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There is a lack of research focused on understanding the different characteristics and healthcare utilization of metastatic breast cancer patients by palliative care use. This study aims to investigate trend of in-patient palliative care and its association with healthcare utilization among hospitalized metastatic breast cancer patients in the US. National Inpatient Sample (NIS) was used to identify nationwide metastatic breast cancer patients (n = 5209, weighted n = 25,961) from 2010 to 2014. We examined the characteristics of the study sample by palliative care and its association with healthcare utilization, measured by discounted hospital charges and length of stay. Multivariable survey regression models were used to identify predictors. Among 26,961 breast cancer patients, 19.0% had palliative care. Percentage of receiving palliative care during the period were gradually increased. Social factors including race, insurance types were also associated with a receipt of palliative care. Survey linear regression results showed that patients with palliative care were associated with 31% lower hospital charges, however, length of stays were not significantly associated. This study found evidence of who was associated with the receipt of palliative care and its relationship with healthcare utilization. This study also emphasizes the importance of receiving palliative care in patients with breast cancer, paving the way for future research into ways to improve palliative care in cancer patients. This study also found social differences and gave evidence of programs that could be used to help vulnerable groups in future health policy decisions.

Background We aimed to investigate the association between fragmented cancer care in the early phase after cancer diagnosis and patient outcomes using national insurance claim data. Methods From a nationwide sampled cohort database, we identified National Health Insurance beneficiaries diagnosed with gastric cancer (ICD-10: C16) in South Korea during 2005–2013. We analyzed the results of a multiple logistic regression analysis using the generalized estimated equation model to investigate which patient and institution characteristics affected fragmented cancer care during the first year after diagnosis. Then, survival analysis using the Cox proportional hazard model was conducted to investigate the association between fragmented cancer care and five-year mortality. Results Of 2879 gastric cancer patients, 11.9% received fragmented cancer care by changing their most visited medical institution during the first year after diagnosis. We found that patients with fragmented cancer care had a higher risk of five-year mortality (HR: 1.310, 95% CI: 1.023–1.677). This association was evident among patients who only received chemotherapy or radiotherapy (HR: 1.633, 95% CI: 1.005–2.654). Conclusions Fragmented cancer care was associated with increased risk of five-year mortality. Additionally, changes in the most visited medical institution occurred more frequently in either patients with severe conditions or patients who mainly visited smaller medical institutions. Further study is warranted to confirm these findings and examine a causal relationship between fragmented cancer care and survival.

Objective The benefits of palliative care for cancer patients were well developed; however, the characteristics of receiving palliative care and the utilization patterns among lung cancer patients have not been explored using a large-scale representative population-based sample. Methods The National Inpatient Sample of the United States was used to identify deceased metastatic lung cancer patients (n = 5,068, weighted n = 25,121) from 2010 to 2014. We examined the characteristics of receiving palliative care use and the association between palliative care and healthcare utilization, measured by discounted hospital charges and LOS (length of stay). The multivariate survey logistic regression model (to identify predictors for receipts of palliative care) and the survey linear regression model (to measure how palliative care is associated with healthcare utilization) were used. Results Among 25,121 patients, 50.1% had palliative care during the study period. Survey logistic results showed that patients with higher household income were more likely to receive palliative care than those in lower-income groups. In addition, during hospitalization, receiving palliative care was associated with11.2% lower LOS and 28.4% lower discounted total charges than the non-receiving group. Conclusion Clinical evidence demonstrates the benefits of palliative care as it is associated with efficient end-of-life healthcare utilization. Health policymakers must become aware of the characteristics of receiving the care and the importance of limited healthcare resource allocation as palliative care continues to grow in cancer treatment.

Background Although survival based outcomes of lung cancer patients have been well developed, institutional transition of cancer care, that is, when patients transfer from primary visiting hospitals to other hospitals, and mortality have not yet been explored using a large-scale representative population-based sample. Methods Data from the Korean National Elderly Sampled Cohort survey were used to identify patients with lung cancer who were diagnosed during 2005–2013 and followed up with for at least 1 year after diagnosis (3738 patients with lung cancer aged over 60 years). First, the authors examined the distribution of the study population by mortality, and Kaplan-Meier survival curves/log-rank test were used to compare mortality based on institutional transition of cancer care. Survival analysis using the Cox proportional hazard model was conducted after controlling for all other variables. Results Results showed that 1-year mortality was higher in patients who underwent institutional transition of cancer care during 30 days after diagnosis (44.2% vs. 39.7%, p = .027); however, this was not associated with 5-year mortality. The Cox proportional hazard model showed that patients who underwent institutional transition of cancer care during 30 days after diagnosis exhibited statistically significant associations with high mortality for 1 year and 5 years (1-year mortality, Hazard ratio [HR]: 1.279, p = .001; 5-year mortality, HR: 1.158, p = .002). Conclusion This study found that institutional transition of cancer care was associated with higher mortality among elderly patients with lung cancer. Future consideration should also be given to the limitation of patients’ choice when opting for institutional transition of care since there are currently no control mechanisms in this regard. Results of this study merit health policymakers’ attention.

Background In Korea, the universal health system offers coverage to all members of society. Despite this, it is unclear whether risk of death from hepatocellular carcinoma (HCC) varies depending on income. We evaluated the impact of low income on HCC mortality. Methods The Korean National Health Insurance sampling cohort was used to identify new HCC cases (n = 7325) diagnosed between 2004 and 2008, and the Korean Community Health Survey data were used to investigate community-level effects. The main outcome was 5-year all-cause mortality risk, and Cox proportional hazard models were applied to investigate the individual- and community-level factors associated with the survival probability of HCC patients. Results From 2004 to 2008, there were 4658 new HCC cases among males and 2667 new cases among females. The 5-year survival proportion of males was 68%, and the incidence per person-year was 0.768; the female survival proportion was 78%, and the incidence per person-year was 0.819. Lower income was associated with higher hazard ratio (HR), and HCC patients with hepatitis B (HBV), alcoholic liver cirrhosis, and other types of liver cirrhosis had higher HRs than those without these conditions. Subgroup analyses showed that middle-aged men were most vulnerable to the effects of low income on 5-year mortality, and community-level characteristics were associated with survival of HCC patients. Conclusion Having a low income significantly affected the overall 5-year mortality of Korean adults who were newly diagnosed with HCC from 2004 to 2008. Middle-aged men were the most vulnerable. We believe our findings will be useful to healthcare policymakers in Korea as well as to healthcare leaders in countries with NHI programs who need to make important decisions about allocation of limited healthcare resources according to a consensually accepted and rational framework.

Aberrant population expansion of follicular helper T cells (TFH cells) occurs in patients with lupus. An unanswered question is whether an altered repertoire of T cell antigen receptors (TCRs) is associated with such expansion. Here we found that the transcription factor Blimp-1 (encoded by Prdm1) repressed expression of the gene encoding cathepsin S (Ctss), a cysteine protease that cleaves invariant chains and produces antigenic peptides for loading onto major histocompatibility complex (MHC) class II molecules. The increased CTSS expression in dendritic cells (DCs) from female mice with dendritic cell-specific conditional knockout of Prdm1 (CKO mice) altered the presentation of antigen to CD4+ T cells. Analysis of complementarity-determining region 3 (CDR3) regions containing the β-chain variable region (Vβ) demonstrated a more diverse repertoire of TFH cells from female CKO mice than of those from wild-type mice. In vivo treatment of CKO mice with a CTSS inhibitor abolished the lupus-related phenotype and reduced the diversity of the TFH cell TCR repertoire. Thus, Blimp-1 deficiency in DCs led to loss of appropriate regulation of Ctss expression in female mice and thereby modulated antigen presentation and the TFH cell repertoire to contribute to autoimmunity.

In our previous study, the Kelch domain-containing 7B (KLHDC7B) was revealed to be hypermethylated at the promoter but upregulated in breast cancer. In this study, we identified a long non-coding RNA, ST8SIA6-AS1 (STAR1), whose expression was significantly associated with KLHDC7B in breast cancer (R2 = 0.3466, P

To identify dysregulated genes by abnormal methylation and expression in breast cancer, we genome-wide analyzed methylation and expression microarray data from the Gene Expression Omnibus and the Cancer Genome Atlas database. One of the genes screened in silico, FLRT2, showed hypermethylation and downregulation in the cancer dataset and the association was verified both in cultured cell lines and cancer patients’ tissue. To investigate the role of FLRT2 in breast cancer, its expression was knocked down and upregulated in mammary cell lines, and the effect was examined through three levels of approach: pathway analysis; cell activities such as proliferation, colony formation, migration, and adhesion; target gene expression. The top pathway was “Cellular growth and proliferation”, or “Cancer”-related function, with the majority of the genes deregulated in a direction pointing to FLRT2 as a potential tumor suppressor. Concordantly, downregulation of FLRT2 increased cell proliferation and cell migration, while overexpression of FLRT2 had the opposite effect. Notably, cell adhesion was significantly decreased by FLRT2 in the collagen I-coated plate. Taken together, our results provide insights into the role of FLRT2 as a novel tumor suppressor in the breast, which is inactivated by hypermethylation during tumor development.

A single nucleotide polymorphism of PRDM1, the gene encoding Blimp-1, is strongly associated with inflammatory bowel disease. Here, we demonstrate that Blimp-1 in CD103(+) dendritic cells (DCs) critically contributes to the regulation of macrophage homeostasis in the colon. Dextran sodium sulfate (DSS)-exposed Blimp-1(cko) mice with a deletion of Blimp-1 in CD103(+) DCs and CD11c(hi) macrophages exhibited severe inflammatory symptoms, pronounced weight loss, high mortality, robust infiltration of neutrophils in epithelial regions of the colon, an increased expression of proinflammatory cytokines and a significant decrease in CD103(+) DCs in the colon compared with DSS exposed wild-type (WT) mice. Purified colonic macrophages from Blimp-1(cko) mice expressed increased levels of matrix metalloproteinase 8, 9 and 12 mRNA. WT macrophages cocultured with colonic DCs but not bone marrow-derived DCs from Blimp-1(cko) produced increased matrix metalloproteinases in an interleukin (IL)-1β- and IL-6-dependent manner. Treatment of Blimp-1(cko) mice with anti-IL-1β and anti-IL-6 abrogated the exaggerated clinical response. Overall, these data demonstrate that Blimp-1 expression in DCs can alter an innate inflammatory response by modulating the activation of myeloid cells. This is a novel mechanism of contribution of Blimp-1 for the pathogenesis of inflammatory bowel diseases, implicating another therapeutic target for the development of inflammatory bowel disease.

Dendritic cells (DCs) that orchestrate mucosal immunity have been studied in mice. Here we characterized human gut DC populations and defined their relationship to previously studied human and mouse DCs. CD103(+)Sirpα(-) DCs were related to human blood CD141(+) DCs and to mouse intestinal CD103(+)CD11b(-) DCs and expressed markers of cross-presenting DCs. CD103(+)Sirpα(+) DCs aligned with human blood CD1c(+) DCs and mouse intestinal CD103(+)CD11b(+) DCs and supported the induction of regulatory T cells. Both CD103(+) DC subsets induced the TH17 subset of helper T cells, while CD103(-)Sirpα(+) DCs induced the TH1 subset of helper T cells. Comparative analysis of transcriptomes revealed conserved transcriptional programs among CD103(+) DC subsets and identified a selective role for the transcriptional repressors Bcl-6 and Blimp-1 in the specification of CD103(+)CD11b(-) DCs and intestinal CD103(+)CD11b(+) DCs, respectively. Our results highlight evolutionarily conserved and divergent programming of intestinal DCs.

Mbu-1 (Csrnp-3) is a mouse gene that was identified in our previous study as showing highly restricted expression to the central nervous system. In this study, to elucidate the regulatory mechanism for tissue specificity of the gene, epigenetic approaches that identify the profiles of CpG methylation, as well as histone modifications at the promoter region were conducted. Methylation-specific PCR revealed that the CpG sites in brain tissues from embryo to adult stages showed virtually no methylation (0.052–0.67%). Lung (9.0%) and pancreas (3.0%) also showed lower levels. Other tissues such as liver, kidney, and heart showed much higher methylation levels ranging from approximately 39–93%. Treatment of 5-aza-2′-deoxycytidine (5-Aza-dC) significantly decreased promoter methylation, reactivating Mbu-1 expression in NG108-15 and Neuro-2a neuronal cells. Chromatin immunoprecipitation assay revealed that 5-Aza-dC decreased levels of acetylated H3K9 and methylated H3K4, and increased methylated H3K9. This result indicates that CpG methylation converses with histone modifications in an opposing sense of regulating Mbu-1 expression.

Epigenetic methylation change is a major process that occurs during cancer development. Even though many tumor-related genes have been identified based on their relationship between methylation and expression, few studies have been conducted to investigate the relevant biological pathways involved in these changes. To identify essential pathways likely to be affected by methylation in breast cancer, we examined a pool of genes in which expression was upregulated after induction of demethylation by 5-Aza-2′-deoxycytidine (Aza) in the MCF-7 breast cancer cell line. Genome-wide demethylation was confirmed by monitoring the demethylation of a previously known gene, SULT1A1. Overall, 210 and 213 genes were found to be upregulated and downregulated (fold change ≥ 2), respectively, in common in cells treated with 5 and 10 μM of Aza. Network analysis of these 423 genes with altered expression patterns identified the involvement of a cancer related network of genes that were heavily regulated by TNF-α in breast tumorigenesis. Our results suggest that epigenetic dysregulation of cellular processes relevant to TNF-α-dependent apoptosis may be intimately involved in tumorigenesis in MCF-7 cells.

Lactoferrin (LF) plays pivotal roles in primary defense against microbial infection and other cellular processing including immuno-modulation and growth stimulation of cells. To understand the molecular mechanism of LF action we stably overexpressed LF in the K562 erythroleukemia cells and examined differential gene expression using a cDNA microarray. One of the genes that were highly upregulated in the LF-overexpressing cells was the IκB family member B cell lymphoma-3 (BCL-3) that is implicated to promote B cell proliferation and chronic lymphocytic leukemia. Northern blot as well as RT-PCR analysis confirmed that BCL-3 was highly induced in LF-transfected cells. Furthermore, by treating the K562 cells with natural LF protein, we observed a significant increase of BCL-3 messages with the peak at 50 μg/mL and 2 h after treatment. These results suggest that LF signals to induce BCL-3 and thereby promotes B cell proliferation and survival.

The biological mechanisms underlying resistance to tamoxifen are of considerable clinical significance. However, little is known about the correlation between tamoxifen resistance and methylation of genes related to drug-metabolizing enzymes. To address this issue, we examined the methylation pattern and expression of the selected genes coding for drug-metabolizing enzymes, including COMT, CYP1A1, CYP2D6, NAT1, and SULT1A1 in tamoxifen-resistant and control breast cancers. Bisulfite genomic sequencing and methylation-specific PCR were carried out to evaluate the methylation patterns of the five genes from control (n = 74) and tamoxifen-resistant tissues (n = 37) chosen by an age-matched sampling method. Also, end-point reverse transcriptase polymerase chain reaction (RT-PCR) and real-time RT-PCR were performed to determine RNA expression of the genes. Bisulfite genomic sequencing revealed methylation of the NAT1 gene in 25 of the control cancers (33.8%) and 23 of the resistant tumors (62.2%). Of the five genes, only NAT1 showed a significant lower methylation rate in the control group than in the resistant group (p = 0.004). No significant difference of the methylation rate was found in the other four genes including COMT, CYP1A1, CYP2D6, and SULT1A1 (p > 0.05). Furthermore, the expression rate of NAT1 mRNA was lower in the tumors from the resistant group than in control tumors (28.6% vs. 65.2%, p = 0.031). Real-time RT-PCR analysis demonstrated that the NAT1 gene was more down-regulated in resistant tissues than in control group (p = 0.023). Moreover, malignant cells from the resistant cases demonstrated a higher percentage of positive staining for Ki67 (p = 0.001) and cyclin D1 (p = 0.043) than those from the control group. Taken together, the higher methylation rate of the NAT1 gene is related to tamoxifen resistance, and this fact supports the hypothesis that hypermethylation of the NAT1 gene might affect the initiation of tamoxifen resistance.

Thyroid-stimulating-hormone-alpha (TSH-α) is the common subunit of the heterodimeric hormone TSH and also of other glycoprotein hormones. Although both expression and promoter-methylation profiles of the gene have been observed in the pituitary gland and placenta, no observation has been reported in the thyroid gland. We examined TSH-α expression in normal and cancer thyroid tissues. Real-time RT-PCR and immunohistochemistry indicated that TSH-a was repressed in normal tissues while activated in cancer tissues. To identify the epigenetic mechanism of upregulation of TSH-α, the methylation status of the seven CpG sites in the TSH-a promoter was examined in sixty thyroid cancer tissues. Two CpG sites showed remarkably higher levels of methylation in cancer (46 and 45%) than in normal tissues (24 and 23%) (p=0.010 and 0.003). These findings indicate that TSH-α is expressed in the thyroid cancer tissue per se and that its expression can be affected by promoter methylation.

Stem cell-based therapy has recently emerged for use in novel therapeutics for incurable diseases. For successful recovery from neurologic diseases, the most pivotal factor is differentiation and directed neuronal cell growth. In this study, we fabricated three different widths of a micro-pattern on polydimethylsiloxane (PDMS; 1, 2, and 4 microm). Surface modification of the PDMS was investigated for its capacity to manage proliferation and differentiation of neural-like cells from umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs). Among the micro-patterned PDMS fabrications, the 1 microm-patterned PDMS significantly increased cell proliferation and most of the cells differentiated into neuronal cells. In addition, the 1 microm-patterned PDMS induced an increase in cytosolic calcium, while the differentiated cells on the flat and 4 microm-patterned PDMS had no response. PDMS with a 1 microm pattern was also aligned to direct orientation within 10 degrees angles. Taken together, micro-patterned PDMS supported UCB-MSC proliferation and induced neural like-cell differentiation. Our data suggest that micro-patterned PDMS might be a guiding method for stem cell therapy that would improve its therapeutic action in neurological diseases.

Background In the year 2000, the South Korean government introduced a program for separation of drug prescribing and dispensing. The goals of the program are to reduce misuse of drugs and to contain drug expenditures. The government also designated exception regions for the program to reduce the inconvenience for people who reside in areas with a shortage of health care resources. However, according to government reports, many adverse events related to drug misuse occurred in these exception regions after the program reforms were introduced. Therefore, it is worth investigating the factors that relate to drug consumption so that misuse in exception regions can be reduced. Methods Data from medical institutions, detailed drug supply data, and community health survey data were included in the analysis. Multilevel linear regression analysis using mixed models that included pharmacy—and regional-level variables were used to examine the associations regarding the percentages of drug types consumed (i.e., antipyretic, analgesic, anti-inflammatory drugs, psychotropic drugs, adrenal cortical hormones, and antibiotics). Results The data used in this analysis were from a total of 16,455 pharmacies. There were 1.9 % pharmacies from program exception regions and 98.1 % pharmacies from program application regions. Compared with the pharmacies in the program application regions, the exception region pharmacies had higher values for percent consumption of the antipyretic, analgesic, anti-inflammatory drugs category, and of the adrenal cortical hormones category (antipyretic, analgesic, anti-inflammatory drugs = β: 3.19, Standard Error (SE): 0.82, t: 3.88, p-value

Background Body mass index (BMI) has been used as an indirect predictor for the risk of metabolic syndrome. However, there are challenges in evaluating the risk of metabolic syndrome using BMI in certain parts of the world. Therefore, it is worth exploring additional factors that could supplement BMI to predict the risk of metabolic syndrome. In this study, we assessed the combined effect of BMI and perception for predicting metabolic syndrome. Methods We used the fifth Korea National Health and Nutrition Examination Surveys (KNHANES V, 2010–12, N = 16,537) in this study. Multivariable logistic regression analysis was performed to examine the association while controlling for potential confounding variables. We also performed an analysis for the combined effect of BMI and perception of body size, and subgroup analysis by age group or moderate physical activity. Results Data from 16,537 participants were analyzed in this study (males: 6,978, females: 9,559). Among them, metabolic syndrome was diagnosed in 1,252 (17.9 %) males and 2,445 (25.6 %) females, respectively. The combination of BMI and body size perception had a positive relation with the presence of metabolic syndrome. People who perceived themselves to be overweight for their body size had a higher risk for metabolic syndrome even if they have the same BMI. Conclusion Our findings suggest that the combination of body size perception and BMI is useful in predicting the risk of metabolic syndrome. The use of complementary predictors could reduce the risk for inaccurate prediction of metabolic syndrome.

Highly hydrophilic, uniform, superparamagnetic and nontoxic maltotrionic acid (MA)-coated magnetite nano-particles (MAM) were prepared and characterized by TEM, DLS, XRD and VSM. MA was used to improve the biocompatibility, monodispersity and non-specific intracellular uptake of nanoparticles. Folic acid (FA) was subsequently conjugated to the MAM to preferentially target KB cells (cancer cells) that have folate receptors expressed on their surfaces and to facilitate nanoparticles in their transit across the cell membrane. Finally, fluorescence isothiocyanate (FITC) was added to the nanoparticles to visualize the nanoparticle internalization into KB cells. After the cells were cultured in a media containing the MAM and MAM-folate conjugate (FAMAM), the results of fluorescence and confocal microscopy showed that both types of nanoparticles were internalized into the cells. Nevertheless, the amount of FAMAM uptake was higher than that of MAM. This result indicated that nanoparticles modified with MA and FA could be used to facilitate the nanoparticle uptake to specific KB cells (cancer cells) for molecular imaging.

To determine whether the mammary gland can be used to secrete large quantities of a bioactive heterodimeric protein into milk, we used a bovine beta-casein promoter to target and express human follicle-stimulating hormone (hFSH) in the mammary gland into the milk of transgenic mice. We also identified the effects of hFSH leaked into the bloodstream. Transgenic mice produced a high level (up to 300 mIU/ml) of recombinant hFSH in the mammary gland. Human FSH was expressed in the mammary gland and brain, as determined by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. In vitro bioactivity was also identified by cyclic AMP (cAMP) assay. The highest activity was showed in the transgenic mice line 11. However, hFSH leaked into the bloodstream was a powerful factor in the generation of breast and ovarian tumors from the transgenic mice line 11. These results suggest that change of endogenous hormones (FSH and progesterone) may affect the morphology and blood cell counts of peripheral blood and, especially, provoke breast and ovarian tumors.

We have developed a transgenic female goat harboring goat beta-casein promoter/human granulocyte colony stimulating factor (G-CSF) fusion gene by microinjection into fertilized one-cell goat zygotes. Human G-CSF was produced at levels of up to 50 microg/ml in transgenic goat milk. Its biological activity was equivalent to recombinant human G-CSF expressed from Chinese hamster ovary (CHO) cell when assayed using in vitro HL-60 cell proliferation. Human G-CSF from transgenic goat milk increased the total number of white blood cells in C57BL/6N mice with leucopenia induced by cyclophosphamide (CPA). The secreted human G-CSF was glycosylated although the degree of O-glycosylation was lower compared to CHO cell-derived human G-CSF.

The origin of the radiative recombination leading to yellow luminescence (YL) has been elucidated by the study of luminescence properties of GaN films grown with two different gas feeding methods. GaN films were grown on a (0001) sapphire substrate in a rapid thermal chemical vapor deposition (RTCVD) reactor. GaN films emitted two different luminescence energies, 2.2 and 3.47 eV, depending on the introducing position of hydrogen gas in the growth reactor. The distribution of the TMGa flow and gas phase reactions in the reactor were investigated to understand the effect of the gas feeding methods on the optical properties of GaN films. The results suggest that YL is related to Ga vacancies in the grown films.

We show that the tumor-specific primary cytotoxic T lymphocytes (CTL) induced in vitro with the MCA205 fibrosarcoma cells transduced with the B7.1 (CD80) gene are highly effective in adoptive-transfer therapy of the parental tumors. The MCA205 fibrosarcoma cell line was transduced with the retroviral vectors encoding the B7.1 gene and tested for their efficiency as stimulators in short-term (5 days) mixed lymphocyte/tumor cell cultures with highly purified syngenic, unprimed T cells as responders. The induction of the CTL required the presence of a low dose of interleukin-2 (25 U/ml). The injection of the CTL prevented colony formation by the intravenously injected tumor cells in a lung colonization assay in which the CTL were injected after inoculation of tumor cells. We also showed that the adoptive transfer of the same T cells was effective in delaying the growth of the subcutaneously injected tumor cells. These results imply that the short-term mixed lymphocyte/tumor cell culture with the tumor cells transduced with the gene for the B7.1 costimulatory molecule is potentially a good source of CTL for adoptive-transfer therapy of tumors.

Background Because equivocal fixed perfusion defects on single photon emission computed tomography (SPECT) often cause a diagnostic dilemma in patients with suspected coronary artery disease (CAD), we used receiver-operating characteristic (ROC) curve analysis to evaluate the degree of increased accuracy provided by adding gated images for interpretation of such cases.

Our laboratory has been studying the impact of low Blimp-1 expression on dendritic cell function in SLE, analyzing both a mouse model of SLE in which there is a deletion of Blimp-1 in CD11c dendritic cells (DC Blimp-1KO mice) and healthy individuals with the SLE risk allele of Blimp-1. This allele leads to reduced Blimp-1 expression in dendritic cells. Low expression of Blimp-1 alters cytokine expression following TLR activation and antigen-processing machinery. This leads to a highly distinct TCR repertoire in T-follicular helper cells in DC Blimp-1KO mice. Much of this phenotype is under estrogen regulation. These data therefore provide an integrated explanation for altered cytokines, autoantibodies and female predisposition in SLE.