There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality.

Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

I and i

다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

Human mesenchymal stem cells are thought to be multipotent cells, which are present in adult marrow, that can replicate as undifferentiated cells and that have the potential to differentiate to lineages of mesenchymal tissues, including bone, cartilage, fat, tendon, muscle, and marrow stroma. Cells that have the characteristics of human mesenchymal stem cells were isolated from marrow aspirates of volunteer donors. These cells displayed a stable phenotype and remained as a monolayer in vitro. These adult stem cells could be induced to differentiate exclusively into the adipocytic, chondrocytic, or osteocytic lineages. Individual stem cells were identified that, when expanded to colonies, retained their multilineage potential.

http://science.sciencemag.org/content/sci/284/5411/143.full.pdf

Multilineage Potential of Adult Human Mesenchymal Stem Cells

抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

article i nfo Myocardial infarction (MI) provokes regional inflammation which facilitates the healing, whereas excessive inflammation leads to adverse cardiac remodelling. Our aim was to determine the role of macrophage migration inhibitory factor (MIF) in inflammation and cardiac remodelling following MI. Wild type (WT) or global MIF deficient (MIFKO) mice were subjected to coronary artery occlusion. Compared to WT mice, MIFKO mice had a significantly lower incidence of post-MI cardiac rupture (27% vs. 53%) and amelioration of cardiac remodelling. These were associated with suppressed myocardial leukocyte infiltration, inflammatory mediators' expression, and reduced activity of MMP-2, MMP-9, p38 and JNK MAPK. Infarct myocardium-derived or exogenous MIF mediated macrophage chemotaxis in vitro that was suppressed by inhibition of p38 MAPK or NF-κB. To further dissecttheroleofMIFderivedfromdifferentcellular sources in post-MIcardiacremodelling, we generatedchimeric mice with MIF deficiency either in bone marrow derived-cells (WT KO

inhibitoryfactorininflammatoryresponsesandcardiacremodellingpost myocardial infarction

We investigated the possibility that amine-containing phospholipids react directly with glucose to form advanced glycosylation endproducts (AGEs). Phospholipid-linked AGEs formed readily in vitro, mimicking the absorbance, fluorescence, and immunochemical properties of AGEs that result from the advanced glycosylation of proteins. Lipid-AGE formation was accompanied by fatty acid oxidation, which occurred in the absence of added, transition metal ions. In additional experiments, incubation of low-density lipoprotein (LDL) with glucose was found to produce AGE moieties that were attached to both the lipid and the apoprotein (ApoB) components. Oxidized-LDL formed concomitantly with AGE-modified LDL. AGE-specific ELISA analysis of LDL specimens isolated from diabetic individuals revealed increased levels of both apoprotein- and lipid-linked AGEs when compared to specimens obtained from normal, non-diabetic controls. Circulating levels of oxidized-LDL were elevated in diabetic patients, and correlated significantly with apoB-AGE and lipid-AGE levels. Lipid-advanced glycosylation may result from intra-molecular redox reactions that occur during advanced glycosylation and presents a facile mechanism to explain lipid oxidation in vivo, where free metals are present in too low a concentration to induce oxidative modification.

Advanced Glycosylation of LDL: Role in Oxidative Modification and Diabetic Complications

Profibrotic Role for a Dysregulated D-Dopachrome Tautomerase-Cullin 3 Signaling Axis in Alveolar Type II Epithelial Cells

There is disclosed a fibrocyte-based vaccine formulation made from isolated fibrocytes. There is further disclosed a method for establishing an immune response against a specific antigen by administering a fibrocyte-based vaccine formulation, such as one made by pulsing fibrocytes in culture with the antigen peptide or protein, or by fusing tumor cells (whole cells or membrane fragments thereof) with fibrocytes.

Richard Bucala

Papers

inhibitoryfactorininflammatoryresponsesandcardiacremodellingpost myocardial infarction

Advanced Glycosylation of LDL: Role in Oxidative Modification and Diabetic Complications

Profibrotic Role for a Dysregulated D-Dopachrome Tautomerase-Cullin 3 Signaling Axis in Alveolar Type II Epithelial Cells

Fibrocyte-based cellular therapy formulations

The Role of CD74 in Bleomycin-Induced Pulmonary Fibrosis