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

Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity

中枢神経系疾患の治療は正常細胞（ニューロン）の機能維持を目的とするが，脳血管障害のように機能障害の原因が細胞の死滅に基づくことは多い．一方，脳腫瘍の治療においては薬物療法や放射線療法といった腫瘍細胞の死滅を目標とするものが大きな位置を占める．いずれの場合にも，細胞死の機序を理解することは各種病態や治療法の理解のうえで重要である．現在のところ最も研究の進んでいる細胞死の型はアポトーシスである．そのなかで重要な位置を占めるミトコンドリアにおける反応および抗アポトーシス因子について概要を紹介する．

Neuroscience 細胞死：最近の知見

A central question in cell biology is how membrane-spanning receptors transmit extracellular signals inside cells to modulate cell adhesion and motility. Focal adhesion kinase (FAK) is a crucial signalling component that is activated by numerous stimuli and functions as a biosensor or integrator to control cell motility. Through multifaceted and diverse molecular connections, FAK can influence the cytoskeleton, structures of cell adhesion sites and membrane protrusions to regulate cell movement.

Focal adhesion kinase: in command and control of cell motility

RNAscope: A Novel in Situ RNA Analysis Platform for Formalin-Fixed, Paraffin-Embedded Tissues

Precipitation transformation pathway and mechanical behavior of nanoprecipitation strengthened Fe-Mn-Al-C-Ni austenitic low-density steel

Schizophrenia is a debilitating mental illness that affects 1.1% of the general population (3 million people in the USA). It is characterized by profound disturbances in thinking, cognition and social functioning. In severe cases, schizophrenia can lead to withdrawal from society, institutionalization and even death. It imposes a huge financial burden on afflicted individuals, families and society. The overall cost of schizophrenia in the USA for 2002 was estimated to be US$63 billion [1]. Although schizophrenia is among the most prevalent of brain disorders, it continues to be one of the least understood. Unlike Alzheimer’s disease, Parkinson’s disease and other neurodegenerative disorders, schizophrenia lacks clear or distinct pathological lesions. Clearly, genetic factors play a role in schizophrenic pathogenesis. The risk of developing schizophrenia is significantly higher among people who have immediate relatives with a history of this or other psychiatric diseases. It is believed that schizophrenia occurs as a result of a combination of genetic predisposition, environmental exposures and/or stresses during pregnancy or childhood. Schizophrenia is thought to be caused by impaired brain development [2–5]. This may include defects in neural genesis, neuron migration, axon pathway and synapse formation. In addition, neurotransmission and its plasticity may be altered at various neurotransmitter pathways including those of glutamate and GABA, major excitatory and inhibitory neurotransmitters, respectively, in addition to the dopaminergic pathway [6–8]. Recently, several susceptibility genes have bene identified for schizophrenia [4]. In particular, mutations or polymorphisms of neuregulin-1 (NRG-1) and ErbB4 appear to support an etiologic role [9–13]. Recent studies appear to have identified schizophrenia-relevant functions of the two proteins and provide the biological basis of the increased risk with two genes. Neuregulin-1 & ErbB-receptor tyrosine kinases Neuregulin-1 was identified in the early 1990s by four independent groups of scientists searching for different biological activities, and was thus named as neu-differentiation factor, heregulin, glial growth factor and acetylcholine-receptor inducible activity [14,15]. It belongs to a family of growth factors encoded by four individual genes. The prototype of neuregulin-1 is a transmembrane protein, which was cleaved to release the EGF-like domain.

Neuregulin-1 signaling in schizophrenia

Compositions that inhibit or block the interaction between Erbin and ErbB2 and methods of their use are provided. Preferred compositions include peptides that inhibit or block Erbin and ErbB2 interaction under physiologic conditions in a subject. One embodiment provides an isolated peptide fragment of ErbB2 including the C-terminal 15 amino acids of ErbB2. The peptide fragment can be about 15 to 27 amino acids in length.

Methods of using ERBB2 conjugate peptides

DOK7 Promotes NMJ Regeneration After Nerve Injury

Enteric glial cells (EGCs) play an important role in visceral hypersensitivity associated with irritable bowel syndrome (IBS). Losartan (Los) is known to reduce pain; however, its function in IBS is unclear. The present study aimed to investigate Los's therapeutic effect on visceral hypersensitivity in IBS rats. Thirty rats were randomly divided into control, acetic acid enema (AA), AA + Los low, medium and high dose groups in vivo. EGCs were treated with lipopolysaccharide (LPS) and Los in vitro. The molecular mechanisms were explored by assessing the expression of EGC activation markers, pain mediators, inflammatory factors and angiotensin-converting enzyme 1(ACE1)/angiotensin II (Ang II)/Ang II type 1 (AT1) receptor axis molecules in colon tissue and EGCs. The results showed that the rats in the AA group showed significantly higher visceral hypersensitivity than the control rats, which was alleviated by different doses of Los. The expression of GFAP, S100β, substance P (SP), calcitonin gene-related peptide (CGRP), transient receptor potential vanilloid 1 (TRPV1), tumor necrosis factor (TNF), interleukin-1β (IL-1β) and interleukin-6 (IL-6) was considerably increased in colonic tissues of AA group rats and LPS-treated EGCs compared with control rats and EGCs, and reduced by Los. In addition, Los reversed ACE1/Ang II/AT1 receptor axis upregulation in AA colon tissues and LPS-treated EGCs. These results show that Los inhibits ACE1/Ang II/AT1 receptor axis upregulation by suppressing EGC activation, resulting in reduced expression of pain mediators and inflammatory factors, thereby alleviating visceral hypersensitivity. 

Lin Mei

Papers

Precipitation transformation pathway and mechanical behavior of nanoprecipitation strengthened Fe-Mn-Al-C-Ni austenitic low-density steel

Neuregulin-1 signaling in schizophrenia

Methods of using ERBB2 conjugate peptides

DOK7 Promotes NMJ Regeneration After Nerve Injury

Losartan attenuates acetic acid enema-induced visceral hypersensitivity by inhibiting the ACE1/Ang II/AT1 receptor axis in enteric glial cells