Adding more portion-size options to a menu: A means to nudge consumers to choose larger portions of healthy food items.

We propose and find that the extremeness aversion bias when choosing portion-sizes is stronger for healthy food as compared to unhealthy food items. In two studies (and a follow-up) we find that adding an extra-large option to a standard menu of small, medium, and large portions increases the choice share of the larger portion-sizes; but more so for healthy food than for unhealthy food. Furthermore, we find evidence for the lay belief that larger portions of healthy food do not have incremental health costs. When health costs of the larger portions of healthy food were made salient by providing calorie information, the above effects disappeared. These findings show (1) a boundary condition to the extremeness aversion effect when choosing portion sizes, and (2) imply that this bias can act as a nudge to increase the consumption of healthy food.

Helping fellow beings: anthropomorphized social causes and the role of anticipatory guilt.

People are often reluctant to comply with social causes because doing so may involve personal sacrifices of time, money, and effort for benefits that are shared by other members of society. In an effort to increase compliance, government agencies and public institutions sometimes employ financial tools to promote social causes. However, employing financial tools to induce prosocial behavior is expensive and often ineffective. We propose that anthropomorphizing a social cause is a practical and inexpensive tool for increasing compliance with it. Across three prosocial contexts, we found that individuals exposed to a message from an anthropomorphized social cause, compared with individuals exposed to a message relating to a nonanthropomorphized social cause, were more willing to comply with the message. This effect was mediated by feelings of anticipatory guilt experienced when they considered the likely consequences of not complying with the cause. The theoretical and practical implications of these findings are discussed.

Minichromosome maintenance protein 3 is a candidate proliferation marker in papillary thyroid carcinoma.

The proliferative capacity of tumor cells is a characteristic feature in the whole growing tumors. Many pathologists and clinicians have used the estimation of cell proliferation for prognostic information. Minichromosome maintenance protein 3 (MCM3) is known to have a role on the initiation and regulation of DNA replication during cell cycle. The aim of this study was to evaluate the potential applicability of one of the MCM proteins, MCM3, as a proliferation marker in papillary thyroid carcinoma (PTC) with correlation to clinicopathological parameters. We performed the immunohistochemical analysis for MCM3 and Ki-67 in 60 cases of PTC and Western blot analysis for MCM3 expression in 6 PTCs and normal thyroid tissues. The comparison of MCM3 labeling index (LI) to tumor size (P=0.031) and extrathyroidal extension (P=0.037) was statistically significant while that of Ki-67 LI to them was not. Moreover, a significant association was not observed between MCM3 and Ki-67, but the MCM3 LI was considerably higher. Western blot analyses revealed that the MCM3 protein expression levels were overexpressed in all PTCs. On the contrary, the levels of MCM3 were very low or absent in all normal thyroid tissues. Our results indicate that MCM3 may be a more reliable proliferation marker than Ki-67 in accessing the growth of tumor and evaluating tumor aggressiveness of PTC.

New quantitative method for bone tracer uptake of temporomandibular joint using Tc-99m MDP skull SPECT.

OBJECTIVES: Quantitative bone SPECT studies have several advantages over qualitative studies for evaluating a temporomandibular joint (TMJ), yet in certain cases additional images are still needed. Accordingly, the current study developed a new easy SPECT quantification method for the bone tracer uptake in a TMJ and evaluated its usefulness and inter-observer variability in patients with TMJ pain. METHODS: Sixty-six adult patients (11 males, 55 females) with a mean age of 31 years (range 22-79 years) suffering from TMJ pain were questioned regarding the history of their condition, and then subjected to an oromaxillofacial examination and bone SPECT. New quantitative data for TMJs (TMJ index) were calculated from a formula using TMJ and skull counts. RESULTS: TMJs with spontaneous pain had higher TMJ indices than those without spontaneous pain (8.87 vs. 6.87, P = 0.032). TMJs with mouth-opening pain or palpatory pain also exhibited higher TMJ indices than those without such pains, although the differences were not statistically significant. Positive TMJs, according to a visual SPECT interpretation, had much higher TMJ indices than the negative ones (8.99 vs. 5.37, P < 0.001). The reference skull count, mean TMJ count and TMJ index obtained using the proposed TMJ quantification method demonstrated an excellent correlation based on two independent observers (r = 0.996, r = 0.993 and r = 0.989, respectively; P < 0.001). CONCLUSIONS: The current results indicate that the proposed quantitative TMJ bone SPECT is easy to perform, plus the resulting TMJ index has a lower inter-observer variability, making it an effective TMJ evaluation method for patients with painful TMJs, and especially useful for serial studies.

Oncoprotein HCCR-1 expression in breast cancer is well correlated with known breast cancer prognostic factors including the HER2 overexpression, p53 mutation, and ER/PR status.

BACKGROUND: Oncoprotein HCCR-1 functions as a negative regulator of the p53 and contributes breast tumorigenesis. The serum HCCR-1 assay is useful in diagnosing breast cancer and mice transgenic for HCCR developed breast cancers. But it is unknown how HCCR-1 contributes to human breast tumorigenesis. METHODS: Oncogene HCCR-1 expression levels were determined in normal breast tissues, breast cancer tissues and cancer cell lines. We examined whether HCCR-1 protein expression in breast cancer is related to different biological characteristics, including ER, PR, p53 genotype, and HER2 status in 104 primary breast cancer tissues using immunohistochemical analyses. RESULTS: HCCR-1 was upregulated in breast cancer cells and tissues compared with normal breast tissues. In this study, overexpression of HCCR-1 was well correlated with known breast cancer prognostic markers including the presence of steroid receptors (ER and PR), p53 mutation and high HER2 overexpression. HCCR-1 was not detected in the ER-negative, PR-negative, p53 negative and low HER2 breast cancer tissues. These data indicate that the level of HCCR-1 in breast cancer tissues is relatively well correlated with known breast cancer factors, including the HER2 overexpression, p53 mutation, and ER/PR status. CONCLUSION: Determination of HCCR-1 levels as options for HER2 testing is promising although it needs further evaluation.

Dual action of apolipoprotein E-interacting HCCR-1 oncoprotein and its implication for breast cancer and obesity.

Obese women have an increased risk for post-menopausal breast cancer. The physiological mechanism by which obesity contributes to breast tumourigenesis is not understood. We previously showed that HCCR-1 oncogene contributes to breast tumourigenesis as a negative regulator of p53 and detection of HCCR-1 serological level was useful for the diagnosis of breast cancer(.) In this study, we found that the HCCR-1 level is elevated in breast cancer tissues and cell lines compared to normal breast tissues. We identified apolipoprotein E (ApoE) interacting with HCCR-1. Our data show that HCCR-1 inhibits anti-proliferative effect of ApoE, which was mediated by diminishing ApoE secretion of breast cancer cells. Finally, HCCR-1 induced the severe obesity in transgenic mice. Those obese mice showed severe hyperlipidaemia. In conclusion, our results suggest that HCCR-1 might play a role in the breast tumourigenesis while the overexpression of HCCR-1 induces the obesity probably by inhibiting the cholesterol-lowering effect of ApoE. Therefore, HCCR-1 seems to provide the molecular link between the obesity and the breast cancer risk.