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Neural Regeneration Research 2025年第8期20卷 2169-2180页

作者： Mingyi Yu Faith Teo En Ning Chang Liu Yu-Chi Liu Tissue Engineering and Stem Cell Group Singapore Eye Research InstituteSingapore yong loo Lin school of medicine National University of SingaporeSingapore Department of Cornea and External Eye Disease Singapore National Eye CenterSingapore Ophthalmology and Visual Sciences Academic Clinical Program Duke-NUS Medical SchoolSingapore

Diabetic corneal neuropathy and diabetic retinopathy are ocular complications occurring in the context of diabetes *** corneal neuropathy refers to the progressive damage of corneal *** retinopathy has traditionally been considered as damage to the retinal ***,growing evidence suggests that diabetic retinopathy is a complex neurovascular disorder resulting from dysfunction of the neurovascular unit,which includes both the retinal vascular structures and neural *** retinopathy is one of the leading causes of blindness and is frequently screened for as part of diabetic ocular ***,diabetic corneal neuropathy is commonly overlooked and underdiagnosed,leading to severe ocular surface *** studies have found that these two conditions tend to occur together,and they share similarities in their pathogenesis pathways,being triggered by a status of chronic *** review aims to discuss the interconnection between diabetic corneal neuropathy and diabetic retinopathy,whether diabetic corneal neuropathy precedes diabetic retinopathy,as well as the relation between the stage of diabetic retinopathy and the severity of corneal *** also endeavor to explore the relevance of a corneal screening in diabetic eyes and the possibility of using corneal nerve measurements to monitor the progression of diabetic retinopathy.

关键词： cornea corneal nerves diabetes diabetic corneal neuropathy diabetic retinopathy retina

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Nitric oxide synthase and heme oxygenase expressions in human liver cirrhosis

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World Journal of Gastroenterology 2006年第4期12卷 588-594页

作者： Beatrice J Goh Bee Tee Tan Wei Min Hon Kang Hoe Lee Hoon Eng Khoo Department of Biochemistry Yong Loo Lin School of Medicine National University ofSingapore Department of medicine Yong Loo Lin School of Medicine National University of Singapore Research Biolabs Pte Ltd

AIM： Portal hypertension is a common complication of liver cirrhosis. Intrahepatic pressure can be elevated in several ways. Abnormal architecture affecting the vasculature, an increase in vasoconstrictors and increased circulation from the splanchnic viscera into the portal system may all contribute. It follows that endogenous vasodilators may be able to alleviate the hypertension. We therefore aimed to investigate the levels of endogenous vasodilators, nitric oxide （NO） and carbon monoxide （CO） through the expression of nitric oxide synthase （NOS） and heme oxygenase （HO）. METHOD： Cirrhotic （n = 20） and non-cirrhotic （n = 20） livers were obtained from patients who had undergone surgery. The mRNA and protein expressions of the various isoforms of NOS and HO were examined using competitive PCR, Western Blot and immunohistochemistry. RESULTS： There was no significant change in either inducible NOS （iNOS） or neuronal NOS （nNOS） expressions while endothelial NOS （eNOS） was up- regulated in cirrhotic livers. Concomitantly, caveolin-1, an established down-regulator of eNOS, was upregulated. Inducible HO-1 and constitutive HO-2 were found to show increased expression in cirrhotic livers albeit in different Iocalizations. CONCLUSION： The differences of NOS expression might be due to their differing roles in maintaining liver homeostasis and/or involvement in the pathology of cirrhosis. Sheer stress within the hypertensive liver may induce increased expression of eNOS. In turn, caveolin-1 is also increased. Whether this serves as a defense mechanism against further cirrhosis or is a consequence of cirrhosis, is yet unknown. The elevated expression of HO-1 and HO-2 suggest that CO may compensate in its role as a vasodilator albeit weakly. It is possible that CO and NO have parallel or coordinated functions within the liver and may work antagonistically in the pathophysiology of portal hypertension.

关键词： Liver cirrhosis Nitric oxide synthase Heine oxygenase Gene expression Competitive PCR

Expression patterns of cytokine,growth factor and cell cycle-related genes after partial hepatectomy in rats with thioacetamide-induced cirrhosis

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World Journal of Gastroenterology 2006年第7期12卷 1063-1070页

作者： Shu Yang Chon Kar Leow Theresa May Chin Tan Department of Biochemistry Yong Loo Lin School of Medicine National University of SingaporeSingapore Department of Surgery Yong Loo Lin School of Medicine National University of Singapore Singapore

AIM： To examine the differences in the responses of normal and cirrhotic livers to partial hepatectomy in relation to the factors influencing liver regeneration.METHODS： Cirrhosis was induced in rats by administration of thioacetarnide. Untreated rats were used as controls. The control rats as well as the cirrhotic rats were subjected to 70% partial hepatectorny. At different time points after hepatectorny, the livers were collected and the levels of cytokines, growth factors and cell cycle proteins were analyzed.RESULTS： After hepatectomy, the cirrhotic remnant expressed significantly lower levels of cyclin D1, its kinase partner, cdk4, and cyclin E as compared to the controls up to 72 h post hepatectomy. Significantly lower levels of cyclin A and cdk2 were also observed while the cdk inhibitor, p27 was significantly higher. In addition, the cirrhotic group had lower IL-6 levels than the control group at all time points up to 72 h following resection.CONCLUSION： The data from our study shows that impaired liver regeneration in cirrhotic remnants is associated with low expression of cyclins and cdks. This might be the consequence of the low IL-6 levels in cirrhotic liver remnant which would in turn influence the actions of transcription factors that regulate genes involved in cell proliferation and metabolic homeostasis during the regeneration process.

关键词： Cirrhosis Partial hepatectomy Cytokines Growth factors Cell cycle

Up-regulation of micro RNA-210 inhibits proliferation of hepatocellular carcinoma cells by targeting YES1

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World Journal of Gastroenterology 2015年第46期21卷 13030-13041页

作者： Weiqi Tan Seng-Gee Lim Theresa MC Tan Department of Biochemistry Yong Loo Lin School of MedicineNational University of Singapore Department of medicine Yong Loo Lin School of MedicineNational University of Singapore

AIM: To determine the expression of micro RNA-210(mi R-210) in hepatocellular carcinoma(HCC) and to examine its role using HCC ***: The expression of mi R-210 was determined in 21 pairs of HCC samples and the corresponding surrounding non-tumor tissues. The effects of mi R-210 on proliferation and cell cycle progression were examined using Hep G2 and Hu H7 cells. Overexpression and inhibition of mi R-210 was achieved by transfection of the cells with mi R-210 mimic or inhibitor. Luciferase reporter constructs were used to identify the mi R-210 interacting site on Yes1. Yes1 expression was examined after mi R-210 transfection,as well as in the HCC ***: mi R-210 was significantly up-regulated by 3.4 fold(P < 0.01) in the tumor samples. The over-expression of mi R-210 significantly reduced cell proliferation compared to the mock-treated cells(68.9% ± 7.4% and 53.6% ± 5.0%,P < 0.05 for the Hep G2 and Hu H7 cells respectively). Analysis of the Hu H7 cells transfected with mi R-210 mimic by flow cytometry showed that the cells took a longer time to reach the G2/M phase. The interaction between mi R-210 and the 3'UTR of the Yes1 transcript was confirmed using a luciferase reporter assay. Over-expression of mi R-210 reduced the expression of Yes1 protein in both Hu H7 and Hep G2 cells. Tumors with a greater than fourfold increase in the expression of mi R-210 showed consistently lower expressions of Yes1 in the *** nocodazole-treated cells with a significant G2/M cell population,Yes1 protein was significantly reduced and pre-inhibition of mi R-210 in Hu H7 cells was able to prevent the reduction of Yes1 protein expression. Knock-down of Yes1 by si RNA also led to reduced cell proliferation(70.8% ± 7.5%,P < 0.05 in the Hu H7 cells).CONCLUSION: Up-regulation of mi R-210 inhibits cell proliferation. Yes1 is a target of mi R-210 and affects cell proliferation in HCC.

关键词： Micro RNA-210 Hepatocellular carcinoma Proliferati

Emergence of life——how and where?——An update based on recent ideas

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Progress in Natural Science:Materials International 2007年第5期17卷 500-510页

作者： Bor Luen Tang Department of Biochemistry yong loo Lin school of medicine National University of Singapore Republic of Singapore

Panspermic origins notwithstanding, life, assuming that it started on Earth, may have taken root as soon as it became geologically permissible. There are multiple possibilities for early biogenesis from complex inorganic/organic geochemistry at diverse geological niches. Recent theoretical calculations have revived the possibility of Earth having a rather reduced early atmosphere, and had refueled arguments for a surface origin of life. Laboratory modeling of possible prebiotic RNA polymerization has seen interesting experimental advances, although a plausible replicator-like molecule has not yet been produced. The hydrothermal origin school of thought has also seen an interesting postulation for life’s early emergence and evolution—within contiguous, porous hydrothermal iron-sulfide (FeS) compartments, leading to a non-free living last universal common ancestor (LUCA). A confined LUCA evolving later into free-living archaebacteria and eubacteria could potentially reconcile some problems of molecular divergence between these two kingdoms. There are, however, many unresolved problems, and experimental evidence for such a scheme is lacking. Here, recent updates and refinements to the mainstay hypotheses for the emergence of life on Earth are reviewed and discussed.

关键词： emergence/origin of life iron-sulfide (FeS) last universal common ancestor (LUCA).

Drugging in the absence of p53

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Journal of Molecular Cell Biology 2019年第3期11卷 255-264页

作者： Obed Akwasi Aning Chit Fang Cheok Institute of Molecular and Cell Biology A*STARSingapore Department of Pathology Yong Loo Lin School of MedicineNational University of SingaporeSingapore Department of Biochemistry Yong Loo Lin School of MedicineNational University of SingaporeSingapore

Inactivation of the p53 gene is a key driver of tumorigenesis in various cancer cohorts and *** quest for a successful p53-based therapy that holds the promise of treating more than half of the cancer population has culminated in extensive knowledge about the role and function of p53 and led to new proposed innovative strategies against p53-defective *** will discuss some of these latest studies with a focus on metabolic regulation and DNA damage response and also highlight novel functions of p53 in these pathways that may provide a contemporary rationale for targeting p53 loss in tumors.

关键词： therapeutics metabolism DNA damage replication stress p53 synthetic lethality

Helicobacter pylori γ-glutamyl transpeptidase:A formidable virulence factor

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World Journal of Gastroenterology 2013年第45期19卷 8203-8210页

作者： Samantha Shi Min ling Khay Guan Yeoh Bow Ho Department of Microbiology Yong Loo Lin School of Medicine National University of Singapore Singapore 117597 Singapore Department of medicine Yong Loo Lin School of Medicine National University of Singapore Singapore 117597 Singapore

Helicobacter pylori(***)produce an enzyme known asγ-glutamyl transpeptidase(HpGGT)that is highly conserved and common to all *** has been gaining increasing attention as an important virulence factor of the bacterium,having been demonstrated to be an important colonization factor in several animal models and has also recently been strongly associated with the development of peptic ulcer *** the results of various independent researcher groups,it is clear that HpGGT acts through several pathways to damage gastric epithelial cells including the induction of apoptosis and cell cycle arrest,production of reactive oxygen species leading to DNA damage,promotion of inflammation by increasing cyclooxygenase-2 and interleukin-8 expression,and upregulation of heparin-binding epidermal growth factor-like growth factor resulting in cell survival and *** addition,the potential role of HpGGT in promoting gastric carcinogenesis will also be discussed in this *** from affecting the gastric epithelium,HpGGT also has immunomodulatory actions on host immune cells where it displays an antiproliferative effect on T cells by inducing cell cycle arrest and also works with other *** virulence factors to skew dendritic cells towards a tolerogenic phenotype,possibly contributing to the persistence of the pathogen in the gastric mucosa.

关键词： Helicobacter pylori Gamma-glutamyl transpeptidase Pathogenesis Immunomodulation Carcinogenesis

A paradigm shift:emerging roles of microglia,a non-neuronal cell,in learning and memory

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Neural Regeneration Research 2021年第10期16卷 1992-1993页

作者： Neelima Gupta S.Thameem Dheen Department of Anatomy Yong Loo Lin School of MedicineNational University of SingaporeSingapore

Microglial cells are non-neuronal cells which serve as the first line of defence against various injuries and insults in the central nervous system(CNS).They act as sentinels that constantly patrol the surrounding parenchyma through their ramified processes in the *** response to any pathological insult,microglia become activated,undergo proliferation,migrate to the site of injury or infection,and release chemokines and cytokines followed by the phagocytosis of dead cells and debris.

关键词： injuries debris migrate

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From blood to brain:amoeboid microglial cell,a nascent macrophage and its functions in developing brain

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Acta Pharmacologica Sinica 2007年第8期28卷 1087-1096页

作者： Charanjit KAUR S Thameem DHEEN Eng-ang ling Department of Anatomy yong loo Lin school of medicine National University of Singapore117597Singapore

Amoeboid microglial cells(AMC)in the developing brain are active *** macrophagic nature of these cells has been demonstrated by many methods,such as the localization of various hydrolytic enzymes and the presence of comple-ment type 3 surface receptors in *** importantly is the direct visualizationof these cells engaged in the phagocytosis of degenerating cells at the ultrastruc-tural *** evidence of them being active macrophages is the avid inter-nalization of tracers administered by the intravenous or intraperitoneal routes indeveloping *** potential involvement of AMC in immune functions is sup-ported by the induced expression of major histocompatibility complex class I andII antigens on them when challenged by lipopolysaccharide or interferon-γ.Im-munosuppressive drugs,such as glucocorticoids and immune function-enhanc-ing drugs like melatonin,affect the expression of surface receptors and antigensand the release of cytokines by *** studies in our laboratory haveshown the expression of insulin-like growth factors,endothelins,2',3'-cyclic nucle-otide 3'-phosphodiesterase,and N-methyl-D-asparate *** along withthe release of chemokines,such as stromal derived factor-la and monocytechemoattractant protein-1,suggests multiple functional roles of AMC in earlybrain development.

关键词： developing brain amoeboid microglial cells functions

miR-106b-25/miR-17-92 clusters: Polycistrons with oncogenic roles in hepatocellular carcinoma

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World Journal of Gastroenterology 2014年第20期20卷 5962-5972页

作者： Weiqi Tan Yang Li Seng-Gee Lim Theresa MC Tan Department of Biochemistry Yong Loo Lin School of Medicine National University of Singapore Singapore S117597 Singapore Department of medicine Yong Loo Lin School of Medicine National University of Singapore Singapore S117597 Singapore

MicroRNAs are small endogenously expressed RNA molecules which are involved in the process of silencing gene expression through translational *** polycistronic miR-17-92 cluster is the first microRNA cluster shown to play a role in *** has two other paralogs in the human genome,the miR-106b-25 cluster and the miR-106a-363 ***,the microRNAs encoded by these clusters can be further grouped based on the seed sequences into four families,namely the miR-17,the miR-92,the miR-18and the miR-19 ***-expression of the miR-106b-25 and miR-17-92 clusters has been reported not only during the development of cirrhosis but also subsequently during the development of hepatocellular *** of these clusters have also been shown to affect the replication of hepatitis B and hepatitis C *** targets of these microRNAs have been identified,and these targets are involved in tumor growth,cell survival and *** this review,we first describe the regulation of these clusters by c-Myc and E2F1,and how the members of these clusters inturn regulate E2F1 expression forming an auto-regulatory *** addition,the roles of the various members of the clusters in affecting relevant target gene expression in the pathogenesis of hepatocellular carcinoma will also be discussed.

关键词： miR-106b-25 cluster miR-17-92 cluster Hepatocellular carcinoma Liver cirrhosis MicroRNAs