Chinese︱Feedback︱Save this page

Login︱Register

• Elaborating Academic Views 　　　　 • Exchanging Innovative Ideas
• Protecting Intellectual Properties 　　• Fast Sharing Science Papers

Sponsored by the Center for Science and Technology Development of the Ministry of Education
Supervised by Ministry of Education of the People's Republic of China

Home > Papers > Basic-Medicine

There are 181 papers published in subject: since this site started.

Results per page:

181 Total, 19 Pages | << First < Previous 7 8 9 10 11 12 13 Next > Last >>

Select Subject

All (8831)

Agronomy (158)

Animal Husbandry,... (64)

Aquatic Science (16)

Astronomy (36)

Aviation (22)

Basic Medicine (184)

Biology (504)

Chemical Engineering (103)

Chemistry (635)

Civil and Archite... (105)

Clinical Medicine (236)

Computer Science ... (924)

Dynamic and Elect... (121)

Earth Science (119)

Economics (67)

Education (31)

Electrics, Commun... (927)

Energy Science an... (67)

Engineering and T... (15)

Environmental Sci... (140)

Food Science and ... (63)

Forestry (36)

Hydraulic Enginee... (40)

Mechanics (240)

Metallurgical Eng... (32)

Mine Engineering ... (38)

Nuclear Science a... (21)

Pharmacy (98)

Physics (920)

Preventive Medici... (37)

Psychology (20)

Security Science ... (17)

Sports Science (6)

Surveying and Map... (15)

Textile Science a... (16)

Traditional Chine... (56)

Transportation En... (57)

Second-level Subject

Biomedical Engineering(43)
Human Anatomy(4)
Human Histology and Embry...(7)
Human Immunology(11)
Human Physiology(11)
Medical Biochemistry(13)
Medical Cell Biology(18)
Medical Genetics(5)
Medical Laboratorial Zoology(2)
Medical Microbiology(11)
Medical Parasitology(1)
Medical Statistics(2)
Other Subjects of Basic M...(3)
Pathology(29)
Pharmacology(22)
Radioactive Medicine(1)

Rank

Results per page:

181 Total, 19 Pages | << First < Previous 7 8 9 10 11 12 13 Next > Last >>

Alert Name:
Alerting to:
Authentication email will be sent to your email address in 24 hours
Frequency:
Email Message Format:	Plain text Graphical(HTML)

Complete the form below and we will recommend the selected titles to your friends on your behalf. * Indicates a required field.
Your name*:
Your email address*:
Recipient's name*:
Recipient's email address*:
(multiple recipient's names and email addresses should be separated with semicolons)
Your comments:	I thought you would find the page(s) useful.

Your name:
Your email address:
Recipient's name:
Recipient's email address:
(multiple recipient's names and email addresses should be separated with semicolons)
Your comments:	I thought you would find this page useful.

Disclaimer: This message was sent to your friend using the "Send it to a friend" facility on the Sciencepaper Online’ WWW site, http://www.paper.edu.cn/en. The Sciencepaper Online is not responsible for the content of this email, and anything said in this email does not necessarily reflect the Sciencepaper Online's views.


	1. Influences of Angiotensin I-Converting Enzyme and Endothelial Nitric Oxide Synthase Gene Polymorphisms on Hepatocellular Carcinoma Risks in China
	YUAN Fang,ZHANG Lushun,LI Hongyu,LIAO Miao,LV Meili※,ZHANG Chongjie※
	Basic Medicine 11 January 2013
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:Aims: Growing evidences suggested that angiotensin-converting enzyme (ACE) gene and endothelial nitric oxide synthase (eNOS) gene have been associated with the risk in a wide range of cancers. The objective of this study was to examine whether two DNA polymorphisms at the ACE insertion/deletion (I/D) and NOS intron 4 variable number of tandem repeats (4a/4b) have been linked with the risk of developing hepatocellular carcinoma (HCC) in a Chinese population. Methods: Polymorphisms of ACE I/D and eNOS 4a/4b were genotyped in 293 HCC patients and 384 healthy control subjects using the polymerase chain reaction (PCR). Results: Frequencies of D allele and DD genotype in ACE gene of HCC patients were significantly different from that in healthy controls. However, no differences were observed in eNOS 4a/4b genotype and allele frequencies between the HCC and controls. Conclusions: These findings indicate that the ACE I/D polymorphism may play a role in HCC progression.
	TO cite this article:YUAN Fang,ZHANG Lushun,LI Hongyu, et al. Influences of Angiotensin I-Converting Enzyme and Endothelial Nitric Oxide Synthase Gene Polymorphisms on Hepatocellular Carcinoma Risks in China[OL].[11 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4511647


	2. Interleukin-6 Regulates Voltage-Gated Sodium channels in a Time- and Dose-Dependent Manner in Rat Cortical Neurons
	SHENG Jiangtao,GAO fenfei,CHEN Weiqiang,DENG Lijuan,GUO Jingfang,WANG Gefei,DAI Jianping,HUANG Zhengyi,SHI Ganggang,LI Kangsheng
	Basic Medicine 10 January 2013
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:The cytokine interleukin-6 (IL-6) is expressed at elevated levels within the CNS in many neurological disorders and may contribute to the histopathological, pathophysiological, and cognitive deficits associated with such disorders. However, the effects of chronic IL-6 exposure on neuronal function in the CNS are largely unknown. A voltage-gated Na+ channel is essential for the excitability and electrical properties of neurons. Therefore, using patch-clamp recording we investigated the effects of chronic IL-6 exposure on voltage-gated Na+ channels. Our results showed that IL-6 suppressed Na+ currents through its receptor in a time- and dose-dependent manner, but did not alter the voltage-dependent activation and inactivation. The spike amplitude was also inhibited by IL-6 in the doses that decreased Na+ currents. The present data reveals chronic exposure to elevated levels of IL-6, such as occurs in various neurological diseases, produces inhibition in the voltage-gated Na+ channels without the alterations in single-channel characteristics. The results support the hypothesis that chronic IL-6 exposure can disrupt normal CNS function and thereby contribute to the pathophysiology associated with many neurological diseases.
	TO cite this article:SHENG Jiangtao,GAO fenfei,CHEN Weiqiang, et al. Interleukin-6 Regulates Voltage-Gated Sodium channels in a Time- and Dose-Dependent Manner in Rat Cortical Neurons[OL].[10 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4513574

Saved Papers

Saved Papers


	3. BH3-only proteins in myocardial ischemia: poison or meal?
	Xin Hong,Bao Guangzhi,Wang Minjun,Zhu Yizhun
	Basic Medicine 10 January 2013
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:Loss of myocardial cells via apoptosis has been characterized in ischemic heart disease. BH3-only proteins of Bcl-2 family are essential initiators of apoptosis during heart ischemia and hypoxia. Multiple BH3-only proteins, such as Bnip3, Nix, Puma, Bid and Bad, have been upregulated and shown to contribute to the cell death via apoptosis pathway during myocardial ischemia. Autophagic flux is activated in ischemic heart disease due to the short supply of nutrients. BH3-only proteins also control the initiation of autophagy which is another important pathway regulating cell survival and death. A novel BH3-only protein, beclin-1, plays a critical role in autophagy. Autophagy functions as cardioprotective pathway to overcome the stress through against apoptosis, but prolonged activation can result in cell death. Here we review the roles of BH-3 only proteins in myocardial ischemia.
	TO cite this article:Xin Hong,Bao Guangzhi,Wang Minjun, et al. BH3-only proteins in myocardial ischemia: poison or meal?[OL].[10 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4513724


	4. Induction of cytopathic effect and cytokines in coxsackievirus B3-infected murine astrocytes
	ZENG Jun,WANG Gefei,LI Weizhong,CHEN Xiaoxuan,XIN Gang,ZHANG Dangui,JIANG Zhiwu,LI Kangsheng
	Basic Medicine 09 January 2013
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:Coxsackievirus commonly infects children and occasionally causes severe meningitis and/or encephalitis in the newborn. The underlying mechanism(s) behind the central nervous system pathology is poorly defined. It is hypothesized that astrocytes may be involved in inflammatory response induced by CVB3 infection. Here we discuss this hypothesis in the context of CVB3 infection and associated inflammatory response in primary mouse astrocytes. CVB3 infected and replicated in astrocytes, with release of infectious virus particles. CVB3 induced cytopathic effect (CPE) and production of proinflammatory cytokines IL-1β, TNF-α, IL-6, and chemokine CXCL10 from astrocytes. These data suggest that direct astrocyte damage and cytokines induction could be a mechanism of virus-induced neuropathology.
	TO cite this article:ZENG Jun,WANG Gefei,LI Weizhong, et al. Induction of cytopathic effect and cytokines in coxsackievirus B3-infected murine astrocytes[OL].[ 9 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4513097


	5. Des-γ-carboxy prothrombin increase the proliferation and migration of human vascular endothelial cells
	Li Yuanyuan,Yuan Yi,Qu Xianjun
	Basic Medicine 07 January 2013
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:Des-γ-carboxy prothrombin (DCP) is an aberrant prothrombin produced by hepatocellular carcinoma (HCC) cells. High level of DCP in serum and tissue is considered to show the malignant potential of HCC. In this paper, we described the proliferation and migration of human vascular endothelial cells by DCP. MTT assay showed that DCP could significantly stimulate HUVEC ECV304 cell proliferation with dose and time dependent manner. A continuous rapid migration of ECV304 cells was seen after treatment with DCP as measured by the scratch wound assay. A continuous rapid invasive activity as evaluated by transwell chamber assay also showed that DCP increased endothelial cells migration through the reconstituted extracellular matrix. The tube formation of vascular endothelial cells on 3-D Matrigel showed an increase of branch points of ECV304 cells exposed to DCP. The expressions of vascular endothelial cell growth-related angiogenic factors and matrix metalloproteinase were examined by Western blotting assay. DCP significantly stimulated the expression levels of epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and matrix metalloproteinase (MMP)-2 (latent and active). Together, these results suggest that DCP is a vascular endothelial growth factor. DCP may play a crucial role of mitogenic and migrative activities in angiogenesis in the development of HCC.
	TO cite this article:Li Yuanyuan,Yuan Yi,Qu Xianjun. Des-γ-carboxy prothrombin increase the proliferation and migration of human vascular endothelial cells[OL].[ 7 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4511380


	6. Selective alpha 1- and alpha 2-adrenoreceptor agonist on galanin expression in cultured dorsal root ganglion neurons
	LIU Zhen,LI Zhenzhong
	Basic Medicine 27 December 2012
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:In this paper, the effects of selective alpha 1- or alpha 2-adrenoreceptor agonist on galanin (Gal) expression in dorsal root ganglion (DRG) neurons were investigated. Alpha-adrenoreceptors are expressed in sympathetic neurons. Interestingly, functional alpha-adrenoreceptors are also expressed in DRG primary sensory neurons and regulate neurogenic inflammation and nociceptive responses. Gal is involved in inflammation and nociception. Whether selective alpha 1- or alpha 2-adrenoreceptor agonist affects Gal expression in DRG neurons is still unclear. In the present study, primary cultured DRG neurons were used to determine effects of alpha 1-adrenoreceptor agonist phenylephedrine (10-5 mol/L) or alpha 2-adrenoreceptor agonist clonidine (10-5 mol/L) on Gal and its mRNA expression. The results showed that alpha 1-adrenoreceptor agonist phenylephedrine promoted Gal mRNA and Gal peptide expression after 4 days incubation. Alpha 2-adrenoreceptor agonist clonidine did not have significant effect on Gal and its mRNA expression. These results imply that activation of alpha 1-adrenoreceptor, but not alpha 2-adrenoreceptor, was involved in Gal expression. These effects may be relevant to noradrenergic pain modulation.
	TO cite this article:LIU Zhen,LI Zhenzhong. Selective alpha 1- and alpha 2-adrenoreceptor agonist on galanin expression in cultured dorsal root ganglion neurons[OL].[27 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4509467


	7. Exposure of selective beta 1- and beta 2-adrenoreceptor agonist or antagonist on galanin expression in sympathetic neurons in vitro
	LIU Zhen,LI Zhenzhong
	Basic Medicine 27 December 2012
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:In this paper, the possible regulation of selective beta 1- and beta 2-adrenoreceptor agonists or antagonists on galanin (Gal) expression in organotypically cultured superior cervical ganglion (SCG) neurons was evaluated. Gal, a 29-amino-acid neuropeptide in most species (30-amino-acid in human), is expressed in SCG neurons and plays a trophic role in the adult animal and acts as an inhibitory modulator of cholinergic and noradrenergic neurotransmission. Whether beta-adrenoreceptors are involved in modulation on Gal expression in SCG neurons remains unknown. In the present study, after acute (4 hours) or chronic (4 days) incubation with these agonists or antagonists, the expression of Gal and its mRNA were estimated by double fluorescent labeling and real time-PCR, respectively. The results showed that the amount of Gal and Gal mRNA expression in organotypically cultured SCG neurons decreased significantly after chronic stimulation with beta 2-adrenoreceptor agonist salbutamol as compared with that in control group. Beta 1-adrenoreceptor agonist denopamine, antagonist metoprolol, and beta 2-adrenoreceptor antagonist ICI118551 chronic stimulation did not have effects on Gal and Gal mRNA expression. The expression of Gal and its mRNA did not significantly change after acute exposure of these agents. These data implicated that Gal may be regulated by chronic activation beta 2-adrenoreceptors, but not beta 1-adrenoreceptors in sympathetic neurons.
	TO cite this article:LIU Zhen,LI Zhenzhong. Exposure of selective beta 1- and beta 2-adrenoreceptor agonist or antagonist on galanin expression in sympathetic neurons in vitro[OL].[27 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4509464


	8. microRNA-133b regulates MMP9 and inhibits migration and invasion in human colorectal carcinoma cells
	Hu Gui,Chen Daojin,Li Xiaorong
	Basic Medicine 19 December 2012
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:Objective: To explore the effect and mechanism of microRNA-133b in the regulation of colorectal cancer cell migration and invasion. Methods: To construct eukaryotic expression vector of microRNA-133b and stable tansfection into human colorectal cancer cell SW-620; wound-healing assay and Matrigel invasion assay was performed to determine the effect of microRNA-133b on in vitro SW-620 migration and invasion; The possible target of miR-133b were predicted by a web-based computer program and verified by Dual-luciferase assay system. Results: The expression of miR-133b was dramatically greater in SW-620-133b compared with SW-620 (P＜0.05); In sw-620 cells, expression of microRNA-133b significantly inhibited tumor cell migration and invasion(P＜0.05); MMP9 was the candidate target of microRNA-133b and verified by Dual-luciferase assay. Conclusions: microRNA-133b suppresses tumor cell migration and invasion through modulation of the MMP9 signaling pathway.
	TO cite this article:Hu Gui,Chen Daojin,Li Xiaorong. microRNA-133b regulates MMP9 and inhibits migration and invasion in human colorectal carcinoma cells[OL].[19 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4506084


	9. Transplantation of parthenogenetic embryonic stem cells ameliorates cardiac dysfunction and remodeling after myocardial infarction
	Liu Yi,Ye Xiaoying,Mao Lina,Cheng Zhaokang,Yao Xinpeng,Jia Xiaohua,Mao Duo,Ou Lailiang,Li Zongjin,Che Yongzhe,Liu Na,Liu Lin,Kong Deling
	Basic Medicine 14 December 2012
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:Aims: Parthenogenetic embryonic stem cells (pESCs) are derived from artificially activated oocytes without fertilization and therefore raise minimal ethical concerns and may serve as attractive candidates for regenerative medicine. We thought to investigate whether pESCs can repair myocardial infarction (MI). Methods and Results: Mice (n=89) survived coronary ligation randomly received undifferentiated pESCs, ESCs, or saline. Sham-operated mice received no treatment (n=21). After 7 days, pESCs transplantation promoted pro-angiogenic factors secretion and reduced infiltrated leukocytes. pESCs-treated hearts, superior to ESC group, showed prevented cardiac remodeling and enhanced angiogenesis in and 30 days post MI. Heart contractile function was notably improved by administration of pESCs by 30 days. Moreover, tissues regenerated from the engrafted pESCs in the infarcted myocardium were positive for cardiomyocyte, endothelial cell and smooth muscle cell markers. Furthermore, teratoma fomation appeared in ESCs-treated mice in high proportion (6/34), but surprisingly not found in pESCs-treated mice (0/30) by 30 days. Conclusions: Cardiac dysfunction and adverse ventricular remodeling post MI were attenuated by pESCs transplantation, which may represent an effective and relatively safer strategy for autologous cell therapy in females.
	TO cite this article:Liu Yi,Ye Xiaoying,Mao Lina, et al. Transplantation of parthenogenetic embryonic stem cells ameliorates cardiac dysfunction and remodeling after myocardial infarction[OL].[14 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4504322


	10. Pseudomonas aeruginosa isolates of distinct sub-genotypes exhibit similar potential of antimicrobial resistance by drugs exposure
	LIU Zhenhong,XU Yan,LIU Guirong,LIU Shulin
	Basic Medicine 11 December 2012
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (0 B)

	Abstract:Pseudomonas aeruginosa, a wide-spread opportunistic pathogen, often complicates clinical treatments due to its resistance to a large variety of antimicrobials, especially in immune compromised patients, occasionally leading to death. However, the resistance to antimicrobials varies greatly among the P. aeruginosa isolates, which raises a question on whether some sub-lineages of P. aeruginosa might have greater potential to develop antimicrobial resistance than others. To explore this question, we divided 160 P. aeruginosa isolates collected from cities of USA and China into distinct genotypes using I-CeuI, a special endonuclease that had previously been proven to reveal phylogenetic relationships among bacteria reliably due to the highly conserved 26-bp recognition sequence. We resolved 10 genotypes by I-CeuI analysis and further divided them into 82 sub-genotypes by endonuclease cleavage with SpeI. Eight of the 10 genotypes contained both multi-drug resistant (MDR) and less resistant isolates based on comparisons of their antimicrobial resistance profiles (ARPs). When the less resistant or susceptible isolates from different genotypes were exposed to eight individual antimicrobials, they showed similar potential to become resistant with minor exceptions. This is to our knowledge the first report to examine correlations between phylogenetic sub-lineages of P. aeruginosa and their potential to become resistant to antimicrobials. This study further alerts the importance and urgency of antimicrobial abuse control.
	TO cite this article:LIU Zhenhong,XU Yan,LIU Guirong, et al. Pseudomonas aeruginosa isolates of distinct sub-genotypes exhibit similar potential of antimicrobial resistance by drugs exposure[OL].[11 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4501720

	Check out RSS, or use RSS reader to subscribe this item