In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

OBJECTIVE To assess prospectively the risk of coronary heart disease associated with elevated plasma levels of homocyst(e)ine.
DESIGN Nested case-control study using prospectively collected blood samples.
SETTING Participants in the Physicians' Health Study.
PARTICIPANTS A total of 14,916 male physicians, aged 40 to 84 years, with no prior myocardial infarction (MI) or stroke provided plasma samples at baseline and were followed up for 5 years. Samples from 271 men who subsequently developed MI were analyzed for homocyst(e)ine levels together with paired controls, matched by age and smoking.
MAIN OUTCOME MEASURE Acute MI or death due to coronary disease.
RESULTS Levels of homocyst(e)ine were higher in cases than in controls (11.1 +/- 4.0 [SD] vs 10.5 +/- 2.8 nmol/mL; P = .03). The difference was attributable to an excess of high values among men who later had MIs. The relative risk for the highest 5% vs the bottom 90% of homocyst(e)ine levels was 3.1 (95% confidence interval, 1.4 to 6.9; P = .005). After additional adjustment for diabetes, hypertension, aspirin assignment, Quetelet's Index, and total/high-density lipoprotein cholesterol, this relative risk was 3.4 (95% confidence interval, 1.3 to 8.8) (P = .01). Thirteen controls and 31 cases (11%) had values above the 95th percentile of the controls.
CONCLUSIONS Moderately high levels of plasma homocyst(e)ine are associated with subsequent risk of MI independent of other coronary risk factors. Because high levels can often be easily treated with vitamin supplements, homocyst(e)ine may be an independent, modifiable risk factor.
A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians.

MicroRNAs are proposed to serve vital functions in the regulation of tumor progression and invasion. However, the expression levels of miR-203 in non-small cell lung cancer (NSCLC) and its clinical significance remain unknown. In the present study, the association between B-cell-specific moloney murine leukemia virus insertion site 1 (Bmi1) and miR-203 was investigated. miR-203 was demonstrated to act as a tumor suppressor by regulating the expression of Bmi1. miR-203 expression levels were downregulated in NSCLC tissues while Bmi1 expression was upregulated in NSCLC tissues and cell lines. Furthermore, downregulated Bmi1 or enhanced miR-203 expression inhibited NSCLC cell proliferation and invasion in vitro. In addition, a dual-luciferase reporter assay was performed, which identified Bmi1 as a novel target of miR-203. In conclusion, the present study demonstrated that miR-203 functions as a tumor suppressor and is important in inhibiting the proliferation of NSCLC cells through targeting Bmi1. These findings indicate that miR-203 may be useful as a novel potential therapeutic target for NSCLC.
MicroRNA-203 inhibits cellular proliferation and invasion by targeting Bmi1 in non-small cell lung cancer.

Latent membrane protein 1 (LMP1), an oncoprotein encoded by EpsteinBarr virus (EBV), is an integral membrane protein, which acts like a constitutively active receptor. LMP1 is critical for some facet of EBV's induction and maintenance of proliferation of infected B cells. It, in part, mimics signaling by the CD40 receptor and has been implicated in regulating proliferation, survival, or both properties of EBV-infected cells. We established a conditional LMP1 allele in the context of the intact EBV genome to define the immediate-early cellular target genes regulated by LMP1 in order to assess its contributions to infected human B cells. The functional analysis of this conditional system indicated that LMP1 specifically induces mitogenic B-cell activation through c-myc and Jun/AP1 family members and confirms its direct role in upregulating expression of multiple genes with opposing activities involved in cell survival. LMP1's signals were found to be essential for the G1/S transition in human B cells; cells lacking LMP1's signals are cell cycle arrested and survive quiescently. LMP1's activities are therefore not required to maintain survival in nonproliferating cells. LMP1 does induce both pro- and antiapoptotic genes whose balance seems to permit survival during LMP1's induction and maintenance of proliferation.
Latent membrane protein 1 of EpsteinBarr virus coordinately regulates proliferation with control of apoptosis