PubMed · 13985899
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S PRADO, O PHILIPPI, R DEL RIO, P DONOSO. 1963. [Acute endocarditis].. https://pubmed.ncbi.nlm.nih.gov/13985899/
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Specific immunotherapies for patients with acute myeloid leukemia (AML) using leukemia-associated antigens (LAA) as target structures might be a therapeutic option to enhance the graft-vs.-leukemia effect observed after allogeneic stem cell transplantation or to prolong a complete remission (CR) achieved by chemotherapy. Significant mRNA expression of LAA is a prerequisite for such immunotherapies. Here, previously characterized antigens associated with solid tumors (TAA) and newly characterized LAA were investigated for their expression in up to 60 AML patients and in leukemia cell lines. To investigate their specificity for leukemic blasts, the mRNA expression was also characterized in PBMN and CD34 positive cells of healthy volunteers and in a panel of normal tissues. The following antigens showed high mRNA expression in AML patients: MPP11 was detected in 43/50 (86%), RHAMM in 35/50 (70%), WT1 in 40/60 (67%), PRAME in 32/50 (64%), G250 in 18/35 (51%), hTERT in 7/25 (28%) and BAGE in 8/30 (27%) of AML patients. Real-time RT-PCR showed a tumor-specific expression of the antigens BAGE, G250 and hTERT, as well as highly tumor-restricted expression for RHAMM, PRAME and WT1. The antigen MPP11 was overexpressed. These antigens might be candidates for immunotherapies of leukemia patients and, because of their simultaneous expression, also for polyvalent vaccines.
The aim of this study was to identify the frequency and possible pathogenic mechanisms of early neurological deterioration in patients with acute small non-lacunar infarction. We studied 46 patients (35 men, 11 women; age, 70.3+/-10.4 years) with acute small non-lacunar infarction. Small non-lacunar infarction was diagnosed using diffusion-weighted magnetic resonance imaging (DWI) as being <15 mm in diameter and located in the cortex and centrum ovale in the middle cerebral artery territory. The patients were divided into two groups; Group D (n=6) had neurological deterioration within 7 days after symptom onset, while Group N (n=40) did not have any neurological deterioration. In Group D, the interval from symptom onset to clinical deterioration was 3.3+/-1.5 days (range 2-6 days). Blood pressure on admission was higher in Group D than in Group N (p<0.05). In Group D, four of these five patients with follow-up DWI had new acute small ischemic lesions in addition to the initial lesions, indicating recurrent attacks of brain infarction. Neurological deterioration occurred within 7 days after symptom onset in 13% of patients. Neurological deterioration was frequently caused by recurrent infarction detected by DWI.
The effect of diesel exhaust particulate (DEP) exposure on innate, cellular and humoral pulmonary immunity was studied using high-dose, acute-exposure rat, mouse, and cell culture models. DEP consists of a complex mixture of petrochemical-derived organics adsorbed onto elemental carbon particles. DEP is a major component of particulate urban air pollution and a health concern in both urban and occupational environments. The alveolar macrophage is considered a key cellular component in pulmonary innate immunity. DEP and DEP organic extracts have been found to suppress alveolar macrophage function as demonstrated by reduced production of cytokines (interleukin-1 [IL-1], tumor necrosis factor- alpha [TNF- alpha]) and reactive oxygen species (ROS) in response to a variety of agents, including lipopolysaccharide (LPS), interferon- gamma (IFN- gamma), and bacteria. Fractionation of DEP organic extract suggests that this activity was predominately in polyaromatic-containing and more polar (resin) fractions. Organic-stripped DEP did not alter these innate pulmonary immune responses. DEP also depressed pulmonary clearance of Listeria monocytogenes and Bacillus Calmette-Guerin (BCG). The contribution of the organic component of DEP is less well defined with respect to acquired and humoral immunity. Indeed, both DEP and carbon black enhanced humoral immune responses (specific immunoglobulin [Ig] E and IgG) in an ovalbumin-sensitized rat model. It is concluded that both the particulate and adsorbed organics may contribute to DEP-mediated immune alterations.