bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of Different Atropine Therapy Strategies on Fenthion‐Induced Organ Dysfunction in Rats
Authors: Fidan Huseyin , Sahin Onder , Ela Yuksel , Kilbas Aynur , Bas Orhan , Yavuz Yucel , Sahin Dursun Ali , Altuntas Irfan 
Published: March 2007

Abstract:  We studied the influence of dose and timing of atropine therapy on fenthion‐induced organ dysfunction. Thirty‐six rats were randomized into six groups. All rats in the five groups except the control group were intoxicated with fenthion. The high‐dose atropine group received 2 mg/kg of atropine, whereas the low‐dose group received 100 µg/kg of atropine every hour for 24 hr. One group received 2 mg/kg of atropine in the first 4 hr of intoxication while the other group received 2 mg/kg of atropine in the last 4 hr before killed, which for all rats was 24 hr after intoxication. Pseudocholinesterase and aspartate aminotransferase and alanine aminotransferase levels and histopathological markers of lung, brain and liver were studied. None of our atropine therapy strategies in this study totally prevented harm on the three organs. Although the high dose of atropine administered for 24 hr had the least harmful markers for lung, it also had the most harmful markers for brain and liver. We did not succeed in finding a unique therapy strategy in our models beneficial for all studied organs in fenthion intoxication in rats. Atropine administration strategy should be oriented for the most affected organ pathology in fenthion intoxication.
Protective Effects of Caffeic Acid Phenethyl Ester, Vitamin C, Vitamin E and N‐Acetylcysteine on Vancomycin‐Induced Nephrotoxicity in Rats
Authors: Ocak Sabahattin , Gorur Sadik , Hakverdi Sibel , Celik Sefa , Erdogan Suat 
Published: March 2007

Abstract:   The objective of this study was to compare the beneficial effects of caffeic acid phenethyl ester (CAPE), vitamin C, vitamin E and N‐acetylcysteine on vancomycin‐induced nephrotoxicity. Thirty rats were randomly devided into six groups: (i) control; (ii) vancomycin, 200 mg/kg administrated via intraperitoneal route; (iii) vancomycin plus CAPE – vancomycin with 10 µmol/kg CAPE; (iv) vancomycin plus vitamin C – vancomycin (intraperitoneally) with 200 mg/dl vitamin C in drinking water; (v) vancomycin plus vitamin E – vancomycin with 1000 mg/kg body weight vitamin E (intramuscularly); and (vi) vancomycin plus N‐acetylcysteine – vancomycin with 10 mg/kg body weight (intraperitoneally) of N‐acetylcysteine. Vancomycin treatments were started 1 day after the first administrations of these agents and continued for 7 days. At the end of the experiments, catalase activity was significantly decreased by vancomycin in kidney homogenates (P < 0.05). Vitamin E, vitamin C, N‐acetylcysteine and CAPE administrations decreased the blood urea nitrogen levels increased by vancomycin, although significant differences were detected only in the vitamins E and C groups (P < 0.05). Increased renal malondialdehyde and nitric oxide levels by vancomycin were significantly suppressed by agents used in the study (P < 0.05). Histopathological examination demonstrated prominent damages in the vancomycin‐treated group. Vitamin E was the most beneficial agent on vancomycin‐induced tubular damage, followed by vitamin C, N‐acetylcysteine and CAPE treatments, respectively. The data suggest that vitamin E, as well as vitamin C, N‐acetylcysteine and CAPE, could be useful for reducing the detrimental effects on vancomycin‐induced toxicity in kidneys.
Detection of Anti-Leishmania(Leishmania)chagasiImmunoglobulin G by Flow Cytometry for Cure Assessment following Chemotherapeutic Treatment of American Visceral Leishmaniasis
Authors: Lemos Elenice Moreira , Gomes Izabelle Teixeira , Carvalho Sílvio Fernando Guimarães , Rocha Roberta Dias Rodrigues , Pissinate Jauber Fornaciari , Martins-Filho Olindo Assis , Dietze Reynaldo 
Published: March 2007

ABSTRACTThe residual serological reactivity observed in patients cured of visceral leishmaniasis (VL) represents the major factor underlying the low efficiency of most anti-Leishmaniaserological approaches to assess posttherapeutic cure in VL. Herein, we have described a detuned flow cytometry-based methodology to detect anti-live (FC-ALPA-immunoglobulin G [IgG]) and anti-fixed (FC-AFPA-IgG)L. chagasipromastigote IgG, along the titration curve (1:2,000 to 1:128,000), as a tool to assess late (12 months after treatment [12 mAT]) and early (2 and 6 mAT) posttherapeutic cure of pediatric American visceral leishmaniasis. Reactivities were reported as the percentage of positive fluorescent parasite (PPFP), using a PPFP of 50% as a cutoff to segregate positive and negative results. Our data demonstrated that both FC-ALPA-IgG at 1:4,000 and FC-ALPA-IgG at 1:32,000 are useful for late cure assessment in VL, with 100% specificity and outstanding likelihood ratio indices. Cure assessment at 6 mAT also showed promising performance indices, identifying 81% and 71.4% of the treated patients with negative results. However, new interpretation parameters were necessary to monitor cure at 2 mAT. We then introduced the differential PPFP (ΔPPFP) of 25% as a new cutoff for early cure assessment at specific serum dilutions to analyze IgG reactivity by FC-ALPA-IgG and FC-AFPA-IgG. Our data demonstrated that at 2 mAT, ΔPPFP was >25% in 60% and 57.1% of treated patients, whereas at 6 mAT, a ΔPPFP of >25% was observed in 100% and 95.2% of samples assayed by FC-ALPA-IgG and FC-AFPA-IgG, respectively. Together, our findings showed the potential of both FC-ALPA-IgG and FC-AFPA-IgG regarding their applicability to detect differential serological reactivity and further contribution to posttherapeutic cure assessment in VL.
Unusual Clinical Presentation of
Mycobacterium fortuitum
Infection in an Immunocompetent Woman
Authors: Serra Corrado , Loi Giovanni , Saddi Barbara , Pautasso Marisa , Manzin Aldo 
Published: March 2007

ABSTRACT

The
Mycobacterium fortuitum
group of rapidly growing nontuberculous mycobacteria is an uncommon cause of renal infection, particularly in otherwise healthy hosts. We describe a case of nephritis due to
M. fortuitum
in an immunocompetent woman with a clinical and radiological diagnosis of renal tuberculosis.
Exceptionally High Representation of
Burkholderia cepacia
among
B. cepacia
Complex Isolates Recovered from the Major Portuguese Cystic Fibrosis Center
Authors: Cunha Mónica V. , Pinto-de-Oliveira Ana , Meirinhos-Soares Luís , Salgado Maria José , Melo-Cristino José , Correia Susana , Barreto Celeste , Sá-Correia Isabel 
Published: March 2007

ABSTRACT

Burkholderia cepacia
, a species found infrequently in cystic fibrosis (CF), was isolated from 85% of patients infected with bacteria of the
B. cepacia
complex that visited the major Portuguese CF center, in Lisbon, during 2003 to 2005. A detailed molecular analysis revealed that this was mainly due to two
B. cepacia
clones. These clones were indistinguishable from two strains isolated from intrinsically contaminated nonsterile saline solutions for nasal application, detected during routine market surveillance by the Portuguese Medicines and Health Products Authority.
Risk Factors for the Presence of High-Level Shedders ofEscherichia coliO157 on Scottish Farms
Authors: Chase-Topping Margo E. , McKendrick Iain J. , Pearce Michael C. , MacDonald Peter , Matthews Louise , Halliday Jo , Allison Lesley , Fenlon Dave , Low J. Christopher , Gunn George , Woolhouse Mark E. J. 
Published: March 2007

ABSTRACTEscherichia coliO157 infections are the cause of sporadic or epidemic cases of often bloody diarrhea that can progress to hemolytic uremic syndrome (HUS), a systematic microvascular syndrome with predominately renal and neurological complications. HUS is responsible for most deaths associated withE. coliO157 infection. From March 2002 to February 2004, approximately 13,000 fecal pat samples from 481 farms with finishing/store cattle throughout Scotland were examined for the presence ofE. coliO157. A total of 441 fecal pats from 91 farms tested positive forE. coliO157. From the positive samples, a point estimate for high-level shedders was identified using mixture distribution analysis on counts ofE. coliO157. Models were developed based on the confidence interval surrounding this point estimate (high-level shedder, greater than 103or greater than 104CFU g−1feces). The mean prevalence on high-level-shedding farms was higher than that on low-level-shedding farms. The presence of a high-level shedder on a farm was found to be associated with a high proportion of low-level shedding, consistent with the possibility of a higher level of transmission. Analysis of risk factors associated with the presence of a high-level shedder on a farm suggested the importance of the pathogen and individual host rather than the farm environment. The proportion of high-level shedders of phage 21/28 was higher than expected by chance. Management-related risk factors that were identified included the type of cattle (female breeding cattle) and cattle stress (movement and weaning), as opposed to environmental factors, such as water supply and feed.
Comparison of Three Methods for Rapid Identification of Mycobacterial Clinical Isolates to the Species Level
Authors: Wu Xueqiong , Zhang Junxian , Liang Jianqin , Lu Yang , Li Hongmin , Li Chuihuan , Yue Jun , Zhang Lishui , Liu Zhihui 
Published: March 2007

ABSTRACT

A new PCR-reverse dot blot hybridization (RDBH) assay was developed for the rapid identification of
Mycobacterium
species in clinical isolates. The assay, which targets the 16S rRNA, was evaluated for 27 mycobacterial reference strains and 340 clinical isolates that were simultaneously identified by DNA sequencing and conventional methods, including growth characteristics, pigment production, colony morphology, and biochemical tests. All reference strains and clinical isolates hybridized to the
Mycobacterium
genus probe (probe M) on the membrane (100% sensitivity). Each probe had only one hybridization signal with the corresponding
Mycobacterium
species or complex (100% specificity). Compared with DNA sequencing, the RDBH assay correctly identified 337 (99.1% accuracy) of the 340 isolates tested. One
M. asia
isolate and one
M. neoaurum
isolate were not identified by the RDBH assay due to the absence of specific probes for the two species on the membrane. Three isolates with different nucleotide sequences from
M. intracellulare
reference strains had a negative hybridization signal with probe c, which is specific for
M. intracellulare.
The whole procedure can be completed within 2.5 h post-PCR processing. A total of 32 of 340 isolates were erroneously identified by conventional methods (90.6% accuracy). Molecular identification based on the 16S rRNA sequence was superior to the conventional approaches in speed, sensitivity, and specificity. Therefore, the RDBH assay can be considered a rapid, simple, and reliable method for routine identification of frequently occurring and clinically relevant mycobacteria.
Gamma Interferon Blocks Gammaherpesvirus Reactivation from Latency in a Cell Type-Specific Manner
Authors: Steed Ashley , Buch Thorsten , Waisman Ari , Virgin Herbert W. 
Published: March 2007

ABSTRACTGammaherpesviruses are important pathogens whose lifelong survival in the host depends critically on their capacity to establish and reactivate from latency, processes regulated by both viral genes and the host immune response. Previous work has demonstrated that gamma interferon (IFN-γ) is a key regulator of chronic infection with murine gammaherpesvirus 68 (γHV68), a virus that establishes latent infection in B lymphocytes, macrophages, and dendritic cells. In mice deficient in IFN-γ or the IFN-γ receptor, γHV68 gene expression is altered during chronic infection, and peritoneal cells explanted from these mice reactivate more efficiently ex vivo than cells derived from wild-type mice. Furthermore, treatment with IFN-γ inhibits reactivation of γHV68 from latently infected wild-type peritoneal cells, and depletion of IFN-γ from wild-type mice increases the efficiency of reactivation of explanted peritoneal cells. These profound effects of IFN-γ on chronic γHV68 latency and reactivation raise the question of which cells respond to IFN-γ to control chronic γHV68 infection. Here, we show that IFN-γ inhibited reactivation of peritoneal cells and spleen cells harvested from mice lacking B lymphocytes, but not wild-type spleen cells, suggesting that IFN-γ may inhibit reactivation in a cell type-specific manner. To directly test this hypothesis, we expressed the diphtheria toxin receptor specifically on either B lymphocytes or macrophages and used diphtheria toxin treatment to deplete these specific cells in vivo and in vitro after establishing latency. We demonstrate that macrophages, but not B cells, are responsive to IFN-γ-mediated suppression of γHV68 reactivation. These data indicate that the regulation of gammaherpesvirus latency by IFN-γ is cell type specific and raise the possibility that cell type-specific immune deficiency may alter latency in distinct and important ways.
Requirement for an Intact T-Cell Actin and Tubulin Cytoskeleton for Efficient Assembly and Spread of Human Immunodeficiency Virus Type 1
Authors: Jolly Clare , Mitar Ivonne , Sattentau Quentin J. 
Published: March 2007

ABSTRACT

Human immunodeficiency virus type 1 (HIV-1) infection of CD4
+
T cells leads to the production of new virions that assemble at the plasma membrane. Gag and Env accumulate in the context of lipid rafts at the inner and outer leaflets of the plasma membrane, respectively, forming polarized domains from which HIV-1 buds. HIV-1 budding can result in either release of cell-free virions or direct cell-cell spread via a virological synapse (VS). The recruitment of Gag and Env to these plasma membrane caps in T cells is poorly understood but may require elements of the T-cell secretory apparatus coordinated by the cytoskeleton. Using fixed-cell immunofluorescence labeling and confocal microscopy, we observed a high percentage of HIV-1-infected T cells with polarized Env and Gag in capped, lipid raft-like assembly domains. Treatment of infected T cells with inhibitors of actin or tubulin remodeling disrupted Gag and Env compartmentalization within the polarized raft-like domains. Depolymerization of the actin cytoskeleton reduced Gag release and viral infectivity, and actin and tubulin inhibitors reduced Env incorporation into virions. Live- and fixed-cell confocal imaging and assay of de novo DNA synthesis by real-time PCR allowed quantification of HIV-1 cell-cell transfer. Inhibition of actin and tubulin remodeling in infected cells interfered with cell-cell spread across a VS and reduced new viral DNA synthesis. Based on these data, we propose that HIV-1 requires both actin and tubulin components of the T-cell cytoskeleton to direct its assembly and budding and to elaborate a functional VS.
Small Interfering RNAs against the TAR RNA Binding Protein, TRBP, a Dicer Cofactor, Inhibit Human Immunodeficiency Virus Type 1 Long Terminal Repeat Expression and Viral Production
Authors: Christensen Helen S. , Daher Aïcha , Soye Kaitlin J. , Frankel Lisa B. , Alexander Marina R. , Lainé Sébastien , Bannwarth Sylvie , Ong Chi L. , Chung Sean W. L. , Campbell Shahan M. , Purcell Damian F. J. , Gatignol Anne 
Published: March 2007

ABSTRACT
RNA interference (RNAi) is now widely used for gene silencing in mammalian cells. The mechanism uses the RNA-induced silencing complex, in which Dicer, Ago2, and the human immunodeficiency virus type 1 (HIV-1) TAR RNA binding protein (TRBP) are the main components. TRBP is a protein that increases HIV-1 expression and replication by inhibition of the interferon-induced protein kinase PKR and by increasing translation of viral mRNA. After HIV infection, TRBP could restrict the viral RNA through its activity in RNAi or could contribute more to the enhancement of viral replication. To determine which function will be predominant in the virological context, we analyzed whether the inhibition of its expression could enhance or decrease HIV replication. We have generated small interfering RNAs (siRNAs) against TRBP and found that they decrease HIV-1 long terminal repeat (LTR) basal expression 2-fold, and the LTR Tat transactivated level up to 10-fold. In the context of HIV replication, siRNAs against TRBP decrease the expression of viral genes and inhibit viral production up to fivefold. The moderate increase in PKR expression and activation indicates that it contributes partially to viral gene inhibition. The moderate decrease in micro-RNA (miRNA) biogenesis by TRBP siRNAs suggests that in the context of HIV replication, TRBP functions other than RNAi are predominant. In addition, siRNAs against Dicer decrease viral production twofold and impede miRNA biogenesis. These results suggest that, in the context of HIV replication, TRBP contributes mainly to the enhancement of virus production and that Dicer does not mediate HIV restriction by RNAi.
Tyrosine 3 of Poliovirus Terminal Peptide VPg(3B) Has an Essential Function in RNA Replication in the Context of Its Precursor Protein, 3AB
Authors: Liu Ying , Franco David , Paul Aniko V. , Wimmer Eckard 
Published: March 2007

ABSTRACT

Poliovirus (PV) VPg is a genome-linked protein that is essential for the initiation of viral RNA replication. It has been well established that RNA replication is initiated when a molecule of UMP is covalently linked to the hydroxyl group of a tyrosine (Y3) in VPg by the viral RNA polymerase 3D
pol
, but it is not yet known whether the substrate for uridylylation in vivo is the free peptide itself or one of its precursors. The aim of this study was to use complementation analyses to obtain information about the true in vivo substrate for uridylylation by 3D
pol
. Previously, it was shown that a VPg mutant, in which tyrosine 3 and threonine 4 were replaced by phenylalanine and alanine (3F4A), respectively, was nonviable. We have now tested whether wild-type forms of proteins 3B, 3BC, 3BCD, 3AB, 3ABC, and P3 provided either in
trans
or in
cis
could rescue the replication defect of the VPg(3F4A) mutations in the PV polyprotein. Our results showed that proteins 3B, 3BC, 3BCD, and P3 were unable to complement the RNA replication defect in dicistronic PV or dicistronic luciferase replicons in vivo. However, cotranslation of the P3 precursor protein allowed rescue of RNA replication of the VPg(3F4A) mutant in an in vitro cell-free translation-RNA replication system, but only poor complementation was observed when 3BC, 3AB, 3BCD, or 3ABC proteins were cotranslated in the same assay. Interestingly, only protein 3AB but not 3B and 3BC, when provided in
cis
by insertion of a wild-type 3AB coding sequence between the P2 and P3 domains of the polyprotein, supported the replication of the mutated genome in vivo. Elimination of cleavage between 3A and 3B in the complementing 3AB protein, however, led to a complete lack of RNA replication. Our results suggest that (i) VPg has to be delivered to the replication complex in the form of a large protein precursor (P3) to be fully functional in replication; (ii) the replication complex formed during PV replication in vivo is essentially inaccessible to proteins provided in
trans
, even if the complementing protein is translated from a different cistron of the same RNA genome; (iii) 3AB is the most likely precursor of VPg; and (iv) Y3 of VPg has an essential function in RNA replication in the context of both VPg and 3AB.
Epstein-Barr Virus-Encoded Protein Kinase (BGLF4) Is Involved in Production of Infectious Virus
Authors: Gershburg Edward , Raffa Salvatore , Torrisi Maria Rosaria , Pagano Joseph S. 
Published: March 2007

ABSTRACT
The Epstein-Barr virus (EBV) BGLF4 gene product is a protein kinase (PK). Although this kinase has been characterized and several of its targets have been identified, its biological role remains enigmatic. We have generated and assessed a BGLF4 knockdown phenotype by means of RNA interference and report the following: (i) BGLF4-targeting small interfering RNA effectively inhibited the expression of its product, the viral PK, during lytic reactivation, (ii) BGLF4 knockdown partially inhibited viral DNA replication and expression of selected late viral genes, (iii) the absence of EBV PK resulted in retention of the viral nucleocapsids in the nuclei, and (iv) as a result of the nuclear retention, release of infectious virions is significantly retarded. Our results provide evidence that EBV PK plays an important role in nuclear egress of the virus and ultimately is crucial for lytic virus replication.
Functional Analysis of
cis
- and
trans
-Acting Replication Factors of Porcine Circovirus Type 1
Authors: Steinfeldt Tobias , Finsterbusch Tim , Mankertz Annette 
Published: March 2007

ABSTRACT
The replication proteins Rep and Rep′ of porcine circovirus type 1 (PCV1) are both capable of introducing and resealing strand discontinuities at the viral origin of DNA replication in vitro underlying genome amplification by rolling-circle replication. The PCV1 origin of replication encompasses the minimal binding site (MBS) of the Rep and Rep′ proteins and an inverted repeat with the potential to form a stem-loop. In this study, both elements of the PCV1 origin were demonstrated to be essential for viral replication in transfected cells. Furthermore, investigation of conserved amino acid motifs within Rep and Rep′ proteins revealed that the mutation of motifs I, II, and III and of the GKS box interfered with viral replication. In vitro studies demonstrated that motifs I to III were essential for origin cleavage, while the GKS box was dispensable for the initiation of viral replication. A covalent link between Rep/Rep′ and the DNA after origin cleavage was demonstrated, providing a mechanism for energy conservation for the termination of replication.
Both Virus and Tumor Necrosis Factor Alpha Are Critical for Endothelium Damage in a Mouse Model of Dengue Virus-Induced Hemorrhage
Authors: Chen Hsuen-Chin , Hofman Florence M. , Kung John T. , Lin Yang-Ding , Wu-Hsieh Betty A. 
Published: March 2007

ABSTRACT

Hemorrhage is a common clinical manifestation in dengue patients. However, the pathogenic mechanism of dengue virus (DV)-induced hemorrhage awaits clarification. We established a mouse model of DV hemorrhage using immunocompetent C57BL/6 mice by injecting DV serotype 2 strain 16681 intradermally. While inoculation of 3 × 10
9
PFU of DV induced systemic hemorrhage in all of the mice by day 3 of infection, one out of three of those injected with 4 × 10
7
to 8 × 10
7
PFU developed hemorrhage in the subcutaneous tissues. The mice that were inoculated with 4 × 10
7
to 8 × 10
7
PFU but that did not develop hemorrhage were used as a basis for comparison to explore the pathogenic mechanism of dengue hemorrhage. The results showed that mice with severe thrombocytopenia manifested signs of vascular leakage and hemorrhage. We observed that high viral titer, macrophage infiltration, and tumor necrosis factor alpha (TNF-α) production in the local tissues are three important events that lead to hemorrhage. Immunofluorescence staining revealed that DV targeted both endothelial cells and macrophages. In addition, the production of high levels of TNF-α in tissues correlated with endothelial cell apoptosis and hemorrhage. By comparing TNF-α
−/−
to IgH
−/−
, C5
−/−
, and wild-type mice, we found that TNF-α was important for the development of hemorrhage. In vitro studies showed that mouse primary microvascular endothelial cells were susceptible to DV but that TNF-α enhanced DV-induced apoptosis. Our mouse model illustrated that intradermal inoculation of high titers of DV predisposes endothelial cells to be susceptible to TNF-α-induced cell death, which leads to endothelium damage and hemorrhage development. This finding highlights the contribution of the innate immune response to dengue hemorrhage.