bluuebunny/crossref_metadata_2025_split huggingface dataset:
Primary chondrification foci in the wing basipodium of Struthio camelus with comments on interpretation of autopodial elements in Crocodilia and Aves
Authors: Kundrát Martin 
Published: October 2008

AbstractThe present analysis consists of (1) description of the primary chondrification patterns and their transformation into ossified elements in the basipodium of Struthio camelus; (2) comparison of these with the conditions found in Alligator and Gallus; and (3) interpretation of the autopodial elements of Archaeopteryx. Conclusions: (1) The existence of five discrete metacarpal condensations in the 16‐day embryo of Struthio argues for unique linear patterning process for each, and these are interpreted as digits 2,3,4 originating from metacarpal condensations 2,3,4. Nine chondrogenic foci appear in the Struthio carpus: radiale, centrale, intermedium, ulnare, pseudoulnare, pisiform, distal carpal 2+3, distal carpal 4, and distal carpal 5. It is evident that: (a) the avian “radiale” represents fused chondrogenic foci of the intermedium plus the radiale; (b) a neomorph carpal element, the pseudoulnare (probably avian autapomorphy), replaces the ulnare cartilage in Struthio; (c) the pseudoulnare in Struthio and Hinchliffe's element “X” are not identical to each other. (2) Spatio‐temporal conditions of the autopodium are less constrained in the development of Struthio than they are in Gallus. This favors the ostrich model as the more appropriate for interpretation of the autopodial skeleton in the oldest birds and their ancestors. (3) An interpretation of the elements of the hand skeleton of Archaeopteryx is as follows: (a) digits 2,3,4; (b) distal carpal 2+3 (the semilunate); (c) distal carpal 4 (a missing element filling the gap between the semilunate and metacarpal IV); (d) the radiale+intermedium complex (the proximal carpal bone); (e) the pseudoulnare (the proximal carpal bone). J. Exp. Zool. (Mol. Dev. Evol.) 312B:30–41, 2009. © 2008 Wiley‐Liss, Inc.
Insights into the early evolution of SOX genes from expression analyses in a ctenophore
Authors: Jager Muriel , Quéinnec Eric , Chiori Roxane , Le Guyader Hervé , Manuel Michaël 
Published: October 2008

AbstractSOX genes encode transcription factors acting in various developmental processes in bilaterian animals, such as stem cell maintenance and the control of specification and differentiation of cell types in a variety of contexts, notably in the developing nervous system. To gain insights into the early evolution of this important family of developmental regulators, we investigated the expression of one subgroup B, two subgroup E, one subgroup F and two divergent SOX genes in the cydippid larva and in the adult of the ctenophore Pleurobrachia pileus. Transcripts of the two unclassified SOX (PpiSOX2/12) were detected in the female germ line and in various populations of putative somatic stem cells/undifferentiated progenitors. The remaining genes had spatially restricted expression patterns in ciliated epithelial cells, notably within neuro‐sensory territories. These data are compatible with an ancient involvement of SOX proteins in controlling aspects of stem cell maintenance, cellular differentiation and specification, notably within neuro‐sensory epithelia. In addition, the results highlight the complexity of the ctenophore anatomy and suggest that the SOX played an important role in the elaboration of the unique ctenophore body plan during evolution, through multiple gene co‐option. J. Exp. Zool. (Mol. Dev. Evol.) 310B:650–667, 2008. © 2008 Wiley‐Liss, Inc.
Tobacco, alcohol, and drug use among hospital patients: Concurrent use and willingness to change
Authors: Katz Ariel , Goldberg David , Smith Jennifer , Trick William E. 
Published: October 2008

AbstractBACKGROUND:Data are limited on concurrent smoking and substance use among hospital patients. To better inform hospital‐based intervention strategies, we evaluated the prevalence and concurrent use of these behaviors. This study evaluated the association between tobacco, alcohol, and other drug use, compared willingness to quit smoking among patients with and without substance use, and evaluated the relationship between willingness to quit smoking and readiness to change substance use.METHODS:This study was a cross‐sectional survey of non–Intensive Care Unit hospital patients at 2 public hospitals (a 464‐bed tertiary‐care hospital and a 100‐bed community hospital) by bedside interview. Severity of use and willingness to change behavior was determined. We evaluated the association between smoking and substance use by multivariable methods.RESULTS:Of 7,391 patients with known smoking status, 2,684 (36%) were current smokers. Among them, 1,376 hospitalized smokers (51%) had concurrent substance use. Among the 1,972 patients with at‐risk alcohol or drug use, the prevalence of smoking was 70% compared to 24% for non‐substance users (P < .01). Compared to other patients who smoked, substance‐dependent patients were more likely (Prevalence Rate Ratio = 1.4, 95% Confidence Interval = 1.1‐1.9) to be moderate to heavy smokers. Regardless of substance use pattern, most patients (60%) expressed a desire to immediately quit smoking.CONCLUSION:Hospital patients who describe at‐risk substance use are likely to smoke and express willingness to quit smoking. Given the prevalence of concurrent smoking and substance use and patients' desire to change both behaviors, there is a need for coordination of substance use and smoking cessation interventions. Journal of Hospital Medicine 2008;3:369–375. © 2008 Society of Hospital Medicine.
Estimating the direct costs of social conflicts: Road blockings in Bolivia
Authors: De Borger Bruno , Verardi Vincenzo 
Published: October 2008

AbstractSocial conflicts are a serious obstacle to economic growth in many Latin American societies, affecting economic activity both in the short and the long run. The purpose of this paper is twofold. First, we develop a methodology to estimate the direct, short‐run impact of frequently occurring exponents of local conflicts, such as road blockings, on economic activity. The methodology is based on using high frequency (daily) data to estimate the relation between a proxy for economic activity and the occurrence of road blockings. Careful analysis of impulse‐response functions traces the effect of such local social conflicts on economic activity. This information is combined with the aggregate annual time series relation between gross domestic product (GDP) and the high frequency proxy for economic activity to estimate the direct cost of local social conflicts for the economy as a whole. Second, we apply the proposed methodology to analyse the direct economic costs of road blockings in Bolivia, using detailed daily information for the year 2003. The results show that these costs are large. Stronger institutions are a critical factor in reducing the prevalence of such conflicts and to avoid the huge economic costs that they imply. Copyright © 2008 John Wiley & Sons, Ltd.
Can mass dissociation patterns of transition‐metal complexes be predicted from electrochemical data?
Authors: Toma Sergio H. , Alexiou Anamaria D. P. , Toma Henrique E. , Araki Koiti , Eberlin Marcos N. 
Published: October 2008

AbstractThe Cooks kinetic method has been very convenient to correlate the relative dissociation rates obtained by collision‐induced fragmentation experiments with the energies of two related bonds in molecules and complexes in the gas phase. Reliable bond energy data are, however, not always available, particularly for polynuclear transition‐metal complexes, such as the triruthenium acetate clusters of the general formula [Ru3 (µ3‐O)(µ‐CH3COO)6(py)2(L)]+, where L = ring substituted N‐heterocyclic ligands. Accordingly, their gas‐phase collision‐induced tandem mass spectrometry (CID MS/MS) dissociation patterns have been analyzed pursuing a relationship with the more easily accessible redox potentials (E1/2) and Lever's EL parameters. In fact, excellent linear correlations of ln(1/2AL/Apy), where Apy and AL are the abundance of the fragments retaining the pyridine (py) and L ligand, respectively, with E1/2 and EL were found. This result shows that those electrochemical parameters are correlated with bond energies and can be used in the analysis of the dissociation data. Such modified Cooks method can be used, for example, to determine the electronic effects of substituents on the metal–ligand bonds for a series of transition‐metal complexes. Copyright © 2008 John Wiley & Sons, Ltd.
Prevalence and molecular epidemiology of noroviruses detected in outbreak and sporadic cases of acute gastroenteritis in Bulgaria
Authors: Mladenova Zornitsa , Korsun Neli , Geonova Tsvetelina , Di Bartolo Ilaria , Fiore Lucia , Ruggeri Franco Maria 
Published: October 2008

AbstractNoroviruses constitute a genetically diverse group of viruses in the Caliciviridae family, and are recognized as an important cause of acute non‐bacterial gastroenteritis worldwide. To date there are no data on the incidence of noroviruses as a cause of gastroenteritis in Bulgaria. Fecal samples from an outbreak, and sporadic cases of diarrhea that occurred between December 2006 and April 2007 were tested for the presence of noroviruses. From a total of 474 stools (341 from sporadic cases and 133 cases from a single outbreak) examined, 72 samples (37 from sporadic cases and 35 from the outbreak) were positive using a norovirus‐specific enzyme immunoassay. Fifty‐nine specimens were confirmed and genotyped by RT‐PCR and sequencing of regions of the RNA‐dependent RNA polymerase and/or capsid. Sequence and phylogenetic analyses of 29 norovirus strains revealed a great diversity of norovirus genotypes among the sporadic cases including: GGII.3, GGII.4/2006a, GGII.4/2006b, GGII.20, and GGII.Karachi. A single norovirus genotype (GGII.4/2006b) was identified as the causative agent of the outbreak. This first investigation on the prevalence and molecular epidemiology of noroviruses demonstrates the significant role of these viruses as etiologic agents in acute gastroenteritis in Bulgaria. J. Med. Virol. 80:2161–2168, 2008. © 2008 Wiley‐Liss, Inc.
Molecular characterization of a variant virus that caused de novo hepatitis B without elevation of hepatitis B surface antigen after chemotherapy with rituximab
Authors: Miyagawa Masami , Minami Masahito , Fujii Kota , Sendo Rei , Mori Kojiro , Shimizu Daisuke , Nakajima Tomoaki , Yasui Kohichiroh , Itoh Yoshito , Taniwaki Masafumi , Okanoue Takeshi , Yoshikawa Toshikazu 
Published: October 2008

AbstractHepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)‐negative patients following treatment with rituximab has been reported increasingly. The aim of this study was to investigate the molecular mechanisms underlying HBV reactivation in an HBsAg‐negative patient. HBV was reactivated in a 75‐year‐old man following chemotherapy with rituximab, without elevation of HBsAg. The patient's full‐length HBV genome was cloned and the entire sequence was determined. Transfection studies were performed in vitro using recombinant wild‐type HBV (wild‐type), the patient's HBV (patient), and two chimeric HBV constructs, in which the preS/S region of the patient and wild‐type virus had been exchanged with one another. Secreted HBsAg and intra‐ and extra‐cellular HBV DNA were measured. The number of amino acid substitutions in HBV from this patient was much higher than in previous reports of HBV mutants, such as occult HBV and vaccine escape HBV mutants. Levels of HBsAg and HBV DNA production in vitro were significantly lower in the patient compared to wild‐type transfections. From analyses of the chimeric constructs, the altered preS/S region was responsible mainly for this impairment. These results show that highly mutated HBV can reactivate after chemotherapy with rituximab, despite an unusually large number of mutations, resulting in impaired viral replication in vitro. Severe immune suppression, probably caused by rituximab, may permit reactivation of highly mutated HBV. These findings have important clinical implications for the prevention and management of HBV reactivation and may explain partially the mechanism of recent, unusual cases of HBV reactivation. J. Med. Virol. 80:2069–2078, 2008. © 2008 Wiley‐Liss, Inc.
p53 gene mutational rate, Gleason score, and BK virus infection in prostate adenocarcinoma: Is there a correlation?
Authors: Russo Giuseppe , Anzivino Elena , Fioriti Daniela , Mischitelli Monica , Bellizzi Anna , Giordano Antonio , Autran‐Gomez Anamaria , Di Monaco Franco , Di Silverio Franco , Sale Patrizio , Di Prospero Laura , Pietropaolo Valeria 
Published: October 2008

AbstractProstate cancer represents the second leading cause of cancer deaths in Western countries. Viral infections could play a role in prostate carcinogenesis. Human polyomavirus BK (BKV) is a possible candidate because of its transforming properties. In this study, BKV sequences in urine, blood, fresh, and paraffin‐embedded prostate cancer samples from 26 patients were searched using Q‐PCR analysis. T antigen (TAg) and p53 localization in neoplastic cells were evaluated by immunohistochemical analysis. Also, the presence of mutations in 5–9 exons of p53 gene was analyzed. Results showed that BKV‐DNA was found in urine (54%), plasma (31%), and in fresh prostate cancer specimens (85%). The analysis of p53 gene evidenced several mutations in high Gleason patients, according to tumor advanced stage. Immunohistochemical analysis results evidenced the localization of p53 and TAg into cytoplasm, whereas in TAg‐negative tumors, p53 was nuclear. This study suggests that BKV acts as cofactor in the pathogenesis of prostate cancer. These observations emphasize previous studies regarding the cellular pathways that may be deregulated by BKV. J. Med. Virol. 80:2100–2107, 2008. © 2008 Wiley‐Liss, Inc.
Efficacy and safety of peginterferon alpha‐2a/ribavirin in treatment‐naive Cameroonian patients with chronic hepatitis C
Authors: Njouom Richard , Sartre Michèle Tagni , Timba Isabelle , Nerrienet Eric , Tchendjou Patrice , Pasquier Christophe , Rousset Dominique 
Published: October 2008

AbstractData were examined from a day‐to‐day clinical practice in Yaounde, Cameroon to evaluate the efficacy and safety of peginterferon alfa‐2a and ribavirin in treatment‐naive Cameroonian patients with chronic hepatitis C. Ninety adults with chronic hepatitis C (mean age, 53 ± 8 years; 79% males; 37.8% genotype 1; 23.3% genotype 2; and 38.9% genotype 4) were given at least 12 weeks of combination therapy between February 2003 and August 2007. Of these, 54 completed the treatment and the 24‐week follow up. Subsequently, 18 continued treatment and 18 (20%) discontinued the treatment, 6 (6.7%) due to adverse effects. An intention‐to‐treat analysis showed that 38 (52.8%) had an end‐of‐treatment virologic response and 34 (47.2%) had a sustained virologic response. Sustained virologic response were significantly higher among patients with hepatitis C virus (HCV) genotype 2 (83.4%) than in those with genotype 1 (31%) or genotype 4 (42.3%) (P < 0.05). Non HCV‐2 genotype, pretreatment fibrosis score >2, HCV RNA level >8.0 × 105 IU/ml and a non‐virologic response at 12 weeks of treatment were associated with poor sustained virologic response (P < 0.05). Thus, HCV can be treated in a Sub‐Saharan African country. It indicates that Cameroonian HCV‐1 and ‐4 patients have a poorer sustained virologic response than the published results for Western and Middle‐East countries. Virus subtype may influence the treatment outcome, since there is a great genetic diversity within Cameroonian HCV‐1 and ‐4 genotypes. J. Med. Virol. 80:2079–2085, 2008. © 2008 Wiley‐Liss, Inc.
HHV8 a subtype is associated with rapidly evolving classic Kaposi's sarcoma
Authors: Mancuso Roberta , Biffi Renato , Valli Marilena , Bellinvia Monica , Athanasia Tourlaki , Ferrucci Silvia , Brambilla Lucia , Delbue Serena , Ferrante Pasquale , Tinelli Carmine , Clerici Mario 
Published: October 2008

AbstractThe link between human herpesvirus 8 (KSHV) and Kaposi's sarcoma (KS) has been proven, but many important aspects including risk factors, genetic predisposition to tumor development, transmission of KSHV, and the pathogenic potential of different genotypes remain to be elucidated. Possible associations between clinical parameters and antibody levels, viral load fluctuations, and viral genotype were analyzed by quantitative real‐time PCR, an in‐house developed IFA assay, and sequence analysis of ORF K1‐VR1 in blood, serum and saliva of 38 subjects with classic KS (cKS). KSHV lytic antibodies were significantly increased in stage IV compared to stage I and II patients (p = 0.006 and p = 0.041, respectively). KSHV blood, serum, and saliva viral load was comparable in all stages. The highest viral loads were detected in saliva, and they decreased in stages III–IV compared to stages I–II patients. Higher concentrations of lytic antibodies and higher viral loads were observed in fast progressing cKS patients, in whom KSHV detection from blood was also more frequent. Type A KSHV strain was almost exclusively present in rapid progressors (12/17 cases), while C type was mainly present in slow progressing patients (6/7 cases). Finally, detection of type A KSHV strain associated with higher blood viral loads. KSHV lytic antibody levels and viral load can be used to monitor clinical evolution of cKS. Infection supported by KSHV A subtype is associated with more rapid progressive disease. Careful monitoring and aggressive therapeutic protocols should be considered in patients with KSHV A‐supported infection. J. Med. Virol. 80:2153–2160, 2008. © 2008 Wiley‐Liss, Inc.
Consistency of quantitation of HCV genotype 4 from egypt across three HCV‐RNA amplification assays
Authors: Sharkawi Fathia Zaky El , Chudy Michael , Hanschmann Kay‐Martin , Kress Julia , Nübling C. Micha 
Published: October 2008

AbstractDifferent quantitative assays for HCV‐RNA are available that report test results in International Units (IU)/ml based on the WHO International Standard. Thus, assays have been calibrated with standard material containing HCV genotype 1, so the consistency of quantitation might differ between assays for other HCV genotypes. Three commercial HCV nucleic acid amplification techniques (HCV–NAT) were compared for quantitation consistency of genotype 4 and 1 specimens from an Egyptian blood donor panel (n = 92). Consistency of quantitation between HCV–NATs was higher for genotype 1 than for genotype 4. Most quantitative results reported by the assays were in the same range, but some genotype 4 samples were missed by two of the assays. The Abbott assay showed higher concentrations for genotype 4 than the two Roche assays. Follow‐up investigations of individuals should use the same assay unless another assay has been validated properly. Standardization of HCV–NAT assays remains an issue. J. Med. Virol. 80:2086–2091, 2008. © 2008 Wiley‐Liss, Inc.
Correlation between polymorphisms at interleukin‐6 but not at interleukin‐10 promoter and the risk of human T lymphotropic virus type I‐associated myelopathy/tropical spastic paraparesis in Brazilian individuals
Authors: Gadelha Sandra Rocha , Junior Alcântara Luiz Carlos , Costa Gisele Calazans , Acosta Angelina Xavier , Rios Domingos , Kashima Simone , Covas Dimas Tadeu , Galvão‐Castro Bernardo 
Published: October 2008

AbstractHTLV‐1 is the etiologic agent of ATL and HAM/TSP. The majority of HTLV‐1‐infected individuals remain asymptomatic, indicating that the infection alone is not sufficient to cause the diseases. It has been reported that cytokine gene polymorphisms, including polymorphisms at IL‐6 and IL‐10 gene, might be important. We analyzed SNP in the promoter region of the IL‐6: −174, −572, −597, and −634 positions, and IL‐10: −592 position to evaluate the role of these polymorphisms in the HAM/TSP pathogenesis in 133 HTLV‐1 infected individuals and in 100 healthy individuals from Salvador, Bahia, Brazil. The −634C allele frequencies were higher among HAM/TSP patients (21.2%) than among oligosymptomatic (6.5%; P = 0.038) and asymptomatic (9.5%; P = 0.025) subjects. Similarly, the −174G allele frequencies were higher in HAM/TSP patients than in oligosymptomatic patients (P = 0.02). Moreover, the −634GC/−174GG genotype combination was identified at a higher frequency (38.5%) in the HAM/TSP patients than in subjects with other clinical status (8.7%; P = 0.016 for oligosymptomatic and 15.5%, P = 0.012 for asymptomatic patients). However, the multivariate logistic regression including the genotypes of the three studied loci showed that only −634 C IL‐6 carriers remain as significant and independent TSP/HAM predictor (odds ratio [OR] = 5.31; 95% [CI] = 1.60–17.56; P = 0.006). We suggest that −634 G C in IL‐6 could contribute to HAM/TSP development and that identification of the collective influence of several cytokine polymorphisms, their prevalence, and their interaction could help to better understand this disease. J. Med. Virol. 80:2141–2146, 2008. © 2008 Wiley‐Liss, Inc.
Different protection of K252a and N‐acetyl‐L‐cysteine against amyloid‐β peptide–induced cortical neuron apoptosis involving inhibition of MLK3–MKK7–JNK3 signal cascades
Authors: Xu Yan , Hou Xiao‐Yu , Liu Yong , Zong Yan‐Yan 
Published: October 2008

AbstractAmyloid‐β peptide (Aβ) has been implicated in the etiopathogenesis of Alzheimer's disease (AD). However, the molecular mechanisms underlying Aβ neurotoxicity remain to be elucidated. This study showed that Aβ treatment resulted in the increased phosphorylation (activation) of MLK3, MKK7, and JNK3 in cultured cortical neurons, which characterized as biphasic activation (first peaked at 1 hr and second peaked at 12 hr after Aβ treatment). K252a blocked Aβ‐induced neuronal apoptosis, both early and late phases of MLK3–MKK7–JNK3 activation, as well as downstream signal events involving p‐JNKs nuclear translocation, c‐Jun phosphorylation, and Bad translocation to the mitochondria. The neuroprotective effect of K252a on Aβ‐induced apoptosis was partially dependent on Akt activation. In contrast, antioxidant N‐acetyl‐L‐cysteine (NAC) reduced early, but not late, MLK3–MKK7–JNK3 activation by Aβ treatment and provided a weak neuroprotective ability in Aβ‐induced apoptosis. Taken together, Aβ neurotoxicity is mainly due to MLK3–MKK7–JNK3 signal cascades. The late signal events of MLK3 activation after Aβ treatment may play an important role in AD neuronal loss and will be a promising pharmacological target for AD therapeutic intervention. © 2008 Wiley‐Liss, Inc.
Content of endoplasmic reticulum and Golgi complex membranes positively correlates with the proliferative status of brain cells
Authors: Silvestre David C. , Maccioni Hugo J.F. , Caputto Beatriz L. 
Published: October 2008

AbstractAlthough the molecular and cellular basis of particular events that lead to the biogenesis of membranes in eukaryotic cells has been described in detail, understanding of the intrinsic complexity of the pleiotropic response by which a cell adjusts the overall activity of its endomembrane system to accomplish these requirements is limited. Here we carried out an immunocytochemical and biochemical examination of the content and quality of the endoplasmic reticulum (ER) and Golgi apparatus membranes in two in vivo situations characterized by a phase of active cell proliferation followed by a phase of declination in proliferation (rat brain tissue at early and late developmental stages) or by permanent active proliferation (gliomas and their most malignant manifestation, glioblastomas multiforme). It was found that, in highly proliferative phases of brain development (early embryo brain cells), the content of ER and Golgi apparatus membranes, measured as total lipid phosphorous content, is higher than in adult brain cells. In addition, the concentration of protein markers of ER and Golgi is also higher in early embryo brain cells and in human glioblastoma multiforme cells than in adult rat brain or in nonpathological human brain cells. Results suggest that the amount of endomembranes and the concentration of constituent functional proteins diminish as cells decline in their proliferative activity. © 2008 Wiley‐Liss, Inc.