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981.
目的:本研究通过建立糖尿病大鼠动物模型,观察海藻溴酚化合物A、B对糖尿病大鼠机体抗氧化水平的影响。方法:采用STZ注射法制作糖尿病(DM)大鼠模型,随机分为空白对照组、糖尿病模型组、化合物A低剂量组及高剂量组、化合物B低剂量组及高剂量组,灌胃给药12周。12周末处死大鼠,测肾匀浆中谷胱甘肽过氧物酶(GSH-Px)的活力及丙二醛(MDA)的含量;并采用透射电镜观察大鼠肾组织的病理改变。结果:与空白对照组相比,糖尿病模型组肾组织匀浆中GSH-Px活力下降,MDA含量升高,差异有统计学意义(P<0.05)。各干预组中GSH-Px的活力较糖尿病模型组有升高的趋势,MDA含量有下降趋势。电镜下各干预组肾小球及肾小管病变较糖尿病组减轻,且高剂量组优于低剂量组。结论:溴酚化合物A、B能提高糖尿病大鼠机体抗氧化水平,并能一定程度的改善肾脏病理改化,但其具体机制有待进一步探讨。 相似文献
982.
p75NTR is a low-affinity nerve growth factor receptor, which promotes cell proliferation as a positive modulator of high-affinity
receptor TrkA, as well as binds with cell ligands to induce apoptosis and mediate death signals. To analyze the regulatory
mechanisms of p75NTR, the present study utilized a new membrane yeast two-hybrid system to screen a human fetal brain cDNA
library. Results identified BFAR, a novel protein that interacts with p75NTR. Interaction specificity was verified by membrane
yeast two-hybrid co-transformation assays, in vitro GST pull-down assays, and in vitro co-immunoprecipitation assays. The fluorescent subcellular localization assay revealed that the two proteins co-localized
within the cytoplasm. BFAR overexpression in PC-12 and HEK293T cells inhibited the NFκB and JNK signaling pathway, as determined
with the luciferase test. Co-transfected p75NTR and BFAR in HEK293T or PC-12 cells, respectively, increased the percentage
of cells in the G2/M phase, decreased the number of S-phase cells, and did not change the number of G0/G1-phase cells. 相似文献
983.
984.
Fengzhi You Kaiming Huo Ruili Wang Dongmei Xu Jie Deng Ying Wei Fenglian Shi Hongyang Liu Guomei Cheng Zhan Zhang Ping Yang Tao Sun Xiaoyang Wang Bo Jacobsson Changlian Zhu 《PloS one》2012,7(10)
Background
Maternal deaths occur mostly in developing countries and the majority of them are preventable. This study analyzes changes in maternal mortality and related causes in Henan Province, China, between 1996 and 2009, in an attempt to provide a reliable basis for introducing effective interventions to reduce the maternal mortality ratio (MMR), part of the fifth Millennium Development Goal.Methods and Findings
This population-based maternal mortality survey in Henan Province was carried out from 1996 to 2009. Basic information was obtained from the health care network for women and children and the vital statistics system, from specially trained monitoring personnel in 25 selected monitoring sites and by household survey in each case of maternal death. This data was subsequently reported to the Henan Provincial Maternal and Child Healthcare Hospital. The total MMR in Henan Province declined by 78.4%, from 80.1 per 100 000 live births in 1996 to 17.3 per 100 000 live births in 2009. The decline was more pronounced in rural than in urban areas. The most common causes of maternal death during this period were obstetric hemorrhage (43.8%), pregnancy-induced hypertension (15.8%), amniotic fluid embolism (13.9%) and heart disease (8.0%). The MMR was higher in rural areas with lower income, less education and poorer health care.Conclusion
There was a remarkable decrease in the MMR in Henan Province between 1996 and 2009 mainly in the rural areas and MMR due to direct obstetric causes such as obstetric hemorrhage. This study indicates that improving the health care network for women, training of obstetric staff at basic-level units, promoting maternal education, and increasing household income are important interventional strategies to reduce the MMR further. 相似文献985.
Guan X Yabuuchi A Huo H Ginsberg E Racowsky C Daley GQ Lerou PH 《Stem cell research》2012,8(3):410-415
Deficiency of the nuclear factor-kappa-B essential modulator (NEMO) is a rare X-linked disorder that presents in boys as hypohydrotic ectodermal dysplasia with immunodeficiency due to defective nuclear factor-κB activation. Here we report on the generation of 2 human embryonic stem cell lines from discarded in vitro fertilization (IVF) embryos ascertained via preimplantation genetic diagnosis. We have derived two human embryonic stem cell lines that carry a T458G hypomorphic mutation in exon 4 of the NEMO (or IKBKG) gene. One of the lines is diploid male; the other is diploid female but has clonally inactivated the X-chromosome that harbors the wild-type IKBKG gene. We show that both lines are pluripotent, have the capacity to differentiate into hematopoietic progenitors, and have defective inhibitor of nuclear factor kappa-B kinase activity. These NEMO deficiency hES cell lines provide an unlimited source for differentiated cell types and may serve as a unique tool to study NEMO deficiency and potentially lead to the development of new therapies for this disease. 相似文献
986.
Zhang Y Su L Manuzzi D de los Monteros HV Jia W Huo D Hou C Lei Y 《Biosensors & bioelectronics》2012,31(1):426-432
In the pursuit of more economical electrocatalysts for non-enzymatic glucose sensors, one-dimensional Cu nanowires (Cu NWs) with uniform size distribution and a large aspect ratio (>200) were synthesized by a facile, scalable, wet-chemistry approach. The morphology, crystallinity, and surface property of the as-prepared Cu NWs were examined by SEM, XRD, and XPS, respectively. The electrochemical property of Cu NWs for glucose electrooxidation was thoroughly investigated by cyclic voltammetry. In the amperometric detection of glucose, the Cu NWs modified glassy carbon electrode exhibited an extraordinary limit of detection as low as 35 nM and a wide dynamic range with excellent sensitivity of 420.3 μA cm(-2) mM(-1), which was more than 10,000 times higher than that of the control electrode without Cu NWs. The performance of the developed glucose sensor was also independent to oxygen concentration and free from chloride poisoning. Furthermore, the interference from uric acid, ascorbic acid, acetaminophen, fructose, and sucrose at the level of their physiological concentration were insignificant, indicating excellent selectivity. Finally, good accuracy and high precision for the quantification of glucose concentration in human serum samples implicate the applicability of Cu NWs in sensitive and selective non-enzymatic glucose detection. 相似文献
987.
Environmental concerns and an increasing global energy demand have spurred scientific research and political action to deliver large-scale production of liquid biofuels. Current biofuel processes and developing approaches have focused on closing the carbon cycle by biological fixation of atmospheric carbon dioxide and conversion of biomass to fuels. To date, these processes have relied on fertilizer produced by the energy-intensive Haber-Bosch process, and have not addressed the global nitrogen cycle and its environmental implications. Recent developments to convert protein to fuel and ammonia may begin to address these problems. In this scheme, recycling ammonia to either plant or algal feedstocks reduces the demand for synthetic fertilizer supplementation. Further development of this technology will realize its advantages of high carbon fixation rates, inexpensive and simple feedstock processing, in addition to reduced fertilizer requirements. 相似文献
988.
L Du H Yang Y Huo H Wei Y Xu Y Wei R Huang 《World journal of microbiology & biotechnology》2012,28(9):2871-2878
Sucrose phosphorylase, an important enzyme mainly involved in the generic starch and sucrose pathways, has now caught the attention of researchers due to its transglycosylation activity. A novel sucrose phosphorylase, unspase, has been isolated, and its transglycosylation properties were characterized. Compared with Bisp, the sucrose phosphorylase from Bifidobacterium adolescentis, unspase had two deleted regions in its C: -terminal. These deleted regions were probably equivalent to the important five-stranded anti-parallel β-sheet domain in sucrose phosphorylase. Unspase has a k(m) of 21.12?mM, a V(max) of 69.24?μmol?min(-1)?mg(-1) and a k(cat) of 31.19?s(-1) with sucrose as substrate. In 3-(N-morpholino) propanesulfonic acid (MOPS) buffer, unspase transferred the glycosyl moiety to L: -arabinose, D: -fructose and L: -sorbose. Much to our surprise, unspase can catalyze the transglycosylation in which a glycosyl moiety was transferred to L: -arabinose in the presence of phosphate, which is an interesting exception to the generally accepted fact that transglycosylation can only occur under the condition of phosphate absence. The final yield of the transglycosylation product (37.9?%) in phosphate buffer was even higher than that (5.8?%) in MOPS buffer. This is a novel phenomenon that a sucrose phosphorylase can catalyze a transglycosylation reaction in the presence of phosphate. 相似文献
989.
990.
Ehsani S Salehzadeh A Huo H Reginold W Pocanschi CL Ren H Wang H So K Sato C Mehrabian M Strome R Trimble WS Hazrati LN Rogaeva E Westaway D Carlson GA Schmitt-Ulms G 《Journal of molecular biology》2012,422(4):556-574
We recently documented the co-purification of members of the LIV-1 subfamily of ZIP (Zrt-, Irt-like Protein) zinc transporters (LZTs) with the cellular prion protein (PrP(C)) and, subsequently, established that the prion gene family descended from an ancestral LZT gene. Here, we begin to address whether the study of LZTs can shed light on the biology of prion proteins in health and disease. Starting from an observation of an abnormal LZT immunoreactive band in prion-infected mice, subsequent cell biological analyses uncovered a surprisingly coordinated biology of ZIP10 (an LZT member) and prion proteins that involves alterations to N-glycosylation and endoproteolysis in response to manipulations to the extracellular divalent cation milieu. Starving cells of manganese or zinc, but not copper, causes shedding of the N1 fragment of PrP(C) and of the ectodomain of ZIP10. For ZIP10, this posttranslational biology is influenced by an interaction between its PrP-like ectodomain and a conserved metal coordination site within its C-terminal multi-spanning transmembrane domain. The transition metal starvation-induced cleavage of ZIP10 can be differentiated by an immature N-glycosylation signature from a constitutive cleavage targeting the same site. Data from this work provide a first glimpse into a hitherto neglected molecular biology that ties PrP to its LZT cousins and suggest that manganese or zinc starvation may contribute to the etiology of prion disease in mice. 相似文献