bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of the Type I Interferon Response in Human Dendritic Cells by Dengue Virus Infection Requires a Catalytically Active NS2B3 Complex
Authors: Rodriguez-Madoz Juan R. , Belicha-Villanueva Alan , Bernal-Rubio Dabeiba , Ashour Joseph , Ayllon Juan , Fernandez-Sesma Ana 
Published: July 2010

ABSTRACT
Dengue virus (DENV) is the most prevalent arthropod-borne human virus, able to infect and replicate in human dendritic cells (DCs), inducing their activation and the production of proinflammatory cytokines. However, DENV can successfully evade the immune response in order to produce disease in humans. Several mechanisms of immune evasion have been suggested for DENV, most of them involving interference with type I interferon (IFN) signaling. We recently reported that DENV infection of human DCs does not induce type I IFN production by those infected DCs, impairing their ability to prime naive T cells toward Th1 immunity. In this article, we report that DENV also reduces the ability of DCs to produce type I IFN in response to several inducers, such as infection with other viruses or exposure to Toll-like receptor (TLR) ligands, indicating that DENV antagonizes the type I IFN production pathway in human DCs. DENV-infected human DCs showed a reduced type I IFN response to Newcastle disease virus (NDV), Sendai virus (SeV), and Semliki Forest virus (SFV) infection and to the TLR3 agonist poly(I:C). This inhibitory effect is DENV dose dependent, requires DENV replication, and takes place in DENV-infected DCs as early as 2 h after infection. Expressing individual proteins of DENV in the presence of an IFN-α/β production inducer reveals that a catalytically active viral protease complex is required to reduce type I IFN production significantly. These results provide a new mechanism by which DENV evades the immune system in humans.
A Novel Model of Lethal Hendra Virus Infection in African Green Monkeys and the Effectiveness of Ribavirin Treatment
Authors: Rockx Barry , Bossart Katharine N. , Feldmann Friederike , Geisbert Joan B. , Hickey Andrew C. , Brining Douglas , Callison Julie , Safronetz David , Marzi Andrea , Kercher Lisa , Long Dan , Broder Christopher C. , Feldmann Heinz , Geisbert Thomas W. 
Published: July 2010

ABSTRACT
The henipaviruses, Hendra virus (HeV) and Nipah virus (NiV), are emerging zoonotic paramyxoviruses that can cause severe and often lethal neurologic and/or respiratory disease in a wide variety of mammalian hosts, including humans. There are presently no licensed vaccines or treatment options approved for human or veterinarian use. Guinea pigs, hamsters, cats, and ferrets, have been evaluated as animal models of human HeV infection, but studies in nonhuman primates (NHP) have not been reported, and the development and approval of any vaccine or antiviral for human use will likely require efficacy studies in an NHP model. Here, we examined the pathogenesis of HeV in the African green monkey (AGM) following intratracheal inoculation. Exposure of AGMs to HeV produced a uniformly lethal infection, and the observed clinical signs and pathology were highly consistent with HeV-mediated disease seen in humans. Ribavirin has been used to treat patients infected with either HeV or NiV; however, its utility in improving outcome remains, at best, uncertain. We examined the antiviral effect of ribavirin in a cohort of nine AGMs before or after exposure to HeV. Ribavirin treatment delayed disease onset by 1 to 2 days, with no significant benefit for disease progression and outcome. Together our findings introduce a new disease model of acute HeV infection suitable for testing antiviral strategies and also demonstrate that, while ribavirin may have some antiviral activity against the henipaviruses, its use as an effective standalone therapy for HeV infection is questionable.
Human APOBEC3G-Mediated Editing Can Promote HIV-1 Sequence Diversification and Accelerate Adaptation to Selective Pressure
Authors: Kim Eun-Young , Bhattacharya Tanmoy , Kunstman Kevin , Swantek Peter , Koning Fransje A. , Malim Michael H. , Wolinsky Steven M. 
Published: July 2010

ABSTRACT

Human apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G, hereinafter referred to as A3G) is an innate virus restriction factor that inhibits human immunodeficiency virus type 1 (HIV-1) replication and induces excessive deamination of cytidine residues in nascent reverse transcripts. To test the hypothesis that this enzyme can also help generate viral sequence diversification and the evolution of beneficial viral variants, we have examined the impact of A3G on the acquisition of (−)2′,3′-dideoxy-3′-thiacytidine (3TC) resistance
in vitro
. That characteristic resistance mutations are rapidly fixed in the presence of A3G and 3TC suggests that A3G-mediated editing can be an important source of genetic variation on which natural selection acts to shape the structure of HIV-1 populations.
Surprising roles for phospholipid binding proteins revealed by high throughput geneticsThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.
Authors: LeBlanc Marissa A. , McMaster Christopher R. 
Published: July 2010

Saccharomyces cerevisiae remains an ideal organism for studying the cell biological roles of lipids in vivo, as yeast has phospholipid metabolic pathways similar to mammalian cells, is easy and economical to manipulate, and is genetically tractable. The availability of isogenic strains containing specific genetic inactivation of each non-essential gene allowed for the development of a high-throughput method, called synthetic genetic analysis (SGA), to identify and describe precise pathways or functions associated with specific genes. This review describes the use of SGA to aid in elucidating the function of two lipid-binding proteins that regulate vesicular transport, Sec14 and Kes1. Sec14 was first identified as a phosphatidylcholine (PC) – phosphatidylinositol (PI) transfer protein required for viability, with reduced Sec14 function resulting in diminished vesicular transport out of the trans-Golgi. Although Sec14 is required for cell viability, inactivating the KES1 gene that encodes for a member of the oxysterol binding protein family in cells lacking Sec14 function results in restoration of vesicular transport and cell growth. SGA analysis identified a role for Kes1 and Sec14 in regulating the level and function of Golgi PI-4-phosphate (PI-4-P). SGA also determined that Sec14 not only regulates vesicular transport out of the trans-Golgi, but also transport from endosomes to the trans-Golgi. Comparing SGA screens in databases, coupled with genetic and cell biological analyses, further determined that the PI-4-P pool affected by Kes1 is generated by the PI 4-kinase Pik1. An important biological role for Sec14 and Kes1 revealed by SGA is coordinate regulation of the Pik1-generated Golgi PI-4-P pool that in turn is essential for vesicular transport into and out of the trans-Golgi.
The inhibitory effect of celecoxib on mouse hepatoma H22 cell line on the arachidonic acid metabolic pathwayThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.
Authors: Xu Zhigang , Zhang Ming , Lv Xiaoyan , Xiang Dan , Zhang Xuewen , Chen Li 
Published: July 2010

Celecoxib is a selective inhibitor of cyclooxygenase-2 (COX-2). It may reduce the risk of cancer formation by affecting the metabolism of arachidonic acid (AA), which has been implicated in the development of cancer. Accordingly, this study was designed to determine the effects of celecoxib on the AA pathway in mouse hepatoma H22 cells. Celecoxib was found to inhibit the proliferation of H22 cells in a dose- and time-dependent manner. Low doses (50 and 100 µmol·L–1) of celecoxib caused an increase in the expression of cytosolic phospholipase A2 (cPLA2), but did not affect the expression of COX-2 in terms of the mRNA and protein levels. Surprisingly, the amount of AA was elevated and the level of prostaglandin E2 (PGE2) was unaltered in the culture supernatant. At higher celecoxib doses (200 and 400 µmol·L–1), the mRNA and protein of both COX-2 and cPLA2 were inhibited. The concentration of AA was increased, and PGE2 level was depressed in H22 cells. The ratio of AA to PGE2 was increased in a dose-dependent manner. Our findings suggest that the imbalance between AA and PGE2, characterized by increased AA at a low dosage and decreased PGE2 at a high dosage of celecoxib, was an important indicator of cytotoxicity of celecoxib on H22 cells.
Effects of leptin on the expression of α1 (I) collagen gene in human osteoblast-like MG63 cellsThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.
Authors: Peng Mian , Chen Shu , Fang Weiqiang , Yu Xuetao 
Published: July 2010

The objective of this study was to examine the effects of leptin on alpha (α) 1 (I) collagen gene expression in a human osteoblast-like MG63 cell line. MG63 cells were incubated with different doses of leptin (10−8, 10−7, and 10−6 mol·L–1) for 24, 48, and 72 h. α1 (I) collagen gene expression in MG63 cells was detected by real-time fluorescence quantitative polymerase chain reaction (FQ-PCR), with 17β-estradiol (17β-E2) as the positive control. Expression of the α1 (I) collagen gene, regulated by leptin, was dose and time dependent, with maximal expression in the 10−7 mol·L–1 group at 72 h of incubation. As a positive control, 17β-E2 reached its maximal effect in the 10−7mol·L–1 group at 24 h. We conclude that leptin has the ability to up-regulate α1 (I) collagen gene expression in MG63 cells, with a more potent effect but a less rapid response than 17β- E2.
Calorie restriction on insulin resistance and expression of SIRT1 and SIRT4 in ratsThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.
Authors: Chen Yong-Ru , Fang Shi-Rong , Fu Yu-Cai , Zhou Xiao-Hui , Xu Ming-Yan , Xu Wen-Can 
Published: July 2010

The sirtuin proteins are nicotinamide adenine dinucleotide dependent deacetylases and adenosine diphosphate (ADP)-ribosyl transferases associated with metabolic balance and lifespan extension. Sirtuin 1 (SIRT1) and sirtuin 4 (SIRT4) have been reported to regulate insulin secretion, but their association with the development of insulin resistance and nonalcoholic fatty liver disease remain undefined. The aim of this study was to determine the expression of SIRT1 and SIRT4 in the liver and pancreas of rats fed with different diets and analyze the association of these proteins with insulin resistance and nonalcoholic fatty liver disease. Male Sprague–Dawley rats were randomly divided into the following 4 diet treatment groups: normal control (NC), calorie restriction (CR), high-fat (HFa), and high-fructose (HFr), and these groups were maintained for 12 weeks. Blood biochemical analysis and histopathology indicated that HFa and HFr groups were insulin resistant and developed nonalcoholic fatty livers. SIRT1 was present in the nucleus and cytoplasm of the pancreatic β-cells, while SIRT4 was located in the cytoplasm. Treatment with the CR diet increased the expression of SIRT1 in both the pancreas and liver, while treatment with the HFa and HFr diets caused a decrease. SIRT4 was upregulated in the liver of rats treated with the HFa diet, but did not change with the CR diet treatment. These data suggest that SIRT1 and SIRT4 were both involved in the development of insulin resistance and nonalcoholic fatty liver disease.
Effects of plant polyphenols on ovarian follicular reserve in aging ratsThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.
Authors: Chen Zhen-Guo , Luo Li-Li , Xu Jin-Jie , Zhuang Xiao-Lan , Kong Xiao-Xia , Fu Yu-Cai 
Published: July 2010

The pool of ovarian primordial follicles is established during embryonic development or at birth. During the development from primordial to primary, secondary, and antral follicles, only a small portion of follicles can mature and successfully ovulate; the others are destined to degenerate through apoptotic or atretic loss. As aging advances, females ultimately enter the cessation phase of the estrous cycle and are no longer capable of fertilization. The presumption is that if we can slow down the process of folliculogenesis or decrease follicle loss, females may have a larger ovarian follicular reserve and a longer reproductive lifespan. In our study, rats underwent intragastric administration with tea polyphenols, quercetin (meletin), genistein, or resveratrol, once a day for 4 months (from age 12 to 15 months), to test whether they have positive effects on follicular reserve or ovarian functions. The results showed that rats treated with tea polyphenols (27.8 ± 3.2) and quercetin (36.5 ± 4.1) had a comparable number of healthy follicles to those of controls (26.9 ± 3.8), although significantly fewer atretic follicles were observed in the tea polyphenol group (43.4 ± 5.9 vs 79.7 ± 7.5; p < 0.001). Remarkably, both genistein- and resveratrol-treated rats had more healthy follicles (respectively, 42.8 ± 3.9, p < 0.05; and 51.9 ± 6.4, p < 0.001) and fewer atretic follicles (respectively, 58.4 ± 8.0, p < 0.05; and 51.0 ± 6.2, p < 0.01) than controls. These results indicate that genistein and resveratrol can increase the ovarian follicular reserve and prolong the ovarian lifespan in rats, and their positive effects may be not only due to their intervention in the transition from primordial to primary follicle, but also due to the inhibiting effect on follicular atresia.
Chronic effects of venlafaxine on synaptophysin and neuronal cell adhesion molecule in the hippocampus of cerebral ischemic miceThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.
Authors: Fang Shaokuan , Yan Bin , Wang Daoyi , Bi Xiaoying , Zhang Yanbo , He Jue , Xu Haiyun , Yang Yi , Kong Jiming , Wu Jiang , Li Xin-Min 
Published: July 2010

Venlafaxine, a novel antidepressant, inhibits serontonin and norepinephrine reuptake in the presynaptic cleft. Unlike typical selective serontonin reuptake inhibitors (SSRIs), venlafaxine may have modulatory effects on nerve terminals and neuronal plasticity. Our preliminary data found that 5 mg·kg–1·d–1 of venlafaxine treatment prevented decreased synaptophysin (SYP) in the hippocampus, which results from chronic restrained stress in the rat model. The present study investigates whether venlafaxine regulates alterations of synaptophysin and neuronal cell adhesion molecule (NCAM) in a post-stroke depression mouse model. We compared the expression level of SYP and NCAM in the hippocampus of global cerebral ischemic (GCI) mice treated with different doses of venlafaxine using immunohistological and Western blot analysis. Pre-treatment with intraperitoneal injection of venlafaxine (2.5 and 5.0 mg·kg–1·d–1) for 14 days significantly prevented the decrease of SYP in the hilus area of the hippocampus in vehicle-treated GCI mice. NCAM was significantly higher in the hippocampus of vehicle-treated GCI mice, and pretreatment with venlafaxine prevented alterations of NCAM, with the high-dose venlafaxine group comparable with vehicle-sham mice. The results suggest the alteration of neuronal remodeling proteins in the hippocampus may be an underlying mechanism of venlafaxine in treating post-stroke depression.
Bronchogenic and alveologenic tumors in mice induced byN-nitrosopiperidineThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.
Authors: Xie Xiao-Yuan , Shen Jian , Xu Li-Yan , Li En-Min , Shen Zhong-Ying 
Published: July 2010

The aim of this study was to explore the histogenesis and carcinogenesis of pulmonary cancer induced by N-nitrosopiperidine (NPIP) in mice. NPIP is a form of N-nitrosamine found in tobacco smoke, which has been shown to be a genotoxic chemical as well as a mutagenic compound for inducing chromosome aberrations and severe clastogenicity. In this study, 80 BALB/C strain mice were injected with 0.2 mmol/kg NPIP intraperitoneally for 8 weeks, and experiments were conducted for a further 16 weeks. For the control group, 40 mice were injected with an equal volume of 0.9% NaCl. Pulmonary tissues and tumors in the NPIP-treated group were examined by light microscopy and transmission electron microscopy and compared with the control group at 4-week intervals. The mRNA levels of p53 (mutant), bcl-2, c-myc, ras, and subunits of telomerase — telomerase reverse transcriptase (TERT) and an RNA component, TR — were assayed by mPCR or RT–PCR. Twenty-two mice in the experimental group were found to develop pulmonary tumors, but none in the control group. All tumors found in the experimental group originated from alveolar type II epithelial cells. In addition, 6 of the 22 mice also developed tumors of bronchogenic origin. The expression of p53, bcl-2, c-myc, ras, and the subunits of telomerase were found to increase in all pulmonary tissues and tumors formed thereafter upon NPIP treatment. In summary, NPIP-induced mouse lung tumors exhibited morphological changes during carcinogenesis, which may be the consequence of overexpression of some genes associated with the development of carcinoma and changes in subunits of telomerase. This mouse model of lung tumor formation may be a useful tool to delineate the histogenesis and carcinogenesis of human pulmonary cancer.
Le kétoconazole antagonise les effets immuno-gonadotropes au test de la nage forcée chez le rat mâle Wistar
Authors: Frih Hacène , Djenidi Réda , Ali Rachedi Bachir , Frih  Nabila , Tahraoui Abdelkrim , Bairi Abdel Majid 
Published: July 2010

On a souvent rapporté que la dépression s’installe suite à des perturbations des activités de l’axe corticotrope et du système immunitaire. L’objectif de cette étude était d’explorer les effets du kétoconazole, un dérivé d’imidazole, inhibiteur de la stéroïdogénèse gonadique et surrénalienne, sur les variations du nombre de leucocytes totaux et des pourcentages de sous-populations leucocytaires, au cours de la nage forcée chez le rat (test de Porsolt), un test consiste à tester l’efficacité des antidépresseurs. Des cathéters ont été implantés, sous anesthésie générale, dans la carotide droite, et des prises de sang (0,2 mL) ont été réalisées à des intervalles de 15 min au cours de l’expérimentation, alors que les animaux pouvaient se comporter librement. Les degrés d’anxiété et d’activité locomotrice des rats ont été mesurés au labyrinthe en croix surélevée et au test des champs ouverts. La nage forcée a provoqué des fluctuations du système immunitaire et de la testostéronémie, lesquelles qui ont été inhibées suite au traitement des animaux au kétoconazole. Cet effet a été obtenu également sur le plan comportemental (labyrinthe en croix surélevée, nage forcée) dans le sens d’une amélioration (effets anxiolytique et antidépresseur). Ces résultats suggèrent que les réponses comportementales et physiologiques sont inter-reliées d’une manière multifactorielle et que la corticostérone joue un rôle clé dans la pathogénie des maladies psychiatriques.
Variation in natural plant products and the attraction of bodyguards involved in indirect plant defenseThe present review is one in the special series of reviews on animal–plant interactions.
Authors: Mumm Roland , Dicke Marcel 
Published: July 2010

Plants can respond to feeding or egg deposition by herbivorous arthropods by changing the volatile blend that they emit. These herbivore-induced plant volatiles (HIPVs) can attract carnivorous natural enemies of the herbivores, such as parasitoids and predators, a phenomenon that is called indirect plant defense. The volatile blends of infested plants can be very complex, sometimes consisting of hundreds of compounds. Most HIPVs can be classified as terpenoids (e.g., (E)-β-ocimene, (E,E)-α-farnesene, (E)-4,8-dimethyl-1,3,7-nonatriene), green leaf volatiles (e.g., hexanal, (Z)-3-hexen-1-ol, (Z)-3-hexenyl acetate), phenylpropanoids (e.g., methyl salicylate, indole), and sulphur- or nitrogen-containing compounds (e.g., isothiocyanates or nitriles, respectively). One highly intriguing question has been which volatiles out of the complex blend are the most important ones for the carnivorous natural enemies to locate "suitable host plants. Here, we review the methods and techniques that have been used to elucidate the carnivore-attracting compounds. Electrophysiological methods such as electroantennography have been used with parasitoids to elucidate which compounds can be perceived by the antennae. Different types of elicitors and inhibitors have widely been applied to manipulate plant volatile blends. Furthermore, transgenic plants that were genetically modified in specific steps in one of the signal transduction pathways or biosynthetic routes have been used to find steps in HIPV emission crucial for indirect plant defense. Furthermore, we provide an overview on biotic and abiotic factors that influence the emission of HIPVs and how this can affect the interactions between members of different trophic levels. Consequently, we review the progress that has been made in this exciting research field during the past 30 years since the first studies on HIPVs emerged and we highlight important issues to be addressed in the future.
Landslide mechanisms in Hong Kong
Authors: Hencher S. R. , Lee S. G. 
Published: July 2010

Abstract
This paper reviews the nature and mechanics of landslides in the weathered terrain of Hong Kong. The vast majority of landslides are very shallow (a few metres depth) and occur during intense rainstorms. Deeper-seated landslides, in contrast, may occur days or weeks after intense rainstorms. The time of occurrence of landslides can be linked to hydrological and hydrogeological factors, and a hydrogeological grouping of landslide mechanisms is introduced related to timing in a storm. A relationship is presented that links intensity of landsliding to 24 h rainfall. The gradual deterioration and internal erosion of slopes prior to detachment is discussed and allows some realistic opportunity for identifying progressive major landslides. In particular, the growth of natural piping systems and infilling of dilated fracture networks are recommended as important indicators of landslide development. The conclusions are supported by case examples of slope failures, the study of some of which has been taken to a forensic level.