In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
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Question: Context: Animal models for hepatic metastases can facilitate the investigation of lymphokine-activated killer (LAK) cell-based immunotherapy. The aim of this study was to investigate the efficacy of ccM4 antibody-targeted LAK cells in inhibiting hepatic micrometastases.', 'Hepatic micrometastases were generated after the intrasplenic injection of HM7 colon carcinoma cells. TAG72 expression was detected in these hepatic micrometastases using ccM4 antibody. The ccM4 antibody was conjugated onto LAK cells by treatment with 17.5% polyethylene glycol 8000. After the intrasplenic injection of HM7 cells, severe combined immunodeficient mice were randomized into five groups (i-v) and received either 10(7) ccM4-LAK cells plus 1000 U interleukin 2 (IL-2; group i), LAK cells plus 50 micrograms ccM4 and IL-2 (group ii), LAK cells plus IL-2 (group iii), IL-2 alone (group iv), or only phosphate-buffered saline (group v).', 'The ccM4-LAK cells retained cytolytic activity and acquired TAG72-binding reactivity. The results showed that group i had significantly fewer hepatic metastases compared with group ii or group iii (P < 0.05) and even fewer hepatic metastases compared with group iv or group v (P < 0.001).\Question: Do antibody-targeted lymphokine-activated killer cells inhibit liver micrometastases in severe combined immunodeficient mice?

Answer: These results show that ccM4 antibody-targeted LAK cells significantly inhibited tumor growth in vivo; thus, they can be potentially useful in treatment of hepatic micrometastases.

Question: Context: To explore the relationship between continuous thrombocytopenia and sepsis in patients with severe burns.', 'Clinical data of 148 severely burned patients admitted to our,two burn centers from January 2007 to December 2011 and conforming to the study criteria were retrospectively analyzed. All patients were divided into sepsis group (n =44) and non-sepsis group (n = 104) according to the presence or absence of sepsis within post burn day (PBD) 30. The data of age, gender, total burn area, full-thickness burn area, fluid infusion volume within post burn hour (PBH) 24, plasma concentration of calcium ion on PBD 1, plasma concentration of albumin on PBD 1, platelet count on PBD 1, acute physiology and chronic health evaluation (APACHE) II score on admission, the presence or absence of hypovolemic shock or inhalation injury on admission, the presence or absence of disseminated intravascular coagulation (DIC) within PBH 48, operation or no operation within PBD 3, thrombocytopenia duration within PBD 10, and mortality were statistically compared between two groups to screen the independent risk factors of sepsis. Data were processed with t test, chi-square test, single factor Logistic regression analysis, and multi-factor Logistic regression analysis.', 'Between two groups, there were statistically significant differences in total burn area, full-thickness burn area, plasma concentration of calcium ion on PBD 1, plasma concentration of albumin on PBD 1, APACHE II score on admission, presence or absence of hypovolem- ic shock on admission, presence or absence of inhalation injury on admission, presence or absence of DIC within PBH 48, and mortality (with t values from 2.433 to 4.082, 2 values from 8. 818 to 31.528, P < 0.05 or P < 0.01). Furthermore, the duration of thrombocytopenia within PBD 10 in sepsis group was (5.2 2.4) d, which was significantly longer than that in non-sepsis group [(2.9 1.9) d, t =6. 189, P <0.01]. There were no statistically significant differences in the other indexes between two groups (with t values from 0.971 to 1. 250, 2 values respectively 0. 054 and 1.529, P values above 0.05). Single factor and multi-factor Logistic regression analysis indicated that APACHE II score on admission and duration of thrombocytopenia within PBD 10 were closely related to occurrence of sepsis (with odds ratio respectively 1. 140 and 1.569, P values below 0.01).\Question: Do [ Clinical significance of continuous thrombocytopenia in predicting sepsis after severe burn ]?

Answer: Duration of thrombocytopenia within PBD 10 is one of the risk factors for sepsis in severely burned patients, which can reflect pathophysiological changes in the body, thus providing predictive value for the occurrence of sepsis.

Question: Context: Coagulation FXII is activated on contact with lipoprotein particles. It has been suggested that contact with subendothelial tissue provides an alternative biological surface for FXII activation. Our aim was to investigate whether activated FXII (FXIIa) is elevated in patients with coronary atherosclerosis, and whether disease status (acute phase or stable state) affects circulating levels of FXIIa.', 'Circulating FXIIa levels were measured in the peripheral blood of 122 patients with coronary atherosclerosis (32, stable angina; 54, unstable angina; 36, nQ myocardial infarction) and in 45 age-matched subjects (Contr).', 'FXIIa levels (median, first and third quartiles; ng/ml) were higher in patients than in Contr: 1.61 (1.26-2.02) vs. 1.34 (1.13-1.81) (p<0.01). FXIIa levels were similar among patients with stable angina [1.66 (1.23-1.91)], unstable angina [1.53 (1.21-2.04)], and nQ myocardial infarction [1.75 (1.34-2.03)]. The three groups of patients had similar prevalence for most atherothrombotic risk factors; patients with stable angina had an increased severity of coronary disease, which did not explain the different levels of FXIIa. Fasting levels of triglycerides were the best predictor of FXIIa levels in our patients.\Question: Do acute coronary syndromes promote prolonged in vivo FXII-dependent prothrombotic activity?

Answer:
The finding of similar FXIIa levels among patients in either acute or chronic phases of coronary atherosclerosis suggests that the initial arterial denudation and the acute-phase response associated to acute coronary syndromes are not major determinants for prolonged FXII activation.