Tracking Public Beliefs About Anthropogenic Climate Change

A simple question about climate change, with one choice designed to match consensus statements by scientists, was asked on 35 US nationwide, single-state or regional surveys from 2010 to 2015. Analysis of these data (over 28,000 interviews) yields robust and exceptionally well replicated findings on public beliefs about anthropogenic climate change, including regional variations, change over time, demographic bases, and the interacting effects of respondent education and political views. We find that more than half of the US public accepts the scientific consensus that climate change is happening now, caused mainly by human activities. A sizable, politically opposite minority (about 30 to 40%) concede the fact of climate change, but believe it has mainly natural causes. Few (about 10 to 15%) say they believe climate is not changing, or express no opinion. The overall proportions appear relatively stable nationwide, but exhibit place-to-place variations. Detailed analysis of 21 consecutive surveys within one fairly representative state (New Hampshire) finds a mild but statistically significant rise in agreement with the scientific consensus over 2010–2015. Effects from daily temperature are detectable but minor. Hurricane Sandy, which brushed New Hampshire but caused no disaster there, shows no lasting impact on that state’s time series—suggesting that non-immediate weather disasters have limited effects. In all datasets political orientation dominates among individual-level predictors of climate beliefs, moderating the otherwise positive effects from education. Acceptance of anthropogenic climate change rises with education among Democrats and Independents, but not so among Republicans. The continuing series of surveys provides a baseline for tracking how future scientific, political, socioeconomic or climate developments impact public acceptance of the scientific consensus.     

Endocrine markers of semistarvation in healthy lean men in a multistressor environment.

We tested the hypothesis that key endocrine responses to semistarvation would be attenuated by changing only the food intake in a multistressor environment that also included sustained workload, inadequate sleep, and thermal strain. Serum hormones were compared within and between two groups of healthy young male volunteers participating in the 8-wk US Army Ranger course, with four repeated cycles of restricted energy intakes and refeeding: group 1 (n = 49) and group 2 (n = 48); energy deficits averaged 1,200 and 1,000 kcal/day, respectively. After 8 wk, most of group 1 achieved a minimum body fat, serum 3,5,3'-triiodothyronine (T(3)) was below normal (78 +/- 20 ng/dl), testosterone (T) approached castrate levels (4.5 +/- 3.9 nmol/l), insulin-like growth factor I (IGF-I) declined by one-half (75 +/- 25 microg/l), and cholesterol rose from 158 +/- 31 to 217 +/- 39 mg/dl. Bioavailable T(3) and T were further reduced by increases in their specific binding proteins in response to declining insulin. Refeeding, even with continuation of the other stressors, produced prompt recovery of T(3), T, and IGF-I. Higher energy intakes in group 2 attenuated the subclinical hypothyroidism and hypercholesterolemia, whereas consistent luteinizing hormone suppression indicated centrally mediated threshold effects on gonadal hormone suppression. We conclude that low T, T(3), and IGF-I remained reliable markers of acute energy deficits in the presence of other stressors; elevated cholesterol and cortisol provided information about chronic status, corresponding to diminishing body fat stores.     

Clear cell dysplasia of the bladder. Report of a case with flow cytometric analysis.

Clear cell dysplasia of the bladder is a well-described morphologic entity that has been found in association with transitional cell carcinoma of the bladder. Its biologic role in bladder tumorigenesis is unknown, and no instances of its polidy analysis have been reported. The authors describe a case of clear cell dysplasia of the bladder found in association with a primary adenocarcinoma of the bladder. Flow cytometric analysis of bladder tissue involved by clear cell dysplasia, adenocarcinoma and cystitis cystica (all from the same bladder) demonstrated no DNA aneuploid populations. Cells from the area of clear cell dysplasia had an S + G2 + M fraction of 7%, indicating that it was a proliferative lesion. Cells from the adenocarcinoma had an S + G2 + M phase of 18%, and cells from an area of cystitis cystica had an S + G2 + M phase of 4%.     

Cardiolipin biosynthesis and remodeling enzymes are altered during development of heart failure

Cardiolipin (CL) is responsible for modulation of activities of various enzymes involved in oxidative phosphorylation. Although energy production decreases in heart failure (HF), regulation of cardiolipin during HF development is unknown. Enzymes involved in cardiac cardiolipin synthesis and remodeling were studied in spontaneously hypertensive HF (SHHF) rats, explanted hearts from human HF patients, and nonfailing Sprague Dawley (SD) rats. The biosynthetic enzymes cytidinediphosphatediacylglycerol synthetase (CDS), phosphatidylglycerolphosphate synthase (PGPS) and cardiolipin synthase (CLS) were investigated. Mitochondrial CDS activity and CDS-1 mRNA increased in HF whereas CDS-2 mRNA in SHHF and humans, not in SD rats, decreased. PGPS activity, but not mRNA, increased in SHHF. CLS activity and mRNA decreased in SHHF, but mRNA was not significantly altered in humans. Cardiolipin remodeling enzymes, monolysocardiolipin acyltransferase (MLCL AT) and tafazzin, showed variable changes during HF. MLCL AT activity increased in SHHF. Tafazzin mRNA decreased in SHHF and human HF, but not in SD rats. The gene expression of acyl-CoA: lysocardiolipin acyltransferase-1, an endoplasmic reticulum MLCL AT, remained unaltered in SHHF rats. The results provide mechanisms whereby both cardiolipin biosynthesis and remodeling are altered during HF. Increases in CDS-1, PGPS, and MLCL AT suggest compensatory mechanisms during the development of HF. Human and SD data imply that similar trends may occur in human HF, but not during nonpathological aging, consistent with previous cardiolipin studies.