Background {#Sec1}
==========

Endometrial cancer (EC) is the 5th most common form of female cancer in the USA, with 61,380 new cases diagnosed in 2017, and responsible for 10,920 deaths over the same year \[[@CR1]\]. According to the FIGO 2009 classification, 80% of EC are diagnosed in stages I-II, with 5-year survival rates of 89.6% in stage I, decreasing to 78.3% in stage II, 61.9% in stage III, and 21.1% in stage IV \[[@CR2]\]. Although EC diagnosed in early stages is potentially curative with surgery followed by adjuvant radiotherapy +/− chemotherapy, about 15% of these patients present an increased risk of cancer progression \[[@CR3]\]. This risk is assessed by the ESMO-ESGO-ESTRO risk stratification, based on tumour characteristics \[[@CR4], [@CR5]\].

However, the impact of other factors, such as systemic inflammation, is gaining importance as an indicator of poor prognostic in cancer patients \[[@CR6], [@CR7]\]. The interest of this host-dependent response, expressed through prognostic ratios composed of circulating white blood cells, lies mainly on circulating neutrophils, which have been studied as neutrophil-to-lymphocytes ratio (NLR) \[[@CR8], [@CR9]\]. Nonetheless, the role of other subpopulations of leukocytes, such as eosinophils, has been largely overlooked in tumour progression \[[@CR10]\]. Although some reports dating from the 1950s already suggested the role of circulating eosinophils as a biomarker of tumour persistence or recurrence after radiotherapy, recent studies confirm that eosinophils act as an important modulator and effector of both innate and adaptive immune response \[[@CR11]--[@CR15]\]. Eosinophils link two different mechanisms of host defence: against allergens and against malignancies, as they secret cytokines, which guide CD8 (+) T cells and enhance their infiltration into the tumour, and induce the barrier permeability \[[@CR16]--[@CR19]\]. Recently, a high level of blood eosinophils was associated with better survival in metastatic melanoma \[[@CR20]\].

Nonetheless, their role in cancer progression remains controversial as they may be considered as tumour-associated tissue eosinophilia (TATE) or as tumour-associated blood eosinophilia (TABE) \[[@CR16], [@CR21], [@CR22]\]. Classically, TATE is more often reported in the literature and generally considered as a favourable prognosticator, while TABE is usually described as a consequence of tumour necrosis in advanced disease, hence related to poorer outcomes \[[@CR23], [@CR24]\]. Some authors suggest that the release of damage-associated molecular patterns (DAMPs) during tumour necrosis causes immunosuppression in tumour microenvironment and recruits diverse inflammatory cells, including circulating eosinophils, which limit the biologic activity of DAMPs \[[@CR25], [@CR26]\]. This mechanism may clarify why TATE has been long associated with an improved prognosis and may be the reason for the inverse association between atopic disease and the risk of cancer \[[@CR27], [@CR28]\].

The aim of the present study was to explore the impact of the level of pre-treatment circulating eosinophils and lymphocytes, expressed as ratios, on survival outcomes in EC patients.

Methods {#Sec2}
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After the Institutional Review Board approval, a review of our department's database of patients with EC treated at our institution with external beam radiotherapy (EBRT) and/or High Dose Rate Brachytherapy (HDR-BT) in a period of five years was conducted. All patients included signed the informed consent for treatment and data processing.

Patients' characteristics {#Sec3}
-------------------------

The data of 163 patients diagnosed with histologically confirmed EC and treated with postoperative radiotherapy at our centre from January 2011 to December 2015 were retrospectively reviewed. All patients underwent hysterectomy as a first treatment, with laparoscopic pelvic paraaortic lymphadenectomy in 107 cases (81.7%), and had pre-treatment blood test results done within 3 months before surgery. Patients diagnosed with acute or chronic infections, including human immunodeficiency virus (HIV), any type of immunodeficiency, other active malignancies, haematological disorders, steroid or anti-inflammatory treatment for any reason, were excluded. The median age at diagnosis was 65 years (y), mean 64.79, range 41--90. The most frequent histology was endometrioid carcinoma (73.3%). The disease stage was classified as non-advanced (stage I-II) in 98 patients (74.8%).

The combination of EBRT and HDR-BT was administered to 88 patients (65.2%), with a mean dose of 53.4 Gray (Gy) (range 21--75). Only 43 patients (32.8%) were treated exclusively with HDR-BT (mean dose 10.0 Gy, range 7--20). All patients were stratified into six risk groups according to ESMO-ESGO-ESTRO anatomopathological features \[[@CR4]\]. Patients' characteristics are detailed in Table [1](#Tab1){ref-type="table"}.Table 1Characteristics of all patients included in the study (*n* = 163), comparison of these characteristics according to ELR (cut-off ≥ 0.1) and ENLR (cut-off ≥ 0.5)Patients' characteristicsAll patients included (*n* = 163, % of total)ELR \< 0.1 *n* = 117 (%)ELR ≥ 0.1 *n* = 46 (%)*p*-value\*ENLR \< 0.5 *n* = 118 (%)ENLR ≥0.5 *n* = 45 (%)*p*-value\*Age at diagnosis (years):  \<  65 years:74 (45.4%)4 (73.0%)20 (27.0).75753 (71.6%)21 (28.4%).410  ≥ 65 years:89 (54.6%)63 (70.8%)26 (29.2)65 (73.0%)24 (27.0%)FIGO 2009 stage at diagnosis: • IA4 (26.0%)34 (7.1%)9 (0.9%).07033 (76.7%)10 (23.3%).136 • IB54 (33.2%)33 (61.1%)21(38.9%)35 64.8%)19 (35.2%) • II24 (14.0%)19 (79.2%)5 (20.8%)18 (75.0%)6 (25.0%) • IIIA9 (5.5%)4 (44.4%)5 (55.6%)5 (55.6%)4 (44.4%) • IIIB00000 • IIIC115 (9.2%)13 (86.7%)2 (13.3%)14 (93.3%)1 (6.7%) • IIIC27 (4.3%)7(100%)07 (100%)0 • IVA9 (5.5%)6 (66.7%)3 (33.3%)5 (55.6%)4 (44.4%) • IVB2 (1.2%)1 (50%)1 (50%)1 (50.0%)1 (50.0%)Patients in advanced stage (FIGO I-II vs. FIGO III-IV) (n,%): No (FIGO I-II)121(74.2%)85 (70.2%)36(29.8%).46185 (70.2%)36 (29.8%).299 Yes (FIGO III-IV)42 (25.8%)32 (76.2%)10(23.8%)33 (78.6%)9 (21.4%)Tumour grade (n,%): 136 (22.1%)24 (66.7%)12(33.3%).73626 (72.2%)10 (27.8%).772 261 (37.4%)45 (73.8%)16(26.2%)46 (75.4%)15 (24.6%) 366 (40.5%)48 (72.7%)18(27.3%)46 (69.7%)20 (30.3%)Patients with tumour grade 3 vs. tumour grade 1--2 (n,%): Grade 1--297 (59.5%)66 (68.0%)31(32.0%).86572 (74.2%)25 (25.8%).593 Grade 366 (40.5%)46 (69.7%)20(30.3%)46 (69.7%)20 (30.3%)Tumour histology (n,%): Endometrioid119 (73%)85 (71.4%)34(28.6%).30587 (73.1%)32 (26.9%).424 Serous-papillary14 (8.6%)12 (85.7%)2 (14.3%)10 (71.4%)4 (28.6%) Clear cell5 (3.1%)5 (100%)05 (100%)0 Squamous6 (3.7%)3 (50.0%)3 (50.0%)3 (50.0%)3 (50.0%) Villoglandular2 (1.2%)1 (50.0%)1 (50.0%)1 (50.0%)1 (50.0%) Sarcoma (not LMS or carcinosarcoma)2 (1.2%)2 (100%)02 (100%)0 Leiomyosarcoma3 (1.8%)1 (33.3%)2 (66.7%)1 (33.3%)2 (66.7%) Carcinosarcoma12 (7.4%)8 (66.7%)4 (33.3%)9 (75.0%)3 (25.0%)Lymphadenectomy (n,%): No29 (17.8%)19 (65.6%)10(34.5%).40919 (65.5%)10 (34.5%).361 Yes134 (82.2%)98 (73.1%)36(26.9%)99 (73.9%)35 (26.1%)ESMO-ESGO-ESTRO (ESMO 2015) risk groups (n,%): 1 - Low28 (17.2%)21 (75.0%)7 (25.0%).77521 (75.0%)7 (25.0%).440 2 - Intermediate31 (19.0%)20 (64.5%)11(35.5%)21 (67.7%)10 (32.3%)  3- High-Intermediate13 (8.0%)9 (69.2%)4 (30.8%)8 (61.5%)5 (38.5%) 4 - High75 (46.0%)57 (76.0%)18(24.0%)59 (78.7%)16 (21.3%) 5 - Advanced14 (8.6%)9 (64.3%)5 (35.7%)8 (57.1%)6 (42.9%) 6 - Metastatic2 (1.2%)1 (50.0%)1 (50.0%)1 (50.0%)1 (50.0%)Patients in high-risk groups according to ESMO-ESGO-ESTRO risk classification (n,%): Low (risk group 1--3)72 (44.2%)47 (65.3%)25(34.7%).49650 (69.4%)22 (30.6%).484 High (risk group 4--6)91 (55.8%)65 (71.4%)26(28.6%)68 (74.7%)23 (25.3%)Brachytherapy exclusive (n,%): No110 (67.5%)75 (68.2%)35(31.8%).14277 (70.0%)33 (30.0%).325 Yes53 (32.5%)42 (79.2%)11(20.8%)41 (77.4%)12 (22.6%)Chemotherapy (n,%): No104 (63.8%)72 (69.2%)32(30.8%).33771 (68.3%)33 (31.7%).118 Yes59 (36.2%)45 (76.3%)14(23.7%)47 (79.7%)12 (20.3%)\* *X2 test* or *T-student test*

Follow-up results {#Sec4}
-----------------

The follow up (FU) was performed, as suggested by ESMO guidelines, every 3--4 months for the first 2 years, and then every 6 months for the next 3 years.

Systemic inflammation biomarkers {#Sec5}
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The level of eosinophils in pre-treatment blood tests was analysed. We created two groups using a 0.1 cut-off according to the best receiver operating characteristics (ROC) curve value: patients with absolute eosinophil count (AEC) ≥ 0.1 (*n* = 112) vs. AEC \<  0.1 (*n* = 19), and we evaluated the influence of high AEC on patients' survival outcomes.

Afterwards, we described two new systemic inflammatory biomarkers, expressed as follows: Eosinophil-to-Lymphocytes Ratio (ELR) and Eosinophil\*Neutrophil-to-Lymphocytes Ratio (ELR multiplied by the absolute neutrophil count, ENLR), and we analysed their impact on overall survival (OS) and progression free survival (PFS). Additionally, we evaluated the same ratios based on post-treatment blood tests.

Statistical analysis {#Sec6}
--------------------

All statistical tests were two-sided and statistical significance was defined as *p* \<  0.05. Summarized data are presented as numbers and percentages unless otherwise stated.

The primary endpoint was OS and the secondary endpoint was PFS. Predefined subgroup analysis was conducted based on the ESMO-ESGO-ESTRO risk stratification, which subsequently was converted into a binary variable by creating a low (groups 1--3) and a high-risk cohort (groups 4--5).

Afterwards, the study population was subdivided into two groups, based on the cut-offs for ELR and ENLR, separately. Both ELR and ENLR were defined as binary variables by finding the cut-off value from a ROC curve. The binary variables' balance across prognostic characteristics was assessed using Chi-square test (X2 test). Frequencies were compared using Fisher's exact test for categorical variables. Kaplan Meier's curves were displayed to evaluate the prognostic value of ELR and ENLR for OS and PFS. Survival outcomes were calculated from the date of surgery to the event occurrence, which is progression or cancer-related death in the case of PFS, or any death in the case of OS. If no event occurred, patients were censored at the time they were last known to be event free. All survival outcomes were analysed using Log rank test (LR), Breslow test (BR) was additionally applied.

The univariate and multivariate Cox regression models were used to assess the prognostic effect of inflammatory biomarkers and included binary variables: ELR (≥ 0.1 vs. \< 0.1), ENLR (≥ 0.5 vs. \< 0.5), age (≥ 65y vs. \< 65y), ESMO-ESGO-ESTRO high-risk (groups 4--6) vs. low-risk (groups 1--3), high grade (grade 3 vs. grade 1--2), advanced FIGO 2009 stage (stage III-IV vs. stage I-II), endometrioid histology (vs. other tumour histology). All statistical analyses were performed using SPSS v. 23.

Results {#Sec7}
=======

Survival outcomes of the entire cohort {#Sec8}
--------------------------------------

All survival outcomes were expressed in months. After a median follow-up of 54.8 (range 24.6--58.4), progression was observed in 36 patients (22.1%). There was no exclusive local recurrence and only one patient developed exclusive regional recurrence (progression in pelvic node). Both local and regional recurrence, were observed in 10.7% of patients (*n* = 14), while 17.6% (*n* = 23) presented distant metastasis. Median PFS for the entire cohort was of 23.1 (range 0.2--62.2). At the moment of data collection, 21 deaths were reported (12.33%), 20 of them were related to cancer (12.27%). All details concerning the survival outcomes according to the ESMO-ESGO-ESTRO risk groups are included in Table [2](#Tab2){ref-type="table"}.Table 2Patients's status at the end of the study according to ESMO-ESGO-ESTRO modified risk assessment (ESMO 2015)ESMO 2015 risk groupStatus of patients at the end of the study (n = 163)Alive (no evidence of disease)Disease progressionCancer-related deathNon cancer related deathTotal127 (20.8%)1 (8.33%)0028 (17.2%)230 (23.1%)001 (100%)31 (19.0%)311 (8.4%)02 (10%)013 (8.0%)457 (43.8%)7 (58.33%)11 (55%)075 (46.0%)55 (3.9%)4 (33.33)5 (25%)014 (8.6%)6002 (10%)02 (1.2%)Total130 (100%)12 (100%)20 (100%)1 (100%)163 (100%)

ELR {#Sec9}
---

The mean value of ELR was 0.08 (SD 0.065, range 0.0--0.31, median 0.063). Using the cut-off of 0.1 according to the ROC with the Area Under Curve (AUC) of 0.61, we divided the entire cohort into two groups: ELR ≥ 0.1 (*n* = 46) and ELR \<  0.1 (*n* = 117). Patients' characteristics of the two comparative groups are included in Table [1](#Tab1){ref-type="table"}.

OS in the group with ELR ≥ 0.1 was 50.7 months (IC 95% 43.8--57.6) vs. 62.3 months (IC 95% 59.0--65.5) in the group with ELR \<  0.1 (LR *p* = 0.004, X2 = 6.3; BR *p* = 0.026, X2 = 4.9), HR 2.9, *p* = 0.017 (Fig. [1](#Fig1){ref-type="fig"}).Fig. 1Overall survival of patients with endometrial cancer (*n* = 163) according to the Eosinophil-to-Lymphocytes Ratio (ELR, cut-off ≥ 0.1), *p* = 0.004

Eleven events were reported in the high ELR group (23.9% of patients) vs. 10 events (8.6%) in the low ELR group (LR: p = 0.01, X2 = 6.5; BR: p = 0.026, X2 = 4.9).

Regarding the data of the entire cohort, PFS of patients according to ELR level was not significantly different (LR *p* = 0.095, BR *p* = 0.08). However, the number of events was higher in patients with ELR ≥ 0.1 (14 events vs. 22 events, which meant 30.4% vs. 18.8% patients with progression, respectively).

ELR was not correlated with patient's age (*p* = 0.90), FIGO stage at diagnosis (*p* = 0.77), tumour histology (*p* = 0.94) or tumour grade (*p* = 0.86).

ENLR {#Sec10}
----

The mean value of ENLR was 0.448 (SD 0.59, range 0--5.54, median 0.31). Using the cut-off of 0.5 (ROC curve AUC = 0.621), we divided the entire cohort into two groups: ENLR ≥0.5 (*n* = 45) and ENLR \< 0.5 (*n* = 118). Patients' characteristics of the two comparative groups are included in Table [1](#Tab1){ref-type="table"}.

Median OS in the group with ENLR ≥ 0.5 was 49.8 months (IC 95% 43.8--55.8) vs. 61.9 months (IC 95% 58.6--65.2) in the group with ENLR \< 0.5 (LR: *p* = 0.01, X2 = 6.6; BR: *p* = 0.026, X2 = 4.9, HR = 3.0, *p* = 0.015, Fig. [2](#Fig2){ref-type="fig"}). Ten events were reported in the high ENLR group (which meant 22.2% of patients) vs. 11 events (9.3%) in the low ENLR group.Fig. 2Overall survival of patients with endometrial cancer (*n* = 163) according to the Eosinophil\*Neutrophil-to-Lymphocytes Ratio (ENLR, cut-off  ≥ 0.5), *p* = 0.010

Median PFS according to ENLR level was not significantly different (LR: *p* = 0.1, BR: *p* = 0.09).

ENLR \< 0.5 was not correlated with patients' age (*p* = 0.81), FIGO stage at diagnosis (*p* = 0.22), tumour histology (*p* = 0.63) or tumour grade (*p* = 0.59).

ELR and ENLR as independent prognostic factors {#Sec11}
----------------------------------------------

On univariate analysis, worse OS was associated with ELR ≥ 0.1 (HR = 2.9, *p* = 0.017), ENLR ≥ 0.5 (HR 3.0, *p* = 0.015), ESMO-ESGO-ESTRO high-risk (HR = 4.7, *p* = 0.014), tumour grade 3 (HR = 8.1, *p* = 0.001) and advanced stage (HR = 3.4, *p* = 0.007), while endometrioid histology was associated with better prognosis (HR = 0.3, *p* = 0.003). Age ≥ 65 years did not reach significance, *p* = 0.055 (Table [3](#Tab3){ref-type="table"}). All variables included in univariate analysis were evaluated in all patients using X2 tests (Table [1](#Tab1){ref-type="table"}, Additional file [1](#MOESM1){ref-type="media"}: Figure S1, Additional file [2](#MOESM2){ref-type="media"}: Figure S2, Additional file [3](#MOESM3){ref-type="media"}: Figure S3, Additional file [4](#MOESM4){ref-type="media"}: Figure S4, and Additional file [5](#MOESM5){ref-type="media"}: Figure S5).Table 3Impact of ELR and ENLR on overall survival (OS): Kaplan Meier survival analysis, univariate and multivariate Cox regression (models for ELR and ENLR, respectively), *n* = 163VariablesKaplan-Meier survival analysisUNIVARIATE Cox regressionMULTIVARIATE Cox regression for ELR ≥ 0.1 modelMULTIVARIATE Cox regression for ENLR ≥0.5 modelX2*p*-valueHR (IC 95%)*p*-valueHR (IC 95%)*p*-valueHR (IC 95%)*p*-valueAge ≥ 65 years (vs. \<  65 years)3.9**0.047**2.6 (0.98--6.7)0.0552.8 (1.0--8.2)0.0592.8 (1.03--7.8)**0.043**FIGO advanced stage III (vs. stage I-II)8.3**0.004**3.4 (1.4--8.4)**0.007**3.1 (0.9--9.8)0.0602.8 (0.9--8.5)0.065Tumour grade 3 (vs. grade 1--2)15.8**0.000**8.1 (2.4--27.4)**0.001**6.8 (1.9--24.7)**0.003**5.8 (1.6--21.2)**0.007**Endometroid histology (vs. other histology)10.1**0.001**0.3 (0.1--0.63)**0.003**0.4 (0.1--1.1)0.0680.4 (0.14--1.2)0.099ESMO-ESTRO-ESGO High Risk groups 4--6 (vs. groups 1--3)7.4**0.007**4.7 (1.4--15.8)**0.014**1.2 (0.2--6.5)0.8561.3 (0.2--6.9)0.770ELR ≥ 0.1 (vs. \< 0.1)6.3**0.004**2.9 (1.2--6.8)**0.017**4.9 (1.9--12.4)**0.001**----ENLR ≥ 0.5 (vs. \<  0.5)6.6**0.010**3.0 (1.2--7.3)**0.015**----3.9 (1.6--9.8)**0.003**All entries in boldface reflect *p*-values \< 0.05

On multivariate analysis, carried out separately for ELR and ENLR, the impact of variables used in univariate analysis on the principal endpoint (OS) was evaluated. Three variables reached statistical significance: ELR ≥ 0.1 (HR = 4.9, *p* = 0.001), ENLR ≥0.5 (HR = 3.9, *p* = 0.003), and tumour grade 3 (*p* = 0.003 in ELR model and *p* = 0.007 in ENLR model). Age ≥ 65 was statistically significant only in ENLR model (*p* = 0.043) (Table [3](#Tab3){ref-type="table"}).

Subgroups according to ESMO-ESGO-ESTRO modified risk assessment {#Sec12}
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According to the ESMO-ESGO-ESTRO risk classification, all patients were allocated to six different risk groups (Table [1](#Tab1){ref-type="table"}). Thus, we divided the entire cohort into two groups: low-risk (groups 1--3) and high-risk cohort (groups 4--6).

In the high-risk cohort (*n* = 91), 34.6% of patients with ELR ≥ 0.1 died and OS was of 44.9 months (IC 95% 35.9--53.9) vs. 59.6 months (54.7--64.5) in the low ELR group with 13.8% of patients dead at the end of the study (LR: *p* = 0.009, X2 = 6.8, BR: *p* = 0.015, X2 = 5.9, Additional file [6](#MOESM6){ref-type="media"}: Figure S6). PFS was not significantly different between the two groups (*p* = 0.10).

Patients in the ENLR ≥ 0.5 cohort showed a worse OS of 45.5 months (IC 95%, 36.2--54.9) vs. 59.0 months in ENLR \< 0.5 (IC 95%, 54.1--64.0, LR: *p* = 0.020, X2 = 5.4, BR: *p* = 0.047, X2 = 3.9, Additional file [7](#MOESM7){ref-type="media"}: Figure S7). PFS was not significantly different between the two groups (*p* = 0.18).

In the low-risk cohort (*n* = 72), patients with ELR ≥ 0.1 (*n* = 25) and patients with ENLR ≥ 0.5 (*n* = 22) failed to show statistically significant differences regarding OS and PFS.

Absolute eosinophil count (AEC) {#Sec13}
-------------------------------

Pre-treatment blood eosinophilia, defined as an absolute eosinophils count ≥ 0.65 × 10^9^/L, was detected in our cohort only in 6 patients (4.6%), all of them alive and with no evidence of disease progression at the moment of data collection. The mean value of AEC was 0.1 (SD 0.13, range 0--0.8, median 0.152). There were no statistical differences in OS (55.6 months vs. 61.35 months, *p* = 0.154, X2 = 2.04) nor PFS (*p* = 0.772, X2 = 0.08) between the group with AEC ≥ 0.1 and the one with AEC \< 0.1.

Leucocytosis, neutrophilia and NLR {#Sec14}
----------------------------------

Patients that presented a high level of circulating WBC (leukocytes \> 11,000 × 10^9^/L or neutrophils \> 7000 × 10^9^/L) or NLR ≥ 2.4 (cut-off according to ROC curve, AUC 0.516) at cancer diagnosis did not show statistical difference in OS compared to patients with lower levels (*p* = 0.51, *p* = 0.23 and *p* = 0.63, respectively).

Discussion {#Sec15}
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Systemic inflammation is a recognised feature of cancer progression, and inflammatory biomarkers are a key subject of research on anti-tumour response. However, the role of eosinophils in this field has long been ignored. Even though tumour-associated blood eosinophilia is described in a wide range of tumours \[[@CR11], [@CR12], [@CR27]\], and is easily diagnosed, this finding is not so frequent in clinical practice, and only accounts for 1--7% of all eosinophilia's diagnoses \[[@CR21], [@CR29]\]. In accordance with these reports, we concluded that eosinophilia at cancer diagnosis was really infrequent in our cohort and had no impact on survival outcome. We hypothesise that it is not eosinophils alone, but the ratios between circulating eosinophils and lymphocytes, that may reflect the host's immunosuppression status at cancer diagnosis, and may help to achieve a more precise risk stratification of patients diagnosed with EC.

Here, we describe new eosinophil-based prognostic ratios, expressed as a relationship between different subtypes of WBC. To our best knowledge, we are the first to propose these ratios as prognostic biomarkers in malignant tumours and to apply inflammatory biomarkers as a tool to refine the ESMO-ESGO-ESTRO risk stratification in EC.

We focused our study on EC because, in spite of its generally favourable prognosis, recent studies claim that the survival outcomes depend on factors beyond the classically established risk indicators \[[@CR30]\]. Moreover, the scientific evidence of the inflammatory biomarkers in EC is significantly lower than in other malignancies \[[@CR7]--[@CR9]\].

Our study is based on a uniformly treated cohort that includes patients of all FIGO stages if they underwent hysterectomy as a first treatment. According to the ESMO guidelines, a complete macroscopic cytoreduction is recommended even for advanced disease, while systematic pelvic lymphadenectomy should not be performed routinely, hence lymphadenectomy was performed only in 80% of patients in our study \[[@CR4]\]. Most patients with EC usually present a low recurrence risk, but in our study 55.8% of patients (*n* = 91) belonged to the high-risk group, which may be explained by the reference status of our institution, where patients with high-risk factors are usually addressed. Although distant relapses often account for only one-third of recurrences in the literature, they were observed in 63.9% of all relapses in our cohort \[[@CR4], [@CR30]\]. As most EC relapses occur within 3 years after the primary treatment, we considered that our median FU of 55.9 months (range 52.4--59.4) was long enough \[[@CR4]\].

Due to the correlation between ELR and ENLR, two multivariate analysis models were evaluated: one for ELR ≥ 0.1 (*p* = 0.001, HR = 4.9, IC 95%, 1.9--12.4) and one for ENLR ≥ 0.5 (*p* = 0.003, HR = 3.9, IC 95%, 1.6--9.8). Holding the other covariates constant, higher values of ELR and ENLR were strongly associated with an increased risk of death and were independent indicators of poorer overall survival. Contrarily, ratios based on post-treatment blood tests had no impact on patients' prognosis.

Similarly, pre-treatment ELR and ENLR showed an impact on OS and PFS in the high-risk group, but not in the low-risk group (*p* = 0.21 and *p* = 0.18, respectively), in which a limited number of events was observed.

On univariate analysis of the entire cohort, the variable age ≥ 65y only trended toward significance (*p* = 0.055) but was maintained in multivariate analysis as a clinically important factor, and was significantly associated with worse OS in ENLR Cox model. In the high-risk patients (groups 4--6), age ≥ 65y was an indicator of poor survival (*p* = 0.014 in univariate analysis) and was proven to be an independent prognostic factor in both Cox regression models \[Table [4](#Tab4){ref-type="table"}\]. By contrast, FIGO advanced stage and endometrioid histology were not significant prognosticators in the univariate analysis of high-risk patients.Table 4Impact of ELR and ENLR on overall survival (OS): Kaplan-Meier survival analysis, univariate and multivariate Cox regression (models for ELR and ENLR, respectively) in high-risk patients (ESMO-ESGO-ESTRO groups 4--6, *n* = 91)VariablesKaplan-Meier survival analysisUNIVARIATE Cox regressionMULTIVARIATE Cox regression for ELR ≥ 0.1 modelMULTIVARIATE Cox regression for ENLR ≥0.5 modelX2*p*-valueHR (IC 95%)*p*-valueHR (IC 95%)*p*-valueHR (IC 95%)*p*-valueAge ≥ 65 years (vs. \<  65 years)6.9**0.008**3.7 (1.3--10.5)**0.014**3.2 (1.03--10.3)**0.045**3.2 (1.1--9.7)**0.038**FIGO advanced stage III (vs. stage I-II)2.20.1352.1 (0.8--5.7)0.1432.6 (0.8--8.6)0.1092.5 (0.8--7.7)0.104Tumour grade 3 (vs. grade 1--2)6.7**0.010**5.6 (1.3--24.5)**0.022**6.9 (1.5--31.6)**0.013**5.8 (1.3--26.3)**0.023**Endometroid histology (vs. other histology)1.70.1940.5 (0.2--1.4)0.2020.5 (0.2--1.5)0.1950.5 (0.2--1.6)0.257ELR ≥ 0.1 (vs. \< 0.1)3.9**0.047**3.3 (1.3--8.7)**0.014**4.6 (1.7--12.5)**0.002**----ENLR ≥0.5 (vs. \<  0.5)5.4**0.020**3.0 (1.1--7.7)**0.026**----3.9 (1.6--9.8)**0.011**All entries in boldface reflect *p*-values \< 0.05

ENLR was described in order to demonstrate the importance of the relation between eosinophils and lymphocytes. Subsequently, we observed that the impact on OS was constant and not influenced by the neutrophil count. As both eosinophil-based ratios have proved to be independent prognostic factors for OS, while NLR has not, we concluded that the relation between eosinophils and lymphocytes was not affected by the presence of neutrophils, which may be interpreted as a superiority of eosinophil-based ratios over NLR and Platelet-to-Lymphocytes Ratio (PLR) (Additional file [8](#MOESM8){ref-type="media"}: Figure S8).

Our study presents some limitations, being a retrospective single institution cohort with a relatively small number of patients, which may produce potential confounding biases. However, almost all studies that deal with systemic inflammation biomarkers are of retrospective nature \[[@CR7]--[@CR9], [@CR29], [@CR30]\]. Confirming the cut-off points for ELR and ENLR in a larger cohort, preferably in a multicentre study, would be important for any future investigation.

In our opinion, the most important potential bias in the application of the biomarkers of systemic inflammation in clinical practice is the short life span of the WBC in systemic circulation. Consequently, it is difficult to completely rule out a potential influence of some temporary acute immunological changes, such as asymptomatic infections, on the systemic inflammatory response.

We are convinced that our investigation may contribute to a new stratification of EC and to further immunotherapy research that aim at the eosinophilic-mediate anti-tumour response.

Conclusions {#Sec16}
===========

Our study presents a new concept of the role of eosinophils in cancer progression that may be used as a novel prognostic tool for EC stratification. Increased values of eosinophil-related ratios based on pre-treatment blood tests are associated with worse OS in all EC patients and in high-risk patients of the ESMO-ESGO-ESTRO modified risk assessment. Impact of ELR and ENLR on PFS did not achieve statistical significance.

According to these results, the described ratios are of interest for EC prognosis and should be considered in the pre-treatment analysis. To our best knowledge, this is the first report that describes and analyses eosinophil-related ratios as prognostic indicators in cancer patients.

Additional files
================

 {#Sec17}

Additional file 1:**Figure S1.** Overall survival according to FIGO stage (*n* = 163). Kaplan-Meier survival analysis (*p* = 0.004 Log Rank, *p* = 0.013 Breslow test). (DOCX 64 kb) Additional file 2:**Figure S2.** Overall survival according to tumour grade (*n* = 163). Kaplan-Meier survival analysis (*p* = 0.001 Log Rank, *p* = 0.023 Breslow test). (DOCX 70 kb) Additional file 3:**Figure S3.** Overall survival according to ESMO-ESGO-ESTRO risk assessment (*n* = 163): high-risk (groups 1--3) vs. low-risk (groups 4--6). Kaplan-Meier survival analysis (*p* = 0.007 Log Rank, *p* = 0.005 Breslow test). (DOCX 77 kb) Additional file 4:**Figure S4.** Overall survival according to tumour histology (n = 163): endometrioid vs. non endometrioid (*p* = 0.001 Log Rank, *p* = 0.004 Breslow test). (DOCX 66 kb) Additional file 5:**Figure S5.** Overall survival according to patients' age at diagnosis (n = 163). Kaplan-Meier survival analysis (*p* = 0.047 Log Rank, *p* = 0.036 Breslow test). (DOCX 70 kb) Additional file 6:**Figure S6.** Overall survival of patients in High Risk (risk groups 4--6 of ESMO 2015 classification) stratified by Eosinophil-to-Lymphocytes Ratio (ELR) according to cut-off 0.1. (DOCX 65 kb) Additional file 7:**Figure S7.** Overall survival of patients in High Risk (Risk groups 4--6 of ESMO 2015 classification) stratified by Eosinophil\*Neutrophil-to-Lymphocytes Ratio (ENLR) according to cut-off 0.5. (DOCX 65 kb) Additional file 8:**Figure S8.** ROC curves for ELR, ENLR, NLR and Platelet--to-Lymphocytes Ratio (PLR). (DOCX 81 kb)

AUC

:   Area Under Curve

BR

:   Breslow test

DAMPs

:   Damage-associated molecular patterns

EBRT

:   External Beam Radiotherapy

EC

:   Endometrial Cancer

ELR

:   Eosinophil-to-Lymphocytes Ratio

ENLR

:   Eosinophil\*Neutrophil-to-Lymphocytes Ratio

ESMO-ESGO-ESTRO

:   European Society for Medical Oncology, European Society for Radiotherapy & Oncology, European Society of Gynaecological Oncology

FIGO

:   International Federation of Gynaecology and Obstetrics

Gy

:   Gray

HDR-BT

:   High Dose Rate Brachytherapy

HIV

:   Human Immunodeficiency Virus

HR

:   Hazard Ratio

LR

:   Log rank test

NLR

:   Neutrophil-to-Lymphocytes ratio

OS

:   Overall Survival

PFS

:   Progression Free Survival

TABE

:   Tumour-associated blood eosinophilia

TATE

:   Tumour-associated tissue eosinophilia

X2

:   Chi-square test

y

:   Years

This work was supported by a grant from the University of Barcelona.

Funding {#FPar1}
=======

There was no specific funding for this study.

Availability of data and materials {#FPar2}
==================================

The datasets used and/or analysed during the current study are available as supplementary material.

This article was principally written by KH, with review contributions from AB. Both authors have read and approved the final version of the manuscript. Some preliminary results of this study were presented last year at the 36th ESTRO Annual Meeting held in Vienna and at the 55th Annual Meeting of the Japanese Society of Clinical Oncology in Yokohama, Japan.

Ethics approval and consent to participate {#FPar4}
==========================================

Our study was approved by the Ethical Committee of Hospital Clinic de Barcelona. All patients included in the study signed the informed consent for treatment, data processing and publication.

Competing interest {#FPar3}
==================

The authors declare no conflict of interest.

Publisher's Note {#FPar5}
================

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.


Ralph Lauren present their Varick jeans in a flattering deep indigo shade. Wear with a blouse and blazer to create a preppy daytime look. Styled with a figure hugging super skinny shape and made from soft cotton blend denim with added stretch. Features include five pocket styling and a button and zip fly fastening.


Q:

webBrowser component throws exception occasionally codenameone

I used WebBrowser component to view the url that occasionally throws following exception and the webBrowser is not displayed if there is an exception. What is the issue here? My code is at the end. thanks
Received exception: Unknown host
java.lang.Throwable: Unknown host
    at javafx.scene.web.WebEngine$LoadWorker.describeError(WebEngine.java:1402)
    at javafx.scene.web.WebEngine$LoadWorker.dispatchLoadEvent(WebEngine.java:1341)
    at javafx.scene.web.WebEngine$LoadWorker.access$1100(WebEngine.java:1219)
    at javafx.scene.web.WebEngine$PageLoadListener.dispatchLoadEvent(WebEngine.java:1206)
    at com.sun.webkit.WebPage.fireLoadEvent(WebPage.java:2387)
    at com.sun.webkit.WebPage.fwkFireLoadEvent(WebPage.java:2231)
    at com.sun.webkit.network.URLLoader.twkDidFail(Native Method)
    at com.sun.webkit.network.URLLoader.notifyDidFail(URLLoader.java:843)
    at com.sun.webkit.network.URLLoader.lambda$didFail$93(URLLoader.java:826)
    at com.sun.webkit.network.URLLoader$$Lambda$168/1472224915.run(Unknown Source)
    at com.sun.javafx.application.PlatformImpl.lambda$null$164(PlatformImpl.java:292)
    at com.sun.javafx.application.PlatformImpl$$Lambda$64/2085765319.run(Unknown Source)
    at java.security.AccessController.doPrivileged(Native Method)
    at com.sun.javafx.application.PlatformImpl.lambda$runLater$165(PlatformImpl.java:291)
    at com.sun.javafx.application.PlatformImpl$$Lambda$63/817822539.run(Unknown Source)
    at com.sun.glass.ui.InvokeLaterDispatcher$Future.run(InvokeLaterDispatcher.java:95)
    at com.sun.glass.ui.win.WinApplication._runLoop(Native Method)
    at com.sun.glass.ui.win.WinApplication.lambda$null$141(WinApplication.java:102)
    at com.sun.glass.ui.win.WinApplication$$Lambda$55/1412924864.run(Unknown Source)
    at java.lang.Thread.run(Thread.java:745)

My code:
InfiniteProgress ip = new InfiniteProgress();
f.addComponent(BorderLayout.NORTH, ip);
WebBrowser view = new WebBrowser() {

    @Override
    public void onStart(String url) {
        System.out.println("del ip");
        f.removeComponent(ip);
    }

};
view.setURL("https://docs.google.com/gview?embedded=true&url=" + pdfUrlSelected);
f.addComponent(BorderLayout.CENTER, view);
f.revalidate();

A:

That generally means your web connection or DNS is problematic.
If the host isn't found networking can't really proceed.


Ionic core-shell dendrimers with an octacationic core as noncovalent supports for homogeneous catalysts.
Ionic core-shell dendrimers with an octacationic core have been applied as noncovalent supports for homogeneous catalysts. Catalytically active arylpalladium complexes, which bear a tethered sulfato group, were noncovalently attached to the ionic core-shell dendritic supports via a straightforward ion-exchange reaction under mild conditions. Diagnostic shifts in (1)H NMR and Overhauser contacts show that the sulfato groups of the catalysts are located close to the octacationic core of the dendritic support in the resulting assemblies. The location of the catalytic Pd(II) sites has been varied via two strategies: by increasing the dendrimer generation and/or by shortening of the sulfato tether. In addition, a metallodendritic assembly was prepared, which bears an alternative shell of apolar dodecyl groups. Both the dendrimer size and the nature of the dendritic shell have no influence on the binding properties of the dendritic supports, i.e., the octacationic dendrimers of generations 1-3 form discrete 1:8 assemblies with the arylpalladium complexes. The structural aspects and the nature of the metallodendritic assemblies have been studied by means of pulse gradient spin-echo NMR diffusion methods, Overhauser spectroscopy, and electron microscopy (TEM). These techniques showed that the dendritic supports and arylpalladium complexes are strongly associated in solution to give unimolecular assemblies of nanoscopic dimensions. Membrane dialysis can recover these metallodendritic assemblies due to their nanoscopic size. The catalytic performances of the metallodendritic assemblies are comparable, but slightly lower than the performance of the unsupported catalyst.


<?php

namespace Fisharebest\Localization\Script;

/**
 * Class ScriptKhoj - Representation of the Khojki script.
 *
 * @author    Greg Roach <fisharebest@gmail.com>
 * @copyright (c) 2019 Greg Roach
 * @license   GPLv3+
 */
class ScriptKhoj extends AbstractScript implements ScriptInterface
{
    public function code()
    {
        return 'Khoj';
    }

    public function number()
    {
        return '322';
    }

    public function unicodeName()
    {
        return 'Khojki';
    }
}


Q:

how to extract data using awk or grep from git log?

I have to extract commit message as well as the corresponding files changed from git log.
Basically, I have BUC IDs given in my commit message. So, for certain set of files I want to get BUC IDs.
Output of my command:    git log --dirstat
  commit bcc9d8be62b6ac9b8dc02c0bf56d0f433df59466
  Author:
  Date:   Tue Sep 5 12:08:04 2017 +0530

  BUC:BUC3565-EPIC14 | Review Page Manage permission and junit

 Change-Id: Ice73d25f77d9f6c4afe647e35bdf9ec280dd7dcf

 31.3% manager/src/main/java/com/ericsson/cm/manager/web/listner/
 68.6% manager/src/test/java/com/ericsson/cm/manager/web/listners/

 commit ab70d068b2bcea4060028a3457551cd1cc35a1f1
 Author:
 Date:   Tue Sep 5 11:30:29 2017 +0530

 BUC:BUC12345 MADE some changes

Change-Id: I7e6733afaf8064c1279e5b217c8d4fba469fd061

  59.0% webui/servermanagement/src/servermanagement/regions/left/
  40.9% webui/servermanagement/src/servermanagement/regions/main/

Now I want to get BUC ID for only changes made in webui/.
How can I achieve that?

A:

The command will delete blank lines from output, filter by webui and print 2 lines before the webui match.
git log --dirstat | grep -ve '^$' | grep webui -B 2


Exploiting the Ground-Level Explosion Hoax

Instead, photos and videos from several angles
clearly showed that the collapse initiated at the fire and impact floors
and the collapse progressed from the initiating floors downward,
until the dust clouds obscured the view of the towers.
(p 146/196)

Obviously, a controlled demolition can be engineered
to destroy a building in any order desired.

NIST exploits a common misconception that demolitions
must proceed from the ground up.

NIST's reply works hand-in-glove with productions like
9/11 Eyewitness
to exploit the distraction of ground-level explosions.


A Probabilistic Method for Image Enhancement With Simultaneous Illumination and Reflectance Estimation.
In this paper, a new probabilistic method for image enhancement is presented based on a simultaneous estimation of illumination and reflectance in the linear domain. We show that the linear domain model can better represent prior information for better estimation of reflectance and illumination than the logarithmic domain. A maximum a posteriori (MAP) formulation is employed with priors of both illumination and reflectance. To estimate illumination and reflectance effectively, an alternating direction method of multipliers is adopted to solve the MAP problem. The experimental results show the satisfactory performance of the proposed method to obtain reflectance and illumination with visually pleasing enhanced results and a promising convergence rate. Compared with other testing methods, the proposed method yields comparable or better results on both subjective and objective assessments.


This invention relates to alarm clocks and particularly to a novel microcomputer-controlled solid-state alarm clock having a 10-key input keyboard for setting time, date, and the alarm times of two independently operating alarms that may be set to operate at any desired time at any day or days of the week.
The alarm clock of the invention is controlled by a microcomputer system, such as the F8 Microcomputer System manufactured by Fairchild Camera and Instrument Corporation. The Fairchild F8 Microcomputer System is a versatile family of components comprising a central processing unit to which is added associated components, such as program storage units, memory interfaces, peripheral input/output units, and memories, in accordance with the requirements of the user. The solid state alarm clock of the invention utilizes a 3850 central processing unit, a 3861 peripheral input/output unit, a 3853 memory interface, and a 2708 erasable PROM, all interconnected through a control line bus and the system 8-bit data bus. The CPU is operated by a two-megahertz crystal operated clock and the associated read-only memory is programmed so that the input/output ports of the system will accept the necessary input data and produce output displays of real time, alarm times, month and date, days of the week, and furthermore controls the audible alarm circuitry.


Brain involvement in myotonic dystrophies: neuroimaging and neuropsychological comparative study in DM1 and DM2.
The objective of this study was to determine the degree of brain involvement in a cohort of myotonic dystrophy type 1 and type 2 (DM1, DM2) patients by brain studies and functional tests and to compare the results of the two groups. DM1, DM2 are multisystemic disorders due to polynucleotide expansions. Previous studies on brain involvement by neuroimaging and functional methods have led to contradictory results. Fifty molecularly defined DM1 patients and 14 DM2 patients, were recruited for the study. Age at recruitment, age at disease onset, disease duration and educational level were recorded. Neuromuscular assessment was done by MIRS. An extensive neuropsychological battery was performed in 48/50 DM1 and in a control group of 44 healthy matched subjects. Forty six of 50 DM1 and 12/14 DM2 underwent brain MRI; 21/50 DM1 and 9/14 DM2 underwent brain perfusion SPECT, with semiquantitative analysis of the results. MRI images were classified by ARWMC (age-related white matter changes) score, in order to quantify recurrence, localization and patterns of distribution of white matter hyperintense lesions (WMHLs) in our two cohorts. MRI results were matched to SPECT and to neuropsychological results. Thirty-seven of 46 DM1 and 10/12 DM2 had abnormal MRI imaging, showing scattered supratentorial, bilateral, symmetrical focal or diffuse WMHLs. A typical temporo-insular diffuse subcortical pattern was seen in DM1 subjects only, with no correlation with cognitive involvement. Major cognitive involvement was seen in the case of diffuse frontal lesions. A relationship with CTG expansion size was documented for DM1 subjects. SPECT showed minimal hypoperfusion in the posterior cortex planes in DM1 and, to a lesser extent, in DM2. Very mild degrees of involvement in the DM2 cohort were seen. Neuroimaging and functional investigations confirmed a more severe involvement of the brain in DM1 compared to DM2. A temporo-insular diffuse lesional pattern, specific for DM1, was found on MRI. This confirms greater expansion size as a risk factor for more extensive brain involvement in DM1.


543 F.Supp. 431 (1982)
In the Matter of the Complaint of AMF as Owner of LAURIE, seeking exoneration from or limitation of liability.
No. 82 Civ. 76 (WK).
United States District Court, S. D. New York.
July 21, 1982.
Haight, Gardner, Poor & Havens by David P. H. Watson, New York City, for plaintiff AMF.
Schneider, Kleinick & Weitz, P.C. by Brian J. Shoot, Ian Gura, New York City, for claimant Merryl Wilson.

*432 MEMORANDUM AND ORDER
WHITMAN KNAPP, District Judge.
On March 9, 1980, while traveling northwest along the Main Channel of the Port of Miami, an area also known as Government Cut, David Richardson's 23-foot pleasure boat struck a wake allegedly caused by another pleasure vessel, the LAURIE, owned by AMF (hereinafter the "Owner"). As a result of this incident, one of Richardson's passengers  Mrs. Merryl Wilson  claims to have sustained severe and permanent back injuries.
On June 26, 1981, Mrs. Wilson filed a complaint in New York Supreme Court, New York County, against both Richardson and the Owner claiming that her injuries were caused by the negligent operation of the two pleasure boats, and seeking damages in the sum of two million five hundred thousand dollars (the "state court action").[1] A summons and complaint were served on the Owner on or about July 9, 1981. Shortly thereafter, Richardson filed a cross-claim against the Owner seeking "indemnity and/or contribution" for any liability assessed against him as a result of Mrs. Wilson's state court action.
Less than six months after service on it of the state court summons and complaint, the Owner filed with this court a complaint seeking exoneration from or limitation of liability pursuant to 46 U.S.C. §§ 183-185, 188. This complaint alleges that the accident was not caused by any negligence on the part of the Owner, who should therefore be exonerated from liability. It further alleges that the accident occurred without the Owner's privity or knowledge, that the net value of the LAURIE does not exceed $396,000, and that the Owner is therefore entitled to limit its liability to that amount.
On February 8, 1982, we entered an order approving the Owner's stipulation of value; staying until determination of the action before us further prosecution of any and all actions commenced or to be commenced against the LAURIE in respect to claims arising from the March 9, 1980 incident; and directing the Clerk of the Court to notify all persons asserting such claims to file them in this action on or before April 5, 1982. To date, only Merryl Wilson has filed such a claim. The possibility nevertheless remains that Richardson might apply for leave to file a belated claim, and that such leave might be granted. Supplemental Rule F(4), F.R.Civ.P. No one has suggested any other potential claims against the LAURIE.
At a pre-trial conference held before us on April 13, 1982, counsel for Mrs. Wilson asked that we lift the injunction against prosecution of her state court action. Accepting this as an oral motion, we directed the parties to brief the issue. For reasons and on the terms set forth below, we conclude that Mrs. Wilson should be permitted to try her claim in state court.
The considerations which should guide our discretion in dealing with the instant application seem to us to have been laid out by the Supreme Court in Langnes v. Green (1931) 282 U.S. 531, 51 S.Ct. 243, 75 L.Ed. 520. The Court there opened its discussion of applicable guidelines with the following observation (at 541):
"The term `discretion' denotes the absence of a hard and fast rule. When invoked as a guide to judicial action it means a sound discretion, that is to say, a discretion exercised not arbitrarily or wilfully, but with regard to what is right and equitable under the circumstances and the law, and directed by the reason and conscience of the judge to a just result." (Citation omitted.)
The Court went on to specify the two basic values that should be protected: 1) the right of the claimant to a jury trial whenever possible; and 2) the right of the shipowner to the full protection of the limitation of liability statute against personal judgments totaling more than the value of his interest *433 in the vessel. See also In re Moran Transp. Corp. (2d Cir. 1950) 185 F.2d 386, cert. denied (1951) 340 U.S. 953, 71 S.Ct. 573, 95 L.Ed. 687; In re Red Star Barge Line, Inc. (2d Cir. 1947) 160 F.2d 436.
The problem which Langnes thus enjoins us to solve is how to protect the legitimate rights of the LAURIE's Owner with the least possible interference with those of Mrs. Wilson. It is clear in the first place that (unless this court intervenes to fragment the litigation), there will be only one law suit concerning the incident that gave rise to Mrs. Wilson's alleged injury. The Owner is threatened with no other claims. However, that single law suit could itself give rise to separate claims against the Owner totaling more than the value of the LAURIE.
The complaint in the state court action demands $2,500,000 in damages. Let us arbitrarily assume that the state jury were to fix Mrs. Wilson's damages at $2,000,000; find her free of contributory negligence; and find Richardson and the LAURIE to have been equally at fault. Let us further assume that, having entered judgment in the amount of $2,000,000 against both Richardson and the Owner, Mrs. Wilson were to levy on the LAURIE, succeed in selling it for $400,000, and then actually collect $1,500,000 from Richardson. On this set of assumptions, the Owner  having lost the ship  would nevertheless be faced with an unsatisfied judgment in the amount of $100,000 in Mrs. Wilson's hands; and an unsatisfied claim over of $500,000 by Richardson.[2] This is precisely the result that the limitation of liability act was designed to avoid.
It is apparent, however, that these supposed dangers could only arise after Mrs. Wilson had obtained a judgment in the state court action. The LAURIE's Owner would therefore be fully protected were we to continue in effect as to all other actions the stay entered in our order of February 8, 1982; permit the state court action to proceed, for the moment unfettered, in that court; but stay entry of judgment and consequent enforcement of any recovery there secured against the Owner  whether on Wilson's direct claim or on Richardson's cross-claim  pending resolution in this court of the Owner's right to limit its liability.
This procedure vindicates Mrs. Wilson's right to a jury trial, and saves her the expense and inconvenience of litigating the same alleged incident in two separate forums. Yet, it also provides the Owner with all the protection the statute intends it to enjoy since it is protected from recovery in excess of the value of the LAURIE. This court would be free, in the event of further proceedings here, to take such action as implementation of the limitation of liability act might dictate.
We shall modify Paragraph 5 of our February 8, 1982 Order accordingly. Further, as the Court suggested in Langnes, we shall retain jurisdiction to protect the Owner from any unanticipated developments. Should it develop after verdict has been achieved that any party or parties' right for post-verdict relief (either by appeal or otherwise) were compromised by inability to enter judgment, such party or parties (Wilson, Richardson and/or the Owner) could move for further modification of our order. We could then fashion relief which would allow the parties fully to exploit their state remedies without interfering with any federal rights we are charged with vindicating.
Let the Owner submit a proposed order on five days' notice. Should no order be received in Chambers on or before July 28, 1982, we shall ourselves fashion appropriate relief.
SO ORDERED.
NOTES
[1]  This was Mrs. Wilson's third action with respect to the March 9, 1980 incident. She had previously brought two actions, naming only Richardson, in New York Supreme Court, each of which she appears to have voluntarily discontinued.
[2]  Section 1402 of New York's Civil Practice Law and Rules provides that the "amount of contribution to which a person is entitled shall be the excess paid by him over and above his equitable share of the judgment recovered by the injured party...." (Emphasis supplied.) On the facts supposed, Richardson could accordingly enforce any claim against the Owner only to the extent of monies actually paid by him to Mrs. Wilson in excess of his equitable (50%) share of the $2,000,000 judgment secured.


Rianna Valdes

Rianna Tei Valdes (born 3 September 1996) is an American tennis player.

Valdes has a career-high WTA singles ranking of 498, achieved on 11 May 2015. She also has a career-high WTA doubles ranking of 434, set on 25 November 2019.

Valdes won her first ITF title at the 2019 Thoreau Tennis Open in the doubles draw partnering Angela Kulikov.

She played college tennis at the University of Southern California.

ITF finals

Doubles (1–1)

References

External links

Category:1996 births
Category:Living people
Category:American female tennis players
Category:Sportspeople from Boca Raton, Florida
Category:USC Trojans women's tennis players
Category:Tennis people from Florida


In many ways, Rust has always been something of a digital social experiment: What happens when people are thrown together in a primitive, isolated environment, with no rules beyond "survive?" (Answer: It's Lord of the Flies, every single time.) Back in March, the experiment got a little deeper (and the uproar, a little louder) when the game was updated to arbitrarily assign unchangeable faces and skin tones to players, and now an even more sensitive bit of anatomy has been adjusted in a manner that will likely please some players more than others.

The hot tip came from Reddit, of course, (via PCGamesN), in the form of a video showing the effects of different Steam IDs on penis size. The actual workings of the system remain a closely-guarded mystery, but Rust creator Garry Newman confirmed that the report is accurate. "Like tallness, face, head size, jaw definition, race, and limb size, penises are also randomized," he said. And, like those other features, it's tied to your Steam ID and cannot be changed; if you come up short, so to speak, you're just going to have to deal with it. Maybe buy a big pickup truck or something.

Despite the many variations in "features," everyone in Rust shares one common attribute: They're all dudes. That may change in the not-too-distant future, however, as Facepunch revealed in its latest blog post that it has begun the process of adding a female model to the game. But don't get too wound up over the prospect of being trapped on an island filled with naked swimsuit models.

"We really don’t want to make the female model unrealistic in the sense of her being aesthetically idealized," Tom—presumably Facepunch artist Thomas Butters—wrote. "In the same way that our male models aren’t perfect specimens of the male body, neither should the female be. No huge boobs nor four-inch waists here."

That's as it should be, and as it has to be, really. Unlike the ESRB, I don't have a problem with nudity in videogames, but a game filled with male schlubs and female supermodels would look pretty weird. Butters added that in-game testing of the female model could begin as soon as next week.


Q:

$a, b, c$ form a geometric sequence and $\log_c a, \log_ b c, \log_a b$ form an arithmetic sequence.

The common difference of the arithmetic sequence can be expressed as $\frac mn$, where $m$ and $n$ are relatively prime positive integers. Find $m+n.$
So far, I rearranged the sequences to be
1: $a$, $ar$, $ar^2$
2: $\log_c a, \log_c a + d, \log_c a + 2d$
I plugged in a, ar and ar^2 to the corresponding a, b, and c in the log sequence.
Then, I don't know what to do!

A:

Solution
We have to constrain that,  $a,b,c$ are all positive numbers which do not equal $1$. According to the assumption conditions, we have $$b^2=ac,\tag1$$and$$2\log_b c=\log_a b+\log_c a.\tag2$$
From $(1)$, $b=\sqrt{ac}$. Put it into $(2)$ and apply the base-changing formula.  Thus, $$\frac{4\ln c}{\ln a +\ln c}=\frac{\ln a+\ln c}{2\ln a}+\frac{\ln a}{\ln c}.\tag3$$Denote $t=\dfrac{\ln a}{\ln c}.$ Then,we can obtain the equation$$2t^3+3t^2-6t+1=(t-1)(2t^2+5t-1)=0.\tag4$$
By solving it,we have the roots $$t_1=1,t_2=\frac{-5-\sqrt{33}}{4},t_3=\frac{-5+\sqrt{33}}{4}.$$ On the other hand,let the common difference be $d$,then $$d=\log_c-\log_c a=\frac{\ln c}{\ln b}-\frac{\ln a}{\ln c}=\frac{2-t^2-t}{t+1}\tag5.$$

If $t=t_1=1$, then $d=0$. In this case, $a=b=c$,which is trivial;
If $t=t_2$ or $t_3$, then $t^2=\dfrac{1-5t}{2}$.Thus, $d=\dfrac{2-t^2-t}{t+1}=\dfrac{3(t+1)}{2(t+1)}=\dfrac{3}{2}$.

Summing up the above, it follows that $d=0$ or $d=\dfrac{3}{2}.$ We are done.


JoJo’s Bizarre Adventure 10 – FUCK THA POLICE

Not gonna lie: I stood up and clapped at this moment. I loved this whole god damn episode, but fuck me, this sold me 100 percent on “Battle Tendency.” JoJo taking out a Tommy gun and blasting a vampire on a cold night in New York and telling the vamp to go fuck himself for murdering Speedwagon? Yes. YES. YES! Do with me what you will, Joseph Joestar. I am ready.

I’m someone who doesn’t like to raise his expectations sky high before watching something, for various reasons, but I couldn’t help but get hyped up for “Battle Tendency.” So many people have extolled its greatness on Twitter and elsewhere — would it pay off? Well, I can’t speak for the arc as a whole, but based on the first episode, yes, there is plenty of reason to be excited.

The first thing to notice, clearly, is that Joseph Joestar is a different breed of Joestar altogether. Jonathan Joestar is the gentleman bruiser, a polite, gentle young man who resorts to violence only when it’s absolutely necessary. (Of course, being JoJo, it often is absolutely necessary.) Joseph, meanwhile, seems to be more a man of the streets, wild and impulsive, but also smart and in tune with the world in his own way. I find it interesting that the episode goes out of its way to point out that Joseph was raised in Britain, since his behavior seems more in line with the hot-headed American type characters we so often see in anime. But, of course, a hot-headed British badass is fine, too.

And, of course, because it’s 1930s America, segregation is in full force and the cops are racist assholes. (Quick question for anyone who knows more history than me: Would a place that fancy have let Smokey eat in 1930s New York? I doubt that would be the case. My understanding is that appealing to pure economics (“As long as he pays, he eats.”) didn’t happen so often. You were either the “right” type of person, or your money was no good, no matter how much of it you had. But maybe it was different in certain places in New York? Or perhaps the owner is just a nice guy — or he’s truly driven by profit, which is why he’s cool with the Mafia being all over the place, too. Anyway, enough of that tangent! Just a curiosity on my part.) I like seeing that the Joestar crew are firmly anti-racist and not in a way that’s condescending or done to show what great, AMAZING people they are for being so good to the black man. Joseph is just one dude helping another out of a jam. It’s cool.

Also, name alert — Smokey is almost certainly named for Motown legend Smokey Robinson. Will he be the new Speedwagon figure? I like his pluck, and you definitely need a normal sort of fellow to stand around and be amazed about how FUCKING BANANAS the heroes and villains are. And another thing: I’m actually going to be sad that Erina will likely disappear from the story soon! Wow, it took just a single episode for my whole opinion of her to turn around. Evolving into a badass grandma who I could ABSOLUTELY see as a steely mob boss will do that for a gal. And Speedwagon as an oil baron? Capitalism hasn’t been this moe since Kaiji!

Erina, you are the coooooooooooooooooooooooooooooooooolest~

Look, people, I’m going to drop any pretense of coherency. There is just too much I enjoyed about this episode. JoJo caving in the face of racist asshole cop. JoJo using the ripple to break the other cop’s finger with a BOTTLE CAP and swigging the drink down afterward. The flashback to the plane hijacking. JoJo predicting every move of the Mafia henchman and then fearlessly destroying the leader. JOJO TOTING A FUCKING TOMMY GUN WITH HIM AND BLASTING A VAMPIRE. (Yes, I know I mentioned that already, but it’s so great that it has to be mentioned again.) And, perhaps most of all, the fact that this is turning into more of a globetrotting adventure. It’s like the evolution from Uncharted to the second game, where it has the grand, globe-spanning setting it probably should have had in the first place. I can’t wait for Joseph to hightail it to Mexico!

One more fun thing before I go, though! There is an amusing anachronism in this episode: In this flashback, Joseph Joestar of the early 1930s is reading a magazine/comic with a Get Smart-based ad on the back. For all of you who are unaware, Get Smart was a 1965-70 comedy series that satirized the secret agent genre that had exploded with the James Bond flicks. It was created by Mel Brooks (yes, that Mel Brooks) and Buck Henry and starred Don Adams, whom I am sure is most well known to you all as the voice of Inspector Gadget. But that’s not all!

Yes, the ad on this episode is based on an actual Get Smart ad! My peek at the manga reveals Joseph was reading a Superman comic, so SOMEONE on the JoJo anime staff is either a Get Smart fan, really into old American advertisements or possibly both! This has no real bearing on anything; I just thought it an interesting detail that caught my eye during the course of the episode.

I have a hard time believing that Straits is gonna be our main bad guy this time around. There’s gotta be a Dio OR THE DIO waiting somewhere in the wings. I might even be disappointed a bit if this is not the case.

Yeah, I don’t think Straits is dead by a long shot (bullets don’t kill vampires!), but I’d bet on that vampire (?) frozen among the masks in Mexico being the main villain, with Straits as an upper-tier mid-boss.

I fucking adored this episode with one caveat: that scene of Jojo drinking his soda should have been accompanied by the music from those infamous 90′s Diet Coke adverts (yeah, I know it hadn’t been invented yet, but whatever!). Just a little something for the ladies.

As someone who has read this part of the manga relatively recently and knew exactly what was going to happen, this adaptation was above and beyond anything my wildest dreams could have conjured. David Production is taking an already-awesome manga and improving on it in every way.

Especially all the artistic flourishes that they took with the lighting and color and texture to give it a very modern-art feel. It’s like they saw Araki’s super-fabulous art and thought, “this isn’t NEARLY fabulous enough.” So they turned it up to twelve and made it even more eye-poppingly stylin’. Not to mention that Part 2 already dialed up the level of JoJo poses from where it was in Part 1, and seeing them brought to life in the anime was delightfully giggle-inducing.

And then Taku Iwasaki’s music came in and melded perfectly together with the wacked-out art style and crazy action and it was just… yes.

Oh right, and also cool things happened in this episode, but I already knew about those from the manga. I will try to refrain talking about the plot because I’ll probably spoil something by mistake.

What I will say is that by this point in the manga, I thought Joseph was a pretty cool guy. But every chapter I’ve read so far has raised the bar on his character even further into the clouds. So believe me when I say, “You ain’t seen nothin’ yet.”

Just… everything about this adaptation takes the over-the-top manga and makes it even more balls-to-the-wall ridiculous and I am running out of colorful adjectives and I cannot wait to see what happens when things get even more… well… bizarre.

Yep, it’s not the most well animated show, but the art really makes it stand out. It reminds me a lot of the recent Lupin III TV series like that: Even when it was poorly animated, I still loved looking at it because the art was so unique.

“There is an amusing anachronism in this episode: In this flashback, Joseph Joestar of the 1920s is reading a magazine/comic with a Get Smart-based ad”

So it doesnt seem anachronistic to you, that he is reading a comic at all ? Whatever its contents ? Surely there werent any mass-produced comics in the 20′s, all they had then were newspaper strips and the like.

” It was created by Mel Brooks (yes, that Mel Brooks)”

It is very surprising that Mel Brooks, for once, made something that was merely average, and not shit, like most his other stuff is. Zeus, Mel Brooks is a shitty comic/writer.

I’m still not sure where the hell that Tommy Gun came from, but it’s a little difficult to care at this point. Joseph’s introduction is everything I hoped it would be, and can’t wait to see everything else he does get into the anime.

I also find it interesting that more people have enjoyed the Smokey Robinson reference than those who have complained about there being a black character named “Smokey Brown”. I thought for sure that would have been a major complaint.

A giant man must have giant pockets. That’s my explanation for the Tommy gun, and I’m sticking to it!

As for Smokey, did this episode ever make reference to his last name? Maybe the narrator mentioned it … I honestly don’t recall. But just calling him Smokey is an obvious reference to Smokey Robinson, so I didn’t mind it much.

Actually, one thing I do recall about America is that in 1929 they had the Wall Street crash, causing the biggest depression in American history. Things were so bad I don’t think life would be like how it was portrayed in the anime, but then it does lend credence to the restaurant serving anyone as long as they pay, they were desperate times.

As long as they were in the company of Whitey, black folks could eat in non-black establishments in New York. There wasn’t an official “No black folks allowed” policy, but being in the company of a white person made the difference between their soup being either mostly lentils or mostly assorted dubious juices.

Racism in New York was actually one of the most interesting segments of my Race and Ethnicity class.

On the episode itself, the whole thing made me incredibly happy from start to finish.

So yeah, I finally watched it (or finally caught up to Jojo). And yes, I’m still looping the last minute or so with Joseph Joestar, in Gintoki’s (Tomokazu Sugita) voice, pulling out the Tommy Gun and basically about to screw Straits over. Probably. I might need help for this, someone stop me from looping this scene


To make it easy to find the pattern you are looking for click on a picture below to go to the project details. We only have the projects that are currently completed, but we will add more and eventually have all of them here for you to navigate through.

Wednesday, June 1, 2011

Pattern #51 Cabled-Cuff Mittens

Hey Everybody! It is Em!

Today I will be talking about Pattern #51, the Cabled-Cuff Mittens.

Would you like to know a secret... I have been dreading making these mittens.

I'm not a fan of the provisional cast-on. I just really like to avoid crochet. My better half, Brittany, is a crocheting expert. Me? I am lucky if I am able to chain something. I'm just not made to crochet. Trust me.

So because of my fear of crocheting, I have avoided anything that requires a provisional cast on. I'll sit and make excuses, but I will not touch that evil hook!!! Well, my friend Sarah really wants some cabled-cuffed mittens. Since Sarah is such a great person, I decided to cave in and attempt to make these mittens.

To my surprise, the provisional cast on is actually...SIMPLE!!! Once I was able to figure out HOW to make a chain (which took the longest to master because I suck at crocheting) it took no time. All I had to do was pick up stitches from this little chain. My friend Viki showed me a trick on how to pick up stitches. I found it to be a lot easier to do her way because the material was so tiny.

This is how you pick up, Viki's way:

1) Stick your needle into the crochet material
2) Wrap the yarn around
3) Pull it through with your fingers.

Yes, I know, pulling it through with your fingers may seem somewhat amateur to some, but let me tell you...It made a lot more sense to me.

Then comes the grafting. In all honesty, I hate this stitch. My friend Zoe has taught it to me several times and I still epically fail at it. I would YouTube this. You can find a great Kitchner's stitch tutorial if you click here! Also, I really love Debbie Stoller's instructions that you can find in "Stitch n Bitch Superstar Knitting: Go Beyond the Basics." You can purchase it online here.

If you want to avoid the graft, you can do a 3 needle bind off. However, I do not advise using this for mittens. You see, if one does a 3 needle bind off, there will be a nice seam. For example, below is a yellow hat that I made using the 3 needle bind off.

As you can see there is a seam. This seam is a nice one and, because it is a hat, one will not feel that seam. However, when one grafts there is no seam, as seen below:

My ONE complaint about this pattern is the actual mitten is kinda roomy inside. The cuff is nice and tight, but the space between the thumb and the end of the cabled part is a little baggy.

I ended up decreasing by 5 stitches. Even though it didn't seem like a lot (the original pattern calls for 40 stitches) it sure is!


Q:

reverse map-projection: how to get lat/lon coordinates from projected coordinates

I have a set of lat/lon coords which I can project using, for example, Mollweide projection.
library(mapproj)
set.seed(0)
n <- 100
s <- data.frame(lon = rnorm(n, 0, 60),
                lat = rnorm(n, 0, 40))
p <- mapproject(s$lon, s$lat, proj="mollweide", par=NULL,
                orientation=c(90,200,0))

# plot projected coors
plot(p$x, p$y, type="n", asp=1/1, bty="n")
map.grid(c(-180, 180, -90, 90), nx=20, ny=20,
         font=1, col=grey(.6), labels=F)
points(p$x, p$y, pch="x", cex = .8)

# a point to reverse project
points(1,0, pch=16, col="red", cex=2)

Now, I have a scenario where I need to do some calculations on the projected coordinates and reverse project the results back to lat/lon coords. For example, how can I reverse project the red point [1,0]?
Any ideas how that can be done?

A:

I don't know if there's a reason you need to use mapproject to project in the fist place. If you can use spTransform instead, then this becomes easier because you can also use spTransform to reverse the same process.
Assuming that you do need to use mapproject, we can still use spTransform to convert points from your projected coordinate system into lat-long coordinates, but a little more fiddling is required to deal with the non-standard format of the mapproject projections I.e. the points are normalised to lie between -1 to 1 latitude and -2 to 2 longitude. In more standard map projections the lat/long are expressed in distances (usually meters).
So, first we can use spTransform to find out the conversion factors we need to convert the normalised mapproject coordinates into actual distances:
library(rgdal)
my.points = data.frame(x=c(0,180),y=c(90,0))
my.points = SpatialPoints(my.points, CRS('+proj=longlat'))
my.points = spTransform(my.points, CRS('+proj=moll'))
# SpatialPoints:
#             x       y
# [1,]        0 9020048
# [2,] 18040096       0
# Coordinate Reference System (CRS) arguments: +proj=moll +ellps=WGS84

Now we can use these references to convert from normalised mapproject coordinates into distances in meters:
my.points = data.frame(x=p$x * 18040096/2 , y=p$y * 9020048)
my.points = SpatialPoints(my.points, CRS('+proj=moll'))

And reproject these into lat/long geographic coordinates:
my.points = as.data.frame(spTransform(my.points, CRS('+proj=longlat')))

Finally we need to rotate these points by longitude, to undo the rotation that was performed in mapproject.
my.points$x = my.points$x + 200
my.points$x[my.points$x > 180] = my.points$x[my.points$x > 180] - 360

And lets check that it worked:
head(my.points)
#           x          y
# 1  75.77725  31.274368
# 2 -19.57400 -31.071065
# 3  79.78795 -24.639597
# 4  76.34576   1.863212
# 5  24.87848 -45.215432
# 6 -92.39700  23.068752

head(s)
#         lon        lat
# 1  75.77726  31.274367
# 2 -19.57400 -31.071065
# 3  79.78796 -24.639596
# 4  76.34576   1.863212
# 5  24.87849 -45.215431
# 6 -92.39700  23.068751


Co-evolution of the branch site and SR proteins in eukaryotes.
Serine-arginine-rich (SR) proteins are essential for splicing in metazoans but are absent in yeast. By contrast, many fungi have SR protein homologs with variable arginine-rich regions analogous to the arginine-serine-rich (RS) domain in metazoans. The density of RS repeats in these regions correlates with the conservation of the branch site signal, providing evidence for an ancestral origin of SR proteins and indicating that the SR proteins and the branch site co-evolved.


Effects of gonadectomy on immunoreactivity for choline acetyltransferase in the cortex, hippocampus, and basal forebrain of adult male rats.
Androgens are known to affect cognitive and mnemonic aspects of spatial processing. The cholinergic system is thought to play an important role in cognition and memory, but little is known about the interaction between androgen and cholinergic neurons. The present study focused on the effects of testosterone on the cholinergic neurons in the anterior cingulate cortex, the posterior parietal cortex, the hippocampus, and the basal forebrain including the medial septum, i.e., regions related to spatial processing. We examined choline acetyltransferase (ChAT) immunoreactivity in three groups of adult male rats: sham-operated (Sham), 28-day gonadectomized (GDX), and 28-day gonadectomized with immediate implantation of testosterone propionate (GDX+TP). Comparison of the Sham and GDX+TP groups demonstrated that the GDX group had significantly decreased cell counts of ChAT-immunoreactive neurons in anterior cingulate cortex layer II/III, posterior parietal cortex layer II/III, and the medial septum, but not in the other basal forebrain subregions examined (the horizontal part of the diagonal band of Broca and the substantia innominata). The GDX group also had significantly reduced hippocampal ChAT-immunoreactive fiber pixel density. The GDX+TP group maintained ChAT-immunoreactive cell counts in the anterior cingulate cortex, posterior parietal cortex, and medial septum equivalent to those in the Sham group. Less than 1% of identified cells showed colocalization of immunoreactivity for ChAT and androgen receptor in the cell bodies of the cortex and basal forebrain. Our observations demonstrate that the presence or absence of testosterone for 4 weeks influenced the cholinergic population region-specifically in the adult rat brain.


disable_query_log;
#
# Check if server has support for loading plugin
#
if (`SELECT @@have_dynamic_loading != 'YES'`) {
  --skip The connection_control plugin requires dynamic loading
}

#
# Check if the variable PLUGIN_AUTH is set
#
if (!$PLUGIN_AUTH) {
  --skip The connection_control plugin requires the environment variable \$PLUGIN_AUTH to be set (normally done by mtr)
}

enable_query_log;


Q:

MySQL Group by conditioning

Is there a way to only group by certain rows when a specific value is set?
i.e. I have the following table:
USERNO  |   FIRSTNAME   |   NAME    |   CUSTOMER    |   YEAR
1       |   Jon         |   Snow    |   0           |   2014
2       |   Williams    |   Spear   |   1           |   2015
1       |   John        |   Snow    |   1           |   2015
3       |   Sam         |   Wells   |   0           |   2014
3       |   Sam         |   Wells   |   0           |   2013

When CUSTOMER is 1, it should group by USERNO. So I want the following result:
USERNO  |   FIRSTNAME   |   NAME    |   CUSTOMER    |   YEAR
1       |   Jon         |   Snow    |   1           |   2014
2       |   Williams    |   Spear   |   1           |   2015
3       |   Sam         |   Wells   |   0           |   2014
3       |   Sam         |   Wells   |   0           |   2013

Is this possible?
Thanks in advance!

A:

You can use UNION for getting this type of results like this:
SELECT *
FROM tablename
WHERE CUSTOMER != 1
UNION
SELECT *
FROM tablename
WHERE CUSTOMER = 1
GROUP BY USERNO;

OR You can also use CASE but you have to specify the ELSE part to group records when condition is not satisfied:
SELECT *
FROM tablename
GROUP BY CASE WHEN CUSTOMER  = 1 THEN USERNO ELSE columnname END;

OR You can use GROUP_CONCAT like this if you want your results to be grouped as a COMMA delimited list:
SELECT
  GROUP_CONCAT(DISTINCT CAST(USERNO) AS CHAR),
  GROUP_CONCAT(DISTINCT CAST(FIRSTNAME) AS CHAR),
  GROUP_CONCAT(DISTINCT CAST(NAME) AS CHAR),
  CUSTOMER,
  GROUP_CONCAT(DISTINCT CAST(YEAR) AS CHAR)
FROM tablename
GROUP BY CUSTOMER;


Cults, rituals and underground movements were explored in Zal Batmanglij's unjustly overlooked "Sound Of My Voice," and this year he returns to the Sundance Film Festival with collaborator Brit Marling for "The East," another picture exploring those similar themes. And following its premiere in Park City over the weekend, Fox Searchlight is using the buzz to drop the first teaser trailer for what looks like an equally gripping experience.

Cults, rituals and underground movements were explored in Zal Batmanglij's unjustly overlooked "Sound Of My Voice," and this year he returns to the Sundance Film Festival with collaborator Brit Marling for "The East," another picture exploring those similar themes. And following its premiere in Park City over the weekend, Fox Searchlight is using the buzz to drop the first teaser trailer for what looks like an equally gripping experience.

Starring Marling, Ellen Page, Alexander Skarsgard and Patricia Clarkson, the film centers on a young woman who works for a private intelligence firm who is tasked with infiltrating an anarchist collective. And once she does, she soon finds herself in over her head, and caught up in their campaigns and covert operations, and begins to question her own motives. Our review out of Sundance called it a "stylish thriller" that also serves as "a terrific companion piece for anyone who enjoyed 'Sound Of My Voice.'" This teaser doesn't give too much away, but sets everything up for what looks like a pretty white knuckle little ride.

No release date yet, but "The East" is expected to hit theaters later this year.


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	"./_base",
	"dijit/_WidgetBase",
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				Query("*", this.domNode).orphan();
				this.domNode.innerHTML = this.template.render(this.context);
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			declaredClass: "dojox.dtl.Inline",
			buildRendering: function(){
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				var node = this.srcNodeRef;
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				this.template = new dd.Template(lang.trim(node.text), true);
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				this.context = (this.context.get === dd._Context.prototype.get) ? this.context : new dd._Context(this.context);
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