Expression,purification, and breast cancer cell inhibiting effect of recombinant human lactoferrin C-lobe

Lactoferrin (LTF), a multifunctional glycoprotein of the transferrin family mainly found in exotic secretions in mammals, is an important defense molecule against not only microbial invasion but also tumors. It folds into two globular domains (N- and C-lobes) each containing an iron-binding site. The cationic antimicrobial peptide in N-lobe is known to exert anti-tumor effect via a non-receptor-mediated pathway. However, whether LTF C-lobe also contributes to its anti-tumor activity remains to be investigated. In this study, a human LTF fragment (amino acid residues 343–682) covering the C-lobe was expressed with a histidine tag in E. coli and the purified polypeptide refolded through a series of buffer changing procedure. The resultant recombinant protein caused significant growth arrest of breast carcinoma cells MDA-MB-231 in a dose- and time-dependent manner, evidently via induction of apoptosis of the cell. Our data suggest a positive role for the C-lobe of human LTF in controlling tumors in vitro.     

老年冠心病患者血清Lp-PLA2、hs-CRP、IL-27及MMP-9水平与Gensini积分的相关性研究*

目的:探讨老年冠心病患者血清脂蛋白相关磷脂酶A2(Lp-PLA2)、高敏C反应蛋白(hs-CRP)、白细胞介素-27(IL-27)及基质金属蛋白酶-9(MMP-9)水平与Gensini积分的相关性。方法:选取2015年10月至2018年2月我院收治的冠心病患者142例为研究对象,将所有患者按照不同的冠心病类型分为不稳定型心绞痛(UAP)组54例、稳定型心绞痛(SAP)组40例和急性心肌梗死(AMI)组48例。同时根据患者Gensini积分将其分为轻度47例、中度51例和重度44例。比较不同冠心病类型、不同严重程度的Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分,并分析冠心病患者上述指标水平与Gensini积分的相关性。结果:AMI组患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分均高于UAP组和SAP组,且UAP组高于SAP组(P0.05)。重度患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平及Gensini积分均高于中度和轻度患者,且中度患者高于轻度患者(P0.05)。经Spearman相关性分析结果显示,冠心病患者Lp-PLA2、hs-CRP、IL-27、MMP-9水平与Gensini积分均呈正相关(P0.05)。结论:老年冠心病患者Lp-PLA2、hs-CRP、IL-27及MMP-9水平与患者冠状动脉病变Gensini积分均呈正相关。临床根据Lp-PLA2、hs-CRP、IL-27及MMP-9水平的变化,有助于评估老年冠心病患者的病情严重程度。     

Macular retinal thickness and flow density change by optical coherence tomography angiography after posterior scleral reinforcement

Optical coherence tomography angiography(Angio-OCT) has introduced a new non-invasive, quantitative method to assess superficial and deep capillary networks of the retina. In this study, we investigated macular retinal thickness and flow density change following posterior scleral reinforcement(PSR) surgery, using an RTVue XR Avanti Angio-OCT, in patients with pathological myopia. A total of 13 patients with pathological myopia were recruited and all patients completed the 6 months follow-up visit. Data from 22 eyes were used in this study. The mean age was 36.23±15.29 years, and 43%(n=6) were men.Spherical equivalent refractive error(SE) ranged from –8.0 to –24.0 D. Postoperative axial length, best-corrected visual acuity and SE did not change significantly at each follow-up, compared with pre-operative measures(P0.05). Postoperative flow density of superficial and deep retinal layers at each sector did not change significantly at each follow-up, compared with preoperative measures(P0.05). However, we found significant decrease in retinal thickness of parafovea-inferior sector after PSR surgery(P0.01), indicating potential relaxation of vitreofoveal traction after PSR surgery.     

Application of an efficient indole oxygenase system from Cupriavidus sp. SHE for indigo production

Bioprocess and Biosystems Engineering - Indigo, one of the most widely used dyes, is mainly produced by chemical processes, which generate amounts of pollutants and need high energy consumption....     

CPI-17-mediated contraction of vascular smooth muscle is essential for the development of hypertension in obese mice

Several factors have been implicated in obesity-related hypertension, but the genesis of the hypertension is largely unknown. In this study, we found a significantly upregulated expression of CPI-17(C-kinasepotentiated protein phosphatase 1 inhibitor of 17 kDa) and protein kinase C(PKC) isoforms in the vascular smooth muscles of high-fat diet(HFD)-fed obese mice. The obese wild-type mice showed a significant elevation of blood pressure and enhanced calcium-sensitized contraction of vascular smooth muscles. However, the obese CPI-17-deficient mice showed a normotensive blood pressure, and the calcium-sensitized contraction was consistently reduced. In addition, the mutant muscle displayed an abolished responsive force to a PKC activator and a 30%-50% reduction in both the initial peak force and sustained force in response to various G protein-coupled receptor(GPCR) agonists. Our observations showed that CPI-17-mediated calcium sensitization is mediated through a GPCR/PKC/CPI-17/MLCP/RLC signaling pathway. We therefore propose that the upregulation of CPI-17-mediated calcium-sensitized vasocontraction by obesity contributes to the development of obesity-related hypertension.