头孢藻属中国新记录种

头孢藻属(Cephaleuros)是一类寄生性藻,在分类学上位于绿藻门石莼纲橘色藻目橘色藻科。国内对头孢藻属的研究多见于它对经济作物和观赏植物的危害,而分类学研究较缺乏。为了全面系统地了解中国头孢藻属的多样性,于2012-2018年先后在多个省份采集头孢藻属标本60余份,并对其进行了形态分类学研究。结果显示,头孢藻属中国新记录种有6种,分别为:寄生头孢藻(Cephaleuros parasiticus Karsten)、德鲁特头孢藻(Cephaleuros drouetii Thompson&Wujek)、肿毛头孢藻(Cephaleuros tumidae-setae Thompson&Wujek)、散生头孢藻(Cephaleuros diffusus Thompson&Wujek)、宽阔头孢藻(Cephaleuros expansa Thompson&Wujek)、亨宁头孢藻(Cephaleuros henningsii Schmidle),对6个种的形态学特征进行了详细描述,并提供了照片资料。     

The role of EMT-related lncRNA in the process of triple-negative breast cancer metastasis

Triple-negative breast cancer (TNBC) is the most malignant and fatal subtype of breast cancer, which has characterized by negativity expression of ER, PR, and HER2. Metastasis is the main factor affecting the prognosis of TNBC, and the process of metastasis is related to abnormal activation of epithelial–mesenchymal transition (EMT). Recent studies have shown that long non-coding RNA (LncRNA) plays an important role in regulating the metastasis and invasion of TNBC. Therefore, based on the metastasis-related EMT signaling pathway, great efforts have confirmed that LncRNA is involved in the molecular mechanism of TNBC metastasis, which will provide new strategies to improve the treatment and prognosis of TNBC. In this review, we summarized many signal pathways related to EMT involved in the transfer process. The advances from the most recent studies of lncRNAs in the EMT-related signal pathways of TNBC metastasis. We also discussed the clinical research, application, and challenges of LncRNA in TNBC.     

SRC-3 Deficiency Exacerbates Neurological Deficits in a Mouse Model of Intracerebral Hemorrhage: Role of Oxidative Stress

Intracerebral hemorrhage (ICH) causes long term neurological abnormality or death. Oxidative stress is closely involved in ICH mediated brain damage. Steroid receptor cofactor 3 (SRC-3), a p160 family member, is widely expressed in the brain and regulates transactivation of Nrf2, a key component of antioxidant response. Our study aims to test if SRC-3 is implicated in ICH mediated brain injury. We first examined levels of SRC-3 and oxidative stress in the brain of mice following ICH and analyzed their correlation. Then ICH was induced in wild type (WT) and SRC-3 knock out mice and how SRC-3 deletion affected ICH induced brain damage, oxidative stress and behavioral outcome was assessed. We found that SRC-3 mRNA and protein expression levels were reduced gradually after ICH induction in WT mice along with an increase in oxidative stress levels. Correlation analysis revealed that SRC-3 mRNA levels negatively correlated with oxidative stress. Deletion of SRC-3 further increased ICH induced brain edema, neurological deficit score and oxidative stress and exacerbated ICH induced behavioral abnormality including motor dysfunction and cognitive impairment. Our findings suggest that SRC-3 is involved in ICH induced brain injury, probably through modulation of oxidative stress.

     

冷驯化对松墨天牛幼虫脂代谢的影响

【目的】在低温环境下,昆虫会启用体内的生理调控机制稳定自身代谢,脂肪代谢在昆虫抵御低温的过程中发挥重要作用。本研究旨在探究松墨天牛Monochamus alternatus幼虫脂肪代谢在低温条件下的变化及其对耐寒性的影响。【方法】将室内25℃下饲养的松墨天牛4龄幼虫分别置于25℃(对照)和4℃(冷驯化)恒温培养箱,7 d后解剖幼虫,收集其脂肪体,观察冷驯化后脂滴变化,测定脂肪体内脂肪含量;利用气相色谱 质谱分析,检测脂肪体内游离脂肪酸组分及含量;并用RT-qPCR方法检测脂肪体内脂肪酸β-氧化关键酶(CPT1, 4KCT, VLCAD, ECH和3HCD-1)基因的相对表达量。【结果】冷驯化(4℃)7 d后松墨天牛4龄幼虫脂肪体中脂滴较对照变小,密度降低,脂肪含量下降;但其脂肪酸组成种类未变,对照组和冷驯化组主要脂肪酸均为C16∶0, C16∶1, C18∶0, C18∶1和C18∶2,其中C18∶2的相对含量在两组中均最高,由未驯化时的31.83%±8.82%降至冷驯化后的25.16%±2.88%。冷驯化后,松墨天牛4龄幼虫脂肪体中C16∶0,C16∶1和C18∶2脂肪酸含量减少,C18∶0与C18∶1的相对含量上升。在5种主要脂肪酸中,冷驯化后各脂肪酸的相对丰度较对照均有所减少,其中C16∶0, C16∶1及C18∶2的相对丰度则显著下降。但冷驯化后松墨天牛4龄幼虫脂肪体中游离脂肪酸的双键指数较对照上升3.88%。且冷驯化组脂肪体中VLCAD基因表达量较对照组显著上调。【结论】低温环境中松墨天牛幼虫通过消耗脂肪维持基本代谢,幼虫脂肪体的脂肪酸分解代谢水平提高;不饱和脂肪酸在松墨天牛的耐寒性中起关键作用。脂代谢调控为松墨天牛应对低温的重要生存策略。     

Feedback regulation of coronary artery disease susceptibility gene ADTRP and LDL receptors LDLR/CD36/LOX-1 in endothelia cell functions involved in atherosclerosis

A high level of low-density lipoprotein cholesterol (LDL) is one of the most important risk factors for coronary artery disease (CAD), the leading cause of death worldwide. However, a low concentration of LDL may be protective. Genome-wide association studies revealed that variation in ADTRP gene increased the risk of CAD. In this study, we found that a low concentration of oxidized-LDL induced the expression of ADTRP. Further analyses showed that knockdown of the expression of LDL receptor genes LDLR, CD36, or LOX-1 significantly downregulated ADTRP expression, whereas overexpression of LDLR/CD36/LOX-1 markedly increased ADTRP expression through the NF-κB pathway. Like ADTRP, LDLR, CD36 and LOX-1 were all involved in endothelial cell (EC) functions relevant to the initiation of atherosclerosis. Downregulation of LDLR/CD36/LOX-1 promoted monocyte adhesion to ECs and transendothelial migration of monocytes by increasing expression of ICAM-1, VCAM-1, E-selectin and P-selectin, decreased EC proliferation and migration, and increased EC apoptosis, thereby promoting the initiation of atherosclerosis. Opposite effects were observed with the overexpression of ADTRP and LDLR/CD36/LOX-1 in ECs. Interestingly, through the NF-κB and AKT pathways, overexpression of ADTRP significantly upregulated the expression of LDLR, CD36, and LOX-1, and knockdown of ADTRP expression significantly downregulated the expression of LDLR, CD36, and LOX-1. These data suggest that ADTRP and LDL receptors LDLR/CD36/LOX-1 positively regulate each other, and form a positive regulatory loop that regulates endothelial cell functions, thereby providing a potential protective mechanism against atherosclerosis. Our findings provide a new molecular mechanism by which deregulation of ADTRP and LDLR/CD36/LOX-1 promote the development of atherosclerosis and CAD.     

LncRNA H19 rs4929984 Variant is Associated with Coronary Artery Disease Susceptibility in Han Chinese Female Population

Biochemical Genetics - Long non-coding RNAs (lncRNAs) have been reported to play an important role in cardiovascular diseases. The present study aimed to investigate the levels of lncRNA H19 in...     

HN1L promotes migration and invasion of breast cancer by up-regulating the expression of HMGB1

Recent reports showed that haematological and neurological expressed 1-like (HN1L) gene participated in tumorigenesis and tumour invasion. However, the expression and role of HN1L in breast cancer remain to be investigated. Here, bioinformatics, western blot and immunohistochemistry were used to detect the expression of HN1L in breast cancer. Wound healing, transwell assay, immunofluorescence assay and mass spectrum were used to explore the role and mechanism of HN1L on the migration and invasion of breast cancer, which was confirmed in vivo using a nude mice model. Results showed that HN1L was significantly over-expressed in breast cancer tissues, which was positively correlated with M metastasis of breast cancer patients. Silencing HN1L significantly inhibited the invasion and metastasis of breast cancer cells in vitro and lung metastasis in nude mice metastasis model of breast cancer. Mechanistically, HN1L interacted with HSPA9 and affected the expression of HMGB1, playing a key role in promoting the invasion and metastasis of breast cancer cell. These results suggested that HN1L was an appealing drug target for breast cancer.     

Superior japonica rice variety YJ144 with improved rice blast resistance,yield, and quality achieved using molecular design and multiple breeding strategies

Molecular Breeding - The stem color of young mung bean is a very useful tool in germplasm identification. Flowering time and plant height (PH) are known to be strongly correlated with crop adaption...