bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chemokine regulation of the inflammatory response to a low-dose influenza infection in CCR2–/– mice
Authors: Wareing Mark D , Lyon Ashley , Inglis Chandra , Giannoni Francesca , Charo Israel , Sarawar Sally R 
Published: December 2006

AbstractInfluenza virus infections induce chemokines and cytokines, which regulate the immune response. The chemokine receptor CCR2 plays an important role in macrophage recruitment and in the development of T1 immunity. In the present study, we addressed the role of CCR2 in influenza A virus infection. CCR2 knockout (−/−) mice are protected against influenza A virus infection, despite delayed recruitment of macrophages. We show that low-dose influenza infection of CCR2−/− mice leads to increased neutrophilia between Days 5 and 10 after infection and decreased monocyte/macrophage and CD4+ T cell recruitment to the lungs between Days 5 and 7 after infection. These changes in leukocyte recruitment did not result from or cause increased viral titers or delayed viral clearance. Neutrophilia in the lungs correlated with increased keratinocyte-derived chemokine (KC) and/or MIP-2 expression in CCR2−/− mice between Days 5 to 10 after infection, although the kinetics of neutrophil recruitment was not altered. MIP-2 mRNA and protein expression was increased three- to fivefold, and KC protein levels were increased two- to threefold in CCR2−/− compared with CCR2 wild-type mice at Day 5 after infection. This preceded the peak neutrophil influx, which occurred 7 days after infection. In vitro studies confirmed that MIP-2 and KC accounted for neutrophil chemotactic activity in the bronchoalveolar lavage. CCR2 deficiency also resulted in increased MIP-1α, MIP-1β, MCP-1, and IFN-inducible protein 10 and decreased RANTES mRNA expression. Furthermore, IL-6 and TNF-α cytokine production were elevated after infection. These studies suggest that CCR2 plays a multifactorial role in the development of the immune response to influenza.
Multiple Endocrine Neoplasia Type 1 (MEN1): Loss of One MEN1 Allele in Tumors and Monohormonal Endocrine Cell Clusters But Not in Islet Hyperplasia of the Pancreas
Authors: Perren Aurel , Anlauf Martin , Henopp Tobias , Rudolph Thomas , Schmitt Anja , Raffel Andreas , Gimm Oliver , Weihe Eberhard , Knoefel Wolfram T. , Dralle Henning , Heitz Philipp U. , Komminoth Paul , Klöppel Günter 
Published: December 2006

Abstract
Context: The occurrence of multiple small pancreatic endocrine tumors in patients suffering from multiple endocrine neoplasia type 1 (MEN1) represents a unique possibility to study early neoplasms and their potential precursor lesions. To date, it is unknown whether small islet-like endocrine cell clusters found in MEN1 patients are neoplastic or rather hyperplastic. It is also unclear whether microadenomas develop from islets.
Design: We hypothesized that monohormonal endocrine cell clusters observed in MEN1 patients are small neoplasms with loss of heterozygosity of the MEN1 locus. Using a technique combining fluorescence in situ hybridization of the MEN1 locus and the centromeric region of chromosome 11q with hormone immunostaining, we examined resection specimens from four MEN1 patients. We focused our investigations on the following: 1) typical microadenomas; 2) monohormonal endocrine cell clusters; 3) endocrine and exocrine structures entrapped in microadenomas; and 4) morphologically normal islets.
Results: Loss of one MEN1 allele was found in all 27 microadenomas and 19 of 20 (95%) monohormonal endocrine cell clusters. By contrast, it was absent in islets and ductal or acinar structures. Our results indicate that monohormonal endocrine cell clusters represent a minute form of microadenomas.
Conclusion: The frequent presence of single nonneoplastic insulin cells in microadenomas and the occurrence of microadenomas in islets suggest an islet origin of microadenomas. Islet hyperplasia does not seem to be an obligatory stage in pancreatic MEN1-associated tumor development.
Possible Association between Diabetes and Bisphosphonate-Related Jaw Osteonecrosis
Authors: Khamaisi Mogher , Regev Eran , Yarom Noam , Avni Batia , Leitersdorf Eran , Raz Itamar , Elad Sharon 
Published: December 2006

Abstract
Context: Bisphosphonate-related osteonecrosis (BON) of the jaws is a newly identified condition for which the exact mechanism involved in its pathogenesis remains obscure.
Objective: The objective of the study was to evaluate whether diabetes mellitus (DM) may be a contributing factor in the development of BON.
Design: From 2004 to 2006, 31 patients were diagnosed with BON. The diagnosis of BON was based on the medical and dental history of each patient as well as the observation of clinical signs and symptoms of this pathological process. DM was based on two consecutive fasting blood glucose levels above 7 mmol/liter.
Setting: The study was completed in the Hebrew University-Hadassah Hospital referral center.
Results: Of the 31 patients with BON, 18 (58%) were found to have DM or impaired fasting glucose. The proportion of diabetic patients was much higher than expected relative to the incidence of DM in the general population (14%) and compared with the proportion of diabetic patients in a control group of oncological patients treated with bisphosphonates and without BON (12%) (P = 0.00003).
Conclusions: This finding indicates that DM may be a risk factor for BON and that DM patients treated with bisphosphonates should be carefully monitored. We discuss here the bone metabolic pathways characteristic of DM patients and the way in which these pathways can augment the effects of bisphosphonates.
Identification of potential anti-photoageing algal compounds using an in-vitro model of photoageing
Authors: Debacq-Chainiaux F , Borlon C , De Hertogh B , Remacle J , Morvan P-Y , Vallée R , Toussaint O 
Published: December 2006

Abstract
Stress-induced premature senescence (SIPS) has been proposed as an in-vitro model for testing the long-term effects of stressful events and to find molecules/natural extracts that protect against such stress. Premature senescence of human skin diploid fibroblasts (HDFs) can be induced by repeated subcytotoxic exposure to UVB, with the appearance of so-called biomarkers of senescence such as growth arrest, senescence-associated β-galactosidase activity, senescence-associated gene over-expression and the common 4977-bp mitochondrial DNA deletion. This model of UVB-induced premature senescence has been acknowledged as a robust in-vitro model in photoageing research. In this study, the potential anti-photoageing effects of a series of algal extracts were tested. The appearance of the biomarkers of UVB-induced premature senescence of HDFs was studied with or without algal extracts. One algal extract was shown to be particularly protective against UVB-induced SIPS. The results obtained here reinforce the notion that UVB-induced premature senescence of HDFs can be used to screen potential anti-photoageing compounds.
Haloperidol is an inhibitor but not substrate for MDR1/P-glycoprotein
Authors: Iwaki Koichi , Sakaeda Toshiyuki , Kakumoto Mikio , Nakamura Tsutomu , Komoto Chiho , Okamura Noboru , Nishiguchi Kohshi , Shiraki Takashi , Horinouchi Masanori , Okumura Katsuhiko 
Published: December 2006

Abstract
The involvement of the multidrug resistant transporter MDR1/P-glycoprotein in the penetration of haloperidol into the brain and absorption in the intestine was investigated to examine its role in inter/intra-individual variability, using the porcine kidney epithelial cell line LLC-PK1 and its MDR1-overexpressing transfectant, LLC-GA5-COL150. The inhibitory effect of haloperidol on other MDR1 substrates was also investigated in terms of the optimization of haloperidol-based pharmacotherapy. The transepithelial transport of [3H]haloperidol did not differ between the two cell lines, and vinblastine, a typical MDR1 substrate, had no effect on the transport, suggesting that haloperidol is not a substrate for MDR1, and it is unlikely that MDR function affects haloperidol absorption and brain distribution, and thereby the response to haloperidol. However, haloperidol was found to have an inhibitory effect on the MDR1-mediated transport of [3H]digoxin and [3H]vinblastine with an IC50 value of 7.84 ± 0.76 and 3.60 ± 0.64 μM, respectively, suggesting that the intestinal absorption, not distribution into the brain, of MDR1 substrate drugs could be altered by the co-administration of haloperidol in the clinical setting, although further clinical studies are needed.
Cyto-reduction of neuroendocrine tumours using Sandostatin LAR® in combination with Infergen®: results of a case series
Authors: Wang Hank S , Oh David S , Ohning Gordon V , Pisegna Joseph R 
Published: December 2006

Abstract
Historically, limited trials evaluating biotherapy in treating metastatic neuroendocrine tumours have yielded mixed results. In this study, the efficacy of a novel combination therapy featuring long-acting Sandostatin LAR® plus α-interferon was evaluated. In a prospective case series, 12 patients with unresectable metastatic neuroendocrine tumours refractory to treatment initiated therapy with Infergen® and Sandostatin LAR®. Radiological response was followed serially at 3-month intervals. A biochemical response was considered significant if marker levels decreased by ≥50% compared with baseline. Inhibition of tumour growth lasting for greater than 3 months (mean response 22.6 ± 17.7 months) was seen in eight patients. Complete tumour regression was observed in one patient, lasting for 40 months; three patients exhibited partial tumour regression (mean response 29.3 ± 24.0 months), and four patients maintained a stable tumour response (mean response 13.3 ± 9.2 months). Four patients showed no response to therapy (mean response 5.0 ± 6.0 months). All enrolled patients are alive currently. The biochemical response seen in seven patients did not correlate with the radiological response. These results suggest that the novel combination of long-acting Sandostatin LAR® with an α-interferon may be at least as effective as either combination therapy with short-acting octreotide or monotherapy with Sandostatin LAR®.
Inhibitory effect of apigenin on benzo(a)pyrene-mediated genotoxicity in Swiss albino mice
Authors: Khan Tajdar Husain , Jahangir Tamanna , Prasad Lakshmi , Sultana Sarwat 
Published: December 2006

Abstract
Apigenin, a bioflavonoid, is abundantly present in fruits and vegetables and possesses potential chemopreventive properties against a wide variety of chronic diseases. In this study we investigated the anti-genotoxic effects of apigenin against a known genotoxicant, benzo(a)pyrene (B(a)P) (125 mg kg−1 orally) toxicity in Swiss albino mice. B(a)P administration led to induction of cytochrome P-450 (CYP), aryl hydrocarbon hydroxylase (AHH) and DNA strand breaks (P &lt; 0.001), which was suppressed by apigenin (2.5 and 5 mg kg−1 orally) dose dependently (P &lt; 0.001). B(a)P-induced depletion in the level of reduced glutathione (GSH), quinone reductase (QR) and glutathione-S-transferase (GST) was also shown to be restored by apigenin pre-treatment (P &lt; 0.001). A simultaneous significant and dose-dependent reduction was noted in DNA strand breaks and in-vivo DNA damage (P &lt; 0.001), which gives some insight into restoration of DNA integrity in modulator groups. These results strongly support the protective nature of apigenin against B(a)P-induced toxicity.
Analysis of the mechanism of antinociceptive action of niga-ichigoside F1 obtained from Rubus imperialis (Rosaceae)
Authors: Ardenghi Juliana Vargas , Kanegusuku Márcia , Niero Rivaldo , Filho Valdir Cechinel , Monache Franco Delle , Yunes Rosendo Augusto , De Souza Márcia Maria 
Published: December 2006

Abstract
We have previously verified that niga-ichigoside F1 (NI), a triterpene isolated from Rubus imperialis, exhibits significant and potent antinociceptive action when evaluated in some pharmacological models of pain in mice. This effect was confirmed in other experimental models and also the mechanism of action has been evaluated. The antinociception caused by NI (60 mg kg−1) in both phases of the formalin test was significantly attenuated by intraperitoneal injection of mice with haloperidol (a dopaminergic antagonist, 0.20 mg kg−1) and L-arginine (precursor of nitric oxide, 600 mg kg−1). Regarding the cholinergic system, atropine (a cholinergic antagonist 60 mg kg−1) reverted only the second phase. The effect of NI was not affected by treatment of mice with yohimbine (an alpha2-adrenoceptor antagonist, 0.15 mg kg−1). The same pharmacological profile was observed for the administration of naloxone (an opioid receptor antagonist, 1 mg kg−1). On the other hand, intraperitoneal injection caused dose-related and significant effects against glutamate- and capsaicin-induced pain, respectively. In conclusion, the marked antinociception of NI appears to be related to the dopaminergic, cholinergic, glutamatergic, tachykininergic and oxinitrergic systems, supporting the ethnomedical use of Rubus imperialis (Rosaceae).
Cordycepin (3‘-deoxyadenosine) inhibits human platelet aggregation induced by U46619, a TXA2 analogue
Authors: Cho Hyun Jeong , Cho Jae Youl , Rhee Man Hee , Lim Chang Ryul , Park Hwa Jin 
Published: December 2006

Abstract
Cordycepin (3′-deoxyadenosine), which comes from Cordyceps militaris, the Chinese medicinal fungal genus Cordyceps, is known to have anti-tumour activity. In this study, we investigated the novel effect of cordycepin on human platelet aggregation that was induced by U46619, a thromboxane A2 (TXA2) analogue. TXA2 is an aggregation-inducing autacoidal molecule that is produced in various agonist-activated platelets. Cordycepin completely inhibited U46619-induced platelet aggregation and simultaneously reduced cytosolic free Ca2+ ([Ca2+]i), which was increased by U46619 (5 μM) up to 66%. Furthermore, the U46619-stimulated phosphorylation of Ca2+-dependent proteins (20 kDa of a myosin light chain and 47 kDa of pleckstrin) was strongly inhibited by cordycepin. These results suggest that cordycepin may have a beneficial effect on autacoidal TXA2-mediated thrombotic diseases by inhibiting TXA2-induced platelet aggregation via suppression of the Ca2+ level.
Preparation of Gold and Platinum Nanoparticles Using Visible Light Activated FeIII-complex
Authors: Lee Jaesang , Ryu Jungho , Choi Wonyong 
Published: December 2006

Abstract
Iron(III)–citrate photochemical system can generate Au and Pt nanoparticles under the visible light illumination with playing the dual role as a precursor of reducing radicals and a stabilizer.
Electron Transfer in Tris(bipyridine)ruthenium(II) Complex Films on ITO
Authors: Kanaizuka Katsuhiko , Kato Shinji , Moriyama Hiroshi , Pac Chyongjin 
Published: December 2006

Abstract
The packing density of Ru(bpy)3 units was shown to be a crucial factor in constructing thin films having reversible redox functions. We have succeeded in controlling the surface of Ru(bpy)3 thin films using a bottom-up fabrication procedure. The redox function of the resulting multilayered films is highly predictable and reliable, although the productivity of the stepwise film growth of 1 is not high.
Chemical Synthesis of Face-centered-tetragonal FePt Film Using Sol–Gel Method
Authors: Su Hailin , Tang Nujiang , Wang Ruilong , Nie Bai , Tang Shaolong , Lv Liya , Du Youwei 
Published: December 2006

Abstract
A simple sol–gel spin-coating technique was developed to prepare FePt films. The calcining temperature was found to have great influences on the film’s crystalline structure and magnetic properties. For this method, pure face-centered-tetragonal FePt film was finally obtained by calcining at 370 °C and subsequently reducing at 470 °C.
N-Terminus Methylation of Desulfovibrio vulgaris (Miyazaki) F Cytochrome c3
Authors: Iida Shin , Kawano Yusuke , Asakura Noriyuki , Tabata Kenji , Okura Ichiro , Kamachi Toshiaki 
Published: December 2006

Abstract
Cytochrome c3 from Desulfovibrio vulgaris (Miyazaki) F is an electron-transfer protein between hydrogenase and ferredoxin and other types of cytochromes. In this study, an N-terminus of the cytochrome c3 has been identified as an N-methylated alanine residue by cleavage with peptidase, liquid chromatography/mass spectrometry (LC/MS) and nuclear magnetic resonance (NMR) analysis. Heterologous expression of the cytochrome c3 with Shewanella oneidensis TSP-C is not methylated, this indicate that the N-methylation occur in vivo in D. vulgaris.
1,3-Dipolar Cycloaddition of Ethyl Diazoacetate to Alkynes in the Pores of Zeolite NaY
Authors: Kobayashi Keijiro , Igura Yuta , Imachi Shouhei , Masui Yoichi , Onaka Makoto 
Published: December 2006

Abstract
Zeolite NaY promotes 1,3-dipolar cycloaddition of ethyl diazoacetate to alkynes having an electron-withdrawing group to afford the corresponding functionalized pyrazoles in high yields. The activation of the dipolarophile inside the pores of NaY is proposed based on the 13C MAS NMR analysis.
Exercise and Calcium Combined Results in a Greater Osteogenic Effect Than Either Factor Alone: A Blinded Randomized Placebo-Controlled Trial in Boys
Authors: Bass Shona L , Naughton Geraldine , Saxon Leanne , Iuliano-Burns Sandra , Daly Robin , Briganti Esther M , Hume Clare , Nowson Caryl 
Published: December 2006

Abstract
We examined the combined effects of exercise and calcium on BMC accrual in pre- and early-pubertal boys. Exercise and calcium together resulted in a 2% greater increase in femur BMC than either factor alone and a 3% greater increase in BMC at the tibia–fibula compared with the placebo group. Increasing dietary calcium seems to be important for optimizing the osteogenic effects of exercise.
Introduction: Understanding the relationship between exercise and calcium during growth is important given that the greatest benefits derived from these factors are achieved during the first two decades of life. We conducted a blinded randomized-controlled exercise–calcium intervention in pre- and early-pubertal boys to test the following hypotheses. (1) At the loaded sites (femur and tibia–fibula), exercise and calcium will produce greater skeletal benefits than either exercise or calcium alone. (2) At nonloaded sites (humerus and radius–ulna), there will be an effect of calcium supplementation.
Materials and Methods: Eighty-eight pre- and early-pubertal boys were randomly assigned to one of four study groups: moderate impact exercise with or without calcium (Ca) (Ex + Ca and Ex + placebo, respectively) or low impact exercise with or without Ca (No-Ex + Ca and No-Ex + Placebo, respectively). The intervention involved 20 minutes of either moderate- or low-impact exercise performed three times a week and/or the addition of Ca-fortified foods using milk minerals (392 ± 29 mg/day) or nonfortified foods over 8.5 months. Analysis of covariance was used to determine the main and combined effects of exercise and calcium on BMC after adjusting for baseline BMC.
Results: At baseline, no differences were reported between the groups for height, weight, BMC, or bone length. The increase in femur BMC in the Ex + Ca group was ∼2% greater than the increase in the Ex + placebo, No-Ex + Ca, or No-Ex + Placebo groups (all p &lt; 0.03). At the tibia–fibula, the increase in BMC in the Ex + Ca group was ∼3% greater than the No-Ex + placebo group (p &lt; 0.02) and 2% greater than the Ex + Placebo and the No-Ex + Ca groups (not significant). No effect of any group was detected at the humerus, ulna–radius, or lumbar spine for BMC, height, bone area, or volume.
Conclusions: In this group of normally active boys with adequate calcium intakes, additional exercise and calcium supplementation resulted in a 2–3% greater increase in BMC than controls at the loaded sites. These findings strengthen the evidence base for public health campaigns to address both exercise and dietary changes in children for optimizing the attainment of peak BMC.
Osteoporosis-Related Kyphosis and Impairments in Pulmonary Function: A Systematic Review
Authors: Harrison Robyn A , Siminoski Kerry , Vethanayagam Dilini , Majumdar Sumit R 
Published: December 2006

Abstract
We conducted a systematic review to examine the relationship between osteoporotic vertebral fractures, kyphosis, and pulmonary function. Findings suggest modest but predictable declines in vital capacity related to the degree of kyphosis. However, there were only four studies, and all had significant methodologic limitations. Further high-quality research is needed.
Introduction: Our objective was to systematically review the extent to which osteoporosis-related vertebral fractures and kyphosis affect pulmonary function.
Materials and Methods: We used a literature search from 1966 to 2006 (using Medline, EMBASE, and hand searches of references) for studies examining pulmonary function in patients without known lung disease who had vertebral fractures or kyphosis secondary to osteoporosis. Two reviewers independently abstracted data. Heterogeneity precluded formal meta-analysis.
Results: Initial searches yielded 453 articles. After applying eligibility criteria, only four case-control studies of limited quality (e.g., only one study was blinded) remained. Since 1966, only 109 patients (6 men) have been studied. All four studies reported reductions in vital capacity (VC), with values ranging from 68% to 94% of predicted values. This was quantified as a 9% reduction in predicted VC per vertebral fracture in one study. The degree of kyphosis clinically (one study) or radiographically (three studies) correlated with declines in VC; impairments were most notable at kyphotic angles &gt;55°. Statistically significant differences in percent predicted VC were obtained only when arm span or recalled height, rather than measured height, was used (two studies).
Conclusions: Despite conventional teaching, the evidence relating osteoporotic vertebral fractures or kyphosis to pulmonary function is limited. On the basis of available studies, declines in VC secondary to kyphosis seem modest and directly related to the number of vertebral fractures or degree of kyphosis. Future studies need longitudinal follow-up of larger numbers of men and women, appropriate proxies for height, standardized measures for pulmonary function and kyphosis, and efforts to blind outcomes ascertainment.