In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".

Abstract: Orai1 and stromal interaction molecule 1 (STIM1) mediate store-operated Ca(2+) entry (SOCE) in immune cells. STIM1, an endoplasmic reticulum (ER) Ca(2+) sensor, detects store depletion and interacts with plasma membrane (PM)-resident Orai1 channels at the ER-PM junctions. However, the molecular composition of these junctions in T cells remains poorly understood. Here, we show that junctophilin-4 (JP4), a member of junctional proteins in excitable cells, is expressed in T cells and localized at the ER-PM junctions to regulate Ca(2+) signaling. Silencing or genetic manipulation of JP4 decreased ER Ca(2+) content and SOCE in T cells, impaired activation of the nuclear factor of activated T cells (NFAT) and extracellular signaling-related kinase (ERK) signaling pathways, and diminished expression of activation markers and cytokines. Mechanistically, JP4 directly interacted with STIM1 via its cytoplasmic domain and facilitated its recruitment into the junctions. Accordingly, expression of this cytoplasmic fragment of JP4 inhibited SOCE. Furthermore, JP4 also formed a complex with junctate, a Ca(2+)-sensing ER-resident protein, previously shown to mediate STIM1 recruitment into the junctions. We propose that the junctate-JP4 complex located at the junctions cooperatively interacts with STIM1 to maintain ER Ca(2+) homeostasis and mediate SOCE in T cells.. Title: Mutant KRAS is a druggable target for pancreatic cancer.
no

Abstract: CONTEXT Whether immunosuppressive treatment adversely affects survival is unclear.
OBJECTIVE To assess whether immunosuppressive drugs increase mortality.
DESIGN Retrospective cohort study evaluating overall and cancer mortality in relation to immunosuppressive drug exposure among patients with ocular inflammatory diseases. Demographic, clinical, and treatment data derived from medical records, and mortality results from United States National Death Index linkage. The cohort's mortality risk was compared with US vital statistics using standardised mortality ratios. Overall and cancer mortality in relation to use or non-use of immunosuppressive drugs within the cohort was studied with survival analysis.
SETTING Five tertiary ocular inflammation clinics. Patients 7957 US residents with non-infectious ocular inflammation, 2340 of whom received immunosuppressive drugs during follow up. Exposures Use of antimetabolites, T cell inhibitors, alkylating agents, and tumour necrosis factor inhibitors.
MAIN OUTCOME MEASURES Overall mortality, cancer mortality.
RESULTS Over 66 802 person years (17 316 after exposure to immunosuppressive drugs), 936 patients died (1.4/100 person years), 230 (24.6%) from cancer. For patients unexposed to immunosuppressive treatment, risks of death overall (standardised mortality ratio 1.02, 95% confidence interval [CI] 0.94 to 1.11) and from cancer (1.10, 0.93 to 1.29) were similar to those of the US population. Patients who used azathioprine, methotrexate, mycophenolate mofetil, ciclosporin, systemic corticosteroids, or dapsone had overall and cancer mortality similar to that of patients who never took immunosuppressive drugs. In patients who used cyclophosphamide, overall mortality was not increased and cancer mortality was non-significantly increased. Tumour necrosis factor inhibitors were associated with increased overall (adjusted hazard ratio [HR] 1.99, 95% CI 1.00 to 3.98) and cancer mortality (adjusted HR 3.83, 1.13 to 13.01).
CONCLUSIONS Most commonly used immunosuppressive drugs do not seem to increase overall or cancer mortality. Our results suggesting that tumour necrosis factor inhibitors might increase mortality are less robust than the other findings; additional evidence is needed.. Title: Overall and cancer related mortality among patients with ocular inflammation treated with immunosuppressive drugs: retrospective cohort study.
yes

Abstract: Circadian rhythms are associated with the preference for sleep-wake timing, also known as morningness-eveningness (ME). Both circadian rhythms and ME are influenced by genetic factors. Studies show an association between eveningness and depression. This study investigates the heritability of ME and whether ME and depression share common genetic influences. Study participants (n = 1237) were from the Vietnam Era Twin Study of Aging, a longitudinal study of aging with a baseline in midlife. Participants received the Morningness-Eveningness Questionnaire (MEQ) and the Center for Epidemiologic Studies Depression (CES-D) Scale as part of an extensive neurocognitive and psychosocial assessment. MEQ correlations between members of twin pairs were 0.41 (95% CI 0.31-0.49) for monozygotic (MZ) twins and 0.28 for dizygotic (DZ) twins (95% CI 0.19-0.41). CES-D correlations were 0.38 (95% CI 0.28-0.46) for MZ twins and 0.24 (95% CI 0.14-0.36) for DZ twins. Greater eveningness (i.e. lower MEQ scores) was significantly related to more depression symptoms (phenotypic correlation = -0.15 (95% CI -0.21 to -0.09). In the best fitting model, the heritability estimates are 0.42 for the MEQ and 0.37 for the CES-D. A significant genetic correlation of -0.21 indicated that ME and depression share a significant amount of their underlying genetic variance. The genetic covariance between ME and depression accounted for 59.1% of the phenotypic correlation. Of the CES-D sub-scales, Depressed Mood and Interpersonal Difficulties were significantly heritable, while only Well-Being had a significant genetic correlation with ME. ME and depression are both heritable (ME 0.42, depression 0.37) and share common genetic factors, suggesting an overlap in etiology and the relevance of circadian rhythms to depression. Further study of this relationship may help elucidate etiological factors in depression and targets for treatment.. Title: A twin-study of genetic contributions to morningness-eveningness and depression.
yes