bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytoplasm‐localized SIRT1 enhances apoptosis
Authors: Jin Qihuang , Yan Tingting , Ge Xinjian , Sun Cheng , Shi Xianglin , Zhai Qiwei 
Published: May 2007

AbstractIn general, SIRT1 is localized in nuclei. Here, we showed that endogenous and exogenous SIRT1 were both able to partially localize in cytoplasm in certain cell lines, and cytoplasm‐localized SIRT1 was associated with apoptosis and led to increased sensitivity to apoptosis. Furthermore, we demonstrated that translocation of nucleus‐localized SIRT1 from nuclei to cytoplasm was the main pathway leading to localization of SIRT1 in cytoplasm. In HeLa cells, wild type SIRT1 was completely localized in nuclei. By truncation of two predicted nuclear localization signals or fusion with an exogenous nuclear export signal, SIRT1 was partially localized in cytoplasm of HeLa cells and resulted in increased sensitivity to apoptosis. The apoptosis enhanced by cytoplasm‐localized SIRT1 was independent of its deacetylase activity, but dependent on caspases. SIRT1 was distributed in cytoplasm at metaphase during mitosis, and overexpression of SIRT1 significantly augmented apoptosis for cells at metaphase. In summary, we found SIRT1 is able to localize in cytoplasm, and cytoplasm‐localized SIRT1 enhances apoptosis. J. Cell. Physiol. 213: 88–97, 2007. © 2007 Wiley‐Liss, Inc.
Increased Ca2+ storage capacity of the skeletal muscle sarcoplasmic reticulum of transgenic mice over‐expressing membrane bound calcium binding protein junctate
Authors: Divet Alexandra , Paesante Silvia , Grasso Cristiano , Cavagna Dario , Tiveron Cecilia , Paolini Cecilia , Protasi Feliciano , Huchet‐Cadiou Corinne , Treves Susan , Zorzato Francesco 
Published: May 2007

AbstractJunctate is an integral sarco(endo)plasmic reticulum protein expressed in many tissues including heart and skeletal muscle. Because of its localization and biochemical characteristics, junctate is deemed to participate in the regulation of the intracellular Ca2+ concentration. However, its physiological function in muscle cells has not been investigated yet. In this study we examined the effects of junctate over‐expression by generating a transgenic mouse model which over‐expresses junctate in skeletal muscle. Our results demonstrate that junctate over‐expression induced a significant increase in SR Ca2+ storage capacity which was paralleled by an increased 4‐chloro‐m‐cresol and caffeine‐induced Ca2+ release, whereas it did not affect SR Ca2+‐dependent ATPase activity and SR Ca2+ loading rates. In addition, junctate over‐expression did not affect the expression levels of SR Ca2+ binding proteins such as calsequestrin, calreticulin and sarcalumenin. These findings suggest that junctate over‐expression is associated with an increase in the SR Ca2+ storage capacity and releasable Ca2+ content and support a physiological role for junctate in intracellular Ca2+ homeostasis. J. Cell. Physiol. 213: 464–474, 2007. © 2007 Wiley‐Liss, Inc.
Dystroglycan expression is reduced during prostate tumorigenesis and is regulated by androgens in prostate cancer cells
Authors: Sgambato A. , De Paola B. , Migaldi M. , Di Salvatore M. , Rettino A. , Rossi G. , Faraglia B. , Boninsegna A. , Maiorana A. , Cittadini A. 
Published: May 2007

AbstractProstate cancer, the most frequently diagnosed cancer in Western men, can display a high variability in term of clinical aggressiveness and prognosis and none of the available markers is able to accurately predict its clinical course. Dystroglycan (DG), a non‐integrin adhesion molecule, is a complex formed by two subunits, α‐ and β‐DG, which bind to extracellular matrix molecules and cytoskeleton, respectively. DG expression is frequently reduced in human cancers and has been related to tumor grade and aggressiveness. This study investigated the role of DG in human prostate tumorigenesis and its suitability as a prognostic marker. The expression level of extracellular α‐DG subunit was frequently reduced in human prostate cancer cell lines and primary tumors and the percentage of positive tumor cells was significantly further decreased in vivo following androgen ablation therapy (median = 1%) compared to pre‐treatment samples (median = 28%). A significant relationship was observed between α‐DG staining on the post‐treatment samples and tumor recurrence. A dose‐ and time‐dependent decrease of DG expression also occurred in human prostate cancer cells following treatment with the anti‐androgen flutamide. Stable expression of an exogenous DG cDNA in the LNCaP human prostate carcinoma cell line resulted in a marked inhibition of both anchorage‐dependent and independent growth and of the in vivo tumorigenicity. These findings confirm and extend previous evidence that disturbances in the function of the DG complex might contribute to the definition of the malignant behavior of prostate cancer cells and suggest that androgens might regulate DG expression in these cells. J. Cell. Physiol. 213: 528–539, 2007. © 2007 Wiley‐Liss, Inc.
Mechanisms of uremic erythrocyte‐induced adhesion of human monocytes to cultured endothelial cells
Authors: Pandolfi Assunta , Di Pietro Natalia , Sirolli Vittorio , Giardinelli Annalisa , Di Silvestre Sara , Amoroso Luigi , Di Tomo Pamela , Capani Fabio , Consoli Agostino , Bonomini Mario 
Published: May 2007

AbstractIn end‐stage renal disease (ESRD) endothelium may represent a key target for the action of circulating elements, such as modified erythrocytes (RBC) and/or plasmatic factors, that may facilitate inflammation and the vasculopathy associated with uremia. We have previously demonstrated that phosphatidylserine (PS) exposure on the surface of RBC from ESRD patients increases RBC‐human umbilical vein endothelial cell (HUVEC) interactions and causes decreased nitric oxide (NO) production. We postulated that, besides the pro‐inflammatory effects due to decreased NO bio‐availability, enhanced ESRD‐RBC‐HUVEC interactions might directly stimulate pro‐inflammatory pathways leading to increased vascular adhesion molecule expression. ESRD‐RBC‐endothelial cell interactions induced a time‐dependent up‐regulation of VCAM‐1 and ICAM‐1 (measured by Western blot (WB) and real‐time PCR), associated with mitogen‐activated protein kinase (MAPK) activation and impairment of the Akt/endothelial nitric oxide synthase (eNOS) signaling cascade, measured by WB. In reconstitution experiments, normal RBC incubated with uremic plasma showed increased PS exposure and significantly increased VCAM‐1 and ICAM‐1 mRNA levels when incubated on HUVEC. Interestingly, ESRD‐RBC induced increased expression of adhesion molecules was prevented by Annexin‐V (AnV, able to mask PS on RBC surface), anti‐integrin‐αvβ3, anti‐thrombospondin‐1 (TSP‐1), and PD98059 (a selective inhibitor of MAPK phosphorylation). Moreover, AnV reversed the ESRD‐RBC effects on MAPK and Akt/eNOS signaling pathways. Our data demonstrate that, possibly via a direct interaction with the endothelial thrombospondin‐(αvβ3) integrin complex, ESRD‐RBC‐HUVEC adhesion induces a vascular inflammatory phenotype. Thus, intervention targeting ESRD‐RBC increased adhesion to endothelium and/or MAPK and Akt/eNOS pathways may have the potential to prevent vascular lesions under uremic conditions. J. Cell. Physiol. 213:699–709. © 2007 Wiley‐Liss, Inc.
Bone morphogenetic protein 4 induces epithelial‐mesenchymal transition through MSX2 induction on pancreatic cancer cell line
Authors: Hamada Shin , Satoh Kennichi , Hirota Morihisa , Kimura Kenji , Kanno Atsushi , Masamune Atsushi , Shimosegawa Tooru 
Published: May 2007

AbstractIn our study, we found that bone morphogenetic protein 4 (BMP4) has a novel effect as an inducer of epithelial‐mesenchymal transition (EMT) on Panc‐1 cells, a human pancreatic carcinoma cell line. BMP4‐treated Panc‐1 cells showed loose cell contacts and a scattered, fibroblast‐like appearance along with E‐cadherin downregulation, Vimentin upregulation and enhanced cell migration, which are characteristic of EMT. BMP4 treatment also induced homeobox gene MSX2 expression, which we previously showed to be associated with EMT in pancreatic carcinoma cells. BMP4 treatment activated the Smad signaling pathway, and extracellular signal‐related kinase (ERK) and p38 mitogen‐activated kinase (MAPK) pathways in these cells. MSX2 was markedly induced by BMP4 through the ERK and p38 MAPK pathways in collaboration with the Smad signaling pathway. The repression of E‐cadherin, induction of Vimentin and enhanced cell migration disappeared when siRNA‐based MSX2 downregulated pancreatic cancer cells were treated with BMP4. These findings indicate that BMP4 may be involved in pancreatic carcinoma development through the promotion of EMT and that MSX2 is indispensable to this process. J. Cell. Physiol. 213:768–774. © 2007 Wiley‐Liss, Inc.
Deer antler regeneration: Cells, concepts, and controversies
Authors: Kierdorf Uwe , Kierdorf Horst , Szuwart Thomas 
Published: May 2007

AbstractThe periodic replacement of antlers is an exceptional regenerative process in mammals, which in general are unable to regenerate complete body appendages. Antler regeneration has traditionally been viewed as an epimorphic process closely resembling limb regeneration in urodele amphibians, and the terminology of the latter process has also been applied to antler regeneration. More recent studies, however, showed that, unlike urodele limb regeneration, antler regeneration does not involve cell dedifferentiation and the formation of a blastema from these dedifferentiated cells. Rather, these studies suggest that antler regeneration is a stem‐cell‐based process that depends on the periodic activation of, presumably neural‐crest‐derived, periosteal stem cells of the distal pedicle. The evidence for this hypothesis is reviewed and as a result, a new concept of antler regeneration as a process of stem‐cell‐based epimorphic regeneration is proposed that does not involve cell dedifferentiation or transdifferentiation. Antler regeneration illustrates that extensive appendage regeneration in a postnatal mammal can be achieved by a developmental process that differs in several fundamental aspects from limb regeneration in urodeles. J. Morphol., 2007 © 2007 Wiley‐Liss, Inc.
Association Between HLA‐DRB1 polymorphism, high‐risk HPV infection and cervical neoplasia in southern Chinese
Authors: Chan Paul K.S. , Cheung Tak‐Hong , Lin C. K. , Siu Shing‐Shun N. , Yim So‐Fan , Lo Keith W.K. , Cheung Jo L. K. , Tam Ann O.Y. , Tang Julian W. 
Published: May 2007

AbstractMultiple determinants are involved in the progression of human papillomavirus (HPV)‐infected cervical lesion to invasive cancer. Human leukocyte antigen (HLA) polymorphism seems to play a role. This study examined the association between HLA‐DRB1 polymorphism, high‐risk HPV infection, and the development of cervical neoplasia in southern Chinese. Three hundred and seventy women with cervical neoplasia (43 cervical intraepithelial neoplasia grade II, 154 grade III, and 173 invasive cancers) and 323 controls were recruited for HLA‐DRB1 typing by a sequence‐based approach. Cervical specimens were collected for HPV detection by a consensus primer‐based polymerase chain reaction, and with the type of HPV identified by hybridization with type‐specific oligonucleotide probes. A protective effect of HLA‐DRB1*12 for cervical neoplasia was observed, and with stronger associations when subgroup analyses were carried out for patients infected with HPV16 and HPV58. The protective effect of HLA‐DRB1*13 that had been reported from other populations was not observed. The data obtained in this study showed that HLA‐DRB1*03 conferred a higher risk for HPV18‐infected, but not for HPV16‐, HPV52‐, or HPV58‐infected cervical lesions. Although, HPV52 was reported as uncommon worldwide, it was found to be the second most prevalent type in the southern Chinese population. However, no additional risk association was observed when subgroup analyses were performed for HPV52‐infected patients. The current study shows that, among southern Chinese, the outcome of HPV‐infected cervical lesions is associated with HLA‐DRB1 polymorphism. These associations often vary with the type of HPV infection. J. Med. Virol. 79:970‐976, 2007. © 2007 Wiley‐Liss, Inc.
Anti‐HTLV‐1 tax antibody and tax‐specific cytotoxic T lymphocyte are associated with a reduction in HTLV‐1 proviral load in asymptomatic carriers
Authors: Akimoto Masaki , Kozako Tomohiro , Sawada Takashi , Matsushita Kakushi , Ozaki Atsuo , Hamada Heiichiro , Kawada Hideaki , Yoshimitsu Makoto , Tokunaga Masahito , Haraguchi Koichi , Uozumi Kimiharu , Arima Naomichi , Tei Chuwa 
Published: May 2007

AbstractPrevious studies have suggested that higher anti‐human T‐lymphotropic virus 1 (HTLV‐1) antibody titer and lower anti‐HTLV‐1 Tax antibody reactivity are risk factors for adult T‐cell leukemia/lymphoma. In the present study, we analyzed the relationships between these factors and clarified their significance. Forty‐five carriers were examined for anti‐HTLV‐1 and anti‐Tax antibody by ELISA. In addition, 43 of the 45 carriers with HLA‐A*0201 and/or A*2402 were examined for frequency of Tax‐specific cytotoxic T lymphocytes (CTLs) using HTLV‐1/HLA tetramers, and 44 were examined for proviral load by real‐time PCR. The relationships between these factors were analyzed statistically. The frequencies of Tax11‐19 and Tax301‐309‐specific CTLs were significantly higher in the anti‐Tax antibody‐positive group as compared with the antibody‐negative group (P = 0.002 and 0.033, respectively). Anti‐HTLV‐1 antibody titer had a positive correlation with proviral load (P = 0.019), whereas anti‐Tax antibody did not show a significant correlation. Higher frequencies of both Tax11‐19 and Tax301‐309‐specific CTLs are related to a reduction in proviral load (P = 0.017 and 0.015, respectively). Synergistic interactions of humoral and cellular immunity against Tax protein were demonstrated in HTLV‐1 carriers. Tax‐specific CTL may reduce HTLV‐1 proviral load to prevent asymptomatic carriers from developing adult T‐cell leukemia/lymphoma. J. Med. Virol. 79:977‐986, 2007. © Wiley‐Liss, Inc.
Molecular characterization of hepatitis A virus isolates from Argentina
Authors: Munné María S. , Vladimirsky Sara , Otegui Lucio , Soto Sonia , Brajterman Leonardo , Castro Raúl , Velasco María C. Cañero , Bonnano Alicia , Fernández Eduardo , Remondegui Carlos , Passeggi Carlos , Rodríguez Claudia , Pizarro Marta , Fabre Adriana , Moreiro Rita , Quarleri Jorge , González Jorge E. 
Published: May 2007

AbstractHepatitis A, a vaccine preventable disease, is now of transitional or intermediate endemicity in Argentina, as the epidemiologic pattern of the disease has shifted with improvements in living conditions in some parts of the country. Increase in the susceptibility of older children and adults has led to increasing disease incidence. Molecular epidemiology has played an important role in the understanding of HAV infection by identifying modes of spreading and by permitting the monitoring of changes in circulating virus brought about by prevention programs. South American isolates characterized are limited. Eighty‐two sporadic and outbreak isolates from Argentina were sequenced in the VP1/2A region of HAV genome over a 9‐year period. All the isolates belonged to subgenotype IA. All our sequences grouped into two big clusters. Apparently, at least two lineages have been co‐circulating in the same place at the same time. Despite great genetic variability, few point amino acid changes could be deduced. Four sequences showed an Arg → Lys substitution at 1–297 which characterized the genotype IB at the amino acid level. Many isolates carried a conservative amino acid substitution Leu → Ile at position 42 of the 2A domain, previously described as a possible fingerprint of HAV sequences in Brazil. The other rare changes have been found before, except for a 1–277 Asn → Ser substitution displayed in two isolates that has not been previously reported. Argentina recently implemented universal vaccination in 1‐year‐old children. Molecular tools would be useful in an active surveillance program. J. Med. Virol. 79:887–894, 2007. © 2007 Wiley‐Liss, Inc.
Genotyping of recent measles virus strains from Russia and Vietnam by nucleotide‐specific multiplex PCR
Authors: Kremer Jacques R. , Nguyen Giang H. , Shulga Sergey V. , Nguyen Phuc H. , Nguyen Ut T. , Tikhonova Nina T. , Muller Claude P. 
Published: May 2007

AbstractThe nucleoprotein genes of 49 measles virus (MV) strains circulating in Russia between 2000 and 2006 and in Vietnam in 2003 were analyzed by genotype‐specific PCR and the results were compared with their sequences. The sequences revealed the presence of genotypes H1 and H2 in the center (Nha Trang) and the north (Hanoi) of Vietnam, respectively. The relative diversity of the H2 strains suggested an endemic circulation of these viruses in the capital. In contrast genotype H1 strains from Nha Trang were homogenous genetically, which may indicate a recent importation. The strains obtained from 12 different regions of the Russian Federation were assigned to the genotypes H1, D4, and D6. Most strains (81.4%) were correctly genotyped by a multiplex PCR method which was sensitive to genotype‐specific mutations [Kremer et al. (2004): J Clin Microbiol 42: 3017–3022]. Ambiguous or negative results for some clade H and genotype D6 strains were due to point mutations in the type‐specific primer binding sites. After exchanging a single nucleotide in both the clade H‐ and the genotype D6‐specific primers, all strains were assigned correctly to their genotype. A simplified procedure for use in Vietnam was developed to distinguish directly between genotypes H1 and H2 and any non‐H genotype. These results demonstrate that our multiplex PCR method can be adapted easily to new sequence variants or specific epidemiological situations, and thus be very useful for rapid genotyping of large number of samples even in laboratories which do not have sequencing facilities. J. Med. Virol. 79:987‐994, 2007. © 2007 Wiley‐Liss, Inc.
Application of molecular and serological assays to case based investigations of rubella and congenital rubella syndrome
Authors: Jin Li , Thomas Brenda 
Published: May 2007

AbstractRubella and congenital rubella syndrome continue to be important health problems worldwide. The detection of rubella RNA directly in clinical specimens is a critical factor in early laboratory diagnosis of recent or congenital infection, in addition to detection of rubella‐specific IgM. In order to comply with recent WHO recommendations for establishing uniform genetic analysis protocols for rubella virus we have developed a new block based PCR assay (PCR‐E317), which extends the sequence generated by the block based PCR‐E592 currently in use, to cover the minimum acceptable 739 nucleotides (nt) window at the E1 gene. In addition, a real‐time PCR assay has been developed to allow rapid detection of the virus in the laboratory. The assays were applied to a number of clinical specimens collected from patients including recent rubella incidences in the UK, Ethiopia and Turkey, two prenatal and two congenital rubella syndrome cases. Rubella RNA was detected in specimens from two patients that were collected too early for IgM detection, in two amniotic fluids for prenatal diagnosis and in the follow up specimens from the two infant with congenital rubella syndrome tested for viral secretion. At least four genotypes were identified among these patients. The results showed that molecular assays are important tools in the early diagnosis of rubella and congenital rubella syndrome, in the provision of molecular epidemiological information for tracking transmission pathways and in adding to the knowledge of rubella strain distribution worldwide. J. Med. Virol. 79:1017‐1024, 2007. © 2007 Wiley‐Liss, Inc.
Seroepidemiology of hepatitis E virus in patients with non‐A, non‐B, non‐C hepatitis in Hungary
Authors: Haagsman Annika , Reuter Gábor , Duizer Erwin , Nagy Gyuláné , Herremans Tineke , Koopmans Marion , Szücs György 
Published: May 2007

AbstractMany cases of acute hepatitis remain undiagnosed and the hepatitis E virus (HEV) is emerging in industrialized countries. The aim of this study was to assess the role HEV as causative agent in acute non‐A, non‐B, and non‐C hepatitis patients in Hungary. 10.5% of the 264 acute non‐A, non‐B, and non‐C hepatitis patients tested had anti‐HEV IgG and 1.9% had anti‐HEV IgM as tested by ELISA. After confirmation by Western blot 6.1% of the acute non‐A, non‐B, and non‐C hepatitis patients had anti‐HEV IgG antibodies only and 1.1% of the patients had both IgG and IgM. All 19 patients that were positive for anti‐HEV IgG and/or IgM tested negative for HEV RNA by PCR. Only a small proportion of the acute hepatitis cases in the southwest of Hungary are assumed to be attributed to HEV infection, however, hepatitis E should be considered along with hepatitis A, B, and C in the diagnosis of acute hepatitis. J. Med. Virol. 79:927–930, 2007. © 2007 Wiley‐Liss, Inc.
Different genotype pattern of varicella‐zoster virus obtained from patients with varicella and zoster in Germany
Authors: Sauerbrei A. , Wutzler P. 
Published: May 2007

AbstractThe general use of the varicella vaccine requires the surveillance of varicella‐zoster virus (VZV) strains in patients infected with VZV. This paper reports the data achieved from a prospective study of genotyping VZV in Germany, analyzing the restriction fragment length polymorphism (RFLP) of the open reading frames (ORF) 38, 54, and 62 as well as the polymorphism of the R5 repeat region. The study included 177 patients with varicella. Seventy‐eight patients with zoster served as controls. Results revealed that 78% of VZV strains in patients with varicella had the genetic profile of the dominant wild‐genotype occurring in Europe and 22% had the markers of African or Asian strains. Varicella patients with the profile of African or Asian strains were significantly younger than patients with varicella caused by the dominant genotype. By contrast, all zoster patients exhibited strains representing the majority of wild‐type strains in Europe. In conclusion, VZV strains from patients with varicella have a significantly higher genetic variability than viral strains from zoster patients. Since variants with the markers of African or Asian strains could only be found in young children with chickenpox, the results suggest a changing scene of VZV genotypes in Germany. As reasons, the spread of viruses, which may be imported originally by persons immigrating from warmer climates, or the recombination between wild‐and vaccine‐type viruses have to be considered. J. Med. Virol. 79:1025‐1031, 2007. © 2007 Wiley‐Liss, Inc.