BACKGROUND:The Mediterranean diet has been consistently associated with reduced mortality risk. Few prospective studies have examined whether the benefits from a Mediterranean diet are equally shared by obese individuals with varying metabolic health.OBJECTIVE:The objective of this study was to investigate the association between Mediterranean diet, metabolic phenotypes and mortality risk in a representative obese US population.METHODS:Data from 1739 adults aged 20-88 years were analyzed from participants of the National Health and Nutrition Examination Survey III, 1988-1994 followed up for deaths until 31 December 2011 in a prospective cohort analysis. Mediterranean Diet Scores (MDS) were created to assess the adherence to Mediterranean diet. Participants were classified as metabolically healthy obese (MHO) phenotype (0 or 1 metabolic abnormality) or metabolically unhealthy obese (MUO) phenotype (two or more metabolic abnormalities), based on high glucose, insulin resistance, blood pressure, triglycerides, C-reactive protein and low high-density lipoprotein cholesterol.RESULTS:The MHO phenotype (n=598) was observed in 34.8% (s.e., 1.7%) of those who were obese (mean body mass index was 33.4 and 34.8 in MHO and MUO phenotypes, respectively). During a median follow-up of 18.5 years, there were 77 (12.9%) and 309 (27.1%) deaths in MHO and MUO individuals, respectively. In MHO individuals, the multivariable-adjusted hazard ratio (HR) of all-cause mortality in the highest tertile compared with the first tertile of MDS was 0.44 (95% confidence interval (CI), 0.26-0.75; P for trend <0.001), after adjustment for potential confounders. A five-point (1 s.d.) increment in the adherence to MDS was associated with a 41% reduction in the risk of all-cause mortality (HR, 0.59; 95% CI, 0.37-0.94). Similar findings were obtained when we restricted our analyses to those with or without prevalent diabetes mellitus and hypertension. We did not observe mortality risk reduction in either individuals with MUO phenotype or all obese participants combined.CONCLUSIONS:Adherence to a Mediterranean dietary pattern appears to reduce mortality in the MHO phenotype, but not among the MUO phenotype in an obese population.

Apicidin is a fungal metabolite shown to exhibit anti-proliferative, anti-invasive, and anti-inflammatory properties by the inhibition of histone deacetylase (HDAC). However, the effects of apicidin on the maturation and immunostimulatory function of dendritic cells (DCs) remain unknown. In this study, we investigated whether apicidin modulates surface molecule expression, cytokine production, endocytosis capacity, and underlying signaling pathways in murine bone marrow-derived DCs. We observed that apicidin significantly attenuated surface molecule expression in LPS-stimulated DCs, suppressed production of interleukin (IL)-12 and proinflammatory cytokines (IL-6 and TNF-α) by DCs, and reduced IFN-γ production by T cells. The apicidin-treated DCs were found to be highly efficient in antigen capture via mannose receptor-mediated endocytosis. Apicidin also inhibited LPS-induced MAPK activation and NF-κB nuclear translocation in DCs. Moreover, the apicidin-treated DCs were incapable of inducing Th1 responses and normal cell-mediated immune responses. These novel findings not only provide new insights into the immunopharmacological role of apicidin in terms of its effects on DCs, but also broaden current perspectives of the immunopharmacological functions of apicidin, and have implications for the development of therapeutic adjuvants for the treatment of DC-related acute and chronic diseases.

METHODS: From January 1, 1996 to December 31, 1999, 2,082 subjects who took the Pap test and the Human papillomavirus test at the OB/GYN clinic of Samsung Jeil hospital for screening of uterine cervical cancer were selected. Cox's proportional hazards regression model was used to estimate hazard ratio of progression of high-risk HPV infection among atypical squamous cells of undetermined significance (ASCUS) and low-grade squamous intraepithelial lesions (LSIL) groups.

Catechol 1,2-dioxygenase I-1 (CDI1) is the first enzyme of the beta -ketoadipate pathway in Acinetobacter lowffii K24. CDI1 has two cysteines (155, 202) and its enzyme activity is inhibited by the cysteine inhibitor, AgNO3. Two mutants, CDI1 C155V and CDI1 C202V, were obtained by site-directed mutagenesis. The two mutants were overexpressed and the mutated amino acid residues (Cys --> Val) were characterized by peptide mapping and amino acid sequencing. Interestingly, CDI1 C155V was inhibited by AgNO3, whereas CDI1 C202V was not inhibited. This suggests that Cys(202) is the sole inhibition site by AgNO3 and is close to the active site of the enzyme. However, the results of the biochemical assay of mutated CDI(1)s suggest that the two cysteines are not directly involved in the activity of the catechol 1,2-dioxygenase of CDI1.

Carcinoembryonic antigen (CEA) is a tumor-associated antigen which is expressed largely in gastrointestinal tract tumors. Some monoclonal antibodies to CEA have already been produced by us and the immunological characteristics of the antibodies characterizes. CEA 79 antibody showed the highest affinity for CEA (1.93 x 10(9) M(-1)). In this study CEA 79 antibody was reduced to the monovalent form and was conjugated with recombinant human angiogenin using the two-step maleimide chemical cross-linking method. Then its cytotoxic effect on SNUC4, which is a human adenocarcinoma cell line established from gastrointestinal tract tumor by the Korean Cell Line Bank (KCLB) and which expresses CEA on its surface, was examined. The resulting monovalent CEA 79 antibody conjugated with recombinant human angiogenin (CEA 79/angiogenin) showed cytotoxic effect at concentrations of 5 x 10(-9) M or higher, while both unconjugated human angiogenin and CEA 79 antibody did not show a corresponding cytotoxic effect, indicating that CEA 79/angiogenin can be used as an immunotoxin toward tumor cells expressing CEA on their surface.

The distribution of the transverse energy in jets has been measured in p $($) over bar$$ p collisions at root s = 1.8 TeV using the DO detector at Fermilab. This measurement of the jet shape is made as st function of jet transverse energy in both the central and forward rapidity regions. Jets are shown to narrow both with increasing transverse energy and with increasing rapidity. Next-to-leading order partonic QCD calculations are compared to the data. Although the calculations qualitatively describe the data, they are shown to be very dependent on renormalization scale, parton clustering algorithm, and jet direction definition and they fail to describe the data in all regions consistently.