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’

As the current Arthritis & Rheumatology ( A&R ) editorial team approaches halfway into our 5-year term, we took stock of what is working and where we can make improvements. COVID-19 and COVID-19 manuscripts dominated the lives of our authors, reviewers, and editors for much of year 1 of the term. With many investigators out of the research setting, articles were ﬁ nished and submitted, leading to a 50% increase in submissions for the ﬁ rst 6 months of our term. An amazing editorial team, staff, and academic editors handled the “ surge ” with characteristic grace. We balanced the need to publish COVID-19 work quickly with the requirement for scienti ﬁ c rigor, and only time will tell if A&R succeeded in achieving balance.

Arthritis & Rheumatology: “Mid‐Term” Report

In various aspects and embodiments the invention provides methods for the treatment of a MIF-mediated disease. In one aspect, the invention provides a method of treating a fibrotic disease in a male subject in need thereof, the method comprising administering to the male subject an effective amount of at least one MIF agonist. In various embodiments, the fibrotic disease is lung fibrosis. In another aspect, the invention provides a method of treating chronic obstructive pulmonary disease (COPD) in a female subject in need thereof, the method comprising administering to the female subject an effective amount of at least one MIF agonist. In various embodiments, the COPD is emphysema type COPD.

Compounds and methods for treating copd and/or lung fibrosis

Sex Steroids are important to the pathogenesis of SLE, a disease which affects females in preference to males (13:1). Abnormalities of estrogen metabolism and androgen metabolism in the human have been described. Increased 16 hydroxylation of estrone has been found in males and females, whereas increased oxidation of testosterone (C-17) has been found only in females with the disease. Females with SLE have low plasma androgens. Patients with active disease have the lowest levels. The compound 16 alpha hydroxyestrone, a unique and potent estrogen, has been shown to bind covalently to plasma proteins and cell membranes. This compound is a product of 16 hydroxylation, and may be important to the pathogenesis of SLE.

Role of Sex Steroids in Systemic Lupus Erythematosus (SLE)

In this study, we evaluate the role of the MIF/CD74 axis in the functionality of CD4+ T lymphocytes (CD4TL) during HIV infection. MDMs from healthy donors were infected with a R5-tropic or Transmitted/Founder (T/F) HIV strain. At day 11 post-MDM infection, allogeneic co-cultures with uninfected CD4TLs plus MIF stimulus were performed. Cytokine production was evaluated by ELISA. MIF plasma levels of people with HIV (PWH) were evaluated by ELISA. The phenotype and infection rate of CD4TLs from PWH were analyzed after MIF stimulus. Intracellular cytokines and transcription factors were evaluated by flow cytometry. Data were analyzed by parametric or non-parametric methods. The MIF stimulation of HIV-infected MDMs induced an increased expression of IL-6, IL-1β and IL-8. In CD4TL/MDM co-cultures, the MIF treatment increased IL-17A/RORγt-expressing CD4TLs. Higher concentrations of IL-17A in supernatants were also observed. These results were recapitulated using transmitted/founder (T/F) HIV-1 strains. The MIF treatment appeared to affect memory CD4TLs more than naïve CD4TLs. MIF blocking showed a negative impact on IL17A+CD4TL proportions. Higher MIF concentrations in PWH-derived plasma were correlated with higher IL-17A+CD4TL percentages. Finally, MIF stimulation in PWH-derived PBMCs led to an increase in Th17-like population. MIF may contribute to viral pathogenesis by generating a microenvironment enriched in activating mediators and Th17-like CD4TLs, which are known to be highly susceptible to HIV-1 infection and relevant to viral persistence. These observations establish a basis for considering MIF as a possible therapeutic target.

/pdf/macrophage-migration-inhibitory-factor-mif-promotes-30canjqf.pdf

Richard Bucala

Papers

Arthritis & Rheumatology: “Mid‐Term” Report

Compounds and methods for treating copd and/or lung fibrosis

Role of Sex Steroids in Systemic Lupus Erythematosus (SLE)

Macrophage Migration Inhibitory Factor (MIF) Promotes Increased Proportions of the Highly Permissive Th17-like Cell Profile during HIV Infection

a CD74-Dependent Manner Cell Migration to the Bone Marrow in and Chronic Lymphocytic Leukemia TAp63 Regulates VLA-4 Expression