bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of the ULBP ligands for NKG2D by B‐NHL cells plays an important role in determining their susceptibility to rituximab‐induced ADCC
Authors: Inagaki Atsushi , Ishida Takashi , Yano Hiroki , Ishii Toshihiko , Kusumoto Shigeru , Ito Asahi , Ri Masaki , Mori Fumiko , Ding Jianmin , Komatsu Hirokazu , Iida Shinsuke , Ueda Ryuzo 
Published: February 2009

AbstractAntibody‐dependent cellular cytotoxicity (ADCC) is a major antitumor mechanism of action of therapeutic monoclonal antibodies (mAbs). The aim of this study was to identify tumor‐associated factors which determine susceptibility to rituximab‐induced ADCC. Thirty different CD20+ non‐Hodgkin lymphoma cell lines were phenotyped for characteristics such as level of expression of NKG2D ligands, and the influence thereof on susceptibility to rituximab‐induced ADCC was established. The present study demonstrated that tumor cell susceptibility to rituximab‐induced ADCC was determined by 3 major tumor‐associated factors: (i) the amount of the target molecule, CD20; (ii) the amount of the ligands for inhibitory killer Ig‐like receptors, major histocompatibility complex class I; and (iii) the amounts of some of the NKG2D ligands, especially UL16‐binding protein (ULBP) 1–3. The importance of the ULBPs was confirmed using antibody blockade. In conclusion, this is the first report to show the importance for rituximab‐induced ADCC of ULBPs expressed on tumor cells. The ULBPs could be valuable diagnostic biological markers and significant targets for immunotherapy to improve efficacy not only of rituximab but also of other therapeutic mAbs. © 2009 UICC
Effects of low‐level light therapy on hepatic antioxidant defense in acute and chronic diabetic rats
Authors: Lim Jinhwan , Ali Zeeshan M. , Sanders Ruth A. , Snyder Ann C. , Eells Janis T. , Henshel Diane S. , Watkins John B. 
Published: February 2009

AbstractDiabetes causes oxidative stress in the liver and other tissues prone to complications. Photobiomodulation by near infrared light (670 nm) has been shown to accelerate diabetic wound healing, improve recovery from oxidative injury in the kidney, and attenuate degeneration in retina and optic nerve. The present study tested the hypothesis that 670 nm photobiomodulation, a low‐level light therapy, would attenuate oxidative stress and enhance the antioxidant protection system in the liver of a model of type I diabetes. Male Wistar rats were made diabetic with streptozotocin (50 mg/kg, ip) then exposed to 670 nm light (9 J/cm2) once per day for 18 days (acute) or 14 weeks (chronic). Livers were harvested, flash frozen, and then assayed for markers of oxidative stress. Light treatment was ineffective as an antioxidant therapy in chronic diabetes, but light treatment for 18 days in acutely diabetic rats resulted in the normalization of hepatic glutathione reductase and superoxide dismutase activities and a significant increase in glutathione peroxidase and glutathione‐S transferase activities. The results of this study suggest that 670 nm photobiomodulation may reduce, at least in part, acute hepatic oxidative stress by enhancing the antioxidant defense system in the diabetic rat model. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:1–8, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20257
Pyrogallol inhibits the growth of human pulmonary adenocarcinoma A549 cells by arresting cell cycle and triggering apoptosis
Authors: Han Yong Hwan , Kim Suhn Hee , Kim Sung Zoo , Park Woo Hyun 
Published: February 2009

AbstractPyrogallol (PG) is a polyphenol compound and has been known to be an Ogenerator. We evaluated the effects of PG on the growth of human pulmonary A549 cells in relation to the cell cycle and apoptosis. Treatment with 50 or 100 μM PG significantly inhibited the cell growth of A549 for 72 h. DNA flow cytometric analysis indicated that PG slightly induced a G1 phase arrest of the cell cycle at 24 or 48 h, but did not induce the specific cell cycle arrest at 72 h. Intracellular GSH depletion was observed in PG‐treated cells. PG induced apoptosis in A549 cells, as evidenced by sub‐G1 cells, annexin V staining cells, and the loss of mitochondrial membrane potential (Δ Ψm). The intracellular ROS (reactive oxygen species) level including Oincreased in PG‐treated A549 cells at 24 and 48 h, and persisted at 72 h. The changes in GSH as well as ROS levels by PG affected the cell viability in A549 cells. In conclusion, PG inhibited the growth of human pulmonary A549 cells by inducing cell cycle arrest as well as triggering apoptosis. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:36–42, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20263
Regulation of cytochrome P450 2C9 expression in primary cultures of human hepatocytes
Authors: Sahi Jasminder , Shord Stacy S. , Lindley Celeste , Ferguson Stephen , LeCluyse Edward L. 
Published: February 2009

AbstractCytochrome P450 2C9 (CYP2C9) expression is regulated by multiple nuclear receptors including the constitutive androstane receptor (CAR) and pregnane X receptor (PXR). We compared coregulation of CYP2C9 with CYP2B6 and CYP3A4, prototypical target genes for human CAR and PXR using human hepatocyte cultures treated for three days with the PXR activators clotrimazole, rifampin, and ritonavir; the CAR/PXR activator phenobarbital (PB); and the CAR‐selective agonists CITCO, (6‐(4‐chlorophenyl)imidazo[2,1‐β][1,3]thiazole‐5‐carbaldehyde‐O‐(3,4‐dichlorobenzyl)oxime) and phenytoin. Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4. We observed EC50values of 519 μM (phenobarbital), 11 μM (phenytoin), and 0.75 μM (rifampin), similar to those for CYP3A4 induction. Avasimibe, a potent PXR activator, produced nearly identical concentration‐dependent CYP2C9 and CYP3A4 activity profiles and EC50values. In 17 donors, rifampin increased mean basal CYP2C9 activity from 59 ± 43 to 143 ± 68 pmol/mg protein/min; fold induction ranged from 1.4‐ to 6.4‐fold. Enzyme activity and mRNA measurements after rifampin, CITCO and PB treatment demonstrated potency and efficacy consistent with CYP2C9 regulation being analogous to CYP3A4 rather than CYP2B6. We demonstrate that hepatic CYP2C9 is differentially regulated by agonists of CAR and PXR, and despite sharing common regulatory mechanisms with CYP3A4 and CYP2B6; this enzyme exhibits an induction profile more closely aligned with that of CYP3A4. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:43–58, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20264
Desensitization of β‐adrenergic receptors in lung injury induced by 2‐chloroethyl ethyl sulfide, a mustard analog
Authors: Kabir Syeda M. , Mukherjee Shyamali , Rajaratnam Veera , Smith Milton G. , Das Salil K. 
Published: February 2009

Abstract2‐Choloroethyl Ethyl Sulfide (CEES) exposure causes inflammatory lung diseases, including acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. This may be associated with oxidative stress, which has been implicated in the desensitization of beta‐adrenergic receptors (β‐ARs). The objective of this study was to investigate whether lung injury induced by intratracheal CEES exposure (2 mg/kg body weight) causes desensitization of β‐ARs. The animals were sacrificed after 7 days and lungs were removed. Lung injury was established by measuring the leakage of iodinated‐bovine serum albumin ([125I]‐BSA) into lung tissue. Receptor‐binding characteristics were determined by measuring the binding of [3H] dihydroalprenolol ([3H] DHA) (0.5–24 nM) to membrane fraction in the presence and absence ofDLDL‐propranolol (10 μ M). Both high‐ and low‐affinity β‐ARs were identified in the lung. Binding capacity was significantly higher in low‐affinity site in both control and experimental groups. Although CEES exposure did not changeKDandBmaxat the high‐affinity site, it significantly decreased bothKDandBmaxat low affinity sites. A 20% decrease in β2‐AR mRNA level and a 60% decrease in membrane protein levels were observed in the experimental group. Furthermore, there was significantly less stimulation of adenylate cyclase activity by both cholera toxin and isoproterenol in the experimental group in comparison to the control group. Treatment of lungs with 3‐isobutyl‐1‐methylxanthine (IBMX), an inhibitor of phosphodiesterase (PDE) could not abolish the difference between the control group and the experimental group on the stimulation of the adenylate cyclase activity. Thus, our study indicates that CEES‐induced lung injury is associated with desensitization of β2‐AR. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:59–70, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20265
Intracellular localization of porcine single‐strand binding protein 2
Authors: Kato Yukio , Kato Takako , Ono Tetsuo , Susa Takao , Kitahara Kousuke , Matsumoto Kaori 
Published: February 2009

AbstractWe have previously cloned cofactor CLIM2 (Ldb1/NL1) as a binding protein for LIM homeodomain transcription factor and now seek a protein interacting with CLIM2. Ultimately, SSBP2 was cloned as CLIM2 binding protein from the adult porcine pituitary cDNA library by the Yeast Two‐Hybrid System. The amino acid sequence of porcine SSBP2 shows a high identity (99%) with those of other mammalian species, man, and mouse. Using fluorescence protein‐fused SSBP2 and its deletion mutants, we observed that SSBP2 overexpressed in CHO cells predominantly localizes in mitochondria. Expression of mutant SSBP2s demonstrated that the first 241 amino acid residues are responsive for the mitochondrial localization. When CLIM2 vector was co‐transfected, SSBP2 changed its location to nuclei. The similar translocation was also observed when CLIM2 vector was transfected 17 h after the transfection of SSBP2 vector. The first 120 residues of SSBP2 are responsible for the nuclear localization by guidance with CLIM2. RT‐PCR demonstrated that SSBP2 was expressed in the porcine pituitary from fetal 40 days to postnatal 230 days in both genders and in the variety of pituitary and non‐pituitary tumor cell lines, indicating that SSBP2 is present ubiquitously and plays a universal function during fetal and postnatal pituitary development. J. Cell. Biochem. 106: 912–919, 2009. © 2009 Wiley‐Liss, Inc.
Cancer metastasis directly eradicated by targeted therapy with a modified Salmonella typhimurium
Authors: Hayashi Katsuhiro , Zhao Ming , Yamauchi Kensuke , Yamamoto Norio , Tsuchiya Hiroyuki , Tomita Katsuro , Hoffman Robert M. 
Published: February 2009

AbstractCancer metastasis is the life‐threatening aspect of cancer and is usually resistant to standard treatment. We report here a targeted therapy strategy for cancer metastasis using a genetically‐modified strain of Salmonella typhimurium. The genetically‐modified strain of S. typhimurium is auxotrophic for the amino acids arginine and leucine. These mutations preclude growth in normal tissue but do not reduce bacterial virulence in cancer cells. The tumor‐targeting strain of S. typhimurium, termed A1‐R, and expressing green fluorescent protein (GFP), was administered to both axillary lymph and popliteal lymph node metastasis of human pancreatic cancer and fibrosarcoma, respectively, as well as lung metastasis of the fibrosarcoma in nude mice. The bacteria were delivered via a lymphatic channel to target the lymph node metastases and systemically via the tail vein to target the lung metastasis. The cancer cells expressed red fluorescent protein (RFP) in the cytoplasm and GFP in the nucleus linked to histone H2B, enabling color‐coded real‐time imaging of the bacteria targeting the metastatic tumors. After 7–21 days of treatment, the metastases were eradicated without the need of chemotherapy or any other treatment. No adverse effects were observed. This new strategy demonstrates the clinical potential of targeting and curing cancer metastasis with engineered bacteria without the need of toxic chemotherapy. J. Cell. Biochem. 106: 992–998, 2009. © 2009 Wiley‐Liss, Inc.
Osmotic responses of Dunaliella to the changes of salinity
Authors: Chen Hui , Jiang Jian‐Guo 
Published: February 2009

AbstractSome species in genus Dunaliella are unique in their remarkable abilities to accumulate large numbers of β‐carotene and thrive in media containing a wide range of NaCl concentrations ranging from about 0.05 M to saturation (around 5.5 M). The algae contain no rigid polysaccharide cell wall and thus have been found to be able to rapidly change their volume and shape in response to changes in the extracellular hypo‐ or hyper‐osmotic pressure. In osmotic adjustment, the osmoregulatory response of Dunaliella functions to maintain osmotic balance at high salinities by synthesis and varying the intracellular concentration of glycerol. In this review, we describe the osmotic response process of Dunaliella under salinity stress, including the changes of cell volume, intracellular ions concentration, intracellular glycerol concentration, and the expression of some salt‐induced genes. Some specific proteins and enzymes can be induced by different salinities in osmotic response process. In addition, we introduce the exogenous expression of salt‐related genes of Dunaliella salina in plants and microorganisms for the purpose of confirming the functions of related genes, proteins, and enzymes. The aim of this review is to emphasize the importance of the studies on the mechanisms of osmotic adjustments of Dunaliella in order to develop its unique osmotic characteristics. It is prospected that future research should pay attention to the specific signal transduction pathway and the mechanism of osmoregulation, and to improve the salt tolerance of higher plants by using salt‐tolerant genes of Dunaliella. J. Cell. Physiol. 219: 251–258, 2009. © 2009 Wiley‐Liss, Inc.
Adenovirus‐mediated hPNPaseold‐35 gene transfer as a therapeutic strategy for neuroblastoma
Authors: Van Maerken Tom , Sarkar Devanand , Speleman Frank , Dent Paul , Weiss William A. , Fisher Paul B. 
Published: February 2009

AbstractCurrent treatment options for neuroblastoma fail to eradicate the disease in the majority of high‐risk patients, clearly mandating development of innovative therapeutic strategies. Gene therapy represents a promising approach for reversing the neoplastic phenotype or driving tumor cells to self‐destruction. We presently studied the effects of adenovirus‐mediated gene transfer of human polynucleotide phosphorylase (hPNPaseold‐35), a 3′,5′‐exoribonuclease with growth‐inhibitory properties, in neuroblastoma cells. Transgene expression was driven by either the cytomegalovirus (CMV) promoter or by a tumor‐selective promoter derived from progression elevated gene‐3 (PEG‐3). Our data demonstrate that efficient adenoviral transduction of neuroblastoma cells and robust transgene expression are feasible objectives, that the PEG‐3 promoter is capable of selectively targeting gene expression in the majority of neuroblastoma cells, and that hPNPaseold‐35 induces profound growth suppression and apoptosis of malignant neuroblastoma cells, while exerting limited effects on normal neural crest‐derived melanocytes. These findings support future applications of hPNPaseold‐35 for targeted gene‐based therapy of neuroblastoma and suggest that combination with the PEG‐3 promoter holds promise for creating a potent and selective neuroblastoma therapeutic. J. Cell. Physiol. 219: 707–715, 2009. © 2009 Wiley‐Liss, Inc.
Investigation on human adrenocortical cell response to adenovirus and adenoviral vector infection
Authors: Matkovic Urska , Pacenti Monia , Trevisan Marta , Palù Giorgio , Barzon Luisa 
Published: February 2009

AbstractAfter systemic administration, adenoviral vectors (AdVs) are sequestered in the liver and adrenal glands. Adenoviral vector transduction has been shown to cause cytopathic effects on human hepatocytes and to induce an inflammatory response, whereas the effect of AdVs on human adrenocortical cells has never been investigated. In this study, human adrenocortical carcinoma cell lines and primary cell cultures were used to assess the effects of wild‐type adenovirus (Ad5WT) and E1/E3‐deleted AdVs on cell proliferation and steroidogenesis. Ad5WT could efficiently replicate in adrenocortical cells, leading to S phase induction, followed by cell death, whereas high titer AdVs transduction had only mild effects on adrenocortical cell proliferation, with accumulation of cells in G2/M. Both AdVs and Ad5WT induced expression of inflammatory cytokines, such as interleukin‐6 and tumor necrosis factor‐α, but, most importantly, they led to a marked and dose‐dependent increase of cortisol and other steroid hormone production and consistently modulated expression of key steroidogenic enzymes and regulators of steroidogenesis. This effect, which was already apparent at 6 h post‐infection, probably represented a response to adenoviral entry and/or early phases of infection. The result of this study contribute to the understanding of host response to adenoviral vector administration. J. Cell. Physiol. 220: 45–57, 2009. © 2009 Wiley‐Liss, Inc.
Daily and seasonal changes in the stickiness of viscous capture threads in Argiope aurantia and Argiope trifasciata orb‐webs
Authors: Opell Brent D. , Lipkey Genine K. , Hendricks Mary L. , Vito Stephen T. 
Published: February 2009

AbstractThe spirally arrayed viscous capture threads of spider orb‐webs are formed of small, regularly spaced adhesive droplets and are responsible for retaining insects that strike the web, giving a spider more time to subdue these prey. These sticky threads are deposited from the perimeter of the web inward. We tested the hypothesis that depletion of silk reserves during web construction affects the properties of capture threads spun by adult female Argiope aurantia and Argiope trifasciata. In both species the droplet volume (DV) per millimeter thread length was the same in outer and inner capture threads and in early and late season webs. However, the outer threads of both species were stickier than their inner threads and, consequently, had a greater stickiness per DV. Thus, dwindling silk reserves during web construction appeared to reduce the stickiness of both species' threads by changing the composition rather than the volume of their viscous droplets. In A. trifasciata, which we studied later in the fall than A. aurantia, there were also seasonal declines in both thread stickiness and stickiness per DV, which may result from either the depletion of silk reserves or the reallocation of these resources. Early season webs of A. trifasciata also had greater stickiness per square centimeter of capture area than late season webs, better equipping these early webs to retain insects. J. Exp. Zool. 311A:217–225, 2009. © 2009 Wiley‐Liss, Inc.
New imidazole derivatives of 2(3H)‐benzazolones as potential antifungal agents
Authors: Petrov Ognyan , Gerova Mariana , Petrova Katya , Ivanova Yordanka 
Published: February 2009

Abstract
magnified imageA series of new imidazole derivatives containing 2(3H)‐benzoxazolone or 2(3H)‐benzothiazolone ring were synthesized as analogues of the antifungal drug bifonazole. All compounds were tested in vitro against Candida albicans, Candida parapsilosis, and Candida krusli. J. Heterocyclic Chem., (2009).
Synthesis of 7,8‐dihydroxy‐3‐(3,4‐dihydroxyphenyl)‐2H‐chromen‐2‐one derivatives of crown ethers
Authors: Gündüz Cihan , Bulut Mustafa 
Published: February 2009

Abstract
magnified imageThe novel 1‐(3,4‐dimethoxyphenyl)‐2‐(2,3,4‐trimethoxyphenyl)acrylonitrile was prepared from the condensation of the mixture of 2,3,4‐trimethoxybenzaldehyde and 3,4‐dimethoxyphenylacetonitrile in ethanol at 70°C with 20% aqueous sodium hydroxide solution. Cyclization and demethylation of the acrylacetonitrile was performed using pyridine hydrochloride. The obtained 7,8‐dihydroxy‐3‐(3,4‐dihydroxyphenyl)‐2H‐chromen‐2‐one was reacted with the poly(ethylene glycol) ditosylates in CH3CN/alkali carbonate to afford bis‐[12]crown‐4, ‐[15]crown‐5, and ‐[18]crown‐6 chromenones. The chromatographically purified novel chromenone crown ethers were identified by IR, 1H NMR, 13C NMR, and MALDI‐TOF mass spectrometry and elemental analysis. J. Heterocyclic Chem., (2009).
A simple three‐component condensation: Highly efficient microwave‐assisted one‐pot synthesis of polyfunctional pyridine derivatives
Authors: Tu Shujiang , Zhou Dianxiang , Cao Longji , Li Chunmei , Shao Qingqing 
Published: February 2009

Abstract
magnified imageA simple facile one‐step microwave‐enhanced synthesis of methyl 4‐substituted‐6‐amino‐5‐cyano‐2‐methylpyridine‐3‐carboxylate derivatives via a three‐component reaction of aromatic aldehydes, malononitrile, and methyl 3‐aminobut‐2‐enoate has been developed. It is an efficient and promising synthetic strategy to build the polyfunctional pyridine skeleton. J. Heterocyclic Chem., (2009)
The implications of benefit package design: the impact on poor Thai households of excluding renal replacement therapy
Authors: Prakongsai Phusit , Palmer Natasha , Uay‐Trakul Preecha , Tangcharoensathien Viroj , Mills Anne 
Published: February 2009

AbstractWhen the Thai universal coverage (UC) scheme was established, the government decided to exclude renal replacement therapy (RRT) for end‐stage renal disease (ESRD) patients from the benefit package, though RRT was included in two other public health insurance schemes. Access to RRT for UC members thus depended on the ability to pay. This study assessed the economic impact of RRT costs on Thai households of different economic status focusing on three issues: (1) the use of RRT; (2) the financial burden of health care payments and (3) household strategies for coping with RRT costs. In‐depth case studies of 20 households covered by the UC scheme and having ESRD patients were undertaken using three qualitative data collection approaches: semi‐structured and in‐depth interviews, and direct observation. Poorer and richer households in urban and rural areas of Nakorn Ratchasima province, a large province in the Northeast where more than 20 per cent of households live below the national poverty line, were purposively selected. The study was conducted in early 2005 and households were visited every 2 weeks for 3 months. Interviews were transcribed and analysed using a thematic approach. The decision to exclude RRT from the UC benefit package created financial barriers to RRT and had a substantial economic impact on poorer ESRD patients. Inadequate dialyses and erythropoietin injections to correct anaemia appeared to be a major cause of death for poorer patients. Household expenditure on RRT took 25–68 per cent of total income or 31–52 per cent of total expenditure, which meant all poorer patients faced catastrophic health spending. In contrast, richer patients had adequate dialyses, resulting in a higher survival rate and quality of life than poorer counterparts. Various coping strategies were employed by poorer patients; these included reducing frequency of dialyses, reducing food consumption, using public transportation to hospitals and taking high interest loans. The RRT cost burden not only impacted patients but also their household members and relatives who provided financial support. Given the two UC policy objectives of equitable access to health care and financial risk protection, the catastrophic impact of RRT costs on poorer households questions the appropriateness of excluding RRT from the UC benefit package. This issue requires further serious attention by the Thai government. Copyright © 2009 John Wiley & Sons, Ltd.