bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isolation of antibacterial compounds from Quercus dilatata L. through bioassay guided fractionation
Authors: Jamil Maryam , ul Haq Ihsan , Mirza Bushra , Qayyum Mazhar 
Published: May 2012

Abstract

Background
Four medicinal plants (Chrozophora hierosolymitana Spreng, Chrysanthemum leucanthemum L., Ephedra gerardiana Wall. ex Stapf, and Quercus dilatata L.) used by indigenous healers to treat various infectious diseases were selected for the present study. The major objective of the present study was isolation and characterization of antimicrobial components from the crude plant extracts using bioassay guided fractionation.

Methods
Seven methanolic extracts of the four plants were screened to identify any antimicrobial agents present in them. The active crude plant extract was fractionated first by solvent partitioning and then by HPLC. Characterization of the active fractions was done by using spectrophotometer.

Results
All the seven methanolic extracts showed low antifungal activity, however, when these extracts were tested for antibacterial activity, significant activity was exhibited by two extracts. The extract of aerial parts of Q. dilatata was most active and therefore, was selected for further analysis. Initially fractionation was done by solvent-solvent partitioning and out of six partitioned fractions, ethanol fraction was selected on the basis of results of antibacterial activity and phytochemical analysis. Further, fractionation was carried out by RP- HPLC and purified active subfractions were characterized by comparing their absorption spectra with that of the known natural products isolated from the plants of Quercus genus.

Discussion and conclusion
The results suggest that this is the first report of the isolated antibacterial compounds from this genus.
The OGF-OGFr axis utilizes the p21 pathway to restrict progression of human pancreatic cancer
Authors: Cheng Fan , McLaughlin Patricia J , Verderame Michael F , Zagon Ian S 
Published: May 2012

Abstract

Background
Pancreatic cancer is the 4th leading cause of death from cancer in the U.S. The opioid growth factor (OGF; [Met5]-enkephalin) and the OGF receptor form an inhibitory growth regulatory system involved in the pathogenesis and treatment of pancreatic cancer. The OGF-OGFr axis influences the G0/G1 phase of the cell cycle. In this investigation, we elucidate the pathway of OGF in the cell cycle.

Results
Using BxPC-3 cells, OGF decreased phosphorylation of retinoblastoma (Rb) protein without changing total Rb. This change was correlated with reduced cyclin-dependent kinase protein (Cdk) 2 kinase activity, but not total Cdk2. OGF treatment increased cyclin-dependent kinase inhibitor (CKI) p21 protein expression in comparison to controls, as well levels of p21 complexed with Cdk2. Naloxone abolished the increased expression of p21 protein by OGF, suggesting a receptor-mediated activity. p21 specific siRNAs blocked OGF's repressive action on proliferation in BxPC-3, PANC-1, and Capan-2 cells; cells transfected with negative control siRNA had no alteration in p21 expression, and therefore were inhibited by OGF.

Conclusion
These data are the first to reveal that the target of cell proliferative inhibitory action of OGF in human pancreatic cancer is a p21 CKI pathway, expanding strategies for diagnosis and treatment of these neoplasias.
EBV-positive Hodgkin lymphoma is associated with suppression of p21cip1/waf1 and a worse prognosis
Authors: Liu Ting-Yun , Wu Shang-Ju , Huang Mi-Hsin , Lo Fei-Yun , Tsai Mong-Hsun , Tsai Ching-Hwa , Hsu Su-Ming , Lin Chung-Wu 
Published: May 2012

Abstract

Background
About 30-50% of Hodgkin lymphomas (HLs) harbor the Epstein-Barr virus (EBV), but the impact of EBV infection on clinical outcomes has been unclear. EBV-encoded small RNAs (EBER s) are presented in all EBV-infected cells, but their functions are still less understood.

Results

EBER1 was transfected into two HL cell lines, KMH2 and L428, and microarrays were used to screen for EBER1-induced changes. We found that EBER1 suppressed p21
cip1/waf1 transcription in HL cell lines. In addition, positive regulators of p21
cip1/waf1 transcription, such as p53, EGR1, and STAT1, were decreased. Suppression of p21
cip1/waf1 in the EBER1
+ HL cell lines was associated with increased resistance to histone deacetylase inhibitors or proteasome inhibitors, drugs known to cause apoptosis by increasing p21cip1/waf1 levels. On biopsy specimens, EBV+ HLs had weaker expression of both p21cip1/waf1 and active caspase 3. Clinically, suppression of p21cip1/waf1 in EBV+ HLs was associated with a worse 2-year disease-free survival rate (45% for EBV+ HLs vs. 77% for EBV- HLs, p = 0.002).

Conclusion
Although the underlying mechanisms are still relatively unclear, EBER1 inhibits p21
cip1/waf1 transcription and prevents apoptosis through down-regulation of p53, EGR1, and STAT1. The anti-apoptotic activity of EBER1 may be important in the rescue of Reed-Sternberg cells from drug-induced apoptosis and in the clinical behaviors of EBV+ HLs.
Impact of contractile reserve on acute response to cardiac resynchronization therapy
Authors: Moonen Marie , Senechal Mario , Cosyns Bernard , Melon Pierre , Nellessen Eric , Pierard Luc , Lancellotti Patrizio 
Published: May 2012

Abstract

Background
Cardiac resynchronization therapy (CRT) provides benefit for congestive heart failure, but still 30% of patients failed to respond to such therapy. This lack of response may be due to the presence of significant amount of scar or fibrotic tissue at myocardial level. This study sought to investigate the potential impact of myocardial contractile reserve as assessed during exercise echocardiography on acute response following CRT implantation.

Methods
Fifty-one consecutive patients with heart failure (LV ejection fraction 27% ± 5%, 67% ischemic cardiomyopathy) underwent exercise Doppler echocardiography before CRT implantation to assess global contractile reserve (improvement in LV ejection fraction) and local contractile reserve in the region of the LV pacing lead (assessed by radial strain using speckle tracking analysis). Responders were defined by an increase in stroke volume ≥ 15% after CRT.

Results
Compared with nonresponders, responders (25 patients) showed a greater exercise-induced increase in LV ejection fraction, a higher degree of mitral regurgitation and a significant extent of LV dyssynchrony. The presence of contractile reserve was directly related to the acute increase in stroke volume (r = 0.48, p < 0.001). Baseline myocardial deformation as well as contractile reserve in the LV pacing lead region was greater in responders during exercise than in nonresponders (p < 0.0001).

Conclusion
The present study showed that response to CRT largely depends not only on the extent of LV dyssynchrony and the severity of mitral regurgitation but also on the presence of contractile reserve.
Genomic expression dominance in allopolyploids
Authors: Rapp Ryan A , Udall Joshua A , Wendel Jonathan F 
Published: May 2012

Abstract

Background

Allopolyploid speciation requires rapid evolutionary reconciliation of two diverged genomes and gene regulatory networks. Here we describe global patterns of gene expression accompanying genomic merger and doubling in inter-specific crosses in the cotton genus (Gossypium L.).

Results

Employing a micro-array platform designed against 40,430 unigenes, we assayed gene expression in two sets of parental diploids and their colchicine-doubled allopolyploid derivatives. Up to half of all genes were differentially expressed among diploids, a striking level of expression evolution among congeners. In the allopolyploids, most genes were expressed at mid-parent levels, but this was achieved via a phenomenon of genome-wide expression dominance, whereby gene expression was either up- or down-regulated to the level of one of the two parents, independent of the magnitude of gene expression. This massive expression dominance was approximately equal with respect to direction (up- or down-regulation), and the same diploid parent could be either the dominant or the recessive genome depending on the specific genomic combination. Transgressive up- and down-regulation were also common in the allopolyploids, both for genes equivalently or differentially expressed between the parents.

Conclusion

Our data provide novel insights into the architecture of gene expression in the allopolyploid nucleus, raise questions regarding the responsible underlying mechanisms of genome dominance, and provide clues into the enigma of the evolutionary prevalence of allopolyploids.
Detection of porcine circovirus genotypes 2a and 2b in aborted foetuses from infected swine herds in the State of São Paulo, Brazil
Authors: de Castro Alessandra MMG , Cruz Taís F , Salgado Vanessa R , Kanashiro Tatiana M , Ferrari Karen L , Araujo João P , Brandão Paulo E , Richtzenhain Leonardo J 
Published: May 2012

Abstract

Background
Porcine circovirus type 2 (PCV2) has been associated with several disease complexes, including reproductive failure. The aim of this study was to identify the subtypes of PCV2 that are associated with reproductive failure in pigs from the State of São Paulo, Brazil and to investigate co-infections with other infectious organisms.

Findings
Samples of 168 aborted foetuses or mummified foetuses from five farrow-to-finish swine farms known to be infected with PCV2 and located in the State of São Paulo were tested for PCV2 by polymerase chain reaction (PCR). Positive samples were additionally tested for porcine parvovirus (PPV), Leptospira spp. and Brucella spp. by PCR. PCV2 was detected in 18 of the samples (10.7%). PPV, Brucella spp. and Leptospira spp were found in 2, 10 and 0 cases, respectively. Eleven PCV2 strains were sequenced and determined to be either genotype 2a (n = 1) or 2b (n = 10).

Conclusions
The findings indicate that the frequency of PCV2 infections in aborted porcine foetuses from the State of São Paulo is rather low (10.7%) and that co-infection with other pathogens is common and may be involved in PCV2 associated reproductive failure. No repeatable, characteristic amino acid motifs for regions of the PCV2 capsid protein seemed to be associated with abortion in sows.
Fibronectin glycation increases IGF-I induced proliferation of human aortic smooth muscle cells
Authors: Corrêa-Giannella Maria Lúcia , de Azevedo Maria Regina Andrade , LeRoith Derek , Giannella-Neto Daniel 
Published: May 2012

AbstractThe advanced glycation end products, namely AGEs, contribute to long-termed complications of diabetes mellitus, including macroangiopathy, where smooth muscle cells (SMC) proliferation stimulated by platelet-derived growth factor (PDGF) isoforms and insulin-like growth factor-I (IGF-I) plays an important role. The objective of the present study was to investigate the effect of an AGE-modified extracellular matrix protein on IGF-I induced SMC proliferation and on the IGF-I-IGF binding protein 4 (IGFBP-4) axis under basal conditions and after stimulation with PDGF-BB. IGF-I resulted in significantly higher thymidine incorporation in SMC seeded on AGE-modified fibronectin (AGE-FN) in comparison to cells seeded on fibronectin (FN). This augmented proliferation could not be accounted for by increased expression of IGF-IR, by decreased secretion of IGFBP-4, a binding protein that inhibits IGF-I mitogenic effects or by increased IGF-IR autophosphorylation. PDGF-BB did not modulate IGF-IR and IGFBP-4 mRNA expression in any of the substrata, however, this growth factor elicited opposite effects on the IGFBP-4 content in the conditioned media, increasing it in cells plated on FN and diminishing it in cells plated on AGE-FN. These findings suggest that one mechanism by which AGE-modified proteins is involved in the pathogenesis of diabetes-associated atherosclerosis might be by increasing SMC susceptibility to IGF-I mitogenic effects.
Biomarkers characterization of circulating tumour cells in breast cancer patients
Authors: Nadal Rosa , Fernandez Ana , Sanchez-Rovira Pedro , Salido Marta , Rodríguez María , García-Puche José Luis , Macià Marta , Corominas Josep Maria , Delgado-Rodriguez Miguel , Gonzalez Lucas , Albanell Joan , Fernández Mónica , Solé Francesc , Lorente José Antonio , Serrano María José 
Published: May 2012

Abstract
Introduction
Increasing evidence supports the view that the detection of circulating tumor cells (CTCs) predicts outcomes of nonmetastatic breast cancer patients. CTCs differ genetically from the primary tumor and may contribute to variations in prognosis and response to therapy. As we start to understand more about the biology of CTCs, we can begin to address how best to treat this form of disease.

Methods
Ninety-eight nonmetastatic breast cancer patients were included in this study. CTCs were isolated by immunomagnetic techniques using magnetic beads labelled with a multi-CK-specific antibody (CK3-11D5) and CTC detection through immunocytochemical methods. Estrogen receptor, progesterone receptor and epidermal growth factor receptor (EGFR) were evaluated by immunofluorescence experiments and HER2 and TOP2A by fluorescence in situ hybridization. We aimed to characterize this set of biomarkers in CTCs and correlate it with clinical-pathological characteristics.

Results
Baseline detection rate was 46.9% ≥ 1 CTC/30 ml threshold. CTC-positive cells were more frequent in HER2-negative tumors (p = 0.046). In patients younger than 50 years old, HER2-amplified and G1-G2 tumors had a higher possibility of being nondetectable CTCs. Heterogeneous expression of hormonal receptors (HRs) in samples from the same patients was found. Discordances between HR expression, HER2 and TOP2A status in CTCs and their primary tumor were found in the sequential blood samples. Less that 35% of patients switched their CTC status after receiving chemotherapy. EGFR-positive CTCs were associated with Luminal tumors (p = 0.03).

Conclusions
This is the largest exploratory CTC biomarker analysis in nonmetastatic BC patients. Our study suggests that CTC biomarkers profiles might be useful as a surrogate marker for therapeutic selection and monitoring since heterogeneity of the biomarker distribution in CTCs and the lack of correlation with the primary tumor biomarker status were found. Further exploration of the association between EGFR-positive CTCs and Luminal tumors is warranted.
The maize (Zea mays) desynaptic (dy) mutation defines a pathway for meiotic chromosome segregation, linking nuclear morphology, telomere distribution and synapsis
Authors: Murphy Shaun P. , Bass Hank W. 
Published: May 2012

Summary
Meiosis involves a dramatic reorganization of the genetic material, along with changes in the architecture of the nucleoplasm and cytoplasm. In the opisthokonts, nuclear envelope and meiotic chromosome behavior are coordinated by forces generated in the cytoplasm and transferred to the nucleus by the nuclear-envelope protein linkers SUN and KASH. During meiotic prophase I, the telomere bouquet arrangement has roles in interhomolog recognition, pairing, synapsis, interlock resolution and homologous chromosome recombination. The maize desynaptic (dy) mutant is defective in homologous chromosome synapsis, recombination, telomere–nuclear envelope interactions and chromosome segregation. A detailed three-dimensional cytological analysis of dy revealed telomere misplacement during the bouquet stage, synaptic irregularities, nuclear envelope distortion and chromosome bridges at anaphase I. Using linkage and B-A translocation mapping, we placed dy on the long arm of chromosome 3, genetic bin 3.06. SSR marker analysis narrowed the mapping interval to 9 cM. Candidate genes in this region include a PM3-type SUN domain protein, ZmSUN3. No obvious genetic lesions were found in the ZmSUN3 allele of dy, but a conspicuous splice variant, ZmSUN3-sv1, was observed in mRNA from dy. The variant message is predicted to result in the synthesis of a truncated ZmSUN3 protein lacking two C-terminal transmembrane domains. Other potential candidate genes relevant to the documented phenotypes were also considered. In summary, this study reveals that dy causes disruption of a central meiotic pathway connecting nuclear envelope integrity to telomere localization and synapsis during meiotic prophase.
All-You-Can-Eat Buffet: Entry Price, the Fat Tax and Meal Cessation
Authors: Siniver Erez , Yaniv Gideon 
Published: May 2012

Abstract
A widespread meal-serving system commonly blamed for contributing to the obesity epidemic is the all-you-can-eat buffet, where customers can help themselves to as much food as they wish to eat in a single meal for a fixed entry price. The paper offers a rational-choice model for addressing the individual's eating dilemma in an-all-you-can-eat buffet, incorporating the motivation of getting-one's-money's-worth as a behavioral constraint on eating. Contrary to previous findings, the model reveals that the individual will not necessarily overeat beyond the point of fullness and will not necessarily increase eating in response to a higher entry price. An experiment conducted in collaboration with a sushi restaurant supports this conclusion. The paper further shows that a fat tax imposed on both buffet and a-la-carte meals will not affect buffet eating, hence subjecting all-you-can-eat buffets to the fat tax program need not be counter-effective as the literature results imply.
Duality theory of weighted Hardy spaces with arbitrary number of parameters
Authors: Lu Guozhen , Ruan Zhuoping 
Published: May 2012

Abstract
In this paper, we use the discrete Littlewood–Paley–Stein
analysis to get the duality result of the weighted product Hardy
space for arbitrary number of parameters under a rather weak condition
on the product weight

w
∈

A
∞

(

ℝ

n
1

×
⋯
×

ℝ

n
k

)

$w \in A_\infty ( {\mathbb {R}}^{n_1} \times \cdots \times {\mathbb {R}}^{n_k})$

. We will show that for any k ≥ 2,

(

H
w
p

(

ℝ

n
1

×
⋯
×

ℝ

n
k

)

)

*

=
C
M

O
w
p

(

ℝ

n
1

×
⋯
×

ℝ

n
k

)

${(H^p_w({\mathbb {R}}^{n_1} \times \cdots \times {\mathbb {R}}^{n_k}))^\ast =\textup {CMO}^p_w({\mathbb {R}}^{n_1} \times \cdots \times {\mathbb {R}}^{n_k})}$

(a generalized Carleson measure),
and obtain the boundedness of singular integral operators on

BMO
w

$\mathrm {BMO}_w$

. Our theorems even when
the weight function w = 1 extend the H
1-BMO duality of Chang–R. Fefferman for
the non-weighted two-parameter Hardy space

H
1

(

ℝ

n

×

ℝ

m

)

$H^1({\mathbb {R}}^n\times {\mathbb {R}}^m)$

to

H
p

(

ℝ

n
1

×
⋯
×

ℝ

n
k

)

$H^p({\mathbb {R}}^{n_1} \times \cdots \times {\mathbb {R}}^{n_k})$

for all

0
<
p
≤
1

$0&lt;p\le 1$

and our weighted theory extends the duality result of
Krug–Torchinsky on weighted Hardy spaces

H
w
p

(

ℝ

n

×

ℝ

m

)

$H^p_w({\mathbb {R}}^n\times {\mathbb {R}}^m)$

for

w
∈

A
r

(

ℝ

n

×

ℝ

m

)

${w\in A_r({\mathbb {R}}^n\times {\mathbb {R}}^m)}$

with

1
≤
r
≤
2

$1\le r\le 2$

and

r
/
2
<
p
≤
1

${r/2&lt;p\le 1}$

to

H
w
p

(

ℝ

n
1

×
⋯
×

ℝ

n
k

)

$H^p_w({\mathbb {R}}^{n_1} \times \cdots \times {\mathbb {R}}^{n_k})$

with

w
∈

A
∞

(

ℝ

n
1

×
⋯
×

ℝ

n
k

)

${w \in A_\infty ( {\mathbb {R}}^{n_1} \times \cdots \times {\mathbb {R}}^{n_k})}$

for all

0
<
p
≤
1

${0&lt;p\le 1}$

.
Cadherin-related protein 24 induces morphological changes and partial cell polarization by facilitating direct cell-cell interactions
Authors: Behrendt Marc , Krahn Michael P. , Al-Bayati Hiam , Amiri Mahdi , Rizk Sandra , Naim Hassan Y. 
Published: May 2012

Abstract
Cadherin-related protein 24 (CDHR24) is a potential tumor suppressor located apically as well as laterally in polarized cells. Here, the role of CDHR24 in contributing to cell morphology and polarity is examined. CDHR24 was predominantly localized at the nonattached part of nonpolarizing cells while another apically sorted protein, aminopeptidase N, was equally distributed over the plasma membrane. Furthermore, CDHR24 expression induced cell aggregation capacity, indicating direct cell-cell interaction. The transepithelial resistance, however, was elevated in polarized MDCK cells, but not in nonpolarizing CHO cells. Our data propose a model in which CDHR24 is directly involved in cell and tissue morphogenesis.
The distribution of speech errors in multi-word prosodic units
Authors: Choe Wook Kyung , Redford Melissa A. 
Published: May 2012

AbstractSequencing errors in natural and elicited speech have long been used to inform models of phonological encoding and to understand the process by which serial ordering is achieved in speech. The present study focused on the distribution of sequential speech errors within multi-word prosodic units to determine whether such units are relevant to speech planning, and, if so, how. Forty native English-speaking undergraduate students were asked to produce sentences that varied in length and in the extent to which certain phonological features were repeated (tongue twisters or not). Participants prepared their utterances in advance of speaking and were coached to be as fluent as possible once they started speaking. The goal was to ensure the production of well-structured utterances, while maximizing the number of errors produced, and minimizing the effects that excessive self-correction might have on prosodic structure. Speech errors were perceptually identified in the recorded speech and categorized. Strong and weak prosodic boundaries were prosodically transcribed in sentences with sequencing errors. Speech error patterns were found to correspond well with the boundaries of the multi-word prosodic units defined by the strong and weak prosodic boundaries. In particular, the number of sequencing errors was found to vary as a function of position within a unit such that the fewest errors were found in initial position, more occurred in early-mid position, and even more occurred in late-mid position. This pattern of increasing errors across the multi-word prosodic unit was referred to as the cumulative error pattern. The analyses also revealed a final position effect. When multi-word prosodic units occurred in utterance-initial or utterance-medial position, a disproportionate number of errors occurred in the final position of the unit. However, when the units occurred in utterance-final position, more errors occurred in late-mid position than in final position. The cumulative error pattern and final position effect are interpreted to suggest the serial activation and decay in activation of multi-word planning domains during phonological encoding.
Deg Xinag Rounding Assimilation: A case study in phonologization
Authors: Hargus Sharon 
Published: May 2012

AbstractAcoustic and video evidence suggest that Deg Xinag, an Athabaskan language, contains Rounding Assimilation, rounding of schwa before a stressed rounded vowel across uvular or laryngeal consonants. Although Rounding Assimilation has received no mention in previous Deg Xinag studies, it appears to be at stage II, phonologization, in the model of sound change proposed by Hyman (1976). Data from the related language Babine-Witsuwit'en is also presented, showing an absence of Rounding Assimilation in one of the contexts where it occurs in Deg Xinag. Babine-Witsuwit'en sheds light on how and why Rounding Assimilation may have developed historically in Deg Xinag.