Fungal mycobiome drives IL-33 secretion and type 2 immunity in pancreatic cancer

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股骨转子间骨折的稳定性重建概念演化与研究进展

目的总结近年来股骨转子间骨折在稳定性重建方面的概念演化与研究进展。方法查阅国内外相关文献并结合自身经验，从股骨转子间骨折的解剖特点、稳定型骨折与不稳定型骨折分类、稳定性复位与不稳定性复位、术中加压初始稳定与术后滑动二次稳定、内固定术后稳定性评估、早期下地站立负重等方面进行总结分析。结果股骨转子间骨折发生于股骨颈干骺端转换区，具有天然的内翻不稳定倾向。骨折复位质量是影响后续内固定物安放的最重要前提因素。判断骨折复位质量有对线和对位两方面，对线采用 Garden 指数；在对位方面，随着皮质对位理念（正性、中性、负性）的提出，特别强调前内侧皮质的相互砥住支撑（解剖、正性），是获得骨折稳定性复位的关键，而不再强调后内侧小转子骨块的作用。术后影像学的稳定性评分为早期下地站立负重提供了量化指标。但术中的前内侧皮质支撑复位，在术后头颈骨块滑动获得二次稳定的过程中，仍有皮质对位丢失现象，需研究其危险因素和防范措施。结论股骨转子间骨折在取得良好对线的基础上，只要获得了前内侧皮质的相互砥住和支撑，并用内固定器械维持住，就获得了术后稳定性。术后稳定性评分优良者，可以安全地早期下地负重、站立行走活动。     

人源化CD33单克隆抗体联合化疗与单用化疗在初次复发或难治性急性髓性白血病治疗中比较的Ⅲ期多中心随机研究的评价

4背景 CD33是一种细胞表面的受体，它只存在于粒单细胞表面。体外研究表明，抗CD33抗体与受体结合后导致了剂量依赖性的细胞凋亡．这与其他抗体如CD22在淋巴系统恶性肿瘤中的方式是相似的。由于CD33在急性髓性白血病（acute myeloid leukemia，AML）的幼稚细胞中广泛表达（〉90％），而在大多数的非血液系统的组织则不表达．故针对CD33的抗体类药物．如联合了刺孢霉素的抗CD33抗体吉姆单抗奥佐米星（Gemtuzumab Ozogamicin，GO）已用于治疗AML的病人。     

DIFF33H参与TRAIL诱导的人Jurkat T淋巴细胞白血病细胞凋亡调控

目的：研究DIFF33H在人T淋巴细胞白血病细胞Jurkat凋亡中的表达规律及其生物学功能。方法：采用PCR扩增DIFF33H cDNA，Northern blot分析DIFF33H的mRNA表达，MTT法测定细胞凋亡。结果：在重组可溶性TRAIL诱导的人T淋巴细胞白血病细胞Jurkat凋亡过程中，DIFF33H mRNA的表达水平随着Jurkat细胞的凋亡而下降，并对重组可溶性TRAIL的作用具有浓度和时间的依赖性。在抗肿瘤药物5-FU诱导肿瘤细胞凋亡过程中，DIFF33H的mRNA表达水平也显著下降。结论：DIFF33H参与人T淋巴细胞白血病细胞Jurkat凋亡的调控。     

Polymorphisms in ADAM33 are associated with allergic rhinitis due to Japanese cedar pollen

BACKGROUND: A recent report provided evidence that a disintegrin and metalloprotease domain 33 (ADAM33), a member of the ADAM family, is a novel susceptibility gene in asthma linked to bronchial hyper-responsiveness. However, there has been no investigation of the genetic role of ADAM33 variants in nasal allergy. OBJECTIVE: The purpose of this study was to test the association between ADAM33 polymorphisms and Japanese cedar pollinosis (JCPsis), a most common seasonal allergic rhinitis in Japan. METHODS: We conducted a case-control association study among a Japanese population, involving 95 adult individuals with JCPsis and 95 normal healthy controls. A total of 22 single-nucleotide polymorphisms (SNPs) in ADAM33 were genotyped using PCR-based molecular methods. RESULTS: Six SNPs of ADAM33 gene, three in introns (7575G/A, 9073G/A and 12540C/T) and three in the coding region (10918G/C, 12433T/C and 12462C/T), were strongly associated with JCPsis (P = 0.0002-0.022 for absolute allele frequencies) and most of the SNPs were in linkage disequilibrium with each other. A higher frequency of the common alleles of these SNPs was noted for the subjects with JCPsis in comparison with healthy controls. We also identified a haplotype associated with the disease susceptibility. In addition, associations were found between ADAM33 polymorphisms and various cedar pollinosis phenotypes including clinical severity, eosinophil counts in nasal secretion and allergen-specific IgE levels in sera, but not total serum IgE levels. CONCLUSION: These results indicate that polymorphisms in the ADAM33 gene are associated with susceptibility to allergic rhinitis due to Japanese cedar pollen, but the functional relationship still needs clarification.     

Eleven single nucleotide polymorphisms and one triple nucleotide insertion of the human TGF-β III receptor gene

We found 11 single nucleotide polymorphisms and one triple nucleotide insertion in the cDNA of the human transforming growth factor β (TGF-β) III receptor gene (TGFBR3) located on 1p33–p32, encoding betaglycan, a component of the TGF-β receptor system. Inside the 5′ untranslated region (UTR), a G→A polymorphism was identified at position 311. In the open reading frame (ORF), a non-conservative T→C polymorphism was identified at position 392, and three conservative polymorphisms were found at positions 563 (G→A), 1548 (G→A), and 2370 (C→T). A triple nucleotide insertion (GCA) was identified at position 1419. Inside the 3′ UTR, six polymorphisms were identified: four G→A, at positions 2918, 3055, 3098, and 3355; one T→A, at position 3183; and one G→C, at position 3966. In addition to these changes, some divergences from the published sequence were observed in all 12 chromosomes tested. These included, in the ORF, an additional C after position 555, two additional G after position 563, and an additional T after position 1388. No T was found at position 1394. The alterations translate to a changed amino acid sequence. Inside the 3′ UTR, additional discrepancies were identified. The discovered changes and polymorphisms may be useful for further genetic studies of TGFBR3 receptor deficiencies. Received: December 22, 1999 / Accepted: February 25, 2000     

An improved method for the isolation of the major protein of the gonococcal outer membrane in an antigenically reactive form

The major outer membrane protein (protein I) has been isolated from Neisseria gonorrhoeae strain P9 in an immunologically reactive form. Membranes were sequentially extracted with the detergents sodium cholate and Empigen BB. Protein I was enriched in the Empigen-soluble fraction and was separated from other proteins and lipopolysaccharide by gel filtration chromatography on Sephadex G-200. The purified protein retained its antigenic activity with antiserum raised against the unfractionated outer membrane complex.     

IL-1, IL-18, and IL-33 families of cytokines

Summary: The interleukin-1 (IL-1), IL-18, and IL-33 families of cytokines are related by mechanism of origin, receptor structure, and signal transduction pathways utilized. All three cytokines are synthesized as precursor molecules and cleaved by the enzyme caspase-1 before or during release from the cell. The NALP-3 inflammasome is of crucial importance in generating active caspase-1. The IL-1 family contains two agonists, IL-1α and IL-1β, a specific inhibitor, IL-1 receptor antagonist (IL-1Ra), and two receptors, the biologically active type IL-1R and inactive type II IL-1R. Both IL-1RI and IL-33R utilize the same interacting accessory protein (IL-1RAcP). The balance between IL-1 and IL-1Ra is important in preventing disease in various organs, and excess production of IL-1 has been implicated in many human diseases. The IL-18 family also contains a specific inhibitor, the IL-18-binding protein (IL-18BP), which binds IL-18 in the fluid phase. The IL-18 receptor is similar to the IL-1 receptor complex, including a single ligand-binding chain and a different interacting accessory protein. IL-18 provides an important link between the innate and adaptive immune responses. Newly described IL-33 binds to the orphan IL-1 family receptor T1/ST2 and stimulates T-helper 2 responses as well as mast cells.     

A metacognitive model of social anxiety: Implications for treatment

This article represents an attempt to clarify questions posed by evidence of varying pathways to change in social anxiety. A new perspective is developed which addresses these questions and, importantly, lays the foundation for an innovative treatment approach. Essentially, social anxiety is construed here as the product of a disorganization in which feelings and cognitions (both conscious and preconscious) about the self, about other people, and about the relations between self and others are organized. Specifically, the socially anxious client experiences others autocentrically: that is, in terms of how the other person perceives, evaluates and affects one's own self. The result is a narrowed capacity for experiencing others. The goal of treatment in the new approach advocated here is to allow the individual to understand, appreciate and share the feelings, thoughts and experience of other people. Therapy is directed toward getting clients out of themselves and into other people.     

Ultrastructural studies on the localization of IgG in the aortic endothelium and subendothelial intima of atherosclerotic and nonatherosclerotic rabbits

Immunoelectron microscopy with peroxidase-conjugated Fab fragments of anti-IgG was used for studying the localization of IgG in the aortic endothelium and subendothelial intima of atherosclerotic and nonatherosclerotic rabbits. Small amounts of IgG were found in the cell coat, in caveolae and vesicles, and also in intercellular clefts of endothelial cells from normocholesterolemic rabbits. Injured endothelial cells exhibited prominent accumulations of IgG in the cytoplasmic matrix, possibly due to leakage through plasma membrane defects. In atherosclerotic lesions from hypercholesterolemic rabbits, there was a striking increase in the amount of IgG-reactive material in the cell coat and vesicles of intact endothelial cells. Also in these animals, injured endothelial cells were characterized by a cytoplasmic IgG accumulation. There were prominent IgG depositions in the subendothelial zone of the lesions. IgG was adhering to collagen fibers, and also coating the surfaces of subendothelial foam cells. The pathophysiological significance of an interaction between such intimal IgG and phagocytes is discussed.