of the CD14 gene is associated with chronic periodontitis. It is estimated that individuals with the T/T genotype are at twice a greater risk for moderate to severe periodontitis than people with C/C and C/T genotypes.nfection ,58. CurrDEFB1 gene and the -159 T/T genotype on the CD14 gene, in parallel with increased serum levels of hBD-2 and soluble CD14. Within the limitations of the study, the present findings suggest that DEFB1 and CD14 gene polymorphisms are significantly associated with chronic periodontitis and could possibly be potential markers for assessment of risk for periodontal disease. Further investigation is warranted to elaborate on the diagnostic values of these potential markers in clinical practice.The current study demonstrates that patients with moderate to severe chronic periodontitis present more commonly with the -1654 A/A genotype on the β-defensin and CD14 gene polymorphism in evaluating the status of chronic Inflammation”.We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work. There is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, the article entitled, “Clinical application of human WTYL conducted the research, performed data collection and data analysis, and participated in manuscript writing. YY and CF, JL and YT conducted the clinical examination and performed data collection. LB performed data collection and data analysis. MW supervised clinical examination and participated in manuscript planning. HL performed data analysis and participated manuscript writing. MNBC conducted the clinical examination and participated in manuscript writing. LWCC participated in manuscript planning and writing. Dr. Liu Qing was responsible for data collection. All authors read and approved the final manuscript.


A number of labyrinthine disorders with sensorineural hearing loss, vertigo, and tinnitus are known to occur to young people without vascular risk factors, thus being classified as “idiopathic” in the absence of satisfactory explanations; in the last decade, this phenomenon has found a reliable explanation by the adverse effect of a sharp decrease of blood pressure values followed by an abnormal vasomotor regulation. This model may not only be applied to healthy subjects, but even had some confirmation in conditions possibly affecting hemodynamic changes, such as heart failure or treated hypertension. In particular, the results of a recent study on the impact of different antihypertensive therapies, which was analyzed by monitoring the onset or enhancement of tinnitus as a symptom of inner ear sufferance, unequivocally demonstrated an increased prevalence of tinnitus in subjects submitted to more “aggressive” treatments. This seems in agreement with recent observations about the model of fluid homeostasis of the inner ear, and suggests, when possible, to resort to treatments with modulatory effects in order to maintain a steady perfusion to the labyrinth thus protecting its function. A relatively frequent problem otorhinolaryngologists and audiologists must deal with is represented by the onset of labyrinthine troubles  affecting young people without vascular risk factors. As most of these affections are labelled as “idiopathic”, in the absence of a precise cause, it seemed logical to look at some hemodynamic features, not necessarily of pathologic nature, which could be at the origin of the phenomena: namely, it was hypothesized - and to some extent demonstrated - that hypotension followed by an abnormal vasomotor regulation could generate a transient ischemia and a consequent sufferance of the inner ear ,2. ActuaThis argument could represent a satisfactory explanation for a number of cases of labyrinthine impairment affecting young healthy subjects in absence of other recognizable causes; accordingly, it should be kept in mind, as it could be responsible for a recurrence of this kind of disorder when the underlying conditions are not modified. Moreover, if in some cases a particular cardiovascular/autonomic profile can be postulated as a basis for explaining this phenomenon ,7, analoTo study the possible effect of different antihypertensive drugs on the inner ear function, tinnitus appears as an available symptom. Actually, it is a non-specific disturbance which can derive from any level of the auditory pathways, but implies a cochlear involvement in a number of cases : this seEven if the study did not investigate any causal factor(s) of tinnitus, which can even present as a symptom deriving from an underlying vascular damage, the reported data seem to confirm a possible involvement of a rapid lowering of blood pressure values, followed by a sharp vasoconstriction, among the threatening factors to the labyrinth. It must be considered that the latter is characterized by a blood supply of terminal type, and therefore represents a typical model of end-organ which can be more easily prone to damages linked to an acute lack of perfusion. In addition, the complexity of the labyrinthine structures is to be considered, as a noteworthy amount of energy is required in order to maintain the homeostasis of fluids: this can result in an overexposure of the inner ear to adverse effects due to hemodynamic variations.Indirect support for this interpretation is provided by the recent report of a therapeutic effect of water intake in Meniere Disease : this laAs already mentioned, the latter seems to be a not negligible factor for maintaining the regulation of the inner ear fluids, which derives from complex processes recently better clarified by focusing on the presence and the role of aquaporins : these pThese observations, along with the results concerning our group of patients with sudden sensorineural hearing loss ,2 are inIn conclusion, it must be firstly precised that the present paper does not aim at discussing about the primary necessity of setting a safe and effective therapy in subjects with hypertension, which obviously must be applied according to the most appropriate modalities in order to avoid major cardiovascular events; moreover, further prospective studies are needed to draw precise conclusions about the relationship between tinnitus and antihypertensive drugs. However, the awareness of some aspects concerning the effects on a peripheral sensory organ could be of some additional utility when choosing the therapy; from this point of view, it should be considered that drugs that block the vascular effect of either sympathetic activation, as alfa-blockers, or tissue renin – angiotensin system, as angiotensin II receptor blockers, seem to be useful to reduce tinnitus , on one


This study indicates that increased level of β-HCH and dieldrin may be associated with the risk of PD.The cause of Parkinson's disease (PD) remains elusive, but environmental chemical exposures have been postulated to be involved in the etiology of PD. We examined the association between the persistent organochlorine pesticides (OCPs) and PD in the North Indian population. This case control study included 70 PD and 75 control subjects in the age group of 50 to 85 years. Blood samples were collected and high-purity grade hexane and acetone (2 : 1 ratio) were used for extraction of organochlorine residues. OCPs (hexachlorocyclohexane (HCH), aldrin, dieldrin, endosulfan, pp′-Dichlorodiphenyldichloroethylene (pp′-DDE), op′-DDE, pp′- Dichlorodiphenyltrichloroethane (pp′-DDT), op′-DDT, pp′-dichlorodiphenyldichloroethane (pp′-DDD) and op′-DDD) were quantitatively estimated by using gas chromatography. The most frequently detected OCP was dieldrin, which was present in 9.3% of control and 61.4% of PD. The strongest predictor was  Neurodegenerative diseases form a subset of pathologies that are characterized by a progressive loss of neurons paralleled by the emergence of misfolded proteins in various cell types, the significance of which is still being debated . ParkinsWorldwide, more than 25 million tons of pesticides are used every year, and 99% of these pesticides are being released aimlessly into the environment . In IndiThis case control study included 145 subjects in the age group of 50 to 85 years, during the period from February 2010 to January 2012, attending the outpatients department of neurology of a tertiary care hospital in New Delhi, India. Out of these, 70 subjects diagnosed with PD were enrolled in the study group. PD was defined by United Kingdom Parkinson's Disease Society Brain Bank Criteria [Blood samples were collected using standard venepuncture technique and stored at −80°C until analysis. Extraction of OCP residues was done by using HPLC- grade hexane and acetone (2 : 1) according to method of Singh et al. . Hexane α-HCH, β-HCH, γ-HCH, aldrin, Dieldrin, α-endosulfan, β-endosulfan, pp′-DDE, p,p′-pp′-DDT, and op′ DDT. The samples were analysed on Perkin Elmer Gas Chromatography equipped with 63Ni electron capture detector under standard operating conditions [The pesticides assayed were nditions . For quaχ2 was performed for analysis of categorical variables, including sex and pesticide detection with the presence or absence of Parkinson's disease. The data was analysed for normality using Kolmogorov Smirnov and Shapiro-Wilk tests. OCPs were expressed as detected in patients (%), detectable range and 25th, 50th, and 75th percentile. Nonparametric test of significance (Mann Whitney Tests) was used to compare pesticide levels in two groups. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated using logistic regression analysis, with β-HCH, Dieldrin, pp′-DDE, age, and sex, as predictor variables for PD versus control status. Before putting the variables for logistic regression, all assumptions of multicollinearity and presence of outliers were tested by collinearity diagnostics and inspection of residuals respectively. Values of tolerance and variance inflation factor (VIF) were calculated to exclude multicollinearity. Variables with tolerance values of less than 0.1 and/or VIF values of more than 10 were excluded from the model. To evaluate the fit of the model to the data, Omnibus tests of model coefficients and computation of residuals using a Hosmer-Lemeshow test were performed. Amount of variation on dependent variable was calculated using Cox and Snell R square and Nagelkerke R square values. Variables with P value < 0.05 at Wald test were considered contributing significantly to the predictive ability of the model. The statistical analysis was carried out by using SPSS version 20. χ2 = 1.161; P = 0.281). A Mann-Whitney U test revealed no significant difference in the age of PD subjects  and controls , U = 2270, z = −1.408, P = 1.59, r = 0.117. Distribution of OCP levels is listed in β-HCH, Dieldrin, and pp′-DDE were present in ≥40% of PD subjects . Further we have divided these three OCP levels  into four different ranges of concentration  as shown in There was no significant difference in both the groups in terms of sex  = 117.266, P < 0.00, indicating that the model was able to distinguish between controls and those suffering from PD. Further, Hosmer and Lemeshow test also supports our model  indicating an excellent fit. The model as a whole explained between 55.5% (Cox and Snell R square) and 74.0% (Nagelkerke R squared) of the variance in disease status, and correctly classified 88.3% of cases, when only 57.1% of cases could be classified without entering our independent variables in our model. Tolerance and VIF values in β-HCH and Dieldrin levels). The strongest predictor was β-HCH, which reported an odds ratio of 2.566 , indicating that, for every additional one unit of increase in β-HCH, subjects had 2.566 times more chances of developing PD. χ2 tests between two groups (pesticides present = 1) revealed significant difference . As shown in Evidence tying pesticide use and PD have surfaced from all over the world although the identification of specific compounds has been more complex. Koller et al.  found thβ-HCH, dieldrin, and p,p-DDE in subjects with PD as compared to controls, which is in accordance with the previous studies [In the present study we found a significantly increased level of OCPs, mainly  studies –19. α-HCH, β-HCH, γ-HCH, and δ-HCH, are of commercial significance. Among the HCH isomers, β-HCH is most slowly excreted from the body. In humans, the concentration of β-HCH in adipose tissue is typically higher than other HCH isomers [β-HCH have been found, which is in accordance with the recent study done by Richardson et al. [β-HCH from 1945 and 2000 at 8,50,000 tons, of which 2,30,000 tons were emitted into the atmosphere over the same period. Recently Richardson et al. [β-HCH have decreased significantly between 2001 and 2008, but the association with PD was still significant and suggested that elevated levels of serum β-HCH in people over 60 years of age might serve as a useful predictor of PD development. Increased β-HCH levels have been linked with older age, rural environment livelihood, and male gender in humans, and these are identified as risk factors for PD. The presence of detectable β-HCH levels in control group holds the fact that other factors, like lifestyle or genetic polymorphism, may act together with β-HCH to increase the risk of development of PD. There may be a possible role of enzymes that regulate the xenobiotic transport and metabolism [β-HCH in blood will increase the risk of PD 2.5 times that is double of what Faroe Islands study showed (OR = 1.44), while Richardson et al. [Chakraborty et al.  conducte isomers . In the n et al. . Li et an et al.  estimaten et al.  reportedtabolism . In the n et al.  showed tβ-HCH and pp′-DDE) were found in only two cases each. We also found that the dieldrin also contributes to risk of PD as the OR calculated was 2.0 in PD subjects. Dieldrin has possibly the best documented toxicity on dopaminergic cells which includes the generation of oxygen radicals, aggregation and fibrillation of α-synuclein, disruption of the ubiquitin-proteasome system and the mitochondrial membrane potential, induction of dopamine release leading to intracellular dopamine depletion, and activation of caspases [α-synuclein expression, and altered dopamine homeostasis [Recently some studies concluded that the Dieldrin is among the more likely candidate to contribute to the development of PD , 17. In caspases , 24, 25.eostasis . Few smaeostasis , 20. Theeostasis , 24. pp′-DDE levels in present study were also significantly high in PD subjects as compared to controls. It is found to be more persistent than DDT. Fleming and coworkers [pp′-DDE in patients with PD versus controls. pp′-DDE induces neural death by apoptosis through the activation of mitogen-activated protein kinases (MAPKAs) [Serum oworkers  found thoworkers  reported(MAPKAs) . β-HCH levels were higher than the other two pesticides in PD subjects when the levels were in the range of <5 ng/mL, suggesting that this OCP is strongly associated with PD risk. Further we also tried to see the detected levels of OCP in both subjects of PD and control and found that one pesticide was higher in controls as compared to the PD subjects, which infers that there are other factors like gene predisposition that are contributing to the risk of PD. Also when the OCPs were subdivided into <5 ng/mL to >10 ng/mL groups, we found that β-HCH and Dieldrin may be associated with the development of PD. Our results support the epidemiology-based studies that associate exposure to pesticides with increased risk of PD. This study also reflects that apart from the environmental factors there are other factors such as genetic that decide the disease development in susceptible individuals. The result obtained from this study clearly indicates that increased serum level of


The cytochrome P450 17α-hydroxylase (CYP17) plays a vital role in androgen biosynthesis. A T-to-C polymorphism in the 5′ promoter region of CYP17 has been implicated as a risk factor for prostate cancer, but the results of individual studies are inconclusive or controversial. To derive a more precise estimation of the relationship, we performed an updated meta-analysis from 31 studies based on 27 publications.A comprehensive search was conducted to examine all the eligible studies of CYP17 polymorphism and prostate cancer risk. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association.P = 0.72, Pheterogeneity < 0.0001; CT vs. TT: OR = 0.99, 95% CI = 0.87-1.12, P = 0.88, Pheterogeneity = 0.0006). In the stratified analysis by ethnicity, there was a significantly increased risk of prostate cancer among individuals of African descent under the recessive model .Overall, individuals with CC/CT genotype were not associated with prostate cancer risk (CC vs. TT: OR = 1.03, 95% CI = 0.86-1.24, This meta-analysis suggested that CYP17 polymorphism might be associated with prostate cancer risk among individuals of African descent. Prostate cancer (PCa) is one of the most common causes of cancer-related death among men in Western countriesGenetic variation in one particular gene in this pathway, the cytochrome P450 17α-hydroxylase (CYP17), has been studied extensively in relation to gonadal development and the synthesis of androgens and estrogensConsidering the possible small effect of the genetic polymorphism on PCa and the relatively small sample size in some studies, any small but real association may be underpowered, which would account for the apparent discrepancies among studies. In an attempt to resolve these contradictory results, a meta-analysis of all available studiesPubMed was searched using the search terms: “CYP17”, “polymorphism” and “prostate cancer” or “prostate” (last search was updated on 5 May 2009). The search was limited to English-language papers. All studies matching the eligible criteria were retrieved, and their references of other relevant studies were hand-searched to find additional eligible studies. When more than one publication involved the same patient population, only the most recent or complete study was included in this meta-analysis.The inclusion criteria were as follows: ① case-control studies; ② the distribution of CYP17 genotypes in prostate cancer cases and in a concurrent control group of the prostate cancer cases were eligible, regardless of whether they had a first-degree relative with prostate cancer or not; ③ disease-free controls, regardless of whether they had benign prostatic hyperplasia (BPH) or not; ④ sufficient published data for evaluating the OR with 95% CI.Two investigators independently extracted the data and reached consensus on all items. The following information was sought from each study: First author's surname, publication data, country, ethnicity of subjects, definition of cases, characteristics of controls, and the number of cases and controls with TT, TC and CC genotypes. Subjects were categorized as being of European, Asian and African descent. For studies in which subjects of different ethnicities were included, the data were analyzed separately according to the ethnicities for subgroup analysis. We did not define a minimum number of patients to include a study in this meta-analysis.2-based Q-test P < 0.05 was considered as statistically significant.ORs with 95% CIs were used to assess the strength of association of CYP17 polymorphism with prostate cancer risk, according to the method of WoolfIn this meta-analysis, a subgroup analysis was performed to evaluate any ethnicity-specific effect. One-way sensitivity analysis was conducted to assess the stability of the results. Namely, a single study in this meta-analysis was deleted each time to reflect the influence of the individual data set to pooled OR.P < 0.05 was considered representative of statistically significant publication bias).An estimate of potential publication bias was carried out by funnel plot, using the standard error of log (OR). An asymmetric plot suggests a possible publication bias. Funnel plot asymmetry was assessed by the method of Egger's linear regression test, a linear regression approach to measure funnel plot asymmetry on the natural logarithm scale of the OR. The significance of the intercept was determined by the T-test suggested by Egger , and the Review Manager Version 4.2 .A total of 27 articles (including 31 studies) were retrieved based on the above search criteria for PCa susceptibility related to CYP17 T27C polymorphism. The main study characteristics are summarized in Prostate cancer was confirmed histologically or pathologically in 21 studies. Of the 31 studies, 9 studies used frequency-matched controls to the cases by age, or ethnicity. A classical polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was conducted in 25 studies, and a TaqMan assay was used in 4 studies. The genotype distributions among the controls of all but four studies were in agreement with Hardy-Weinberg equilibrium.P = 0.013; We observed a wide variation of the 27C allele frequencies across different ethnicities. The frequency of the 27C allele frequencies was 33.87% (95%CI=30.37-37.38) among controls of African descent, which was significantly lower than that in controls of European descent , heterozygote comparison (CT vs.TT: Pheterogeneity = 0.0006), dominant model comparison (CC+CT vs.TT: Pheterogeneity < 0.0001), and recessive model comparison (CC vs.CT+TT: Pheterogeneity = 0.001). Although we assessed the source of heterogeneity by ethnicity, genotyping method, and sample size (more than 200 subjects in both cases and controls) for homozygote comparison, heterozygote comparison, dominant model comparison, and recessive model comparison, we did not find the source of heterogeneity by meta-regression. However, when Galbraith plots were used to evaluate the source of the heterogeneity, we found out the contributors of sources of heterogeneity for the various comparisons .P = 0.164; CT vs. TT: P = 0.349; CT vs. CT+TT: P = 0.241; CC+CT vs. TT: P = 0.256).We used Begg's funnel plot and Egger's test to assess the publication bias of the literature used in this meta-analysis. The shape of funnel plots did not reveal any evidence of obvious asymmetry in all comparison models, and the Egger's test was used to provide statistical evidence of funnel plot symmetry. The results did not show any evidence of publication bias in P = 0.04, Pheterogeneity = 0.65). In addition, the variant allele frequency of 27C across the controls of African, Asian and European descent were 33.87% (95% CI: 30.37-37.38), 44.96% (95% CI=36.43-53.49) and 38.85% (95% CI=36.97-40.73) respectively. The result indicated that the distribution of 27C allele frequency showed a significant difference between individuals of African descent and individuals of Asian or European descent (P < 0.05), and the physiological function of 27C allele might differentiate among different ethnicities. It was suggested that there was a possible role of ethnic differences in genetic backgrounds and the environment they lived in. In Asians and Europeans, the influence of the 27C allele might be masked by the presence of other as-yet unidentified causal genes involved in prostate cancer development. Besides, it is also likely that the observed ethnic differences may be due to chance because studies with small sample size may have insufficient statistical power to detect a slight effect or may have generated a fluctuated risk estimate.The present meta-analysis, including 6226 cases and 6584 controls from 31 published case-control studies, explored the association between CYP17 T27C polymorphism and prostate cancer risk. Several studies have shown that the CYP17 27C allele may be associated with increased risk of prostate cancer. Other studies, however, reported a decreased risk of prostate cancer in subjects with the CYP17 27C allele, or no association. Thus molecular epidemiological studies have presented seemingly contradictory results concerning a potential role of CYP17 T27C polymorphism in prostate cancer risk. In this study, we did not find that CYP17 T27C polymorphism was significantly associated with prostate cancer risk in a worldwide population. However, our analysis indicated that the C allele was significantly associated with prostate cancer among individuals of African descent under the recessive genetic model  is known to mediate two key steps in sex steroid biosynthesisBetween-study heterogeneity may be attributed to many factors including the selection of publications, difference in population characteristics and sample sizes. We have addressed heterogeneity in these studies using a random-effects framework, which evaluates the variation in the pooled ORs based on individual OR of each study. Some limitations of this meta-analysis should be addressed. First, the association in this meta-analysis was investigated in all types of cases . There may be PCa-specific genetic effects among these cases but we could not obtain enough information to further estimate these effects. In addition, controls were not uniformly defined. Although most of the controls were mainly selected from healthy populations, some had BPH, and non-differential misclassification bias was possible because these studies may have included controls that had different risks for developing PCa. Second, lacking of the original information of the reviewed studies limited our further evaluation of potential interactions, because the interactions among gene-gene, gene-environment, and even different polymorphic loci of the same gene may modulate prostate cancer risk. Third, our result was based on unadjusted estimates, while a more precise analysis should be conducted if more detailed individual data were available, which would allow for an adjusted estimate by other factors, such as age. Lacking of information for data analysis may cause serious confounding bias. Fourth, misclassifications of disease status and genotyping may also influence the results because cases in several studies were not confirmed by pathology or other gold standard methods, and the quality control of genotyping was also not well-documented in some studies. In spite of these limitations, our meta-analysis also had some advantages. First, substantial numbers of cases and controls were pooled from different studies, which significantly increased the statistical power of the analysis. Second, the quality of case-control studies included in current meta-analysis was satisfactory and met our inclusion criteria. Third, we did not detect any publication bias, indicating that all pooled results should be unbiased.In summary, this meta-analysis did not provide evidence of an association between CYP17 T27C polymorphism and prostate cancer risk in a pooled worldwide population, but under the recessive model this polymorphism was significantly associated with prostate cancer among individuals of African descent. However, additional large studies are warranted to validate our findings. Further, studies should use standardized unbiased genotyping methods and homogeneous cancer patients and well-matched controls. Moreover, more sophisticated gene-gene and gene-environment interactions should also be considered in further analyses, which should lead to a better, comprehensive understanding of the association between the CYP17 T27C polymorphism and prostate cancer risk.