bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modulation of scratching behavior by silencing an endogenous cyclooxygenase‐1 gene in the skin through the administration of siRNA
Authors: Inoue Tomoyuki , Sugimoto Masanori , Sakurai Takanobu , Saito Rie , Futaki Nobuko , Hashimoto Yuki , Honma Yusuke , Arai Iwao , Nakaike Shiro 
Published: August 2007

AbstractBackgroundRNA interference (RNAi) is rapidly becoming a major tool that is revolutionizing research in the bioscience and biomedical fields. To apply the RNAi technique in vivo, it is crucial to develop appropriate methods of guiding the short interfering RNA (siRNA) molecules to the right tissues and cells. Here, we demonstrate an efficient method for performing gene knockdown in the body skin using the in vivo electro‐transduction of siRNA. Using this method, we examined whether the targeted silencing of the cyclooxygenase (COX) gene in the skin could modulate the scratching behavior of an atopic dermatitis mouse model.MethodsNC/Nga mice were used as the atopic dermatitis model. Using our optimized in vivo electroporation conditions, siRNAs were introduced into the skin; the silencing efficiency was then analyzed by Western blotting, measuring the levels of prostaglandins, and immunohistochemistry. The scratching behaviors of the mice were measured using an automatic system.ResultsTargeted silencing of the COX‐1 gene using our in vivo siRNA technique significantly accelerated the scratching behavior of NC/Nga mice, whereas the COX‐2 siRNA showed no effect. In addition, the effect of COX‐1 siRNA was mimicked by treatment with a COX‐1‐selective inhibitor (SC‐560).ConclusionsWe have demonstrated the successful silencing of endogenous gene expression in the skin using the intradermal transfection of unmodified siRNA via electroporation. Using this method, we revealed that COX‐ 1‐mediated prostaglandins may act as endogenous inhibitors of scratching behavior. Copyright © 2007 John Wiley & Sons, Ltd.
Provider response to insulin‐induced hypoglycemia in hospitalized patients
Authors: Garg Rajesh , Bhutani Himanshu , Jarry Amy , Pendergrass Merri 
Published: August 2007

AbstractBACKGROUNDRisk of hypoglycemia is a major barrier to the implementation of tight blood glucose (BG) control in hospitalized patients. The objective of this study was to evaluate the changes in diabetes treatment after an episode of hypoglycemia.METHODSThe study was a retrospective data analysis of patients who received 50% dextrose for an episode of hypoglycemia. Data on immediate and subsequent changes in the antidiabetic medications the patients received were collected and evaluated by 2 diabetes specialists.RESULTSData from 52 patients were included in the study. Mean BG at the time of dextrose administration was 52.1 ± 9.3 mg/dL (range 31‐68). Mean BG during the 24 hours before the hypoglycemic episode was 137.5 ± 57.0 mg/dL (range 63‐287). Insulin dose was held at the time of the hypoglycemic episode in all 52 patients. Diabetes specialists agreed with this decision 100% of the time. Changes were subsequently made in the treatment of only 21 patients (40%), and diabetes specialists agreed with the changes made for 11 of these patients (52%). Thirty‐one patients (60%) received no changes in treatment, and diabetes specialists agreed with that decision for 10 patients (32%).CONCLUSIONSProvider response in making treatment changes after an episode of hypoglycemia is suboptimal. Standardized protocols to make changes in diabetes treatment after an episode of hypoglycemia need to be tested. Journal of Hospital Medicine 2007;2:258–260. © 2007 Society of Hospital Medicine.
Impact of Society of Hospital Medicine workshops on hospitalists' knowledge and perceptions of health care–associated infections and antimicrobial resistance
Authors: Bush‐Knapp Megan E. , Budnitz Tina , Lawton‐Ciccarone Rachel M. , Sinkowitz‐Cochran Ronda L. , Brinsley‐Rainisch Kristin J. , Dressler Daniel D. , Williams Mark V. 
Published: August 2007

AbstractBACKGROUNDHealth care–associated infections and antimicrobial resistance threaten the safety of hospitalized patients. New prevention strategies are necessary to address these problems. In response, the Society of Hospital Medicine (SHM) in collaboration with the Centers for Disease Control and Prevention developed and conducted workshops to educate hospitalists about conducting quality improvement programs to address antimicrobial resistance and health care–associated infections in hospitalized patients.METHODSSHM collected and analyzed data from pretests and posttests administered to physicians who attended SHM workshops in 2005 in 1 of 3 major cities: Denver, Colorado; Boston, Massachusetts; or Portland, Oregon.RESULTSA total of 69 SHM members attended the workshops, and 50 completed both a pretest and a posttest. Scores on the knowledge‐based questions increased significantly from pretest to posttest (x̄ = 48% vs. 63%, P < .0001); however, perceptions of the problem of antimicrobial resistance did not change. Most participants (85%) rated the quality of the workshop as “very good” or “excellent” and rated the workshop sessions as “useful” (x̄ = 3.9 on a 5.0 scale).CONCLUSIONSHospitalists who attended the SHM workshop increased their knowledge of health care–associated infections, antimicrobial resistance, and quality improvement programs related to these issues. Similar workshops should be considered in efforts to prevent health care–associated infections and antimicrobial resistance. Journal of Hospital Medicine 2007;2:268–273. © 2007 Society of Hospital Medicine.
Respiratory syncytial virus protects against the subsequent development of Japanese cedar pollen‐induced allergic responses
Authors: Liu Beixing , Kimura Yoshinobu 
Published: August 2007

AbstractRespiratory syncytial virus (RSV) infection has been hypothesized to be a risk factor for the development of allergy and asthma, but epidemiologic studies in humans still remain inconclusive. The association between RSV infection and allergic diseases may be dependent on atopic background and previous history of RSV infection. In this study, the influence of the timing of RSV infection on the development of Japanese cedar pollen (JCP)‐induced allergic responses was examined. BALB/c mice were intranasally infected with RSV before or after sensitization to JCP. Production of cytokines in the culture fluid of lung parenchyma cells and the level of antigen‐specific antibodies in the serum were determined. It became clear that JCP was a strong inducer for the elicitation of Th2‐type responses, characterized by production of interleukin (IL)‐4 and IL‐5 in the lung and JCP‐specific IgE antibody in the serum. RSV infection, however, suppressed JCP‐induced allergic responses by decreasing the production of Th2‐like cytokines and Th2‐type antibodies. This phenomenon was observed more clearly in the groups that were infected with RSV, 2 weeks or 2 days before sensitization to JCP. The inhibitory mechanism of RSV infection seems to be due to RSV‐induced Th1 type dominant environment, which down‐regulated the Th2‐type responses subsequently induced by allergen sensitization. On the other hand, JCP‐inoculation altered RSV‐induced immune responses to shift from Th1‐ to Th2‐type dominance, by inhibiting RSV‐induced Th1‐like cytokine production. These data provide evidence that under a certain condition, RSV infection may play a protective role in JCP‐induced allergic responses. J. Med. Virol. 79:1600–1605, 2007. © Wiley‐Liss, Inc.
High prevalence of amantadine‐resistance influenza a (H3N2) in six prefectures, Japan, in the 2005–2006 Season
Authors: Saito Reiko , Li Danjuan , Suzuki Yasushi , Sato Isamu , Masaki Hironori , Nishimura Hidekazu , Kawashima Takashi , Shirahige Yutaka , Shimomura Chieko , Asoh Norichika , Degawa Satoshi , Ishikawa Hidefumi , Sato Maki , Shobugawa Yugo , Suzuki Hiroshi 
Published: August 2007

AbstractSubstantial increase in amantadine‐resistant influenza A (H3N2) was reported in Asia and North America in 2005. In this study the frequency and genetic characteristics of amantadine‐resistant influenza A, circulated in Japan in 2005–2006 season, were investigated. Isolates were tested by amantadine susceptibility test (TCID50/0.2 ml method), and sequencing of the M2 gene to identify mutations that confer resistance. Additionally, the hemagglutinin (HA) and neuraminidase (NA) genes of the viruses were examined. In total, 415 influenza A isolates from six prefectures were screened, and 231 (65.3%) of 354 influenza A (H3N2) were amantadine‐resistant, with a serine to asparagine (S31N) change in the M2 gene. However, none of 61 A (H1N1) isolates were resistant. In addition, genetic analyses of the HA gene showed all amantadine‐resistant viruses clustered in one (named clade N), possessing specific double mutations at 193, serine to phenylalanine (S193F), and at 225, asparatic acid to asparagine (D225N), and sensitive viruses belonged to another group (clade S). The clinical presentations at the clinical visit did not differ between patients shedding clade N virus and those shedding clade S virus. None of the patients had received previous treatment with amantadine. The results indicate an unusually high prevalence and wide circulation of the amantadine‐resistance influenza A (H3N2) in Japan in the 2005–2006 season. These strains had the characteristic double mutations in the HA, in addition to the M2 mutation responsive for resistance. Antiviral resistance monitoring should be intensified and maintained for rapid feedback into treatment strategies, and selection of alternative therapeutic agents. J. Med. Virol. 79:1569–1576, 2007. © Wiley‐Liss, Inc.
Neuraminidase inhibitor resistance in influenza viruses
Authors: Reece Phillip Andrew 
Published: August 2007

AbstractZanamivir and oseltamivir, the currentlymarketed influenza virus neuraminidase inhibitors (NAIs), are prescribed for the treatment and prophylaxis of influenza and are being stockpiled for pandemic influenza. Oseltamivir resistance has been reported in up to 2% of patients in clinical trials of oseltamivir and in up to 18% of treated children. There are also reports in at least three patients treated with oseltamivir for influenza A (H5N1) infections. At this stage, there are no reports of resistance occurring to zanamivir in immunocompetent patients. Zanamivir and oseltamivir bind differently at the neuraminidase catalytic site and this contributes to different drug resistance profiles. The magnitude and duration of NAI concentrations at the site of infection are also expected to be important factors and are determined by route and timing of drug administration, dose, and pharmacokinetic differences between patients. In addition, the type, strain, and virulence of the influenza strain and the nature of the immune response all appear to play a role in determining the likelihood of drug resistance arising. The clinical significance of a particular NAI‐resistant isolate from a patient is often not clear but virus viability and transmissibility are clearly important characteristics. Early initiation of NAI treatment in suspected cases of influenza is important for maximizing efficacy and minimizing the risk of drug resistance. Higher NAI doses and longer periods of treatment may be required for patients with influenza A (H5N1) infections but further work is needed in this area. J. Med. Virol. 79:1577–1586, 2007. © Wiley‐Liss, Inc.
The membrane protein of SARS‐CoV suppresses NF‐κB activation
Authors: Fang Xiaonan , Gao Jinrong , Zheng Hong , Li Baozong , Kong Lingbao , Zhang Yijuan , Wang Wei , Zeng Yingchun , Ye Linbai 
Published: August 2007

AbstractSevere acute respiratory syndrome coronavirus (SARS‐CoV) infects many organs, such as lung, liver, and immune organs and causes life‐threatening atypical pneumonia, SARS causes high morbidity and mortality rates. The molecular mechanism of SARS pathogenesis remains elusive. Inflammatory stimuli can activate IκB kinase (IKK) signalsome and subsequently the nuclear factor kappa B (NF‐κB), which influences gene expression of cyclooxygenase‐2 (Cox‐2) along with other transcription factors. In this work, we found that the membrane (M) protein of SARS‐CoV physically interacted with IKKβ using a co‐immunoprecipitation assay (IPA). Expression of M suppressed tumor necrosis factor alpha (TNF‐α) induced NF‐κB activation using a luciferase reporter assay. Further investigation showed M protein suppressed Cox‐2 expression using a luciferase reporter gene assay, RT‐PCR and Western blot analysis. The carboxyl terminal of M protein was sufficient for the M protein function. Together, these results indicate that SARS‐CoV M suppresses NF‐κB activity probably through a direct interaction with IKKβ, resulting in lower Cox‐2 expression. Suppression of NF‐κB activity and Cox‐2 expression may contribute to SARS pathogenesis. J. Med. Virol. 79:1431–1439, 2007. © Wiley‐Liss, Inc.
Molecular epidemiology of HIV‐1 in Santa Catarina State confirms increases of subtype C in Southern Brazil
Authors: Locateli Dayse , Stoco Patrícia H. , de Queiroz Artur T.L. , Alcântara Luiz C.J. , Ferreira Luiz G.E. , Zanetti Carlos R. , Rodrigues Rosângela , Grisard Edmundo C. , Pinto Aguinaldo R. 
Published: August 2007

AbstractRecent studies have demonstrated an increased prevalence of human immunodeficiency virus type 1 (HIV‐1) subtype C in southern Brazil. Although Santa Catarina State (SC) is located in this area and presents one of the country's highest incidences of HIV/AIDS, knowledge on the molecular epidemiology of HIV‐1 in such State is lacking. The aim of this study was to investigate the HIV‐1 molecular diversity and epidemiological profile of HIV‐1‐infected patients from SC. DNA samples were PCR amplified and HIV‐1 subtypes were determined using both env and gag genes by direct sequencing. Phylogenetic analyses revealed that 48% were subtype C and 23% were subtype B. Possible recombinant forms were observed for both B/C (23%) and B/F (6%) subtypes. Our results, for the first time, identifies HIV‐1 subtype C as a major clade circulating in SC and contributes to the understanding of HIV epidemics in the country by confirming the epidemic spread of the HIV‐1 subtype C in southern Brazil. J. Med. Virol. 79:1455–1463, 2007. © Wiley‐Liss, Inc.
Environmental contamination with rhinovirus and transfer to fingers of healthy individuals by daily life activity
Authors: Winther Birgit , McCue Karen , Ashe Kathleen , Rubino Joseph R. , Hendley J. Owen 
Published: August 2007

AbstractRhinovirus infection may be acquired by inoculation of virus on fingertips to conjunctiva or nose (self‐inoculation). The virus contaminating the fingertips may come from hand contact with someone with a cold or from virus in mucus on environmental surfaces. This study was designed to assess rhinovirus contamination of surfaces by adults with colds and rhinovirus transfer from surfaces to fingertips during normal daily activities. Fifteen adults with natural rhinovirus colds stayed overnight in a local hotel. Ten touched sites in each room were tested for rhinovirusRNA using RT‐PCR. Transfer to fingertips of five subjects was examined by drying 10 µl of virus‐containing mucus from each subject onto light switches, telephone dial buttons and telephone handsets. After an interval of 1 or 18 hr the subject flipped the light switch, pressed the button, held the handset. Fingertip rinses were tested for virus. Thirty five percent of the 150 environmental sites in the rooms were contaminated. Common virus‐positive sites were door handles, pens, light switches, TV remote controls, faucets, and telephones. Rhinovirus was transferredfrom surfaces to fingertips in 18/30 (60%) trials 1 hr after contamination and in 10/30 (33%) of trials 18 hr (overnight) after contamination. Adults with colds commonly contaminate environmental surfaces with rhinovirus; virus on surfaces can be transferred to a fingertip during normal daily activities. J. Med. Virol. 79:1606–1610, 2007. © Wiley‐Liss, Inc.
Dengue neurovirulence in mice: Identification of molecular signatures in the E and NS3 helicase domains
Authors: Bordignon Juliano , Strottmann Daisy M. , Mosimann Ana Luiza P. , Probst Christian M. , Stella Vanessa , Noronha Lucia , Zanata Sílvio M. , dos Santos Claudia N. Duarte 
Published: August 2007

AbstractRecent observations indicate that the clinical profile of dengue virus (DENV) infection is changing, and that neurological manifestations are becoming frequent. The neuro pathogenesis of dengue, and the contribution of viral and host factors to the disease are not well understood. To define the amino acid substitutions in DENV potentially implicated in the acquisition of a neurovirulent phenotype we used a murine model to characterize two neuroadapted strains of DENV‐1, FGA/NA a5c (previously obtained), and FGA/NA P6 (recently obtained). Only three amino acid substitutions were identified in the neurovirulent strains, mapping to the E and NS3 helicase domains. These mutations enhanced the ability of neuroadapted viral strains to replicate in the CNS of infected mice, causing extensive damage with leptomeningitis and encephalitis. J. Med. Virol. 79:1506–1517, 2007. © Wiley‐Liss, Inc.
Prevalence and characterization of enteric adenoviruses in the South of Ireland
Authors: Lennon G. , Cashman O. , Lane K. , Cryan B. , O'Shea H. 
Published: August 2007

AbstractEnteric adenoviruses have been shown to be a substantial cause of pediatric gastroenteritis in various parts of the world, and are considered to be the second most common cause of viral gastroenteritis, next to rotavirus in young children. Genetic characterization of 95 adenovirus isolates obtained from patients with acute gastroenteritis between 2002 and 2007 from the southern regions of Ireland, were characterized by PCR analysis, restriction endonuclease (RE) analysis and sequencing analysis. All isolates were found to be of adenovirus type 41 origin. Genetic analysis of seven hypervariable regions (HVRs) located within the hexon gene has revealed a high level of amino acid sequence homology in samples over the course of this study, with a very close relationship to the D22 genome type. The D22 genome type has been detected in several other countries, thus suggesting Irish isolates have common genome types with other stains worldwide. This is the first such study undertaken in the south of Ireland, to type and genetically characterize adenoviral gastroenteritis isolates, and has revealed a high level of conservation within the isolated analyzed. J. Med. Virol. 79:1518–1526, 2007. © Wiley‐Liss, Inc.
Loss of hepatitis B surface antigen from the serum of patients with chronic hepatitis treated with lamivudine
Authors: Kobayashi Mariko , Suzuki Fumitaka , Akuta Norio , Hosaka Tetsuya , Sezaki Hitomi , Yatsuji Hiromi , Yatsuji Hiromi , Kobayashi Masahiro , Suzuki Yoshiyuki , Arase Yasuji , Ikeda Kenji , Watahiki Sachiyo , Iwasaki Satomi , Miyakawa Yuzo , Kumada Hiromitsu 
Published: August 2007

AbstractAlthough loss of hepatitis B e antigen (HBeAg) from the serum is sought by treatment with lamivudine, clearance of hepatitis B surface antigen (HBsAg) is the eventual goal of any antiviral therapy. In a single hepatology center in the Metropolitan Tokyo, 486 patients with chronic hepatitis B were followed up for longer than 3 years after they started treatment with lamivudine. HBsAg disappeared from the serum in 17 (3.5%). Age ≥50 years and low HBsAg levels (hemagglutination titer ≤27) at the start of lamivudine were significantly more frequent in the patients who did than did not lose HBsAg from the serum. Except for these two factors, there were no differences between the two groups of patients in the prevalence of HBeAg and HBV DNA levels at the baseline, as well as the development of YMDD mutants and breakthrough hepatitis during lamivudine treatment. Using multivariate analysis, age ≥50 years at the start of lamivudine was the only factor predicting the loss of HBsAg (hazard ratio: 2.96 [95% confidence interval: 1.14–7.68], P = 0.028). By the method of Kaplan–Meier performed on the 486 patients, the loss of HBsAg was estimated to occur in 3% and 13% of patients, respectively, who had received lamivudine therapy for 5 and 10 years. These results indicate that loss of HBsAg occurs in a minority (3.5%) of patients with chronic hepatitis B who receive lamivudine therapy and more frequently in those with lower HBsAg titers and older ages at the start of treatment. J. Med. Virol. 79:1472–1477, 2007. © Wiley‐Liss, Inc.
Do G protein‐coupled receptors expressed in human lingual epithelium interact with HPV11?
Authors: Durzyński Lukasz , Gaudin Jean‐Charles , Breuils Laure , Szydłowski Jaroslaw , Goździcka‐Józefiak Anna , Haertlé Thomas 
Published: August 2007

AbstractHuman papillomaviruses infect epithelia but little is known about the nature of cell surface receptors interacting with the viral particles. It has been proposed that glycosaminoglycans and integrins may be involved in the attachment process. In the present study, the putative interactions of virus‐like particles of human papillomavirus type 11 (HPV11), which present a tropism for nasopharyngeal epithelia, with olfactory and taste receptors expressed in the human lingual epithelium were studied. The L1 protein of HPV11 was produced in insect cells. The presence of L1 virus‐like particles was analyzed by ELISA using monoclonal antibodies specific for full‐size particles and by electron microscopy. Using immunofluorescence, it was observed that virus‐like particles interacted with taste buds from murine tongue, with the tagged human olfactory receptor hJCG5 expressed in HEK‐293 but not with the tagged taste receptor hT2R4. This therefore suggests that hJCG5 may be involved in the adsorption process of HPV11 to lingual epithelium serving as a so‐called “adsorption‐adhesive molecule.” J. Med. Virol. 79:1545–1554, 2007. © Wiley‐Liss, Inc.
Polymorphism and drug selected mutations of reverse transcriptase gene in 102 HIV‐1 infected patients living in China
Authors: Liu Li , Lu Hong Zhou , Henry Mireille , Tamalet Catherine 
Published: August 2007

AbstractFew data are available for genotypic patterns within human immunodeficiency virus‐1 (HIV‐1) reverse transcriptase (RT) in drug‐naive patients and RT inhibitor (RTI) treated patients in China. This study aimed at characterizing the polymorphism of RT HIV‐1 in the absence of drug treatment and to identify known and unknown mutations emerging under RTI selective pressure. The HIV‐1 RT gene from 21 drug‐naive patients and 81 RTI treated patients from three provinces in China was analyzed. Most patients (>80%) received a triple regimen including stavudine (d4T) plus didanosine (ddI) and nevirapine (NVP), or d4T plus lamivudine (3TC) and efavirenz (EFV), or zidovudine (AZT) +ddI + NVP. In untreated patients, four highly polymorphic positions were found (122, 200, 207, and 211). In treated patients, two patterns of resistance associated mutations (RAMs) were observed: (1) K65R (9.8%), L74V (7.4%), M184V (7.4%), Q151M (5%), and thymidine analogue mutations (TAMs) (9.3%) including T215Y (5.5%), in patients who underwent ddI + d4T + NVP. (2) T215Y (23%), M184V (20%), and TAMs (15.4%) in patients receiving d4T + 3TC + EFV. In all cases, a high prevalence of non‐nucleoside RTIs (NNRTI) RAMs (41.9%) was found. Four RTI suspected new RAMs were described at position 142, 221, 224, and 228. An association between H221Y and L228H/R with Y181C was noted. These data highlight the predominant spread of NNRTI RAM in China, depict the specific genotypic pattern of RTI selected mutations in China, and suggest the association of newly described mutations with RTI therapy. J. Med. Virol. 79:1593–1599, 2007. © Wiley‐Liss, Inc.