bluuebunny/crossref_metadata_2025_split huggingface dataset:
Positive selection for CD90 as a purging option in acute myeloid leukemia stem cell transplants
Authors: Feller Nicole , Kelder Angèle , Westra Guus , Ossenkoppele Gert J. , Schuurhuis Gerrit J. 
Published: December 2007

AbstractBackground:Several studies showed the benefit of purging of acute myeloid leukemia (AML) stem cell transplants. We reported previously that purging by positive selection of CD34+ and CD133+ cells resulted in a 3–4 log tumor cell reduction (TCR) in CD34− and/or CD133− AML, but has been shown to be potentially applicable in only about 50% of cases. Similar to CD34 and CD133, CD90 marks the hematopoietic CD34 positive stem cells capable of full hematopoietic recovery after myeloablative chemotherapy, and therefore, in the present study, we explored whether a similar purging approach is possible using CD90.Methods:CD90 expression was established by flowcytometry in diagnosis AML on the clonogenic AML CD34+ blast population by flow cytometry. Positivity was defined as >3% CD90 (CD34+) expression on blasts. For the calculation of the efficacy of TCR by positive selection, AML blasts were recognized by either prelabeling diagnosis blasts with CD45‐FITC in spiking model experiments or using expression of leukemia associated marker combinations both in spiking experiments and in real transplants.Results:In 119 patients with AML and myelodysplastic syndrome, we found coexpression of CD34 and CD90 (>3%) in 42 cases (35%). In AML patients 60 years or younger, representing the patients who are eligible for transplantation, only 23% (16/69) of the patients showed CD90 expression. Positive selection for CD90 in transplants containing CD90 negative AML resulted in a 2.8–4 log TCR in the models used.Conclusions:Purging by positive selection using CD90 can potentially be applied effectively in the majority of AML patients 60 years or younger. © 2007 Clinical Cytometry Society
Impact of trisomy 12, del(13q), del(17p), and del(11q) on the immunophenotype, DNA ploidy status, and proliferative rate of leukemic B‐cells in chronic lymphocytic leukemia
Authors: Quijano Sandra , López Antonio , Rasillo Ana , Sayagués José María , Barrena Susana , Sánchez Maria Luz , Teodosio Cristina , Giraldo Pilar , Giralt Manuel , Pérez M. Carmen , Romero Mercedes , Perdiguer Luis , Orfao Alberto 
Published: December 2007

AbstractB‐cell chronic lymphocytic leukemia (B‐CLL) is a well‐defined clinical entity with heterogeneous molecular and cytogenetic features. Here, we analyze the impact of trisomy 12, del(13q), del(17p), and del(11q) as determined by interphase fluorescence in situ hybridization analysis of purified neoplastic B‐CLL cells on their immunophenotype, DNA ploidy status and proliferative rate.Overall, 111 of 180 (62%) B‐CLL cases studied displayed one (50%) or more (12%) genetic abnormalities, del(13q) (35%) being more frequently detected than trisomy 12 (23%) followed by del(11q) (9%) and del(17p) (8%). Trisomy 12 was associated with a higher frequency of DNA aneuploidy, stronger expression of CD19, CD20, CD22, CD24, CD27, CD79b, CD38, and sIg and lower reactivity for CD43 with respect to cytogenetically nonaltered cases. In turn, cases with del(13q) displayed greater reactivity for CD20, FMC7, CD27, CD22, CD5, and bcl2, while del(11q) was associated with brighter expression of CD38, FMC7, CD25, and sIg. Hierarchical clustering analysis of the immunophenotype of B‐CLL cases with cytogenetic abnormalities allowed the identification of three different groups of patients with increasing frequencies of trisomy 12, del(11q), and del(13q). Remarkably, none of the cytogenetic abnormalities analyzed except coexistence of 13q‐ and 17p‐ had a clear impact on the proliferative index of B‐CLL cells. © 2007 Clinical Cytometry Society
A comparision of aspiration cytology and core needle biopsy according to tumor size of suspicious breast lesions
Authors: Barra Alexandre de Almeida , Gobbi Helenice , de L. Rezende César Alencar , Gouvêa Agostinho Pinto , de Lucena Clécio Ênio Murta , Reis João Henrique Pena , Costa e Silva Soraya Zhouri 
Published: December 2007

AbstractThe purpose of the study was to compare the accuracy of FNAC, CNB, and combined biopsy according to tumor size of suspicious breast lesions.FNAC and CNB were performed in 264 patients with suspicious breast lesions from August, 1997 to August, 2002. The procedures were guided by ultrasound and performed in the same session by the same operator. The lesions were divided in four groups according to the tumor size in the histopathology report: lesions smaller than 1 cm, between 1 and 2 cm, between 2 and 5 cm, and lesions greater than 5 cm.The final surgical histopatology results identified 222 (84%) malignant cases and benign lesions summed 42 (16%). For lesions smaller than 1 cm, FNAC, CNB, and combined biopsy were equivalent for all parameters. For lesions between 1 and 2 cm, FNAC and CNB were equivalent. Combined biopsy showed higher absolute sensitivity (P = 0.007) and lower inadequate rate (P = 0.03) when compared to FNAC. However, when combined biopsy and CNB were compared, no difference were found. For lesions between 2 and 5 cm, CNB showed higher absolute sensitivity (P < 0.001) and lower inadequate rate (P < 0.007) when compared to FNAC. Combined biopsy showed higher sensitivity compared to FNAC and CNB alone (P < 0.05) in this group. For lesions greater than 5 cm, FNAC and CNB were equivalent for all parameters. Combined biopsy only showed higher absolute sensitivity (P = 0.04) when compared with FNAC alone.The combination of FNAC and CNB can improve the diagnosis of suspicious breast lesions higher than 1 cm. However, for lesions smaller than 1 cm, our results showed no difference between FNAC, CNB, and combined biopsy, for these lesions any modality has technical limitations. Diagn. Cytopathol. 2008;36:26–31. © 2007 Wiley‐Liss, Inc.
Synchronous metastases to the liver and pancreas from a primary neuroendocrine carcinoma of the breast diagnosed by fine‐needle aspiration
Authors: McIntire Maria , Siziopikou Kalliopi , Patil Jyothi , Gattuso Paolo 
Published: December 2007

AbstractExtrapulmonary neuroendocrine carcinoma is uncommon. Cases of primary neuroendocrine carcinoma of the breast have been reported, though rare. We report the case of a 53‐year‐old woman who underwent a mastectomy for breast carcinoma and presented three years later with synchronous masses in the head of the pancreas and liver. Fine‐needle aspiration of both organs revealed a neuroendocrine carcinoma. The original breast tumor was reviewed and found to express neuroendocrine markers. A diagnosis of a primary neuroendocrine carcinoma of the breast was rendered. Diagn. Cytopathol. 2008;36:54–57. © 2007 Wiley‐Liss, Inc.
Transgenic mouse lines expressing Cre recombinase specifically in posterior notochord and notochord
Authors: Kumar Amit , Yamaguchi Taihei , Sharma Prashant , Kuehn Michael R. 
Published: December 2007

AbstractDuring development, the organizer provides instructive signals to surrounding cells as well as contributing cells to axial structures. To dissect organizer function at different developmental stages, conditional approaches such as the Cre/loxP system for conditional mutagenesis are particularly useful. Here we describe two new Cre transgenic mouse lines, Foxa2 NFP‐Cre and Nodal PNC‐Cre, with activity in two organizer domains, the posterior notochord (PNC) and notochord. These lines were made using defined regulatory elements from the Foxa2 and Nodal genes that direct Cre expression in overlapping domains of the PNC and notochord. Our detailed analysis of the timing and location of Foxa2 NFP‐Cre and Nodal PNC‐Cre activity indicates that these lines are appropriate for conditional mutagenesis of genes expressed from early somite stages onward. genesis 45:729–736, 2007. Published 2007 Wiley‐Liss, Inc.
Generation of mice with a conditional allele of the p120 Ras GTPase‐activating protein
Authors: Lapinski Philip E. , Bauler Timothy J. , Brown Eric J. , Hughes Elizabeth D. , Saunders Thomas L. , King Philip D. 
Published: December 2007

Abstractp120 Ras GTPase‐activating protein (RasGAP) encoded by the rasa1 gene in mice is a prototypical member of the RasGAP family of proteins involved in negative‐regulation of the p21 Ras proto‐oncogene. RasGAP has been implicated in signal transduction through a number of cell surface receptors. In humans, inactivating mutations in the coding region of the RASA1 gene cause capillary malformation arteriovenous malformation. In mice, generalized disruption of the rasa1 gene results in early embryonic lethality associated with defective vasculogenesis and increased apoptosis of neuronal cells. The early lethality in this mouse model precludes its use to further study the importance of RasGAP as a regulator of cell function. Therefore, to circumvent this problem, we have generated a conditional rasa1 knockout mouse. In this mouse, an exon that encodes a part of the RasGAP protein essential for catalytic activity has been flanked by loxP recognition sites. With the use of different constitutive and inducible Cre transgenic mouse lines, we show that deletion of this exon from the rasa1 locus results in effective loss of expression of catalytically‐active RasGAP from a variety of adult tissues. The conditional rasa1 mouse will be useful for the analysis of the role of RasGAP in mature cell types. genesis 45:762–767, 2007. © 2007 Wiley‐Liss, Inc.
Hemispheric and gender related differences in the midcingulum bundle: A DTI study
Authors: Huster Rene J. , Westerhausen Rene , Kreuder Frank , Schweiger Elisabeth , Wittling Werner 
Published: December 2007

AbstractThe midcingulate cortex and therefore the underlying midcingulum bundle (MCB) as well play a major role in attention. Although a specific structure's function does strongly depend on its neuroanatomical characteristics, research assessing the morphological variability of the midcingulate region is rather sparse. The present study examined the micro‐ and macrostructure of the MCB in both hemispheres by means of diffusion‐tensor imaging. Besides, effects of gender (Female = 40, Male = 39) and handedness (Lefthanders = 45, Righthanders = 34) were assessed as well. Measures of fractional anisotropy, mean diffusion, as well as the white matter volumes of the MCBs were assessed. By integration of multi‐modal images, the MCB was isolated and confounding with callosal fibers was avoided. Evidence was found indicating differences between hemispheres and gender regarding both volume and microstructural characteristics of the MCB. Interestingly, gender‐related effects seem to be substantially associated with variations in individual brain volumes. Handedness did not emerge as relevant factor in the analyses. These findings might indicate a higher functional connectivity of the left MCB and in males as compared to females. Hum Brain Mapp, 2009. © 2007 Wiley‐Liss, Inc.
Toward understanding nonparticipation in sigmoidoscopy screening for colorectal cancer
Authors: Blom Johannes , Yin Li , Lidén Annika , Dolk Anders , Jeppsson Bengt , Påhlman Lars , Holmberg Lars , Nyrén Olof 
Published: December 2007

AbstractUnderstanding the reasons for nonparticipation in cancer screening may give clues about how to improve compliance. However, limited cooperation has hampered research on nonparticipant profiles. We took advantage of Sweden's comprehensive demographic and health care registers to investigate characteristics of all participants and nonparticipants in a pilot program for colorectal cancer screening with sigmoidoscopy. A population‐based sample of 1986 Swedish residents 59–61 years old was invited. Registers provided information on each individual's gender, country of birth, marital status, education, income, hospital contacts, place of residence, distance to screening center and cancer within the family. Odds ratios (ORs) with 95% confidence intervals (CIs), modeled with multivariable logistic regression, estimated the independent associations between each background factor and the propensity for nonparticipation after control for the effects of other factors. All statistical tests were 2‐sided. Being male (OR = 1.27, 95% CI = 1.03–1.57, relative to female), unmarried or divorced (OR = 1.69, 95% CI = 1.23–2.30 and OR = 1.49, 95% CI = 1.14–1.95, respectively, relative to married) and having an income in the lowest tertile (OR = 1.68, 95% CI = 1.27–2.23, relative to highest tertile) was associated with increased nonparticipation. Living in the countryside or in small communities and having a documented family history of colorectal cancer was associated with better participation. Distance to the screening center did not significantly affect participation, nor did recent hospital care consumption or immigrant status. To increase compliance, invitations must appeal to men, unmarried or divorced people and people with low socioeconomic status. © 2007 Wiley‐Liss, Inc.
Exercise running and tetracycline as means to enhance skeletal muscle stem cell performance after external fixation
Authors: Shefer G. , Carmeli E. , Rauner G. , Yablonka‐Reuveni Z. , Benayahu D. 
Published: December 2007

AbstractProlonged limb immobilization, which is often the outcome of injury and illness, results in the atrophy of skeletal muscles. The basis of muscle atrophy needs to be better understood in order to allow development of effective countermeasures. The present study focused on determining whether skeletal muscle stem cells, satellite cells, are directly affected by long‐term immobilization as well as on investigating the potential of pharmacological and physiological avenues to counterbalance atrophy‐induced muscle deterioration. We used external fixation (EF), as a clinically relevant model, to gain insights into the relationships between muscle degenerative and regenerative conditions to the myogenic properties and abundance of bona fide satellite cells. Rats were treated with tetracycline (Tet) through the EF period, or exercise trained on a treadmill for 2 weeks after the cessation of the atrophic stimulus. EF induced muscle mass loss; declined expression of the muscle specific regulatory factors (MRFs) Myf5, MyoD, myogenin, and also of satellite cell numbers and myogenic differentiation aptitude. Tet enhanced the expression of MRFs, but did not prevent the decline of the satellite cell pool. After exercise running, however, muscle mass, satellite cell numbers (enumerated through the entire length of myofibers), and myogenic differentiation aptitude (determined by the lineal identity of clonal cultures of satellite cells) were re‐gained to levels prior to EF. Together, our results point to Tet and exercise running as promising and relevant approaches for enhancing muscle recovery after atrophy. J. Cell. Physiol. 215: 265–275, 2008. © 2007 Wiley‐Liss, Inc.
Osteoclast stimulatory transmembrane protein (OC‐STAMP), a novel protein induced by RANKL that promotes osteoclast differentiation
Authors: Yang Meiheng , Birnbaum Mark J. , MacKay Carole A. , Mason‐Savas April , Thompson Benjamin , Odgren Paul R. 
Published: December 2007

AbstractMicroarray and real‐time RT‐PCR were used to examine expression changes in primary bone marrow cells and RAW 264.7 cells in response to RANKL. In silico sequence analysis was performed on a novel gene which we designate OC‐STAMP. Specific siRNA and antibodies were used to inhibit OC‐STAMP RNA and protein, respectively, and tartrate‐resistant acid phosphatase (TRAP)+ multinucleated osteoclasts were counted. Antibodies were used to probe bone tissues and western blots of RAW cell extracts +/− RANKL. cDNA overexpression constructs were transfected into RAW cells and the effect on RANKL‐induced differentiation was studied. OC‐STAMP was very strongly up‐regulated during osteoclast differentiation. Northern blots and sequence analysis revealed two transcripts of 2 and 3.7 kb differing only in 3′UTR length, consistent with predictions from genome sequence. The mRNA encodes a 498 amino acid, multipass transmembrane protein that is highly conserved in mammals. It has little overall homology to other proteins. The carboxy‐terminal 193 amino acids, however, are significantly similar to the DC‐STAMP family consensus sequence. DC‐STAMP is a transmembrane protein required for osteoclast precursor fusion. Knockdown of OC‐STAMP mRNA by siRNA and protein inhibition by antibodies significantly suppressed the formation of TRAP+, multinucleated cells in differentiating osteoclast cultures, with many TRAP+ mononuclear cells present. Conversely, overexpression of OC‐STAMP increased osteoclastic differentiation of RAW 264.7 cells. We conclude that OC‐STAMP is a previously unknown, RANKL‐induced, multipass transmembrane protein that promotes the formation of multinucleated osteoclasts. J. Cell. Physiol. 215: 497–505, 2008. © 2007 Wiley‐Liss, Inc.
Deoxycholyltaurine rescues human colon cancer cells from apoptosis by activating EGFR‐dependent PI3K/Akt signaling
Authors: Raufman Jean‐Pierre , Shant Jasleen , Guo Chang Yue , Roy Sanjit , Cheng Kunrong 
Published: December 2007

AbstractRecent studies indicate that secondary bile acids promote colon cancer cell proliferation but their role in maintaining cell survival has not been explored. We found that deoxycholyltaurine (DCT) markedly attenuated both unstimulated and TNF‐α‐stimulated programmed cell death in colon cancer cells by a phosphatidylinositol 3‐kinase (PI3K)‐dependent mechanism. To examine the role of bile acids and PI3K signaling in maintaining colon cancer cell survival, we explored the role of signaling downstream of bile acid‐induced activation of the epidermal growth factor receptor (EGFR) in regulating both apoptosis and proliferation of HT‐29 and H508 human colon cancer cells. DCT caused dose‐ and time‐dependent Akt (Ser473) phosphorylation, a commonly used marker of activated PI3K/Akt signaling. Both EGFR kinase and PI3K inhibitors attenuated DCT‐induced Akt phosphorylation and Akt activation, as demonstrated by reduced phosphorylation of a GSK‐3‐paramyosin substrate. Transfection of HT‐29 cells with kinase‐dead EGFR (K721M) reduced DCT‐induced Akt phosphorylation. In HT‐29 cells, EGFR and PI3K inhibitors as well as transfection with dominant negative AKT attenuated DCT‐induced cell proliferation. DCT‐induced PI3K/Akt activation resulted in downstream phosphorylation of GSK‐3 (Ser21/9) and BAD (Ser136), and nuclear translocation (activation) of NF‐κB, thereby confirming that DCT‐induced activation of PI3K/Akt signaling regulates both proproliferative and prosurvival signals. Collectively, these results indicate that DCT‐induced activation of post‐EGFR PI3K/Akt signaling stimulates both colon cancer cell survival and proliferation. J. Cell. Physiol. 215: 538–549, 2008. © 2007 Wiley‐Liss, Inc.
Regulation of bim in glucocorticoid‐mediated osteoblast apoptosis
Authors: Espina B. , Liang M. , Russell R.G.G. , Hulley P.A. 
Published: December 2007

AbstractOsteoblasts undergo apoptosis both in vitro and in vivo in response to high dose glucocorticoid (GC) treatment. However, the molecular mechanisms remain elusive, hindering the prevention and treatment of this side‐effect. Apoptosis was induced by dexamethasone (Dex) in murine MBA‐15.4 osteoblasts within 24–48 h of treatment. We found dose‐ and time‐dependent upregulation of Bim protein, a pro‐apoptotic Bcl‐2 family member, with highest levels at 24–48 h for 1 µM Dex. This was also observed in primary human bone marrow stromal cells. Bim is subjected to stringent transcriptional and post‐translational regulation in osteoblasts. Bim mRNA was upregulated in response to 1 µM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex‐induction of Bim protein, indicating transcriptional regulation involving the GC receptor. The proteasome inhibitor, MG132, potently increased Bim protein levels. Bim was also upregulated in osteoblasts undergoing apoptosis in response to serum deprivation and matrix detachment. Gene silencing experiments show that short interference RNA (siRNA) specific for Bim or the downstream effector Bax both reduced apoptosis induced by Dex in osteoblastic cells. These findings suggest that Bim is a novel regulator of osteoblast apoptosis and may be a therapeutic target. J. Cell. Physiol. 215: 488–496, 2008. © 2007 Wiley‐Liss, Inc.
All‐trans retinoic acid attenuates ultraviolet radiation‐induced down‐regulation of aquaporin‐3 and water permeability in human keratinocytes
Authors: Cao Cong , Wan Shu , Jiang Qin , Amaral Ashley , Lu Shan , Hu Gang , Bi Zhigang , Kouttab Nicola , Chu Wenming , Wan Yinsheng 
Published: December 2007

AbstractOne of the major characteristics of human skin photoaging induced by ultraviolet (UV) radiation is the dehydration of the skin. Water movement across plasma membrane occurs via diffusion through lipid bilayer and via aquaporins (AQPs). We find that UV induces aquaporin‐3 (AQP3) down‐regulation in human skin keratinocytes. MEK/ERK inhibitors PD98059 and U0126 inhibit UV‐induced down‐regulation of AQP3. Antioxidant N‐acetyl‐L‐cysteine or NAC blocks UV‐induced MEK/ERK activation and down‐regulation of AQP3. All‐trans retinoic acid or atRA, while alone inducing AQP3 expression, attenuates UV‐induced down‐regulation of AQP3 and water permeability. Using special inhibitors, we find that activation of EGFR and inhibition on ERK activation are involved in atRA's protective effects against UV‐induced AQP3 down‐regulation. Using specific AQP3's water transport inhibitors and siRNA knockdown, we observe that AQP3 is involved in cell migration and in vitro wound healing. UV‐induced AQP3 down‐regulation results in reduced water permeability, decreased cell migration, and delayed wound healing, which are attenuated by atRA pretreatment. We conclude that atRA protects against UV‐induced down‐regulation AQP3 and decrease in water permeability, reduction in cell migration and delayed in vitro wound healing via trans‐activation of EGFR and inhibition on ROS‐mediated MEK/ERK pathway. This novel finding provides evidence to support possible involvement of AQP3 in UV induced skin dehydration. J. Cell. Physiol. 215: 506–516, 2008. © 2007 Wiley‐Liss, Inc.
FGF‐21/FGF‐21 receptor interaction and activation is determined by βKlotho
Authors: Kharitonenkov Alexei , Dunbar James D. , Bina Holly A. , Bright Stuart , Moyers Julie S. , Zhang Chen , Ding Liyun , Micanovic Radmila , Mehrbod Sean F. , Knierman Michael D. , Hale John E. , Coskun Tamer , Shanafelt Armen B. 
Published: December 2007

AbstractFibroblast growth factor‐21 (FGF‐21) is a metabolic regulator that can influence glucose and lipid control in diabetic rodents and primates. We demonstrate that βKlotho is an integral part of an activated FGF‐21‐βKlotho‐FGF receptor (FGFR) complex thus a critical subunit of the FGF‐21 receptor. Cells lacking βKlotho did not respond to FGF‐21; the introduction of βKlotho to these cells conferred FGF‐21‐responsiveness and recapitulated the entire scope of FGF‐21 signaling observed in naturally responsive cells. Interestingly, FGF‐21‐mediated effects are heparin independent suggesting that βKlotho plays a role in FGF‐21 activity similar to the one played by heparin in the signaling of conventional FGFs. Moreover, in addition to conferring specificity for FGF‐21, βKlotho appears to support FGF‐19 activity and mediates the receptor selectivity profile of FGF‐19. All together, these results indicate that βKlotho and FGFRs form the cognate FGF‐21 receptor complex, mediating FGF‐21 cellular specificity and physiological effects. J. Cell. Physiol. 215: 1–7, 2008. © 2007 Wiley‐Liss, Inc.