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Testosterone and metabolic syndrome

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Asian Journal of Andrology 2015年第2期17卷 192-196,I0006页

作者： Glenn R Cunningham departments of Medicine and Molecular and cellular biology Baylor College of Medicine Baylor St. Luke's Medical Center 6624 Fannin Suite 1180 Houston TX 77030 USA.

Controversies surround the usefulness of identifying patients with the metabolic syndrome （MetS）. Many of the components are accepted risk factors for cardiovascular disease （CVD）. Although the MetS as defined includes many men with insulin resistance, insulin resistance is not universal. The low total testosterone （TT） and sex hormone binding globulin （SHBG） levels in these men are best explained by the hyperinsulinism and increased inflammatory cytokines that accompany obesity and increased waist circumference. It is informative that low SHBG levels predict future development of the MetS. Evidence is strong relating low TT levels to CVD in men with and without the MetS; however, the relationship may not be causal. The recommendations of the International Diabetes Federation for managing the MetS include cardiovascular risk assessment, lifestyle changes in diet, exercise, weight reduction and treatment of individual components of the MetS. Unfortunately, it is uncommon to see patients with the MetS lose and maintain a 10% weight loss. Recent reports showing testosterone treatment induced dramatic changes in weight, waist circumference, insulin sensitivity, hemoglobin Alc levels and improvements in each of the components of the MetS are intriguing. While some observational studies have reported that testosterone replacement therapy increases cardiovascular events, the Food and Drug Administration in the United States has reviewed these reports and found them to be seriously flawed. Large, randomized, placebo-controlled trials are needed to provide more definitive data regarding the efficacy and safety of this treatment in middle and older men with the MetS and low TT levels.

关键词： cardiovascular risk metabolic syndrome sex hormone binding globulin testosterone testosterone replacement therapy

Protein Kinase Activity Changes in the Aging Brain

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Biomedical and Environmental Sciences 1991年第1期4卷 173-181页

作者： MICHAE LR.PISANO HOAU-YAN WANG EITAN FRIEDMAN departments of Psychiatry and pharmacology Medical College of PennsylvaniaDepartments of Psychiatry and Pharmacology Medical College of PennsylvaniaDepartments of Psychiatry and Pharmacology Medical College of Pennsylvania Philadelphia Pennsylvania 19129 Philadelphia Pennsylvania 19129Philadelphia Pennsylvania 19129 To whom correspondence should be addressed

The aging process in mammals is correlated with changes in psychomotor performance, cognitive function, and ability to adapt to stress (Montgomery et al., 1982; Lorens et al., 1990). These changes may be related to alterations in neuronal tissue that occur during the aging process. The normal aging process may be conceived of as the neuronal cell’s increasing inability to maintain normal cellular function which ultimately results in a number of morphological and biochemical changes. Morphologically, there is a loss of neuronal cells with increasing age (Brizzee and

关键词： Protein Kinase Activity Changes in the Aging Brain

Inducible heat shock protein 70 kD and inducible nitric oxide synthase in hemorrhage/resuscitation-induced injury

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Cell Research 2004年第6期14卷 450-459页

作者： Juliann G.KIANG Department of cellular Injury Walter Reed Army Institute of Research Silver Spring MD 20910-7500 USA. departments of Medicine and of pharmacology Uniformed Services University of The Health Sciences Bethesda MD 20814-4799

Inducible heat shock protein 70 kD (HSP-70i) has been shown to protect cells, tissues, and organs from harmful assaults in in vivo and in vitro experimental models. Hemorrhagic shock followed by resuscitation is the principal cause of death among trauma patients and soldiers in the battlefield. Although the underlying mechanisms are still not fully understood, it has been shown that nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) over expression play important roles in producing injury caused by hemorrhagic shock including increases in polymorpho nuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B4 (LTB4) generation. Moreover, transcription factors responsible for iNOS expression are also altered by hemorrhage and resuscitation. It has been evident that either up-regulation of HSP-70i or down-regulation of iNOS can limit tissue injury caused by ischemia/reperfusion or hemorrhage/resuscitation. In our laboratory, geldanamycin, a member of ansamycin famil

关键词： inducible HSP-70 iNOS eNOS hemorrhage caspase-3 ATP KLF6 resuscitation

Edaravone protects PC12 cells from ischemic-like injury via attenuating the damage to mitochondria

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2006年第9期7卷 749-756页

作者： SONG Ying LI Meng LI Ji-cheng WEI Er-qing Department of cellular biology School of Medicine Zhejiang University Hangzhou 310031 China Department of pharmacology School of Medicine Zhejiang University Hangzhou 310031 China

Background： Edaravone had been validated to effectively protect against ischemic injuries. In this study, we investigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of Bcl-2/Bax protein expression and recovering from damage to mitochondria after OGD （oxygen-glucose deprivation）-reperfusion. Methods： Viability of PC 12 cells which were injured at different time of OGD injury, was quantified by measuring MTT （2-（4,5-dimethylthia-zol-2-yl）-2,5-diphenyltetrazolium bromide） staining. In addition, PC 12 cells＇ viability was also quantified after their preincubation in different concentration of edaravone for 30 min followed by （OGD）. Furthermore, apoptotic population of PC 12 cells that reinsulted from OGD-reperfusion with or without preincubation with edaravone was determined by flow cytometer analysis, electron microscope and Hoechst/Pl staining. Finally, change of Bcl-2/Bax protein expression was detected by Western blot. Results：（1） The viability of PC12 cells decreased with time （1-12 h） after OGD. We regarded the model of OGD 2 h, then replacing DMEM （Dulbecco＇s Modified Eagle＇s Medium） for another 24 h as an OGD-reperfusion in this research. Furthermore, most PC 12 cells were in the state of apoptosis after OGD-reperfusion. （2） The viability of PC 12 cells preincubated with edaravone at high concentrations （1, 0.1, 0.01 μmol/L） increased significantly with edaravone protecting PC 12 cells from apoptosis after OGD-reperfusion injury. （3） Furthermore, edaravone attenuates the damage of OGD-reperfusion on mitochondria and regulated Bcl-2/Bax protein imbalance expression after OGD-reperfusion. Conclusion： Neuroprotective effects of edaravone on ischemic or other brain injuries may be partly mediated through inhibition of Bcl-2/Bax apoptotic pathways by recovering from the damage of mitochondria.

关键词： Edaravone lschemia Apoptosis Rat pheochromocytoma (PC 12) cells Mitochondria Bax Bcl-2 Oxygen-glucose deprivation (OGD)

Mutant KRAS as a critical determinant of the therapeutic response of colorectal cancer

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Genes & Diseases 2015年第1期2卷 4-12页

作者： Kyle Knickelbein Lin Zhang University of Pittsburgh Cancer Institute Departments of Pharmacology&Chemical BiologyUniversity of Pittsburgh School of MedicinePittsburghPA 15213USA

Mutations in the KRAS oncogene represent one of the most prevalent genetic alterations in colorectal cancer(CRC),the third leading cause of cancer-related death in the *** addition to their well-characterized function in driving tumor progression,KRAS mutations have been recognized as a critical determinant of the therapeutic response of *** studies demonstrate that KRAS-mutant tumors are intrinsically insensitive to clinically-used epidermal growth factor receptor(EGFR)targeting antibodies,including cetuximab and *** resistance to the anti-EGFR therapy was found to be associated with enrichment of KRAS-mutant tumor ***,the underlying molecular mechanism of mutant-KRAS-mediated therapeutic resistance has remained *** intensive efforts,directly targeting mutant KRAS has been largely *** review summarizes the recent advances in understanding the biological function of KRAS mutations in determining the therapeutic response of CRC,highlighting several recently developed agents and strategies for targeting mutant KRAS,such as synthetic lethal interactions.

关键词： Colorectal cancer EGFR KRAS Synthetic lethality Targeted therapy

Extracellular nucleotides and adenosine regulate microglial motility and their role in cerebral ischemia

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Acta Pharmaceutica Sinica B 2013年第4期3卷 205-212页

作者： Zehui Li Wei Li Qin Li Minke Tang Department of Molecular and cellular biology North Dakota State UniversityFargo 58102USA Department of pharmacology Beijing University of Chinese MedicineBeijing 100102China

Acting as immune cells,microglia play a surveillance role in central nervous system injuries and *** nucleotides such as ATP and UTP,and adenosine are reported to regulate the response of microglia to insults and *** activates P2X receptors and triggers several signal cascades,resulting in the activation of ***,UDP binding to the P2Y6 receptor induces phagocytosis by microglia,while adenosine regulates process retraction in *** and adenosine leak out from dead cells and act on their corresponding receptors on microglia,stimulating the release of inflammatory factors and cytokines to provide both neurotrophic and neurotoxic *** this article,we review the regulatory effects of nucleotides and adenosine on microglial chemotaxis,phagocytosis,and process retraction,and summarize the activities of these cells after ischemia.

关键词： Microglia Nucleotides and adenosine signals P2 and adenosine receptors Chemotaxis Phagocytosis Process retraction Cerebral ischemia

Neural regulation of CNS angiogenesis during development

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Frontiers in biology 2015年第1期10卷 61-73页

作者： Shang MA Zhen HUANG departments of Neurology and Neuroscience University of Wisconsin-Madison Madison WI 53706 USA Graduate Program in cellular and Molecular biology University of Wisconsin-Madison Madison WI 53706 USA

Vertebrates have evolved a powerful vascular system that involves close interactions between blood vessels and target tissues. Vascular biology had been mostly focused on the study of blood vessels for decades, which has generated large bodies of knowledge on vascular cell development, function and pathology. We argue that the prime time has arrived for vascular research on vessel-tissue interactions, especially target tissue regulation of vessel development. The central nervous system （CNS） requires a highly efficient vascular system for oxygen and nutrient transport as well as waste disposal. Therefore, neurovascular interaction is an excellent entry point to understanding target tissue regulation of blood vessel development. In this review, we summarize signaling pathways that transmit information from neural cells to blood vessels during development and the mechanisms by which they regulate each step of CNS angiogenesis. We also review important mechanisms of neural regulation of blood-brain barrier establishment and maturation, highlighting different functions of neural progenitor cells and pericytes. Finally, we evaluate potential contribution of malfunctioning neurovascular signaling to the development of brain vascular diseases and discuss how neurovascular interactions could be involved in brain tumor angiogenesis.

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Genetic Encoding of a Photocaged Glutamate for Optical Control of Protein Functions

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CCS Chemistry 2023年第6期5卷 1301-1307页

作者： Xinyu Ling Yi Zuo Heqi Chen Dezhong Ji Jingjing Wang Liying Chang Tao Liu State Key Laboratory of Natural and Biomimetic Drugs Chemical Biology CenterDepartment of Molecular and Cellular PharmacologyPharmaceutical SciencesPeking UniversityHaidian DistrictBeijing 100191

Genetic encoding of photocaged noncanonical amino acids provides a powerful tool to study protein functions through optical control but is not yet available for acidic amino ***,we report the first site-specific genetic encoding of a photocaged glutamate,4-methoxy-7-nitroindolinyl caged glutamate(MNI-Glu),into recombinant proteins via an expanded genetic code through evolved EcLeuRS/tRNA *** two enzymes as examples,we demonstrate that substituting the conserved-active-site glutamate of a secreted alkaline phosphatase and a protease HRV3C to MNI-Glu allows photoregulatory control of their enzymatic *** approach is an important addition to the photocaged noncanonical amino-acid toolbox and provides a general method to photocontrol protein activity based on caging a critical glutamate.

关键词： noncanonical amino acid genetic code expansion MNI-Glu photocaged glutamate optical control

Targeting proliferation and survival pathways in head and neck cancer for therapeutic benefit

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Chinese Journal of Cancer 2012年第7期31卷 319-326页

作者： Daniel E. Johnson departments of Medicine and pharmacology & Chemical biology University of Pittsburgh Cancer InstitutePittsburgh Pennsylvania 15213 USA

Head and neck squamous cell carcinomas (HNSCC) are common human malignancies with poor clinical outcomes. The 5-year survival rates for patients with advanced stage HNSCC have not changed appreciably in the past few decades, underscoring a dire need for improved therapeutic options. Recent studies have elucidated a key signaling axis, the EGFR-STAT3-Bcl-XL signaling axis, that is aberrantly activated in a majority of HNSCC and contributes to the proliferation and survival of malignant cells. Considerable effort is being placed on developing highly specific inhibitors of different components of this pathway. This review highlights the progress that is being made towards achieving potent inhibition of the EGFR-STAT3-Bcl-XL signaling axis in HNSCC and the promising therapeutic strategies that are currently under development for this disease.

关键词：治疗效果头颈部癌症存活增殖鳞状细胞癌头部恶性肿瘤