BackgroundThe incidence of thyroid cancer in Korea has increased by about 25 % every year for the past 10 years. This increase is largely due to a rising incidence in papillary thyroid cancer, which is associated with an overdiagnosis of small tumors that may never become clinically significant. This study was conducted to explore Korean women’s understanding of overdiagnosis and to investigate changes in screening intention in response to overdiagnosis information.MethodsFocus group interviews were conducted among women of ages 30–69 years, who are commonly targeted in Korea for cancer screening. Women were divided into four groups according to thyroid cancer screening history and history of thyroid disease. Of 51 women who were contacted, 29 (57 %) participated in the interviews.ResultsPrior awareness of thyroid cancer overdiagnosis was minimal. When informed about the risks of overdiagnosis, the participants were often surprised. Overcoming initial malcontent, many women remained skeptic about overdiagnosis and trusted in the advice of their physicians. Meanwhile, some of the study participants found explanations of overdiagnosis difficult to understand. Further, hearing about the risks of overdiagnosis had limited impact on the participants’ attitudes and intentions to undergo thyroid cancer screening, as many women expressed willingness to undergoing continued screening in the future.ConclusionA large majority of Korean women eligible for and had undergone thyroid cancer screening were unaware of the potential for overdiagnosis. Nevertheless, overdiagnosis information generally had little impact on their beliefs about thyroid cancer screening and their intentions to undergo future screening. Further research is needed to determine whether these findings could be generalized to the wider Korean population.

Taurine is ubiquitously distributed in mammalian tissues and is highly concentrated in the heart, brain, and leukocytes. Taurine exerts neuroprotective effects in various central nervous system diseases and can suppress infarct formation in stroke. Taurine reacts with myeloperoxidase (MPO)-derived hypochlorous acid (HOCl) to produce taurine chloramine (Tau-Cl). We investigated the neuroprotective effects of taurine using a rat middle cerebral artery occlusion (MCAO) model and BV2 microglial cells. Although intranasal administration of taurine (0.5 mg/kg) had no protective effects, the same dose of Tau-Cl significantly reduced infarct volume and ameliorated neurological deficits and promoted motor function, indicating a robust neuroprotective effect of Tau-Cl. There was neutrophil infiltration in the post-MCAO brains, and the MPO produced by infiltrating neutrophils might be involved in the taurine to Tau-Cl conversion. Tau-Cl significantly increased the levels of antioxidant enzymes glutamate–cysteine ligase, heme oxygenase-1, NADPH:quinone oxidoreductase 1, and peroxiredoxin-1 in BV2 cells, whereas taurine slightly increased some of them. Antioxidant enzyme levels were increased in the post-MCAO brains, and Tau-Cl further increased the level of MCAO-induced antioxidant enzymes. These results suggest that the neutrophils infiltrate the area of ischemic injury area, where taurine is converted to Tau-Cl, thus protecting from brain injury by scavenging toxic HOCl and increasing antioxidant enzyme expression.

Bone absorption is necessary for the maintenance of bone homeostasis. An osteoclast (OC) is a monocyte–macrophage lineage cell that absorbs bone tissue. Extracellular signal-regulated kinases (ERKs) are known to play important roles in regulating OC growth and differentiation. In this study, we examined specific downstream signal pathways affected by ERK inhibition during OC differentiation. Our results showed that the ERK inhibitors PD98059 and U0126 increased receptor activator of NF-κB ligand (RANKL)-induced OC differentiation in RAW 264.7 cells, implying a negative role in OC differentiation. This is supported by the effect of ERK2-specific small interfering RNA on increasing OC differentiation. In contrast to our findings regarding the RAW 264.7 cells, the ERK inhibitors attenuated the differentiation of bone marrow-derived cells into OCs. The ERK inhibitors significantly increased the phosphorylation of adenosine 5′-monophosphate-activated protein kinase (AMPK) but not the activation of p38 MAPK, Lyn, and mTOR. In addition, while the ERK inhibition increased the expression of the RANKL receptor RANK, it decreased the expression of negative mediators of OC differentiation, such as interferon regulatory factor-8, B-cell lymphoma 6, and interferon-γ. These dichotomous effects of ERK inhibition suggest that while ERKs may play positive roles in bone marrow-derived cells, ERKs may also play negative regulatory roles in RAW 264.7 cells. These data provide important information for drug development utilizing ERK inhibitors in OC-related disease treatment.

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