bluuebunny/crossref_metadata_2025_split huggingface dataset:
Asset and Protective Factors for Asian American Children's Mental Health Adjustment
Authors: Zhou Qing , Tao Annie , Chen Stephen H. , Main Alexandra , Lee Erica , Ly Jennifer , Hua Michelle , Li Xiaowei 
Published: June 2012

AbstractAsian Americans (AAs) are the second largest foreign‐born population in the United States. Contrary to the “model minority” stereotype that this group is unitarily well adjusted and high achieving, recent research has revealed substantial differences in mental health adjustment amongAAchildren. Although research to identify the risk processes for mental health problems amongAAchildren is underway, it has paid little attention to related asset and protective processes. This article selectively reviews the theory and empirical evidence on a set of child‐, family‐, and neighborhood‐level characteristics for their potential asset or protective roles inAAchildren's mental health adjustment. These characteristics include (a) child factors (maintenance of heritage culture, bilingualism, coping, and emotion regulation), (b) family factors (authoritative parenting and parental support), and (c) a neighborhood factor (ethnic community). Overall, systematic efforts to identify asset and protective factors forAAchildren's mental health and understand the underlying developmental mechanisms are nascent. Directions for future research in this area are also discussed.
Characterization of a Streptococcus suis tet(O/W/32/O)-Carrying Element Transferable to Major Streptococcal Pathogens
Authors: Palmieri Claudio , Magi Gloria , Mingoia Marina , Bagnarelli Patrizia , Ripa Sandro , Varaldo Pietro E. , Facinelli Bruna 
Published: June 2012

ABSTRACT

Mosaic tetracycline resistance determinants are a recently discovered class of hybrids of ribosomal protection
tet
genes. They may show different patterns of mosaicism, but their final size has remained unaltered. Initially thought to be confined to a small group of anaerobic bacteria, mosaic
tet
genes were then found to be widespread. In the genus
Streptococcus
, a mosaic
tet
gene [
tet
(O/W/32/O)] was first discovered in
Streptococcus suis
, an emerging drug-resistant pig and human pathogen. In this study, we report the molecular characterization of a
tet
(O/W/32/O) gene-carrying mobile element from an
S. suis
isolate.
tet
(O/W/32/O) was detected, in tandem with
tet
(40), in a circular 14,741-bp genetic element (39.1% G+C; 17 open reading frames [ORFs] identified). The novel element, which we designated 15K, also carried the macrolide resistance determinant
erm
(B) and an aminoglycoside resistance four-gene cluster including
aadE
(streptomycin) and
aphA
(kanamycin). 15K appeared to be an unstable genetic element that, in the absence of recombinases, is capable of undergoing spontaneous excision under standard growth conditions. In the integrated form, 15K was found inside a 54,879-bp integrative and conjugative element (ICE) (50.5% G+C; 55 ORFs), which we designated ICE
Ssu32457
. An ∼1.3-kb segment that apparently served as the
att
site for excision of the unstable 15K element was identified. The novel ICE was transferable at high frequency to recipients from pathogenic
Streptococcus
species (
S. suis
,
Streptococcus pyogenes
,
Streptococcus pneumoniae
, and
Streptococcus agalactiae
), suggesting that the multiresistance 15K element can successfully spread within streptococcal populations.
Borrelia burgdorferi Harbors a Transport System Essential for Purine Salvage and Mammalian Infection
Authors: Jain Sunny , Sutchu Selina , Rosa Patricia A. , Byram Rebecca , Jewett Mollie W. 
Published: June 2012

ABSTRACT

Borrelia burgdorferi
is the tick-borne bacterium that causes the multistage inflammatory disease Lyme disease.
B. burgdorferi
has a reduced genome and lacks the enzymes required for
de novo
synthesis of purines for synthesis of RNA and DNA. Therefore, this obligate pathogen is dependent upon the tick vector and mammalian host environments for salvage of purine bases for nucleic acid biosynthesis. This pathway is vital for
B. burgdorferi
survival throughout its infectious cycle, as key enzymes in the purine salvage pathway are essential for the ability of the spirochete to infect mice and critical for spirochete replication in the tick. The transport of preformed purines into the spirochete is the first step in the purine salvage pathway and may represent a novel therapeutic target and/or means to deliver antispirochete molecules to the pathogen. However, the transport systems critical for purine salvage by
B. burgdorferi
have yet to be identified. Herein, we demonstrate that the genes
bbb22
and
bbb23
, present on
B. burgdorferi
's essential plasmid circular plasmid 26 (cp26), encode key purine transport proteins. BBB22 and/or BBB23 is essential for hypoxanthine transport and contributes to the transport of adenine and guanine. Furthermore,
B. burgdorferi
lacking
bbb22-23
was noninfectious in mice up to a dose of 1 × 10
7
spirochetes. Together, our data establish that
bbb22-23
encode purine permeases critical for
B. burgdorferi
mammalian infectivity, suggesting that this transport system may serve as a novel antimicrobial target for the treatment of Lyme disease.
Epstein-Barr Virus Infection and Expression of B-cell Oncogenic Markers in HIV-Related Diffuse Large B-cell Lymphoma
Authors: Chao Chun , Silverberg Michael J. , Martínez-Maza Otoniel , Chi Margaret , Abrams Donald I. , Haque Reina , Zha Hongbin D. , McGuire Michelle , Xu Lanfang , Said Jonathan 
Published: June 2012

Abstract
Purpose: Epstein-Barr virus (EBV)-mediated lymphomagenesis in the setting of HIV infection has been widely accepted. However, little is known about how EBV impacts prognosis. We investigated the hypothesis that EBV infection is associated with expression of specific B-cell oncogenic markers in HIV-related diffuse large B-cell lymphoma (DLBCL) and examined the prognostic use of detecting EBV infection.
Experimental Design: HIV-related DLBCL cases diagnosed between 1996 and 2007 within Kaiser Permanente California were identified. Immunohistochemical staining was used to analyze the expression of selected markers that are cell-cycle regulators, B-cell activators, and antiapoptotic proteins among others. EBV infection was determined by in situ hybridization of EBV RNA. Correlations between EBV and marker expression were examined using Spearman correlation coefficient. The prognostic use of EBV status was examined in multivariable Cox model adjusting for International Prognostic Index (IPI). Receiver-operating characteristics (ROC) analysis was used to evaluate improvement in model discrimination.
Results: Seventy HIV-related DLBCL cases were included (31% EBV±). EBV+ tumor was associated with increased expression of BLIMP1 and CD30 and reduced expression of BCL6 and LMO2. EBV+ tumor was independently associated with elevated 2-year overall mortality [HR, 3.3; 95% confidence interval (CI), 1.6–6.6]. Area under the ROC curve showed improved model discrimination when incorporating tumor EBV status with IPI in the prediction model [0.65 vs. 0.74 (IPI only)].
Conclusion: Our results suggest that EBV infection was associated with expression of several tumor markers that are involved in the NF-κB pathway and that detecting tumor EBV status may have prognostic use in HIV-related DLBCLs. Clin Cancer Res; 18(17); 4702–12. ©2012 AACR.
A 50-Gene Intrinsic Subtype Classifier for Prognosis and Prediction of Benefit from Adjuvant Tamoxifen
Authors: Chia Stephen K. , Bramwell Vivien H. , Tu Dongsheng , Shepherd Lois E. , Jiang Shan , Vickery Tammi , Mardis Elaine , Leung Samuel , Ung Karen , Pritchard Kathleen I. , Parker Joel S. , Bernard Philip S. , Perou Charles M. , Ellis Matthew J. , Nielsen Torsten O. 
Published: June 2012

Abstract
Purpose: Gene expression profiling classifies breast cancer into intrinsic subtypes based on the biology of the underlying disease pathways. We have used material from a prospective randomized trial of tamoxifen versus placebo in premenopausal women with primary breast cancer (NCIC CTG MA.12) to evaluate the prognostic and predictive significance of intrinsic subtypes identified by both the PAM50 gene set and by immunohistochemistry.
Experimental Design: Total RNA from 398 of 672 (59%) patients was available for intrinsic subtyping with a quantitative reverse transcriptase PCR (qRT-PCR) 50-gene predictor (PAM50) for luminal A, luminal B, HER-2–enriched, and basal-like subtypes. A tissue microarray was also constructed from 492 of 672 (73%) of the study population to assess a panel of six immunohistochemical IHC antibodies to define the same intrinsic subtypes.
Results: Classification into intrinsic subtypes by the PAM50 assay was prognostic for both disease-free survival (DFS; P = 0.0003) and overall survival (OS; P = 0.0002), whereas classification by the IHC panel was not. Luminal subtype by PAM50 was predictive of tamoxifen benefit [DFS: HR, 0.52; 95% confidence interval (CI), 0.32–0.86 vs. HR, 0.80; 95% CI, 0.50–1.29 for nonluminal subtypes], although the interaction test was not significant (P = 0.24), whereas neither subtyping by central immunohistochemistry nor by local estrogen receptor (ER) or progesterone receptor (PR) status were predictive. Risk of relapse (ROR) modeling with the PAM50 assay produced a continuous risk score in both node-negative and node-positive disease.
Conclusions: In the MA.12 study, intrinsic subtype classification by qRT-PCR with the PAM50 assay was superior to IHC profiling for both prognosis and prediction of benefit from adjuvant tamoxifen. Clin Cancer Res; 18(16); 4465–72. ©2012 AACR.
Necdin modulates proliferative cell survival of human cells in response to radiation-induced genotoxic stress
Authors: Lafontaine Julie , Tchakarska Guergana , Rodier Francis , Mes-Masson Anne-Marie 
Published: June 2012

Abstract

Background
The finite replicative lifespan of cells, termed cellular senescence, has been proposed as a protective mechanism against the proliferation of oncogenically damaged cells, that fuel cancer. This concept is further supported by the induction of premature senescence, a process which is activated when an oncogene is expressed in normal primary cells as well as following intense genotoxic stresses. Thus, deregulation of genes that control this process, like the tumor suppressor p53, may contribute to promoting cancer by allowing cells to bypass senescence. A better understanding of the genes that contribute to the establishment of senescence is therefore warranted. Necdin interacts with p53 and is also a p53 target gene, although the importance of Necdin in the p53 response is not clearly understood.

Methods
In this study, we first investigated Necdin protein expression during replicative senescence and premature senescence induced by gamma irradiation and by the overexpression of oncogenic RasV12. Gain and loss of function experiments were used to evaluate the contribution of Necdin during the senescence process.

Results
Necdin expression declined during replicative aging of IMR90 primary human fibroblasts or following induction of premature senescence. Decrease in Necdin expression seemed to be a consequence of the establishment of senescence since the depletion of Necdin in human cells did not induce a senescence-like growth arrest nor a flat morphology or SA-β-galactosidase activity normally associated with senescence. Similarly, overexpression of Necdin did not affect the life span of IMR90 cells. However, we demonstrate that in normal human cells, Necdin expression mimicked the effect of p53 inactivation by increasing radioresistance.

Conclusion
This result suggests that Necdin potentially attenuate p53 signaling in response to genotoxic stress in human cells and supports similar results describing an inhibitory function of Necdin over p53-dependent growth arrest in mice.
Analysis of questioning technique during classes in medical education
Authors: Cho Young Hye , Lee Sang Yeoup , Jeong Dong Wook , Im Sun Ju , Choi Eun Jung , Lee Sun Hee , Baek Sun Yong , Kim Yun Jin , Lee Jeong Gyu , Yi Yu Hyone , Bae Mi Jin , Yune So Jung 
Published: June 2012

Abstract

Background
Questioning is one of the essential techniques used by lecturers to make lectures more interactive and effective. This study surveyed the perception of questioning techniques by medical school faculty members and analyzed how the questioning technique is used in actual classes.

Methods
Data on the perceptions of the questioning skills used during lectures was collected using a self‒questionnaire for faculty members (N = 33) during the second semester of 2008. The questionnaire consisted of 18 items covering the awareness and characteristics of questioning skills. Recorded video tapes were used to observe the faculty members’ questioning skills.

Results
Most faculty members regarded the questioning technique during classes as being important and expected positive outcomes in terms of the students’ participation in class, concentration in class and understanding of the class contents. In the 99 classes analyzed, the median number of questions per class was 1 (0–29). Among them, 40 classes (40.4 %) did not use questioning techniques. The frequency of questioning per lecture was similar regardless of the faculty members’ perception. On the other hand, the faculty members perceived that their usual wait time after question was approximately 10 seconds compared to only 2.5 seconds measured from video analysis. More lecture‒experienced faculty members tended to ask more questions in class.

Conclusions
There were some discrepancies regarding the questioning technique between the faculty members’ perceptions and reality, even though they had positive opinions of the technique. The questioning skills during a lecture need to be emphasized to faculty members.
Forelimb EMG-based trigger to control an electronic spinal bridge to enable hindlimb stepping after a complete spinal cord lesion in rats
Authors: Gad Parag , Woodbridge Jonathan , Lavrov Igor , Zhong Hui , Roy Roland R , Sarrafzadeh Majid , Edgerton V Reggie 
Published: June 2012

Abstract

Background
A complete spinal cord transection results in loss of all supraspinal motor control below the level of the injury. The neural circuitry in the lumbosacral spinal cord, however, can generate locomotor patterns in the hindlimbs of rats and cats with the aid of motor training, epidural stimulation and/or administration of monoaminergic agonists. We hypothesized that there are patterns of EMG signals from the forelimbs during quadrupedal locomotion that uniquely represent a signal for the “intent” to step with the hindlimbs. These observations led us to determine whether this type of “indirect” volitional control of stepping can be achieved after a complete spinal cord injury. The objective of this study was to develop an electronic bridge across the lesion of the spinal cord to facilitate hindlimb stepping after a complete mid-thoracic spinal cord injury in adult rats.

Methods
We developed an electronic spinal bridge that can detect specific patterns of EMG activity from the forelimb muscles to initiate electrical-enabling motor control ( eEmc) of the lumbosacral spinal cord to enable quadrupedal stepping after a complete spinal cord transection in rats. A moving window detection algorithm was implemented in a small microprocessor to detect biceps brachii EMG activity bilaterally that then was used to initiate and terminate epidural stimulation in the lumbosacral spinal cord. We found dominant frequencies of 180–220 Hz in the EMG of the forelimb muscles during active periods, whereas these frequencies were between 0–10 Hz when the muscles were inactive.

Results and conclusions
Once the algorithm was validated to represent kinematically appropriate quadrupedal stepping, we observed that the algorithm could reliably detect, initiate, and facilitate stepping under different pharmacological conditions and at various treadmill speeds.
17beta-hydroxysteroid dehydrogenase type 1 modulates breast cancer protein profile and impacts cell migration
Authors: Aka Juliette A , Zerradi Mouna , Houle François , Huot Jacques , Lin Sheng-Xiang 
Published: June 2012

Abstract
Introduction
Human 17beta-hydroxysteroid dehydrogenase type 1 (17β-HSD1) is a steroid-converting enzyme that has long been known to play critical roles in estradiol synthesis and more recently in dihydrotestosterone (DHT) inactivation, showing a dual function that promotes breast cancer cell proliferation. Previously, we reported the first observation of the influence of the enzyme on endogenous estrogen-responsive gene expression. Here, we demonstrate the impact of 17β-HSD1 expression on the breast cancer cell proteome and investigate its role in cell migration.

Methods
17β-HSD1 was stably transfected in MCF7 cells and the proteome of the generated cells overexpressing 17β-HSD1 (MCF7-17βHSD1 cells) was compared to that of the wild type MCF7 cells. Proteomics study was performed using two-dimensional gel electrophoresis followed by mass spectrometry analysis of differentially expressed protein spots. Reverse transcription quantitative real-time PCR (RT-qPCR) was used to investigate the transcription of individual gene. The effect of 17β-HSD1 on MCF7 cell migration was verified by a wound-healing assay.

Results
Proteomic data demonstrate that the expression of more than 59 proteins is modulated following 17β-HSD1 overexpression. 17β-HSD1 regulates the expression of important genes and proteins that are relevant to cell growth control, such as BRCA2 and CDKN1A interacting protein (BCCIP) and proliferating cell nuclear antigen (PCNA) which are down- and upregulated in MCF7-17βHSD1 cells, respectively. RT-qPCR data reveal that 17β-HSD1 increases the mRNA levels of estrogen receptors (ER) alpha and beta by 171 and 120%, respectively, while decreasing that of the androgen receptor by 64%. Interestingly, 17β-HSD1 increases the mRNA transcript (by 3.6 times) and the protein expression of the metastasis suppressor gene nm23-H1 and the expression of the two enzymes are closely correlated. We have further shown that 17β-HSD1 expression is associated with an increase of MCF7 cell migration.

Conclusions
In addition to the regulation of important genes, we have demonstrated for the first time that 17β-HSD1 increases breast cancer cell migration, in spite of its positive regulation of the antimetastatic gene NM23. This is also correlated to its stimulation of breast cancer cell growth, further confirming its targeting in ER positive breast cancer. The novel findings in this study suggest several directions for future research on the contribution of 17β-HSD1 to breast cancer progression and related treatment.
BRCA Mutation Frequency and Patterns of Treatment Response in BRCA Mutation–Positive Women With Ovarian Cancer: A Report From the Australian Ovarian Cancer Study Group
Authors: Alsop Kathryn , Fereday Sian , Meldrum Cliff , deFazio Anna , Emmanuel Catherine , George Joshy , Dobrovic Alexander , Birrer Michael J. , Webb Penelope M. , Stewart Colin , Friedlander Michael , Fox Stephen , Bowtell David , Mitchell Gillian 
Published: June 2012

Purpose The frequency of BRCA1 and BRCA2 germ-line mutations in women with ovarian cancer is unclear; reports vary from 3% to 27%. The impact of germ-line mutation on response requires further investigation to understand its impact on treatment planning and clinical trial design. Patients and Methods Women with nonmucinous ovarian carcinoma (n = 1,001) enrolled onto a population-based, case-control study were screened for point mutations and large deletions in both genes. Survival outcomes and responses to multiple lines of chemotherapy were assessed. Results Germ-line mutations were found in 14.1% of patients overall, including 16.6% of serous cancer patients (high-grade serous, 22.6%); 44% had no reported family history of breast or ovarian cancer. Patients carrying germ-line mutations had improved rates of progression-free and overall survival. In the relapse setting, patients carrying mutations more frequently responded to both platin- and nonplatin-based regimens than mutation-negative patients, even in patients with early relapse after primary treatment. Mutation-negative patients who responded to multiple cycles of platin-based treatment were more likely to carry somatic BRCA1/2 mutations. Conclusion BRCA mutation status has a major influence on survival in ovarian cancer patients and should be an additional stratification factor in clinical trials. Treatment outcomes in BRCA1/2 carriers challenge conventional definitions of platin resistance, and mutation status may be able to contribute to decision making and systemic therapy selection in the relapse setting. Our data, together with the advent of poly(ADP-ribose) polymerase inhibitor trials, supports the recommendation that germ-line BRCA1/2 testing should be offered to all women diagnosed with nonmucinous, ovarian carcinoma, regardless of family history.
Focal adhesion kinase-regulated signaling events in human cancer
Authors: Fu Wei , Hall Jessica E. , Schaller Michael D. 
Published: June 2012

AbstractFocal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase that is highly expressed or activated in many human cancers. Under specific scenarios, FAK can regulate cell proliferation, cell survival, cell migration and invasion, and has been implicated in the control of tumorigenesis and metastasis. FAK has both catalytic and scaffolding activity, and triggers downstream signals by activation of a number of pathways, including the Ras/mitogen-activated protein kinase pathway, the phosphatidylinositol 3′-kinase/Akt pathway, and Rho family GTPases. Recent evidence also suggests novel signaling interactions between FAK and p53. These signaling events were defined primarily from studies on cells in culture, and elucidating which of these signaling pathways are pathologically relevant downstream of FAK in human cancer remains an important goal in determining the molecular mechanisms of tumorigenesis and metastasis. This review discusses select evidence of these signaling pathways with an emphasis on studies linking these to animal models of cancer and human disease. The role of FAK in the process of epithelial-to-mesenchymal transition and in cancer stem cells and recent therapeutic advances targeting FAK are also discussed.
High Integrated Microwave Architecture Using LTCC-SIP Technology in Active Phased Array Antenna Applications
Authors: Zhou Jun , Shi Wei , Dou Wen-Bin , Shen Ya 
Published: June 2012

AbstractA kind of three dimensional Low Temperature Co-fired Ceramic (LTCC)-System in Package (SIP) transition was proposed in this paper. The basic design of SIP with LTCC technology was done by vertical transitions which transmit the microwave signal from the bottom to the surface of the substrate. The measured insertion loss did not exceed 1.5 dB, which contains the insertion loss of the test board about 0.6 dB at 18 GHz and the return loss was better than