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’

Acute kidney injury (AKI) is a challenging clinical condition that affects many hospitalized patients, especially those with critical illness. Among the most common causes for AKI are sepsis, ischemia-reperfusion injury, or nephrotoxins, and studies have revealed a crucial role of the innate and adaptive immune system in AKI pathophysiology. This chapter reviews our current knowledge of various inflammatory processes involved in the complex disease process with the aim to improve our understanding and subsequent treatment of not only AKI but also its long-term consequences: chronic kidney disease and end-stage renal disease.

Adaptive Immunity and Critical Illness

Orthologs of macrophage migration inhibitory factor (MIF) have been identified in dozens of protozoan and nematode parasites, and the properties of many of these have been investigated and reported upon. Crystallographic analyses have revealed close structural similarity of these with human MIF, and many of these parasite MIFs are able to bind directly to the human MIF receptor CD74. Additionally, most parasite MIFs demonstrate tautomerase activity similar to that of the human protein. Parasite MIFs demonstrate many of the pro-inflammatory activities of human MIF, including the ability to regulate macrophage migration, stimulate signal transduction pathways, inhibit apoptosis, and promote production of inflammatory cytokines including IL-8 and TNF-α. These properties indicate that parasite MIFs may be involved in altering the immune response during infection, a role that has been confirmed in a handful of animal model studies. These suggest a mechanism in which parasite MIFs signal to host macrophages to influence the ensuing adaptive immune response in order to promote parasite persistence and transmission. Because of the pathogenic impact of parasite MIFs, therapeutic interventions including small molecule inhibitors and immunizations have been explored. It is hoped that therapies targeting parasite MIFs will provide a novel treatment for an array of chronic, difficult-to-treat infectious diseases.

Parasite MIF Orthologs

830 Can CD74 Predict Treatment Response to Anti-TNF Agents in Inflammatory Bowel Disease?

While immunotherapies have shown durable responses for multiple tumors, their efficacy remains limited in some advanced cancers, including glioblastoma. This may be due to differences in the immune landscape, as the glioblastoma microenvironment strongly favors immunosuppressive myeloid cells, which are linked to an elevation in immune-suppressive cytokines, including macrophage migration inhibitory factor (MIF). We now find that a single-nucleotide polymorphism (SNP) rs755622 in the MIF promoter associates with increased leukocyte infiltration in glioblastoma. Furthermore, we identified lactotransferrin expression as being associated with the rs755622 SNP, which could also be used as a biomarker for immune infiltrated tumors. These findings provide the first example in glioblastoma of a germline SNP that underlies differences in the immune microenvironment and identifies high lactotransferrin as a potential factor promoting immune activation.

Richard Bucala

Papers

Adaptive Immunity and Critical Illness

Parasite MIF Orthologs

830 Can CD74 Predict Treatment Response to Anti-TNF Agents in Inflammatory Bowel Disease?

The MIF SNP rs755622 is a germline determinant of tumor immune activation in Glioblastoma

Ovarian Cancer by Down-Regulating Contributes to the Immune Escape of Macrophage Migration Inhibitory Factor