bluuebunny/crossref_metadata_2025_split huggingface dataset:
Overview of: “Race, Place, and Drug Enforcement: Reconsidering the Impact of Citizen Complaints and Crime Rates on Drug Arrests”
Authors: Engel Robin S. , Smith Michael R. , Cullen Francis T. 
Published: November 2012

Research SummaryInfluential research has reported racial disparities in drug arrests in Seattle, Washington, that could not be explained by race‐neutral factors such as crime rates or community complaints. Based on new data, measures, and methods, we reexamine racial disparities in drug arrests in Seattle and find contradictory evidence. Our analysis, using drug‐related calls for service (CFS) as a benchmark, indicates that African Americans and Hispanics are either evenly represented or underrepresented among those arrested on drug charges in two drug markets examined. Similarly, this analysis reveals a moderate‐to‐strong association among drug arrests, drug‐related CFS, and crime. These results provide support for the “deployment hypothesis,” which argues that as a result of differential police deployment patterns, officers are likely to have increased contact with minority citizens and thus have more opportunities to detect criminal conduct. Our findings demonstrate the importance of selecting an appropriate and conceptually sound benchmark to measure racial disparities in criminal justice outcomes and the importance of selecting an appropriate unit of analysis.Policy ImplicationsOur study cautions against the ready attribution of police practices to racial motives and shows the need for more research, across contexts, into this ongoing policy issue. These findings suggest that racial disparities in drug arrests seem to be more structural in nature rather than based on racial animus and individual police bias. It is, therefore, unlikely that these disparities can be eliminated by popular interventions such as police training in cultural sensitivity or by efforts to monitor and punish officers. This result leads to a consideration of whether focusing police resources based on citizen complaints and reported crimes represents equitable policing and, if not, what would constitute a realistic policy alternative.
Nucleotide oligomerization domain 2 polymorphisms in patients with intestinal failure
Authors: Guerra Juan Francisco , Zasloff Michael , Lough Denver , Abdo Joseph , Hawksworth Jason , Mastumoto Cal , Girlanda Raffaele , Island Eddie , Shetty Kirty , Kaufman Stuart , Fishbein Thomas 
Published: November 2012

AbstractBackgroundNucleotide oligomerization domain 2 (NOD2) has been associated with intestinal immunity after the discovery that its polymorphisms are linked to Crohn's disease (CD). Intestinal failure (IF) represents a wider spectrum of diseases where intestinal homeostasis has been disrupted.AimTo evaluate the prevalence of NOD2 mutations in a population with IF as well as its association with the different conditions causing this problem.MethodsOne hundred ninety‐two consecutive patients with IF and 103 healthy controls were genotyped for the three most common NOD2 polymorphisms. Genotypes were compared between the groups and were related to the entities causing IF.ResultsA high percentage (26%) of patients had at least one of the three most common NOD2 polymorphisms, while only a 4.8% of healthy controls had a mutant genotype. In patients with IF, specific mutations for the 702W, 908R and 1007fs alleles were 11, 5 and 12.5%, respectively, compared with 0.9% (P = 0.0003), 1.9% (P = 0.1) and 1.9% (P = 0.001) in the control group. If we consider patients with any cause of IF other than CD, the percentage is still as high as 18.8%, with specific mutation frequencies of 7.6% (702W; P = 0.01), 5.8% (908R; P = 0.1) and 8.2% (1007fs; P = 0.002). We could not establish an association between a NOD2 mutant genotype with any other specific clinical condition other than CD.ConclusionOur finding supports the importance of NOD2 in the maintenance of intestinal immune homeostasis and may be important to a variety of intestinal stressors.
Analysis of altered microRNA expression profiles in peripheral blood mononuclear cells from patients with primary biliary cirrhosis
Authors: Qin Baodong , Huang Fenglou , Liang Yan , Yang Zaixing , Zhong Renqian 
Published: November 2012

AbstractBackground and AimMicroRNA, as an important regulator of gene expression, has been found to be associated with several diseases. MicroRNA expression profiles have been identified in several autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis. However, the expression profile in peripheral blood mononuclear cells (PBMCs) from primary biliary cirrhosis (PBC) patients and the role of microRNA in PBC remained unclear. The present study aimed to explore abnormal microRNA regulation in PBC.MethodsMicroRNA array was performed in PBMCs obtained from PBC patients versus healthy controls. Then, six of the 17 differentially expressed microRNAs were confirmed using quantitative real‐time polymerase chain reaction. Based on bioinformatics analysis, we identified the potential biological processes and significant signaling pathways affected by these microRNAs, and generated the microRNA–gene network.ResultsAccording to microRNA array, a total of 17 microRNAs were found to be differentially expressed. Six microRNAs have been validated using quantitative real‐time polymerase chain reaction, and the results were consistent with microRNA array analysis. The bioinformatics analysis showed that the potential target genes of these microRNAs were involved in cell proliferation, cell differentiation, apoptosis, and signal transduction. Similarly, these microRNAs also affected endocytosis, mitogen‐activated protein kinase signaling pathway, transforming growth factor‐β signaling pathway, Wnt signaling pathway, calcium signaling pathway, etc.ConclusionIn the present study, 17 microRNAs were identified to be differentially expressed in PBMCs from PBC patients. Functional bioinformatics analysis demonstrated that prediction genes targeted by these microRNAs were involved in multiple biological processes and signaling pathways. The present study offers intriguing new perspectives on the involvement of microRNA in PBC, but the precise mechanisms need to be validated further.
RACK1 identified as the PCBP1‐interacting protein with a novel functional role on the regulation of human MOR gene expression
Authors: Nahar‐Gohad Pranjal , Sultan Hamidah , Esteban Ysabella , Stabile Alyda , Ko Jane L. 
Published: November 2012

AbstractPoly C binding protein 1 (PCBP1) is an expressional regulator of the mu‐opioid receptor (MOR) gene. We hypothesized the existence of a PCBP1 co‐regulator modifying human MOR gene expression by protein–protein interaction with PCBP1. A human brain cDNA library was screened using the two‐hybrid system with PCBP1 as the bait. Receptor for activated protein kinase C (RACK1) protein, containing seven WD domains, was identified. PCBP1‐RACK1 interaction was confirmed via in vivo validation using the two‐hybrid system, and by co‐immunoprecipitation with anti‐PCBP1 antibody and human neuronal NMB cell lysate, endogenously expressing PCBP1 and RACK1. Further co‐immunoprecipitation suggested that RACK1‐PCBP1 interaction occurred in cytosol alone. Single and serial WD domain deletion analyses demonstrated that WD7 of RACK1 is the key domain interacting with PCBP1. RACK1 over‐expression resulted in a dose‐dependent decrease of MOR promoter activity using p357 plasmid containing human MOR promoter and luciferase reporter gene. Knock‐down analysis showed that RACK1 siRNA decreased the endogenous RACK1 mRNA level in NMB, and elevated MOR mRNA level as indicated by RT‐PCR. Likewise, a decrease of RACK1 resulted in an increase of MOR proteins, verified by 3H‐diprenorphine binding assay. Collectively, this study reports a novel role of RACK1, physically interacting with PCBP1 and participating in the regulation of human MOR gene expression in neuronal NMB cells.
Preparation of calcium phosphate nanocapsules including simvastatin/deoxycholic acid assembly, and their therapeutic effect in osteoporosis model mice
Authors: Ito Tomoko , Takemasa Manami , Makino Kimiko , Otsuka Makoto 
Published: November 2012

Abstract

Objectives
Simvastatin has recently been demonstrated to serve as a therapeutic agent for osteoporosis. However, it is hard to dissolve in water and has side effects such as rhabdomyolysis. Solubilization of the drug by deoxycholate was attempted, and the resulting simvastatin/deoxycholate assembly (DeCA/Sim) was coated by calcium phosphate (CaP) to reduce the side effects of simvastatin. The aim of this study was to examine the therapeutic effects of the CaP-coated deoxycholate micelle containing simvastatin in osteoporosis model mice.

Methods
Deoxycholate micelle containing simvastatin coated by CaP (CaP-DeCA/Sim) was prepared by immersion of deoxycholate/simvastatin assembly in simulated body fluid (SBF). The therapeutic effect of CaP-DeCA/Sim on osteoporosis model mice was evaluated by X-ray computed tomography, and also its effect on other body conditions.

Key findings
The CaP coating remarkably reduced cytotoxicity in cultured cells. When CaP-DeCA/Sim was injected into ovariectomized mice, inflammation was suppressed, and led to a whole-body therapeutic effect (body weight, bone mineral content and bone mechanical strength). The deoxycholic acid/simvastatin assembly coated by CaP is thus useful for the treatment of osteoporosis.

Conclusions
Such biocompatible CaP nanocapsules including deoxycholate micelles is expected to be a novel strategy to construct an effective device for delivery of hydrophobic drugs.
Influence of hypertension on pH of saliva in older adults
Authors: Kagawa R , Ikebe K , Enoki K , Murai S , Okada T , Matsuda K , Maeda Y 
Published: November 2012

BackgroundHypertension and/or antihypertensive medication reportedly induce dry mouth; however, an immediate relationship between salivary flow and hypertension has not been elucidated.ObjectivesThe purpose of the present study was to examine the association of hypertension and antihypertensive medication with salivary flow rate and pH in older adults.SubjectsSubjects were independently living volunteers aged 60–78 years taking no medication (n = 138) or only antihypertensive medication (n = 27). Unstimulated saliva and stimulated saliva by the mastication method were collected, and salivary pH was measured. Hypertension was defined as systolic blood pressure of ≥140 mmHg and/or diastolic blood pressure of ≥90 mmHg.ResultsThere was no significant correlation between either hypertension or intake of antihypertensive medication and unstimulated or stimulated salivary flow rate. However, multiple regression analysis showed that hypertension was significantly associated with pH of unstimulated saliva after controlling for other variables (β = −0.270, P = 0.003).ConclusionHypertension regardless of antihypertensive medication was related to a lower pH of unstimulated saliva. Blood pressure might be a required consideration for maintenance of oral health in older individuals.
Neutrophils alter epithelial response to Porphyromonas gingivalis in a gingival crevice model
Authors: Bondy‐Carey J.L. , Galicia J. , Bagaitkar J. , Potempa J.S. , Potempa B. , Kinane D.F. , Veillard F. , Scott D.A. 
Published: November 2012

SummaryA gingival crevice model (epithelial cell–Porphyromonas gingivalis–neutrophil) was established and used to profile gingipain, matrix metalloproteinase (MMP), MMP mediators [neutrophil gelatinase‐associated lipocalin (NGAL) and tissue inhibitor of metalloproteinases 1 (TIMP‐1)] and cytokine networks. Smoking is the primary environmental risk factor for periodontitis. Therefore, the influence of cigarette smoke extract (CSE) was also monitored in the same model. Porphyromonas gingivalis alone induced low levels of interleukin‐1β and interleukin‐8 from epithelial cells, but high levels of both cytokines were produced on the addition of neutrophils. Exposure to CSE (100 and 1000 ng ml−1 nicotine equivalency) significantly compromised P. gingivalis‐induced cytokine secretion (both P < 0.05). P. gingivalis induced impressive secretion of NGAL (P < 0.05) that was not influenced by CSE. The influence of CSE on gingipain production was strain‐specific. Purified gingipains effectively and rapidly degraded both TIMP‐1 and MMP‐9. Induction of large amounts of NGAL, degradation of TIMP‐1, and increased gingipain activity would each be expected to prolong collagen degradation and promote disease progression. However, gingipains also degrade MMP‐9. Hence, P. gingivalis exerts a complex influence on the proteolytic balance of a gingival crevice model. Exposure to CSE reduces the proinflammatory cytokine burden, which may be expected to promote P. gingivalis survival. In addition to novel findings that provide mechanistic insight into periodontal disease progression, these results are in keeping with the recognized clinical dogma of decreased inflammation/increased disease in smokers. This straightforward gingival crevice model is established as a suitable vehicle for the elucidation of mechanisms that contribute to susceptibility to periodontitis.
Measuring the Size‐Independent Fracture Energy of Concrete
Authors: Cifuentes H. , Alcalde M. , Medina F. 
Published: November 2012

Abstract:  The fracture energy of concrete is an important parameter in the analysis of the mechanical behaviour of concrete structures, so it is considered as a material property. However, the most universal test method for measuring the specific fracture energy of concrete (RILEM work‐of‐fracture) has been a subject of intense debate among researchers. The values have been found to vary with the size and shape of the test specimen. In this study, an experimental comparative analysis of the size‐independent fracture energy obtained by two main methods has been carried out. One of these is based on the local fracture energy model of Hu et al. The second is based on the curtailment of the tail of the P–δ curve by Elices et al. Therefore, the relationship between both methods is highlighted. It is shown that both methods give almost identical results.
Capacity of forensic patients to consent to treatment
Authors: Skipworth Jeremy J , Dawson John , Ellis Pete M 
Published: November 2012

Objective: Lack of capacity to consent to psychiatric treatment has been promoted as a better basis for compulsion than mental disorder plus risk of harm. Previous research has examined how that legal change would affect acutely unwell inpatients. There is little research on forensic patients. This research aimed to assess capacity to consent in forensic patients at different stages of recovery and to consider the implications of respecting their competent treatment decisions. Method: Capacity to consent was assessed in a cross-sectional sample of 109 forensic patients both in hospital and in community settings. Results: The majority of participants (67.6%) had treatment-related decision-making capacity. Very few patients with capacity refused treatment. Conclusions: Change to a capacity-based legal approach may alter treatment for some forensic patients but would not necessarily increase risk of harm to others. The implications for release decisions are less clear.
Clonal evolution and devolution after chemotherapy in adult acute myelogenous leukemia
Authors: Parkin Brian , Ouillette Peter , Li Yifeng , Keller Jennifer , Lam Cindy , Roulston Diane , Li Cheng , Shedden Kerby , Malek Sami N. 
Published: November 2012

Abstract
The frequent occurrence of persistent or relapsed disease after induction chemotherapy in AML necessitates a better understanding of the clonal relationship of AML in various disease phases. In this study, we used SNP 6.0 array-based genomic profiling of acquired copy number aberrations (aCNA) and copy neutral LOH (cnLOH) together with sequence analysis of recurrently mutated genes to characterize paired AML genomes. We analyzed 28 AML sample pairs from patients who achieved complete remission with chemotherapy and subsequently relapsed and 11 sample pairs from patients with persistent disease after induction chemotherapy. Through review of aCNA/cnLOH and gene mutation profiles in informative cases, we demonstrate that relapsed AML invariably represents re-emergence or evolution of a founder clone. Furthermore, all individual aCNA or cnLOH detected at presentation persisted at relapse indicating that this lesion type is proximally involved in AML evolution. Analysis of informative paired persistent AML disease samples uncovered cases with 2 coexisting dominant clones of which at least one was chemotherapy sensitive and one resistant, respectively. These data support the conclusion that incomplete eradication of AML founder clones rather than stochastic emergence of fully unrelated novel clones underlies AML relapse and persistence with direct implications for clinical AML research.
Impaired thrombin-induced platelet activation and thrombus formation in mice lacking the Ca2+-dependent tyrosine kinase Pyk2
Authors: Canobbio Ilaria , Cipolla Lina , Consonni Alessandra , Momi Stefania , Guidetti Gianni , Oliviero Barbara , Falasca Marco , Okigaki Mitsuhiko , Balduini Cesare , Gresele Paolo , Torti Mauro 
Published: November 2012

Abstract
In the present study, we used a knockout murine model to analyze the contribution of the Ca2+-dependent focal adhesion kinase Pyk2 in platelet activation and thrombus formation in vivo. We found that Pyk2-knockout mice had a tail bleeding time that was slightly increased compared with their wild-type littermates. Moreover, in an in vivo model of femoral artery thrombosis, the time to arterial occlusion was significantly prolonged in mice lacking Pyk2. Pyk2-deficient mice were also significantly protected from collagen plus epinephrine-induced pulmonary thromboembolism. Ex vivo aggregation of Pyk2-deficient platelets was normal on stimulation of glycoprotein VI, but was significantly reduced in response to PAR4-activating peptide, low doses of thrombin, or U46619. Defective platelet aggregation was accompanied by impaired inside-out activation of integrin αIIbβ3 and fibrinogen binding. Granule secretion was only slightly reduced in the absence of Pyk2, whereas a marked inhibition of thrombin-induced thromboxane A2 production was observed, which was found to be responsible for the defective aggregation. Moreover, we have demonstrated that Pyk2 is implicated in the signaling pathway for cPLA2 phosphorylation through p38 MAPK. The results of the present study show the importance of the focal adhesion kinase Pyk2 downstream of G-protein–coupled receptors in supporting platelet aggregation and thrombus formation.
Association of genetic variations in GNB1 with response to peginterferon plus ribavirin therapy for chronic hepatitis C in a Chinese population in Taiwan
Authors: Lim Yun-Ping , Tsai Fuu-Jen , Liao Wen-Ling , Tien Ni , Hung Dong-Zong , Peng Cheng-Yuan , Wan Lei 
Published: November 2012

AbstractBackgroundThe aim of this study was to evaluate whether polymorphisms in the guanine nucleotide binding (G protein), beta polypeptide 1 (GNB1) gene are associated with a rapid virological response (RVR) among HCV genotype 1 (HCV-1) and 2 (HCV-2) infected patients receiving peginterferon plus ribavirin treatment (PEG-IFNα-RBV).MethodsWe analyzed the association between RVR to PEG-IFNα-RBV therapy and 4 tagging single nucleotide polymorphisms (SNPs) of theGNB1gene. This study included 265 HCV-1 and 195 HCV-2 infected patients in a Chinese population in Taiwan.ResultsAmong theGNB1SNPs examined, the combination of genotypes G/G and G/T populations of rs12126768 was significant inversely correlated with RVR in HCV-1 infected patients (P= 0.0330), whereas HCV-2 infected patients, combination of A/A and A/C genotypes populations at rs4648727 responded better to the PEG-IFNα-RBV treatment (P= 0.0089). However, there were no significant differences in the allele frequencies of those SNPs between RVR responders and non-responders. Several RVR susceptibilityGNB1haplotypes were identified, and the ACAT haplotype of the 4 SNPs may increase the successful outcomes of HCV-1 and HCV-2 infected patients (P= 0.0261 andP= 0.0253, respectively).ConclusionThe data forGNB1SNPs and the association of RVR showed thatGNB1polymorphisms might be associated with the therapeutic outcomes of HCV-1 and HCV-2 infected patients under standard of care (SOC) treatment.
Preclinical evaluation of Gd-DTPA and gadomelitol as contrast agents in DCE-MRI of cervical carcinoma interstitial fluid pressure
Authors: Hompland Tord , Ellingsen Christine , Rofstad Einar K 
Published: November 2012

Abstract

Background
High interstitial fluid pressure (IFP) in the primary tumor is associated with poor disease-free survival in locally advanced cervical carcinoma. A noninvasive assay is needed to identify cervical cancer patients with highly elevated tumor IFP because these patients may benefit from particularly aggressive treatment. It has been suggested that dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) with gadolinium diethylene-triamine penta-acetic acid (Gd-DTPA) as contrast agent may provide useful information on the IFP of cervical carcinomas. In this preclinical study, we investigated whether DCE-MRI with contrast agents with higher molecular weights (MW) than Gd-DTPA would be superior to Gd-DTPA-based DCE-MRI.

Methods
CK-160 human cervical carcinoma xenografts were subjected to DCE-MRI with Gd-DTPA (MW of 0.55 kDa) or gadomelitol (MW of 6.5 kDa) as contrast agent before tumor IFP was measured invasively with a Millar SPC 320 catheter. The DCE-MRI was carried out at a spatial resolution of 0.23 × 0.23 × 2.0 mm3 and a time resolution of 14 s by using a 1.5-T whole-body scanner and a slotted tube resonator transceiver coil constructed for mice. Parametric images were derived from the DCE-MRI recordings by using the Tofts iso-directional transport model and the Patlak uni-directional transport model.

Results
When gadomelitol was used as contrast agent, significant positive correlations were found between the parameters of both pharmacokinetic models and tumor IFP. On the other hand, significant correlations between DCE-MRI-derived parameters and IFP could not be detected with Gd-DTPA as contrast agent.

Conclusion
Gadomelitol is a superior contrast agent to Gd-DTPA in DCE-MRI of the IFP of CK-160 cervical carcinoma xenografts. Clinical studies attempting to develop DCE-MRI-based assays of the IFP of cervical carcinomas should involve contrast agents with higher MW than Gd-DTPA.
Involvement of spinal orexin A in the electroacupuncture analgesia in a rat model of post-laparotomy pain
Authors: Feng Xiao-Ming , Mi Wen-Li , Xia Fang , Mao-Ying Qi-Liang , Jiang Jian-Wei , Xiao Sheng , Wang Zhi-Fu , Wang Yan-Qing , Wu Gen-Cheng 
Published: November 2012

Abstract

Background
Orexin A (OXA, hypocretin/hcrt 1) is a newly discovered potential analgesic substance. However, whether OXA is involved in acupuncture analgesia remains unknown. The present study was designed to investigate the involvement of spinal OXA in electroacupuncture (EA) analgesia.

Methods
A modified rat model of post-laparotomy pain was adopted and evaluated. Von Frey filaments were used to measure mechanical allodynia of the hind paw and abdomen. EA at 2/15 Hz or 2/100 Hz was performed once on the bilateral ST36 and SP6 for 30 min perioperatively. SB-334867, a selective orexin 1 receptor (OX1R) antagonist with a higher affinity for OXA than OXB, was intrathecally injected to observe its effect on EA analgesia.

Results
OXA at 0.3 nmol and EA at 2/15 Hz produced respective analgesic effects on the model (P<0.05). Pre-surgical intrathecal administered of SB-334867 30 nmol antagonized OXA analgesia and attenuated the analgesic effect of EA (P<0.05). However, SB-334867 did not block fentanyl-induced analgesia (P>0.05). In addition, naloxone, a selective opioid receptor antagonist, failed to antagonize OXA-induced analgesia (P>0.05).

Conclusions
The results of the present study indicate the involvement of OXA in EA analgesia via OX1R in an opioid-independent way.