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Having read the original piece (as it was sent through our office via email), this rebuke is fantastic…
Error-Riddled Matt Ridley Piece Lowballs Climate Change, Discredits Wall Street Journal. World Faces 10°F Warming. | ThinkProgress.
Having read the original piece (as it was sent through our office via email), this rebuke is fantastic…
Error-Riddled Matt Ridley Piece Lowballs Climate Change, Discredits Wall Street Journal. World Faces 10°F Warming. | ThinkProgress.
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aThe sizes of the data markers are proportional to the inverse variance of the hazard ratios (HRs). CI indicates confidence interval; HUNT, Nord-Trøndelag Health Study; HR, hazard ratio.
bForty-six participants from the Whickham survey and 3 participants from the Busselton Health Study were not included because follow-up data were only available for death.
cNine participants were excluded from the analysis because of missing cause of death. The Brazilian Thyroid Study was not included in this analysis because of unreliable estimates based on the small number of CHD deaths (n = 10).
aThe sizes of the filled square data markers are proportional to the inverse variance of the HRs. The unfilled squares indicate the reference categories. For the analyses stratified by age, the HRs for CHD events, CHD mortality, and total mortality were adjusted for sex and age as a continuous variable to avoid residual confounding within age strata. CI indicates confidence interval.
bData were available from 7 studies.
cData were available from 10 studies. The Brazilian Thyroid Study was not included because of unreliable estimates based on the small number of CHD deaths (n = 10). Nine participants were excluded from the analysis because of missing cause of death.
dData were available from 11 studies.
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Rodondi N, den Elzen WPJ, Bauer DC, et al. Subclinical Hypothyroidism and the Risk of Coronary Heart Disease and Mortality. JAMA. 2010;304(12):1365–1374. doi:10.1001/jama.2010.1361
© 2020
Author Affiliations: Department of Ambulatory Care and Community Medicine, University of Lausanne, Lausanne, Switzerland (Drs Rodondi, Collet, and Cornuz); Departments of Public Health and Primary Care (Ms den Elzen and Dr Gussekloo) and Gerontology and Geriatrics (Dr Westendorp), Leiden University Medical Center, Leiden, the Netherlands; Departments of Medicine, Epidemiology, and Biostatistics (Drs Bauer and Vittinghoff) and Medicine (Dr Bauer), University of California, San Francisco; Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, School of Medicine, University of Pennsylvania, Philadelphia (Dr Cappola); Department of Endocrinology, Gateshead Health Foundation NHS Trust, Gateshead, England (Dr Razvi); Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, Western Australia (Dr Walsh); Schools of Medicine and Pharmacology (Dr Walsh) and Population Health (Dr Bremner), University of Western Australia, Crawley; Department of Public Health, Norwegian University of Science and Technology, Trondheim, Norway (Dr Åsvold); National Council Research Institute of Clinical Physiology, Pisa, Italy (Dr Iervasi); Department of Clinical Studies, Radiation Effects Research Foundation, Nagasaki, Japan (Dr Imaizumi); Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy (Mr Maisonneuve); Division of Endocrinology, Department of Medicine, Federal University of Sao Paulo, Brazil (Dr Sgarbi); Division of Endocrinology, Faculdade de Medicina de Marília, Marília, Brazil (Dr Sgarbi); Department of Public Health and Primary Care, University of Cambridge, Cambridge, England (Dr Khaw); Department of Endocrinology, Royal Free Hospital, London, England (Dr Vanderpump); Department of Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania (Dr Newman); School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham, England (Dr Franklyn); and the Netherlands Consortium for Healthy Ageing, Leiden (Dr Westendorp).
Context Data regarding the association between subclinical hypothyroidism and cardiovascular disease outcomes are conflicting among large prospective cohort studies. This might reflect differences in participants' age, sex, thyroid-stimulating hormone (TSH) levels, or preexisting cardiovascular disease.
Objective To assess the risks of coronary heart disease (CHD) and total mortality for adults with subclinical hypothyroidism.
Data Sources and Study Selection The databases of MEDLINE and EMBASE (1950 to May 31, 2010) were searched without language restrictions for prospective cohort studies with baseline thyroid function and subsequent CHD events, CHD mortality, and total mortality. The reference lists of retrieved articles also were searched.
Data Extraction Individual data on 55 287 participants with 542 494 person-years of follow-up between 1972 and 2007 were supplied from 11 prospective cohorts in the United States, Europe, Australia, Brazil, and Japan. The risk of CHD events was examined in 25 977 participants from 7 cohorts with available data. Euthyroidism was defined as a TSH level of 0.50 to 4.49 mIU/L. Subclinical hypothyroidism was defined as a TSH level of 4.5 to 19.9 mIU/L with normal thyroxine concentrations.
Results Among 55 287 adults, 3450 had subclinical hypothyroidism (6.2%) and 51 837 had euthyroidism. During follow-up, 9664 participants died (2168 of CHD), and 4470 participants had CHD events (among 7 studies). The risk of CHD events and CHD mortality increased with higher TSH concentrations. In age- and sex-adjusted analyses, the hazard ratio (HR) for CHD events was 1.00 (95% confidence interval [CI], 0.86-1.18) for a TSH level of 4.5 to 6.9 mIU/L (20.3 vs 20.3/1000 person-years for participants with euthyroidism), 1.17 (95% CI, 0.96-1.43) for a TSH level of 7.0 to 9.9 mIU/L (23.8/1000 person-years), and 1.89 (95% CI, 1.28-2.80) for a TSH level of 10 to 19.9 mIU/L (n = 70 events/235; 38.4/1000 person-years; P <.001 for trend). The corresponding HRs for CHD mortality were 1.09 (95% CI, 0.91-1.30; 5.3 vs 4.9/1000 person-years for participants with euthyroidism), 1.42 (95% CI, 1.03-1.95; 6.9/1000 person-years), and 1.58 (95% CI, 1.10-2.27, n = 28 deaths/333; 7.7/1000 person-years; P = .005 for trend). Total mortality was not increased among participants with subclinical hypothyroidism. Results were similar after further adjustment for traditional cardiovascular risk factors. Risks did not significantly differ by age, sex, or preexisting cardiovascular disease.
Conclusions Subclinical hypothyroidism is associated with an increased risk of CHD events and CHD mortality in those with higher TSH levels, particularly in those with a TSH concentration of 10 mIU/L or greater.
Quiz Ref IDControversy persists on the indications for screening and threshold levels of thyroid-stimulating hormone (TSH) for treatment of subclinical hypothyroidism,1-3 defined as elevated serum TSH levels with normal thyroxine (T4) concentrations. Because subclinical hypothyroidism has been associated with hypercholesterolemia4 and atherosclerosis,5 screening and treatment have been advocated to prevent cardiovascular disease.3 However, data on the associations with coronary heart disease (CHD) events and mortality are conflicting among several large prospective cohorts.6-9 Three recent study-level meta-analyses10-12 found modestly increased risks for CHD and mortality, but with heterogeneity among individual studies that used different TSH cutoffs, different confounding factors for adjustment, and varying CHD definitions.10 Part of the heterogeneity might also be related to differences in participants' age, sex, or severity of subclinical hypothyroidism (as measured by TSH level).4 One cohort study suggested particularly high risk in participants with subclinical hypothyroidism and preexisting cardiovascular disease.8
Analysis of individual participant data from large cohort studies may reconcile these conflicting data and define the influence of age, TSH levels, and preexisting cardiovascular disease. Individual participant data analysis is considered the best way for synthesizing evidence across several studies because it is not subject to potential bias from study-level meta-analyses (ecological fallacy)13 and allows performance of time-to-event analyses.14
To clarify the cardiovascular risk of subclinical hypothyroidism, we formed the Thyroid Studies Collaboration and conducted an individual participant data analysis of subclinical hypothyroidism and CHD outcomes.
Identification of potential studies was based on protocols developed for our study-level meta-analysis of prospective cohort studies.10 Briefly, we conducted a systematic literature search of articles in all languages on the association between subclinical thyroid dysfunction and CHD or mortality (cardiovascular and total) published from 1950 to May 31, 2010, in the MEDLINE and EMBASE databases and searched bibliographies of key articles (details are available in the eMethods). To maximize the quality and comparability of the studies, we formulated general inclusion criteria a priori. We included only full-text, published longitudinal cohort studies that (1) measured thyroid function with both serum TSH level and thyroxine (T4) level at baseline in adults, (2) followed up participants systematically over time, (3) assessed CHD events and/or mortality, and (4) had a comparison group with euthyroidism. We excluded studies that only examined persons taking antithyroid medications, thyroxine replacement or amiodarone, or with overt hypothyroidism (defined as low T4 and elevated TSH concentrations). Possible studies for inclusion were independently assessed for suitability by 2 of the authors (N.R., J.G.) and any disagreement was resolved by discussion with a third author (D.C.B). The agreement between the 2 reviewers was 99.9% for the first screen (titles and abstracts, κ = 0.98) and 100% for the full-text screen (κ = 1.00).
Investigators from each eligible study were invited to join the Thyroid Studies Collaboration. We collected detailed information about prespecified outcomes and potential confounding variables for each participant. Requested data included individual demographic characteristics, baseline thyroid function (TSH and T4 levels), baseline cardiovascular risk factors (eg, low- and high-density lipoprotein cholesterol level, diabetes, blood pressure, cigarette smoking), prevalent cardiovascular disease, medication use at baseline (thyroid medication, lipid-lowering and antihypertensive drugs), and outcome data.
To maximize the comparability of the studies, we used a common definition of subclinical hypothyroidism. Based on expert reviews1,2 and definitions used in the Cardiovascular Health Study,6,15 we defined subclinical hypothyroidism as a serum TSH level of 4.5 mIU/L or greater to less than 20 mIU/L, with a normal T4 concentration; and euthyroidism was defined as a serum TSH level of 0.5 mIU/L or greater and less than 4.5 mIU/L. Because the Whickham Survey used a first-generation TSH radioimmunoassay, which gives higher measured TSH values than current assays,16 a TSH range of 6.0 mIU/L or greater to less than 21.5 mIU/L was used for this individual participant data analyses, as in the original and recent analysis of this study.17,18 In that study, a serum TSH level of 6.0 mIU/L corresponded to the 97.5th percentile of the group with negative thyroid antibodies,18 which is close to the modern level of 4.5 mIU/L for the current generation of assays. For T4 level, we used site- and method-dependent specific cutoffs (eTable) because T4 measurements show greater intermethod variation than do sensitive TSH assays. The Whickham Survey measured total T4 level.18 Participants with abnormal T4 values, results suggestive of nonthyroidal illness (low TSH and FT4 levels) or low TSH level (<0.5 mIU/L) were excluded (n = 3023). Some studies had participants with missing T4 values (eTable); we considered participants with a TSH level of 4.5 mIU/L to 19.9 mIU/L and a missing T4 level as having subclinical hypothyroidism because most adults with this degree of TSH elevation have subclinical and not overt hypothyroidism.19 We performed a sensitivity analysis excluding those with a missing T4 level.
Outcome measures were CHD events, CHD mortality, and total mortality. To limit outcome heterogeneity observed with previous study-level meta-analyses,10-12 we used more homogeneous outcome definitions. Similar to the current Framingham risk score,20 we limited cardiovascular mortality to CHD mortality or sudden death (eTable). A CHD event was defined as nonfatal myocardial infarction or CHD death (equivalent to hard events in the Framingham risk score20) and hospitalization for angina or coronary revascularization (coronary artery bypass grafting or angioplasty).6 We performed a sensitivity analysis with hard events only.
Using previously described criteria10 and new information from study authors, we systematically evaluated the following key indicators of study quality13: methods of outcome adjudication and ascertainment, accounting for confounders, and completeness of follow-up ascertainment. Two reviewers (N.R., J.G.) rated all studies for quality.
We used separate Cox proportional hazard models to assess the associations of subclinical hypothyroidism with CHD events and mortality for each cohort (SAS version 9.2, SAS Institute Inc, Cary, North Carolina). Pooled estimates for each outcome were calculated using random-effects models, based on the variance model according to DerSimonian and Laird,21 as recommended14,22 and published in recent 2-stage individual participant data analyses.23 Results were summarized using forest plots (Review Manager version 5.0.24, Nordic Cochrane Centre, Copenhagen, Denmark). The research authors of 1 study with 14 CHD outcomes5,10 declined to participate; as recommended,24 we included the published summary estimate from that study in the random-effects models in a sensitivity analysis. To assess heterogeneity across studies, we used the I2 statistic, which describes the total variation across studies attributable to heterogeneity rather than chance (I2 >50% indicating at least moderate statistical heterogeneity).25
Primary analyses were adjusted for age and sex, and then for traditional cardiovascular risk factors (systolic blood pressure, smoking, total cholesterol, diabetes) that were available in all cohorts (except for the Birmingham Study,26 which was excluded from this analysis). We considered the age- and sex-adjusted model as the primary analysis because some traditional risk factors are potential mediators of the relationship between subclinical hypothyroidism and CHD.4
To explore sources of heterogeneity, we performed several predefined subgroup and sensitivity analyses. We conducted stratified analyses by age, sex, race, TSH concentrations, and preexisting cardiovascular disease. Based on expert reviews1,2 and previous studies,7,15 subclinical hypothyroidism was stratified according to the following TSH concentration categories: 4.5-6.9 mIU/L (mild elevation), 7.0-9.9 mIU/L (moderate elevation), and 10.0-19.9 mIU/L (marked elevation). In the study-specific analyses stratified by age or TSH level, some strata had participants without either CHD deaths or CHD events (for 1 study27). For these study-specific analyses, we used penalized likelihood methods28 to obtain hazard ratios (HRs) and confidence intervals (CIs). As done in previous studies,7,27,29 after including all participants in the primary analyses, we performed sensitivity analyses excluding participants who had thyroid hormone use at baseline and during follow-up. To calculate age- and sex-adjusted rates per 1000 person-years, we first fit Poisson models30 to the pooled data, then standardized the fitted rate in the euthyroidism group to the overall age and sex distribution of the pooled sample. Finally, to obtain rates in the TSH groups consistent with the meta-analytic results, we multiplied the standardized rates in the euthyroidism group by the summary meta-analytic HRs. We checked the proportional hazard assumption using graphical methods and Schoenfeld tests (all P > .05). We used the Egger test31 and age- and sex-adjusted funnel plots to assess for publication bias.
Among 4440 reports identified, 12 prospective studies met eligibility criteria (eFigure) and 11 prospective cohorts in the United States, Europe, Australia, Brazil, and Japan agreed to provide individual participant data (Table 1). The final sample included 55 287 adults comprising 3450 with subclinical hypothyroidism (6.2%) and 51 837 with euthyroidism. Zero to 8.3% of participants reported thyroid hormone use at baseline (all excluded in 5 studies) and 0% to 12.6% reported thyroid hormone use during follow-up. The median follow-up ranged from 2.5 to 20 years, with total follow-up of 542 494 person-years.
All 11 cohort studies reported total and CHD deaths, and 7 studies also reported CHD events among 25 977 participants. For the quality of individual studies, all studies reported outcome adjudication without knowledge of thyroid status; 4 of 7 studies reporting CHD events used formal adjudication procedures6-8,27; and 4 of 11 studies reporting CHD deaths mainly used death certificates.26,33-35 All studies had 5% or less loss to follow-up.
During follow-up, 9664 participants died (2168 of CHD) and 4470 participants had CHD events (among 7 studies). In age- and sex-adjusted analyses, the overall HR for participants with subclinical hypothyroidism compared with euthyroidism was 1.18 (95% CI, 0.99-1.42) for CHD events (24.0 vs 20.3/1000 person-years for participants with euthyroidism), 1.14 (95% CI, 0.99-1.32) for CHD mortality (5.5 vs 4.9/1000 person-years), and 1.09 (95% CI, 0.96-1.24) for total mortality (23.1 vs 21.1/1000 person-years; Figure 1). We found heterogeneity across studies for CHD events (I2 = 59%) and total mortality (I2 = 66%), but not for CHD mortality (I2 = 0%). We subsequently examined whether heterogeneity was related to differences in risks by degree of subclinical hypothyroidism and age. The risk of CHD events (P<.001 for trend) and CHD death (P = .005 for trend) increased with higher TSH level, but not for total mortality (Figure 2). In stratified analyses, participants with TSH levels of 10 mIU/L or greater had significantly increased risk of CHD events (HR, 1.89 [95% CI, 1.28-2.80]; n = 70 events/235; 38.4 vs 20.3/1000 person-years for participants with euthyroidism) and CHD mortality (HR, 1.58 [95% CI, 1.10-2.27]; n = 28 deaths/333; 7.7 vs 4.9/1000 person-years) compared with participants with euthyroidism. The risk for CHD associated with subclinical hypothyroidism appeared to be somewhat higher in younger participants, but the number of outcomes in the younger age group was small, and there was no significant trend in CHD risk across age groups. Otherwise, the risk estimates for CHD events, CHD mortality, and total mortality did not differ significantly according to age, sex, race, or preexisting cardiovascular disease, except an increase in CHD events and CHD mortality among white but not among nonwhite participants with subclinical hypothyroidism (Table 2). All results were similar after further adjustment for traditional cardiovascular risk factors.
Sensitivity analyses yielded similar results, with increased risks of CHD events and mortality in those with TSH levels of 10 mIU/L or greater (Table 3). Risk estimates were slightly higher for those with TSH levels of 10 mIU/L or greater after excluding those who took thyroid medication during follow-up. Estimates were lower for subclinical hypothyroidism overall after limiting the analyses to 4 studies with formal adjudication procedures, but slightly higher for those with TSH levels of 10 mIU/L or greater. The effect of increasing TSH level on CHD events did not significantly differ according to age (P = .87 for interaction). We found no evidence of publication bias, either with visual assessment of age- and sex-adjusted funnel plots or with the Egger test for mortality data (P = .39 for CHD mortality and P = .97 for total mortality) and little evidence of publication bias for CHD events (P = .13 for CHD events).
Quiz Ref IDIn this analysis of 55 287 individual participants from 11 prospective cohort studies, subclinical hypothyroidism was associated with an increased risk of CHD events and CHD mortality in those with higher TSH levels. There was a significant trend of increased risk at higher serum TSH concentrations, and the risk of both CHD mortality and CHD events was significantly increased in participants with TSH levels of 10 mIU/L or greater.Quiz Ref IDThese associations persisted after adjustment for traditional cardiovascular risk factors, and did not significantly differ by age, sex, race, or preexisting cardiovascular disease. Compared with participants with euthyroidism, the overall HR for CHD events with subclinical hypothyroidism was 1.18 (95% CI, 0.99-1.42) and the overall HR for CHD mortality was 1.14 (95% CI, 0.99-1.32). Minimal TSH elevations were not associated with an increased risk of CHD events and CHD mortality. Our results clarify the CHD risk of subgroups of adults with subclinical hypothyroidism, which could not be adequately addressed in previous study-level meta-analyses10-12 or in single cohort studies performed in more limited age groups or without TSH stratification.6,7,26,27
These results are generally consistent with previous study-level meta-analyses showing modest increased risks of CHD events and cardiovascular mortality associated with subclinical hypothyroidism.10,11 However, these meta-analyses could not accurately explore potential differences related to participant characteristics (eg, age, TSH concentrations) because of potential bias without individual participant data analysis (ecological fallacy),13 and they also were limited by clinical heterogeneity,10,36 with individual studies using varying TSH cutoffs, confounding factors for adjustment, and CHD definitions. Among 11 cohorts, only 2 studies previously reported results stratified by TSH level. One study9 reported an increased risk of CHD events in participants with a TSH level of 10.0 mIU/L or greater (HR, 2.2; 95% CI, 1.2-4.2) and the other study7 reported an increased risk of cardiovascular mortality (HR, 2.26; 95% CI, 0.54-9.45) but not CHD events (HR, 0.96; 95% CI, 0.35-2.61) over 4 years among adults aged 70 to 79 years with TSH levels of 10 mIU/L or greater. However, the HR for CHD events increased to 1.28 (95% CI, 0.68-2.39) with extended follow-up to 8 years in the present data. In overall pooled data, we found statistical heterogeneity among individual study findings for CHD events (I2 = 59%), but not for CHD death. Part of the heterogeneity might be related to different CHD risks across age, race, and TSH subgroups.
Our individual participant data analysis found that the CHD outcomes in adults with subclinical hypothyroidism did not differ significantly across age groups. For the specific age group of 80 years or older, there was no significant increased risk of total mortality, CHD mortality, or CHD events in contrast to a single previous study that found reduced mortality associated with increasing TSH concentrations.27,37 Previous study-level meta-analyses have found increased risks of CHD events and cardiovascular mortality associated with subclinical hypothyroidism, particularly in studies with a mean age of younger than 65 years,10,11 but this was not confirmed by our individual participant data analysis. We found some evidence for increased risks of CHD events and mortality in younger adults with subclinical hypothyroidism, but there also were large 95% CIs without significant trend across age groups (Figure 2). Moreover, the effect of increasing TSH level on CHD events did not significantly differ according to age. In contrast to a previous study suggesting that adults with subclinical hypothyroidism and preexisting cardiovascular disease might be at particularly high cardiovascular risk,8 we found no significant effect of baseline preexisting cardiovascular disease on outcomes.
The increased risk of CHD events associated with higher TSH levels in our study might be related to the known effects of thyroid hormone on the heart and metabolism, consistent with the concept that subclinical hypothyroidism is a milder form of overt hypothyroidism.38,39Quiz Ref IDIncreased systemic vascular resistance, arterial stiffness, altered endothelial function, increased atherosclerosis, and altered coagulability have been reported to be associated with subclinical hypothyroidism and may accelerate development of CHD.4,39,40 The fact that adjustment for traditional cardiovascular risk factors did not alter risks could favor this hypothesis. Other potential mechanisms include elevated cholesterol level,4,39 although adjustment for cholesterol level did not remove the associations in our data. Adults with higher TSH concentrations also are more likely to develop overt hypothyroidism,41 and it is possible that this progression explains the association with subclinical hypothyroidism. Alternative explanations for the observed results are bias in the selection of included studies, bias and quality problems in the original studies, publication bias, and unmeasured confounders.42 Sensitivity analyses pooling higher-quality studies yielded similar results. Whereas one randomized controlled trial has shown benefits with thyroxine treatment of subclinical hypothyroidism on intima-media thickness40 and another has shown benefits with thyroxine treatment of subclinical hypothyroidism on brachial artery endothelial function,43 the potential causal relationship can only be proven by randomized controlled trials of thyroxine replacement and clinical outcomes.36
Among the strengths of our study, an individual participant data analysis is the preferred way to perform time-to-event analyses to avoid biases associated with the use of aggregate data in meta-regression for subgroup analysis and to allow standardization of definitions of predictors, outcomes, and adjustment for potential confounders.14,22 We included all available international and published data on these associations. Among the limitations of our study, the individual participant data analysis included predominantly white populations, except for 2 studies conducted in Japan34 and Brazil.35 Results for subgroups at risk of CHD mortality generally had wider 95% CIs than those for CHD events, reflecting less statistical power. However, post hoc calculations showed 80% power to detect meaningful differences between overall subclinical hypothyroidism and euthyroidism groups for each outcome. Specifically, our study had adequate power to detect an HR of 1.18 or higher for CHD events, an HR of 1.30 or higher for CHD mortality, and an HR of 1.13 or higher for total mortality. Even with this very large amount of individual participant data, our power for subgroup analyses was limited among those with TSH levels of 10 mIU/L or greater or adults younger than 50 years because of the limited number of CHD events and deaths. Thyroid function testing was performed only at baseline, and we have no data on how many participants progressed from euthyroidism to subclinical hypothyroidism, from subclinical to overt hypothyroidism, or who normalized their TSH level over time, which is a limitation of all published large cohorts.6,7,33 In addition, free triiodothyronine (T3) was not available in most cohorts, and thus could not be included in thyroid status classification. Commencement of thyroid medication during follow-up by up to 12.6% of participants might have attenuated any true effects of subclinical hypothyroidism, as illustrated by the sensitivity analysis excluding such participants.
In summary, combining all available data from large prospective cohorts among 55 287 individual participants suggests that subclinical hypothyroidism is associated with an increased risk of CHD in those with higher TSH levels. The risk of both CHD mortality and CHD events, but not of total mortality, increases with higher concentrations of TSH and is significantly elevated in adults with TSH levels of 10 mIU/L or greater. Quiz Ref IDConversely, minimal TSH elevations are not associated with an increased risk of CHD events and CHD mortality. Our finding of no increased risk of CHD among the high proportions of adults with minimal TSH elevations is also important because many patients with minimal TSH elevations are currently treated in clinical practice.44 Our results might help refine a TSH threshold at which larger clinical benefits of thyroxine replacement would be expected.4,45 Our study cannot address whether these risks are attenuated or abolished by thyroxine replacement. Given the high prevalence of subclinical hypothyroidism,2,19 this question needs to be addressed in an appropriately powered randomized controlled trial.
Corresponding Author: Nicolas Rodondi, MD, MAS, Department of Ambulatory Care and Community Medicine, University of Lausanne, Bugnon 44, 1011 Lausanne, Switzerland (firstname.lastname@example.com).
Author Contributions: Dr Rodondi had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Rodondi, Bauer, Cornuz, Westendorp, Gussekloo.
Acquisition of data: Rodondi, Bauer, Walsh, Åsvold, Iervasi, Imaizumi, Sgarbi, Khaw, Vanderpump, Newman, Franklyn, Westendorp, Gussekloo.
Analysis and interpretation of data: Rodondi, den Elzen, Bauer, Cappola, Razvi, Åsvold, Iervasi, Imaizumi, Collet, Bremner, Maisonneuve, Sgarbi, Cornuz, Franklyn, Westendorp, Vittinghoff, Gussekloo.
Drafting of the manuscript: Rodondi.
Critical revision of the manuscript for important intellectual content: den Elzen, Bauer, Cappola, Razvi, Walsh, Åsvold, Iervasi, Imaizumi, Collet, Bremner, Maisonneuve, Sgarbi, Khaw, Vanderpump, Newman, Cornuz, Franklyn, Westendorp, Vittinghoff, Gussekloo.
Statistical analysis: Rodondi, den Elzen, Bauer, Vittinghoff.
Obtained funding: Walsh, Iervasi, Sgarbi, Khaw, Vanderpump, Newman, Franklyn, Westendorp, Gussekloo.
Administrative, technical, or material support: Rodondi, Collet, Khaw, Newman, Gussekloo.
Study supervision: Rodondi, Westendorp, Gussekloo.
Financial Disclosures: None reported.
Funding/Support: The Cardiovascular Health Study and the research reported in this article were supported by contract numbers N01-HC-80007, N01-HC-85079 through N01-HC-85086, N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150, N01-HC-45133, grant number U01 HL080295 from the National Heart, Lung, and Blood Institute, with additional funding from the National Institute of Neurological Disorders and Stroke. Additional support was provided through grants R01 AG-15928, R01 AG-20098, AG-027058, and AG-032317 from the National Institute on Aging, grant R01 HL-075366 from the National Heart, Lung, and Blood Institute, and grant P30-AG-024827 from the University of Pittsburgh Claude. D. Pepper Older Americans Independence Center. A full list of principal investigators and institutions of the Cardiovascular Health Study can be found at http://www.chs-nhlbi.org/pi.htm. The thyroid measurements in the Cardiovascular Health Study were supported by an American Heart Association Grant-in-Aid (to Linda Fried). The Health, Aging, and Body Composition Study is supported by National Institute on Aging contract numbers N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106, and in part by the Intramural Research Program of the National Institutes of Health. The National Institute on Aging funded the Health Aging, and Body Composition study. The Leiden 85-plus Study was partly funded by the Dutch Ministry of Health, Welfare, and Sports. The Whickham Survey was supported by the UK Department of Health. The HUNT Study was a collaborative effort of the Faculty of Medicine, Norwegian University of Science and Technology, the Norwegian Institute of Public Health, and the Nord-Trøndelag County Council. The thyroid testing in the HUNT Study was financially supported by Wallac Oy (Turku, Finland). The Nagasaki Adult Health Study was supported by the Radiation Effects Research Foundation, Hiroshima and Nagasaki, Japan, a private, nonprofit foundation funded by the Japanese Ministry of Health, Labor and Welfare and the US Department of Energy, the latter in part through the National Academy of Sciences. This publication was supported by research protocol A-10-08 from the Radiation Effects Research Foundation. The EPIC-Norfolk study was supported by research grants from the UK Medical Research Council and the UK Cancer Research. The Brazilian Thyroid Study was supported by an unrestricted grant from the Sao Paulo State Research Foundation (Fundacão de Amparo a" Pesquisa do Estado de Sao Paulo grant 6/59737-9 to Rui Maciel). Dr Newman is supported by grant AG-023629 from the the National Institute on Aging. Dr Westendorp is supported by grant NGI/NWO 911-03-016 from the Netherlands Organization for Scientific Research.
Role of the Sponsor: The majority of the sponsors had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; or preparation, review, or approval of the manuscript. The National Institute on Aging funded the Health, Aging, and Body Composition study and reviewed the manuscript and approved its publication. The Radiation Effects Research Foundation funded the Nagasaki Adult Health Study and reviewed the manuscript and approved its publication.
Statistical Evaluation: Dr Vittinghoff, professor of biostatistics, in the Department of Epidemiology and Biostatistics, University of California, San Francisco, reviewed the statistical analyses of the article.
Participating Studies of the Thyroid Studies Collaboration:United States: Cardiovascular Health Study; Health, Aging, and Body Composition Study. The Netherlands: the Leiden 85-plus Study. Australia: Busselton Health Study. United Kingdom: Whickham Survey; Birmingham Study; EPIC-Norfolk Study. Italy: Pisa Cohort. Japan: Nagasaki Adult Health Study. Brazil: Brazilian Thyroid Study. Norway: Nord-Trøndelag Health Study (HUNT Study).
Additional Contributions: We thank Sabrina Molinaro (Clinical Physiology Institute, Pisa, Italy) for technical help about data from the Pisa Cohort and from Rui Maciel (Escola Paulista de Medicina, Federal University of Sao Paulo, Brazil) for technical help about data from the Brazilian Thyroid Study. The persons listed in this section did not receive financial compensation.
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Submitted by pfr1968 on Wed, 2008-10-01 11:39.
All the best,
Hi all,
you may have read it already, but anyway there is a new (open source) software: Cleversafe (The company won this years Technology Innovation Award. The software enables you to save data via different (I don't know if it's possible to choose them) servers in encrypted packets. Every server gets only parts hence every connection can be used. A redundancy protocoll ensures restoring date if a server should be down.
I would like to know if anyone is going to use it.
All the best,
Sorry: http://www.cleversafe.com/
Submitted by chadm on Wed, 2008-10-01 14:23.
I haven't used Cleversafe's solution, but it looks pretty interesting. It's listed under filesystems as DSGrid. A number of articles about Cleversafe can be found in the Web Links sidebar from the DSGrid page.


text:
Kozma's progress apparent but future unclear
MILWAUKEE -- Though manager Mike Matheny was effusive with his praise of how Pete Kozma had improved and how professionally he handled two weeks of limited playing time while keeping Mark Ellis' roster spot warm, the 26-year-old shortstop heads to Triple-A with his future within the Cardinals' organization uncertain.
The Cardinals' decision to sign Jhonny Peralta to a four-year contract in November and then boost their organizational depth at short with the March addition of Cuban shortstop Aledmys Diaz sent a message -- whether intended or not -- to Kozma that he was not a central part of the team's long-term plans.
Kozma's struggles last season -- he hit .217 in 143 games -- after being named the team's starting shortstop prompted the Cardinals to look elsewhere. So how does Kozma fit after being optioned to Triple-A Memphis on Tuesday?
"I feel good about Pete in general," Matheny said. "You hate to send out a guy who was such an integral part of our club last year on a team that did win the pennant. But we had some great conversations even leading up to yesterday about how he continues to improve and the faith that we have in him as a player and our hopeful expectation that he just keeps improving, because he can play the shortstop position at this level. Just to keep working on the things that he can work on.
"This was a tough assignment coming in here with bringing in a Jhonny Peralta. But Pete came in and did everything right. He said the right things, worked relentlessly, and very proud of how he handled a tough situation."
Kozma did not make a start during the Cards' first two weeks of games and took only three at-bats. He singled in a ninth-inning at-bat in Monday's win over the Brewers.
"That swing he put on yesterday, I don't think you could count very many times he put a swing like that on a pitch [last year], and we were watching it consistently through batting practice, too," Matheny said, pointing to Kozma's improved mechanics. "He needs to trust himself out over the plate where he can cover all pitches. … Sometimes you need some of the struggles to help open your eyes to some of the holes you have in your game. He's making good strides."
The Cardinals will have Kozma play regularly at short in Memphis, with occasional work at third base in case the Cardinals have the need for a versatile infielder later this season.


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If $X$ is a set and $I$ is an ideal on $X$. Let $\mathbb{P}$ be the forcing poset consisting of $I^+$ subsets of $X$ with the subset partial ordering. Let $G$ be $\mathbb{P}$-generic filter over $M$, where $M$ is the ground model.
As in Jech Lemma 22.13, it can be shown that $G$ is a $M$-ultrafilter on $X$. I presume this means that in $M[G]$, it is proved that $G$ is $M$-ultrafilter.
Then the generic ultrapower is defined in $M[G]$ as follows : it consist of the equivalence classes of function $f : X \rightarrow M$ with $f \in M$ under the usual ultrapower equivalence relation with $\in^{Ult_G(M)}$ defined in the usual way.
I would like to think of the generic ultrapower as a class model in $M[G]$, but it is not immediately clear that it is definable.
The first issue is how exactly is Lemma 22.13 phrased in $M[G]$. How does $M[G]$ talk about $M$?
Then in the construction of the ultrapower, the equivalence class can of course be made into sets by considering element of least rank in each class. However, $M[G]$ still needs to distinguish those $f : X \rightarrow M$ which are in the ground models. Again, the main issue here seems to be whether $M$ is an inner model of $M[G]$.
I am vaguely aware of some result about $M$ being in some sense definable in $M[G]$? I do not know the result precisely to be able to tell if this result could be used to think of the generic ultrapower as a proper class. Nevertheless, it seems that Solovay used the generic ultrapower well before this result was known. How did he handle the definability issue of the generic ultrapower?


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Mozzarella - tokidoki Sticker
Sorry, this product has been archived…meaning it's currently out of stock and may or may not make a return. If you'd like to know *if* we are able to restock this product feel free to send us an email to firstname.lastname@example.com and we'll let you know if we might be able to get it back. Thanks!
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text:
Georgian protesters call for Olympic boycott
Sat., Feb. 1, 2014
TBILISI, Georgia (AP) — Several hundred protesters are rallying in the capital of Georgia to protest the Winter Olympics, which will begin in neighboring Russia on Feb. 7.
Around three hundred people gathered in downtown Tbilisi on Saturday, calling for a boycott of the games which will be held in the Black Sea resort town of Sochi, only 290 miles (460 kilometers) from the Georgian capital.
While the Georgian team in Sochi will have only four athletes, the games have touched a nerve in Georgia, a small nation in the Caucasus mountains that borders Russia. Many in the country remain bitter over a brief 2008 war with Russia, which left two separatist territories outside of Georgia's control, including Abkhazia, a territory just south of Sochi.
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text:
The past several weeks have, no doubt, caused or tempted many investors to sell off. But is that the best course of action? Scott Welch looks back at the market dips in previous years to compare them to the market turmoil today.
Jeremy J Siegel
Senior Investment Strategy Advisor
Jonathan Steinberg
CEO of WisdomTree
Jesper Koll
Senior Advisor
Jeremy Schwartz, CFA
Executive Vice President, Global Head of Research
Christopher Gannatti, CFA
Head of Research, Europe
Christopher Gannatti began at WisdomTree as a Research Analyst in December 2010, working directly with Jeremy Schwartz, CFA®, Director of Research. In January of 2014, he was promoted to Associate Director of Research where he was responsible to lead different groups of analysts and strategists within the broader Research team at WisdomTree. In February of 2018, Christopher was promoted to Head of Research, Europe, where he will be based out of WisdomTree's London office and will be responsible for the full WisdomTree research effort within the European market, as well as supporting the UCITs platform globally. Christopher came to WisdomTree from Lord Abbett, where he worked for four and a half years as a Regional Consultant. He received his MBA in Quantitative Finance, Accounting, and Economics from NYU's Stern School of Business in 2010, and he received his bachelor's degree from Colgate University in Economics in 2006. Christopher is a holder of the Chartered Financial Analyst designation.
Kevin Flanagan
Head of Fixed Income Strategy
Bradley Krom
Director, Research
Tripp Zimmerman, CFA
Director, Research
Rick Harper
Head of Fixed Income & Currency
Gaurav Sinha
Associate Director, Asset Allocation and Modern Alpha
Anita Rausch
Head of Capital Markets
Michael Barrer
Associate Director of Capital Markets
Joseph Tenaglia, CFA
Associate Director, Asset Allocation
Brendan Loftus
Research Analyst
Kara Marciscano, CFA
Senior Research Analyst
Matt Wagner, CFA
Senior Research Analyst
Matt Wagner joined WisdomTree in May 2017 as a member of the Research team. He is responsible for research on WisdomTree's products and communicating the firm's views on the markets. Matt started his career at Morgan Stanley, working as an analyst in Treasury Capital Markets from 2015 to 2017 where he focused on unsecured funding planning, execution and risk management. Matt graduated from Boston College in 2015 with a B.A. in International Studies with a concentration in Economics. Matt is a holder of the Chartered Financial Analyst designation.
Jianing Wu
Research Analyst
Jianing Wu joined WisdomTree as a Research Analyst in October 2018. She is responsible for analyzing market trends and helping support WisdomTree's research efforts. Previously, Jianing completed internships and projects at Geode Capital, Starwint Capital, and Invesco Great Wall Fund Management with a focus in quantitative research. Jianing received her M.S in Finance from the Massachusetts Institute of Technology. She graduated with honors from Boston College with degrees in Mathematics and Philosophy.
Brian Manby
Investment Strategy Analyst
Brian Manby joined WisdomTree in October 2018 as an Investment Strategy Analyst. He is responsible for assisting in the creation and analysis of WisdomTree's model portfolios, as well as helping support the firm's research efforts. Prior to joining WisdomTree, he worked for FactSet Research Systems, Inc. as a Senior Consultant, where he assisted clients in the creation, maintenance and support of FactSet products in the investment management workflow. Brian received a B.A. as a dual major in Economics and Political Science from the University of Connecticut in 2016, and is pursuing the Chartered Financial Analyst designation.
Jeff Weniger, CFA
Director, Asset Allocation
Alejandro Saltiel, CFA
Associate Director of Modern Alpha
Alejandro Saltiel joined WisdomTree as a Quantitative Research Analyst in May 2017. He is responsible for quantitative research on WisdomTree's products and global equity markets. Prior to joining WisdomTree, Alejandro worked at HSBC Asset Management's Mexico City office as Portfolio Manager for multi-asset mutual funds. He started his career working at a boutique hedge fund that specialized on trading options on sector-levered ETFs. Alejandro received his Master's in Financial Engineering degree from Columbia University in 2017 and a Bachelor's in Engineering degree from the Instituto Tecnológico Autónomo de México (ITAM) in 2010. He is a holder of the Chartered Financial Analyst designation.


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At BirthSpirit, we believe that pregnancy is a normal, healthy condition that benefits from a wellness approach. This approach includes good nutrition, moderate exercise, positive childbirth education, and the use of natural therapies instead of medical interventions whenever possible. My role is to monitor and support the natural course of pregnancy by providing regular prenatal care as well as guidance during labor, birth, and the postpartum. My first commitment is always to the safety of both you and your baby. If you choose to have an out-of-hospital birth with BirthSpirit, you will receive high-quality, individualized, comprehensive health care with a strong emphasis on education. You will participate fully in decisions regarding your pregnancy and birth.
I am an apprentice-trained Certified Professional Midwife serving the Northeast Pennsylvania area. I have attended over 850 births since 1992


text: John Coughlin is a pairs figure skater who earned the 2012 U.S. Figure Skating Championships gold medal and 2012 Four Continents Figure Skating Championships silver medal in his first season with partner Caydee Denney. After skating for more than 20 years, Coughlin is en route to making his first Olympic team. Follow John as he blogs about his experiences on his road to the Sochi 2014 Olympic Winter Games.


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maarchk brauchte ein neues Website Design und hat einen Wettbewerb auf 99designs gestartet.
Aus 102 Designs von 30 Designern wurde eine Gewinner gewählt.
This website will work to provide a brief description of our product along with details about its functionality. The product is a DME all-in-one software solution for DME companies. The main page will be a landing sight from google and it should be a simple but effective display of the logo, and message along with links to the different functions of the software. The adjoining pages will be detailed informative pages abut the features of the program along with the usual contact page, company information page, and a request for a demo page.
We are creating a new website for our
company. The goal is to get perspective
clients to view the website and then click through to a demo sign up form and
submit it. The old website is http://www.bonafide.com It is a bit too cluttered on top and does not have much color. We would like to use the bonafide logo on the main page as well as maroon and grey as the primary coloring. We would like to give a breif description of the product and then have a side bar of links to information pages about different features. (Billing, enteral supplies, High-End Rehab, etc) Probably will have 5 categories with 5 sub categories which each link to their own informational page with probably a picture and 2 paragraphs of text.
Also, each page should have a link to "Sign up for a Demo" which will be the contact page.
Can find Logo and colors in this zipped file: http://www.box.net/shared/ox7gzm48w4
- A light weight, clean, and professional website.
- Colored with the Bonafide color scheme and logo.
- Nothing to over whelming or blinding.


text:
Dog food reviews
Member List
Dry Dog Foods
2 Star Dry Dog Food
Previous Product
Next Product
NATIONAL Pet Products, Inc. National Adult Formula
Date of last review
Wed January 2, 2008
Recommended By
Average Price
Average Rating
No recommendations
None indicated
None indicated
Poultry Meal, Kibbled Corn (cooked), Fish Meal, Extruded Rice, Flaked Corn, Pork Fat (preserved with mixed tocopherols), Beet Pulp, Plain, Dried, Feeding Oat Meal, Blood Meal, Sodium Bentonite, Corn Oil (preserved with mixed tocopherols), Cane Molasses, Liver Digest, Flaxseed, Vitamins and Minerals.
Guaranteed Analysis
Crude Protein not less than 26.0%
Crude Fat not less than 15.0%
Crude Fiber not more than 4.5%
Moisture not more than 10.0%
Energy in Kilocalories per lb.
Gross or Total 2,350
Digestible 2,050
Metabolize 1,639
Metabolize Energy in Kilocalories per cup 361
Post a Reply
Registered: October 2005
Posts: 3953
Review Date:
Wed January 2, 2008
Would you recommend the product?
| Price you paid?:
Not Indicated
| Rating:
Third ingredient is a named meat product
Low quality ingredients, products of unidentifiable origin, controversial filler
The first ingredient in this food a low quality meat product. "Poultry" is an ingredient of unidentifiable species, source or quality and such ingredients are usually very cheap and low quality. We note a fish meal ingredient 3rd, but find no guarantee on the manufacturers website that protein sources are ethoxyquin-free (ethoxyquin is a chemical preservative commonly added to fish destined for meal, and is believed to be carcinogenic). Further down the ingredient list, "blood meal" is a further meat related product but unidentifiable by species or quality.
The next ingredient is a low quality grain. Corn is a difficult to digest grain that has limited value and is very commonly linked to allergy problems. Corn Gluten Meal is the dried residue from corn after the removal of the larger part of the starch and germ, and the separation of the bran by the process employed in the wet milling manufacture of corn starch or syrup, or by enzymatic treatment of the endosperm. In plain English, that bit of the corn leftover after most of the nutritious bits have been removed. Extruded rice is a further low quality ingredient, as is flaked corn.
Beet pulp is controversial filler which appears to be used in large quantities in this food. It is a by-product, being dried residue from sugar beets which has been cleaned and extracted in the process of manufacturing sugar. It is a controversial ingredient in dog food, claimed by some manufacturers to be a good source of fibre, and derided by others as an ingredient added to slow down the transition of rancid animal fats and causing stress to kidney and liver in the process. We note that beet pulp is an ingredient that commonly causes problems for dogs, including allergies and ear infections, and prefer not to see it used in dog food. There are less controversial products around if additional fibre is required. Molasses is an unneccessary source of sugar likely to cause or aggravate yeast conditions.
The food has added minerals, but no information about these is given and it may contain synthetics. Likewise, there is not information given about preservatives which could include chemicals such as ethoxyquin, BHT and BHA all of which are allowed in pet products but are banned or heavily regulated in human food due to the belief that they are carcinogenic.
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text:
Avaya and Google Cloud Platform partner to address demand by mid-market customers
About Avaya
Avaya is a leading global provider of solutions for customer and team engagement. The company provides technologies for unified communications and collaboration, contact center and customer experience management, and networking, along with related services to large enterprises, mid-market companies, small businesses, and government organizations around the world.To learn more, visit http://www.avaya.com.
Google Cloud Platform results:
- Google Compute Engine to power subscription-based contact center as a service
- Simple, easy-to-use service answers growing mid-market demand for cloud-based contact management
- Avaya Agent for Chrome software lets users turn a Chromebook and headset into a cost-efficient contact center
Businesses around the world use Avaya's technology and services to enable a higher level of engagement between customers, teams, employees, and partners to improve efficiency and quickly address critical business challenges.
Creating a successful platform for communications is about speed and scalability. As Avaya's mid-market customer base increased, many of its customers were looking for cloud-based services to help support steady growth and seasonal spikes without huge capital expenses. Google Cloud Platform played a key role in helping Avaya bring a new cloud-based customer engagement technology to the mid-market sector.
By collaborating with Google, Avaya can give customers what they want and need. The company's OnAvaya™ customer engagement technology now works as a subscription service powered by Google Compute Engine, and provides hardware and software for "anywhere-anytime" customer experience management.
"Many mid-market sector companies want to avoid making a significant up-front capital investment," says Tony Pereira, director of SMEC business development. "Their time to value is much faster with less up-front costs. Even better, there's no need to manage and care for the technology themselves."
The product, known as Customer Engagement OnAvaya Powered by Google Cloud Platform, includes a subscription-based license and the Avaya Agent for Chrome software, which runs on Google Chromebooks. Users simply provision a Google Chromebook and headset for rapid and cost-efficient contact center implementation.
Avaya wanted a dependable platform based on the latest technology, a key reason behind the company's decision to choose Google Cloud Platform. "Google is one of the world leaders in cloud environments," says Pereira. "They have built an impressive architecture that they are constantly evolving to make the most of cloud efficiencies."
By running on Google Cloud Platform, Pereira says that implementation time should drop from months to weeks — or even days. "Because everything is done in the cloud, our business partners can connect customers much faster," he says. "We'll create an instance in the cloud, stage and prep the solution, and send it back to our business partner to program it to their customer's requirements."
The customer engagement solution is still new to the market, but Pereira says that early users are already able to easily scale to manage peak or seasonal demands, as well as support business continuity and remote agent strategies.
"The Chromebook connection is also a game-changer," says Pereira. All customers need to do is download the Avaya app from Google to turn their Chromebooks into a desktop client. "It's a compelling value," he says. "All you need is a headset, and you can become a contact center while sitting in a Starbucks."
The solution is available to certified Avaya and Google business partners, service providers, and cloud service resellers.
"Through the power of Google Cloud Platform, Avaya and Google are providing a simple, secure and scalable foundation that allows customers and partners to deploy contact centers faster, and agents to work from anywhere."—Joe Manuele, vice president, Global Service Providers, Systems Integrators, Alliances and Cloud GTM, Avaya
About Avaya
Avaya is a leading global provider of solutions for customer and team engagement. The company provides technologies for unified communications and collaboration, contact center and customer experience management, and networking, along with related services to large enterprises, mid-market companies, small businesses, and government organizations around the world.To learn more, visit http://www.avaya.com.


text: Our partners at the National Wildlife Federation (NWF) have designated May "Garden for Wildlife month!" This month's warm weather is perfect for getting out there and sprucing up your home or community garden! NWF's Certified Wildlife Habitat program makes it easy to ensure that your efforts are supporting local wildlife and helping to restore habitats in commercial and residential areas. Our Waterfront park is a certified wildlife habitat! How to create a wildlife-friendly environment: Provide food - Planting native shrubs and trees is the easiest way to provide the foliage, nectar, pollen, berries, seeds and nuts that many species need to survive! Provide water - Animals also need clean water sources to drink and bathe! Give them a helping hand by including a rain garden or bird bath in your garden. Provide shelter - Local wildlife needs shelter from bad weather and predators. Shelter created by native plants and shrubs can also double as a great place for animals to raise their offspring! Get certified! - Show others in your community that your yard is beautifully done AND helping to support the environment! So, ready to get gardening? Share photos of your wildlife habitat with us using #Garden4Wildlife! Tags: certified-wildlife-habitat, community-gardening, Conservation, garden-for-wildlife, garden-for-wildlife-month, gardening, national-aquarium-2, national-wildlife-federation, native-gardens, nwf Categories: Conservation, News Previous Post Next Post


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ALBANY – With the rhetoric getting ugly in the casino revenue-sharing dispute between the state of New York and the Seneca Nation of Indians, the two men at the center of the feud sat at a table last month in a 38th-floor office in a Manhattan skyscraper.
"There was tension. There had to be," said Seneca President Barry Snyder Sr., describing the 90-minute meeting he had with Gov. Andrew M. Cuomo in the governor's New York City office.
"I don't think anybody came in thinking we were going to settle anything that day," he added.
Instead, it was a session for two politicians and government leaders to feel each other out, to see how each other reacted to ideas and to see where there might be common ground.
For Cuomo, accustomed to dealing with legislative leaders, it meant offering a mix of firmness and respect for the elected leader of a sovereign Indian nation. For Snyder, it meant figuring out how to deal with another New York governor, something he has gone through often in his five, two-year terms as Seneca president since he won his first race in 1980.
"It was him understanding who I am and me understanding who he is. It was clear he was not going to give ground and I was not going to give ground," Snyder said.
"He was probably sizing me up as I sized him up," the Seneca leader said in an interview Friday, a day after he and Cuomo signed a deal ending a four-year dispute in which the Senecas withheld millions of dollars in casino revenue-sharing and other payments because of claims the state breached a 2002 compact giving the Senecas exclusive gambling rights in Western New York.
Under the deal, the Senecas get to keep $209 million of the $559.5 million in withheld revenue-sharing payments, and got a promise from Cuomo that no new non-Indian casinos will be located in a huge area from Lake Erie as far east as the central Finger Lakes.
And, according to the memorandum of understanding the state made public Friday, it is all but guaranteed that the tribe's 2002 compact to run casinos in Niagara Falls, Buffalo and Salamanca will run until at least 2023 and not expire, as was possible, in 2016.
"In the end, nobody got 100 percent of what they wanted, but it was very good for both sides," Snyder said.
For Cuomo's part, the negotiating sessions with the Senecas, as well as leaders of the Oneida and St. Regis Mohawks with whom he also recently made casino agreements, took him back to his days as the nation's housing and urban development secretary in the Clinton administration.
"Negotiating with Native Americans is different, much different" than his usual dealings with lawmakers in Albany, the governor explained.
For starters, he said in an interview after signing the agreement, a governor is technically "inferior" to a president of a sovereign Indian nation.
"This is nation-to-state," he said of the protocol of how an Indian leader is to be treated.
Indeed, Snyder said he would not personally meet with Cuomo's representatives unless Cuomo was in the room. Protocol, he explained.
After the May meeting, the two would not meet again until late Wednesday afternoon in Cuomo's Capitol suite. Seneca counselors were already in Albany meeting with various officials, but Snyder said he had a condition for Cuomo when the governor called him and asked him on short notice to get to the Capitol.
"It was the most important meeting, but I was not going to go down until everything was positive," the Seneca president said.
Key officials – including Cuomo's top adviser Howard Glaser and Seneca general counsel Christopher Karns – kept negotiating final clauses. Also in the mix were a team of Cuomo lawyers and aides, while Snyder relied on a group of outsiders for help, including politically wired Albany lobbyist Tracy Lloyd and former Buffalo Mayor Anthony M. Masiello, now a lobbyist for the tribe, as well as lawyers based in Washington.
At 4:24 p.m. Wednesday, a chartered Learjet 35 left Buffalo with Snyder and his team, according to flight tracking service FlightAware. It was in Albany just 37 minutes later and Snyder was on his way to see Cuomo and the waiting Seneca councilors.
At 8:58 p.m., Snyder's jet headed home – with the outlines of a deal in place. Final terms, and some sticking points, needed a last round of lawyer talks Thursday morning before Cuomo felt confident enough that a deal was done.
At 2 p.m. Thursday, the governor ordered two waiting State Police planes to take him and a contingent of Western New York lawmakers to Niagara Falls to announce the deal.
Cuomo and Snyder had talked often via phone over the weeks, and the final talks continued right up until Cuomo's plane departed for Niagara Falls Thursday. But Glaser said the key breakthrough came Wednesday night when Cuomo met Snyder and Seneca Council members in his Capitol office.
"A lot of the complexity in dealing with the Seneca Nation is the need to get consensus by the whole council, and I think the governor really wanted to look them in the eye, face to face," Glaser said.
Glaser said Cuomo then did something he hadn't seen before: he told the Seneca leaders to take time to talk among themselves and to use his private office. They did so for 45 minutes.
"It was a moment of respect," Glaser said.
The governor also acknowledged the problems created by the state that began, the Senecas say, when the state Lottery Division in 2008 let area racetrack "racinos" market themselves as full casinos.
"I think the governor was very direct with the council in saying he understood there had been a breach of trust over the years, and he believed they had a legitimate point and at the end of the day it wasn't about the language of this contract but re-establishing a relationship with the Senecas," said Glaser.
"It's the reboot of the relationship with the Seneca Nation that goes beyond the casino compact itself," Glaser said Friday.
The five-page casino agreement is as interesting for what it includes as for what it omits.
It includes the monetary terms, the new marketing restrictions on three existing area racetrack casinos and paragraphs about the tribe and state holding regular meetings to avoid future conflicts.
But unlike recent deals with the Oneidas, for example, it resolves no other disputes, whether land issues or tax-free sales of cigarettes and gasoline. It also does not compel the Senecas to support a casino expansion referendum that Cuomo hopes to take to voters in November.
The casino-owning Indians, including the Senecas, were seen as major bankrollers of efforts to try to kill the referendum.
"They never asked, and we never offered," Snyder said of the referendum. He would not say if the tribe will take a position on the Cuomo plan to add seven new casinos in the state.
What's more, Snyder said the Senecas might be interested in bidding on the development rights with a partner to run one of the casinos, especially in the Catskills, if the referendum passes. The Senecas years ago made a failed run to develop a Catskills casino.
"We would be interested again. We're looking for partners," Snyder said.
First, though, the memorandum that Snyder and Cuomo signed faces formal approval by the Seneca council; Snyder said he expects approval next week.
Snyder recently told The Buffalo News that Cuomo was "a bully." On Thursday, he apologized to Cuomo for the remark.
But in Friday's interview, Snyder dismissed any notion that the deals Cuomo made with the Oneidas and St. Regis Mohawks put pressure on the Senecas, as Cuomo allies believe. And he said the Senecas were confident they would win the binding arbitration case before a three-member panel where the dispute with Cuomo was taken last year. But, of arbitration he cautioned, "There are no guarantees."
Moreover, Snyder said Cuomo's public threat to locate a new casino, maybe even in downtown Niagara Falls, fell flat with Seneca leaders.
"That was just all political stuff. That was for the news media," he said. Referring to the meeting Thursday, he added: "I told the governor when I met with him that I don't really care if you do or do not put another casino in. I think that settled it. We're a strong gaming entity, and we can compete with anybody."
Snyder said he came to respect Cuomo by the end of the process.
"He's a tough governor. I give him credit. He knows he's a good politician," the Seneca president said.
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'Ikea Monkey' Owner Vows to Fight for Primate's Return
'Ikea Monkey' Owner Vows to Fight for Primate's Return
Dec 11, 2012
"The plan is to try to get him and move out of Toronto where I can own him," Yasmin Nakhuda, a Toronto-based lawyer, told ABCNews.com today.
Nakhuda's monkey, a seven-and-a-half month old Japanese snow macaque named Darwin, was sent to the Story Book Farm Primate Sanctuary in Sunderland, Ont., by Toronto Animal Services yesterday after it escaped from Nakhuda's car while she was shopping at a local Ikea Sunday afternoon.
"I had gone to Ikea before and they had me escorted out and didn't want the monkey in…because they said they had a no pet provision, even though I said he was not a pet , he was my child," said Nakhuda, who obtained Darwin around five months ago from a close friend who is an exotic pet breeder.
"So the next time I went in [to Ikea] I told Darwin he was going to be in the car for a little while," she said. "I guess he got a little bit curious and unlocked the crate by himself and he unlocked he car door, which I wasn't expecting."
By the time Nakhuda, married and the mother of two sons, ages 16 and 12, returned to her car, Animal Services had already left with Darwin. He was taken to Story Book Farm, about an hour outside of Toronto, where the private sanctuary's founder says she was told by Animal Services he'll stay indefinitely.
"He came with the famous coat but the coat has been removed, the diaper has been removed and the harness has been removed," Story Book's Sherri Delaney told ABCNews.com today. "He's just going to be who he is now and that's a monkey."
Delaney confirmed that she had spoken with Nakhuda and told her she can visit Darwin in the future but for now he "needs to settle in" and "familiarize himself with his enclosure and surrounding."
While Darwin settles in at Story Book, he's become an international celebrity, with his own hashtag, Twitter handle, Facebook page and Photoshopped memes devoted to his coat-wearing existence. Helping to fuel that craze are YouTube videos posted by Nakhuda herself, showing her and Darwinbrushing their teeth together and at Nakhuda's office.
Now Nakhuda contends that she is having to learn about her beloved pet's condition only through the media and doesn't believe Darwin is content among his new primate friends like his neighbor, "Sweet Pea," and the "motherly" monkey Delaney says he will soon be paired with.
"They're showing that he's really happy but I don't think that's the actual picture of what's happening," she said. "I don't see him adjusting that easily and he's very fragile in the sense that emotionally he needs someone he's used to."
"What I want to know is whose back he's living off?" Nakhuda said, explaining that Darwin's monkey breed lives off their mothers' backs for the first year. "I was willing to give my back to that monkey. Who is giving her back to Darwin? He's in a cage and he's never been caged by me."
The laws governing ownership of exotic pets are determined by the local municipal governments in Canada and, while it is illegal in Toronto, officials confirmed Sunday they do not plan to press charges against Nakhuda.
A call placed to Animal Services for comment was not immediately returned.
One Response to "'Ikea Monkey' Owner Vows to Fight for Primate's Return"
So it's just fine for "authorities" to grab him in the parking lot and walk off with him. But if you or I did that it'd be stealing.


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Perhaps the most widely known coach in the history of the NFL is John Madden. The former leader of the Oakland Raiders established a virtually unsurpassed record of regular season success during his brief ten-year tenure. Madden won more than 76% of his games. His closest active pursuer, Pittsburgh's Mike Tomlin, has managed only a .672 winning percentage. John Madden also coached the Raiders to an impressive, physical victory over the Minnesota Vikings in Super Bowl XI, 32-14. After leaving the sidelines, Madden carved out the most unique, imposing and meaningful niche in the history of sports broadcasting. And, if that was not sufficient, he also established the premiere video gaming series that has redefined how our society views, plays, and understands football. Simply, John Madden's football legacy is incomparable. In 2006, John Madden was inducted into the Pro Football Hall of Fame.
Madden's successor in Oakland and Los Angeles was the man pictured above, Tom Flores. Back in 1960, Flores shared passing duties with George Blanda and Babe Parilli, but he did most of the heavy lifting in the Raiders first season and over the next 6 seasons. The Raiders laid the foundation for one of the greatest offensive machines in league history. In the popular mind, the preeminent offensive teams were Bill Walsh's San Francisco 49ers and the Miami Dolphins of Dan Marino. However, Al Davis' Raiders ranked in the top 10 in scoring offense every year but 1 from their inception in 1960 until 1984. No team in the league has enjoyed a similar run of offensive prowess…not even the San Francisco 49ers during the era of Walsh and Seifert.
During this run, Tom Flores was the leading passer on the team for five of their first 7 seasons. And, he won two Super Bowls as head coach – one in Oakland and one in Los Angeles.
Time doesn't permit a full exploration of all that Tom Flores achieved on the sidelines, but the recent nominations of Bill Cowher and Bill Parcells for induction into the Pro Football Hall of Fame, suggest a few bullets may be in order.
Consider these facts:
- Tom Flores coached the Raiders for 9 seasons and won 2 Super Bowls. John Madden coached the Raiders for 10 seasons and won 1 Super Bowl.
- Tom Flores amassed an 83-53 record with the Raiders, and a winning percentage of .610. Bill Walsh's career winning percentage is .609. Marty Schottenheimer, another nominee for induction to Canton, has a .613 winning percentage.
- Tom Flores ranks 2nd all-time in playoff win percentage (10 games minimum) behind Vince Lombardi. Bill Parcells has an 11-8 career playoff record. Bill Cowher has a 12-9 career playoff record. Marty Schottenheimer has a 5-13 playoff record. Tom Flores is 8-3.
- After the 4th Super Bowl title of the Pittsburgh Steelers in 1979-80, Tom Flores' Raiders were the only AFC teams to win the Super Bowl until 1997. The NFC dominated the Super Bowl for two decades with powerhouse teams in larger markets like New York, Chicago, Dallas, Washington, and northern California.
- Tom Flores won 2 Super Bowls in 4 years, and in 1983 he handed Washington Redskins head coach Joe Gibbs his only loss in a Super Bowl.
Perhaps the thing that has kept Tom Flores out of the Pro Football Hall of Fame these many years, aside from a bias against Latino excellence and a league-wide contempt for the Raiders, is the fact that he coached in Seattle. The Great Northwest has been the equivalent of a Black Hole for talented football players. It's where careers go to die. Flores coached the Seahawks for 3 years. His teams had a combined record of 14-34.
Flores went from being a coach with a sterling 83-53 record to a rather pedestrian 97-87 (At .527, he's tied with the recently fired Brad Childress…but he's still ranked higher than Dick Vermeil). However, this should not undo the greatness that he achieved in Oakland and Los Angeles for the Silver & Black. Did a stint in Seattle keep Franco Harris from induction? Of course not. Did two 8-8 seasons in Seattle keep Warren Moon out of Canton? Of course not. The remoteness of Seattle and the irrelevance of many of their games may have shattered our collective memory of players like Cortez Kennedy, Kenny Easley and Curt Warner (with a C), but Flores should be teflon in this regard.
Mike Holmgren is still regarded highly even though he's only managed to win one Super Bowl and lost two. Holmgren has a 13-11 playoff record and, unlike Flores, he had prized QB's at the helm in each of his playoff games. Jimmy Johnson and Bill Parcells are still revered though neither has been able to ameliorate the morass or mend the mess that is the Miami Dolphins.
And, Tom Flores' quarterbacks in Seattle were Stan Gelbaugh and Rick Mirer!! That he managed to win as many as 14 games in 3 years with these passers qualifies as a minor miracle.
Some other thoughts to consider on Tom Flores:
- In 1980, the Raiders won the Super Bowl as a Wild Card. Statistically, the Eagles were "better" than the Raiders on both sides of the ball, but Flores and his staff and team figured out a way to win that game.
- Since 1980, Eagles QB Ron Jaworski has become nationally known as a broadcaster and analyst for ESPN. Perhaps he could take up the mantle on behalf of Tom Flores. It's long overdue.
- In 1983, the Raiders beat a team with one of the largest statistical advantages in league history entering a Super Bowl. The Redskins were defending champions and were perceived to be a juggernaut. Jack Squirek did to Joe Theismann what Rod Martin did to Ron Jaworksi. And Marcus Allen did to the Redskins defense what Kenny King had done to the Eagles only three years prior.
- Since 1983, Redskins QB Joe Theismann has become nationally known as a broadcaster and analyst for ESPN and the NFL Network. Perhaps he could take up the mantle on behalf of Tom Flores. It's long overdue.
- Tom Flores won two Super Bowls with an over-the-hill, washed up, washed out quarterback named Jim Plunkett. He beat long odds twice and still stands in the record book — right next to Vince Lombardi as the second-winningest coach in the post-season with an astounding .727 winning percentage.
It's time for Flores to make his speech and be heard…for perhaps the first time.


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No doubt some of those numberless press releases are rattling around like dry old bones in the news morgues of many a Connecticut newspaper.
A few of them relating to internet gambling and the stories they mothered can be fetched from the internet.
Attorney General Blumenthal, as early as 1997, sent out to various newspapers in Connecticut, some of which were much in the habit of reflexively printing his news releases as received, an anti-internet gambling thunderbolt entitled "Blumenthal Urges Effort to Ban Internet Gambling."
Mr. Blumenthal noted in his release that "Gambling and the Internet is a mix that is a recipe for deceit and financial disaster."
Along with other state attorneys general, Mr. Blumenthal appeared at the time before a U.S. Senate subcommittee to endorse legislation he said was essential to preserve state regulation of gambling.
Mr. Blumenthal testified that internet gambling would be, according to his press release, "rife with problems, including no regulation or control over those operating the Internet gambling -- including possibly criminals -- and no protections for those who placed wagers."
That was then.
Coincident with a memo written by Virginia Seitz, head of Justice's Office of Legal Counsel and a possible Obama nominee to the Supreme Court, stating that previous legislation bars only internet betting on sports – not internet betting in general – Governor of Connecticut Dannel Malloy said that "he welcomes the ruling as a way to raise more money for the state," according to a report by WTHN News 8.
The Christian Science Monitor has pointed out that "To win Senate approval to serve on the court, she [Ms. Seitz] would need the support of Senate majority leader Harry Reid (D) of Nevada. Last year, most of Nevada's big casinos became big backers of an effort to overturn the federal Unlawful Internet Gambling Enforcement Act of 2006."
Other cash strapped governors across the fruited plains salivated uncontrollably after the legal opinion that allows states to authorize Web-based, non-sports gambling within their borders.
The ruling breaks open the tax piggy bank at a time when spendthrift legislators and governors had been forced by circumstances to cut spending in their states. The rush of new taxes from newly permitted internet gambling would relieve their anxieties and postpone politically wounding cost saving measures, perhaps beyond the upcoming elections.
It should be noted that internet gambling could not effectively be regulated by current state strictures governing state betting parlors. Internet gambling is a new game that would need new regulations, as well as a federal regulatory apparatus to insure a happy outcome.
Mr. Blumenthal, whose opposition to internet gambling has thawed since 1997, recently told News 8 that "What we really need" are federal regulations that will protect "consumers, so that credit card fraud and identity theft do not come with online gambling."
In 2002, then Attorney General Richard Blumenthal was one of the keynote speakers, along with Danbury Mayor Mark Boughton and Jeff Benedict, author of "Without Reservation," at a public forum sponsored by the Coalition Against Gambling Expansion (CAGE).
In a media release, CAGE noted a series of "facts" surrounding gambling that have not been disputed by Mr. Blumenthal:
"Crime rates in communities with casinos are 84% higher than the national average… Gambling hurts local businesses. One-third of Atlantic City's retail businesses closed within four years of the arrival of casinos… Gambling costs taxpayers money. Every $ 1 in gambling revenue costs states between $ 3 to $ 7 in hidden costs… Gambling eliminates jobs. For every 1 job created by casinos, surrounding communities lose 1 to 2 jobs… Gambling hurts our kids. In states with legalized gambling, 5% to 11% of the teenagers will become compulsive gamblers… Gambling is addictive. A Connecticut study showed that 47% of those who gamble in the state are problem or pathological gamblers… Gambling wrecks lives. In states with legalized gambling: 99% of compulsive gamblers commit crimes; 100% of compulsive gamblers become physically abusive, especially towards children; 25% of compulsive gamblers end up in the legal system…"
Such "facts" cannot be mitigated through regulations. But, then again, inconvenient truths are not likely to weigh heavily on the consciences of Democratic senators and governors whose overriding concern in an era of diminishing tax returns is – how best to raise tax revenue to allow increases in state spending levels without spooking the geese that lay the golden eggs.


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