bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identifying Critical Facilities in Hub‐and‐Spoke Networks: A Hub Interdiction Median Problem
Authors: Lei Ting L. 
Published: April 2013

The hub location problem has been widely used in analyzing hub‐and‐spoke systems. The basic assumption is that a large number of demands exist to travel from origins to destinations via a set of intermediate transshipment nodes. These intermediate nodes can be lost, due to reasons such as natural disasters, outbreaks of disease, labor strikes, and intentional attacks. This article presents a hub interdiction median (HIM) problem. It can be used to identify the set of critical facilities in a hub‐and‐spoke system that, if lost, leads to the maximal disruption of the system's service. The new model is formulated using integer linear programming. Special constraints are constructed to account for origin‐to‐destination demand following the least‐cost route via the remaining hubs. Based on the HIM problem, two hub protection problems are defined that aim to minimize the system cost associated with the worst‐case facility loss. Computational experiment results are presented along with a discussion of possible future work.El problema de la ubicación de la central (hub) ha sido ampliamente analizado para el caso de los sistemas de sistemas radiales (hub‐and‐spoke). La presunción inicial es que existe un gran número de demandas que viajan desde puntos de origen hasta sus puntos de destino a través de un set de nodos intermedios de trasbordo. Estos nodos intermedios pueden perderse por diferentes motivos, como desastres naturales, brotes de enfermedades, huelgas de trabajadores, o ataques intencionales. Este artículo presenta un problema de tipo mediana de interdicción de hub, conocido como hub interdiction median‐HIM. Puede usarse para identificar un set de instalaciones críticas de un sistema tipo hub‐and‐spoke que, si se pierde, conduce a la máxima interrupción del servicio del sistema. El nuevo modelo se ha formulado utilizando programación entera lineal, (integer linear programming‐ILP). El modelo construye restricciones especiales para dar cuenta de la demanda de “origen‐a‐destino” (O‐D), siguiendo la ruta de menor costo, a través de los hubs restantes. Basándonos en el problema de HIM, se definen dos problemas de protección de hub que buscan minimizar el costo asociado al peor caso posible de pérdida de instalaciones. Se presentan además, resultados de experimentos computacionales, así como a una discusión sobre posibles futuros trabajos en la materia.枢纽区位研究已广泛应用于中枢辐射型系统分析，其基本假设条件为起始点到目的地之间存在大量旅行需求的中间转运节点。但自然灾害、突发疾病、劳务罢工和蓄意攻击等因素可能导致中间转运节点的丧失。本文提出了一种枢纽封闭中心模型（HIM），可用于识别中枢辐射型系统的重要节点，一旦这些节点丧失，将导致整个系统服务最大程度的瓦解。新模型通过整数线性规划公式建立。模型特殊约束条件的建立基于最小成本路径通过余下枢纽的花费来解释始发到目的地（ origin‐to‐destination）需求量。基于HIM问题，双枢纽保护问题被定义为旨在最小化系统花费及其与之关联的最坏情况下节点丢失问题。最后，根据计算的经验结果讨论未来可能深入的研究。
Efficient identification of TALEN‐mediated genome modifications using heteroduplex mobility assays
Authors: Ota Satoshi , Hisano Yu , Muraki Michiko , Hoshijima Kazuyuki , Dahlem Timothy J. , Grunwald David J. , Okada Yasushi , Kawahara Atsuo 
Published: April 2013

The heteroduplex mobility assay (HMA) is widely used to characterize strain variants of human viruses. To determine whether it can detect small sequence differences in homologous templates, we constructed a series of deletion constructs (1–10 bp deletions) in the multiple cloning site (MCS) of pBluescript II. After PCR amplification of the MCS using a mixture of wild‐type and one of the deletion constructs, the resulting PCR amplicons were electrophoresed using 15% polyacrylamide gels. Two types of heteroduplexes exhibited retarded electrophoretic migration compared with individual homoduplexes. Therefore, we applied this HMA to detect transcription activator‐like effector nucleases (TALEN)‐induced insertion and/or deletion (indel) mutations at an endogenous locus. We found that TALEN in vivo activity was easily estimated by the degree of multiple HMA profiles derived from TALEN‐injected F0 embryos. Furthermore, TALEN‐injected F0 founder fish produced several unique HMA profiles in F1 embryos. Sequence analysis confirmed that the different HMA profiles contained distinct indel mutations. Thus, HMA is a rapid and sensitive analytical method for the detection of the TALEN‐mediated genome modifications.
Lateral Conduction Switching in Sputtered Ni‐rich NiO Thin Films for Write‐Once‐Read‐Many‐Times Memory Applications
Authors: Liu Zhen , Zhang Hai Yan , Chen Tu Pei , Liu Pan , Zhang Sam , Zhang Wa Li 
Published: April 2013

Magnetron sputtering has been used to deposit Ni‐rich nickel oxide thin films. Based on the switching of lateral current conduction in the nickel oxide thin film between two in‐plane electrodes, a planar write‐once‐read‐many‐times memory device has been demonstrated. The switching from a low‐conductance state (i.e., the OFF state) to a high‐conductance state (i.e., the ON state) is induced by a writing voltage, and it is irreversible due to the formation of tilted conductive filaments that are hard to be dissolved by the Joule heating effect. For 80 devices under test, the writing voltage is in a narrow range of 2.0−3.5 V and the ON/OFF resistance ratio is larger than 105 at the reading voltage of 0.3 V. An excellent reading endurance (106 readings) for both ON and OFF states is demonstrated. The device is promising in low‐power applications as it can operate at ultra‐low voltages (e.g., the reading voltage can be below 100 mV).
Neuraminidase inhibitor susceptibility surveillance of influenza viruses circulating worldwide during the 2011 Southern Hemisphere season
Authors: Okomo‐Adhiambo Margaret , Sleeman Katrina , Lysén Colleen , Nguyen Ha T. , Xu Xiyan , Li Yan , Klimov Alexander I. , Gubareva Larisa V. 
Published: April 2013

BackgroundNeuraminidase (NA) inhibitors (NAIs) are currently the only antivirals effective against influenza infections due to widespread resistance to M2 inhibitors.MethodsInfluenza A and B viruses (n = 1079) collected worldwide between April 01, 2011, and September 30, 2011, were assessed for susceptibility to FDA‐approved NAIs, oseltamivir and zanamivir, and investigational peramivir, using the fluorescent‐based NA‐Fluor™ Influenza Neuraminidase Assay Kit. A subset of viruses (n = 98) were tested for susceptibility to the investigational NAI, laninamivir.ResultsInfluenza A(H1N1)pdm09 viruses (n = 326) were sensitive to all NAIs, except for two (0·6%) with H275Y (N1 numbering; H274Y in N2 numbering) substitution, which exhibited elevated IC50s for oseltamivir and peramivir, and a third with previously unreported N325K substitution, exhibiting reduced susceptibility to oseltamivir. Influenza A(H3N2) viruses (n = 407) were sensitive to all NAIs. Influenza B viruses (n = 346) were sensitive to all NAIs, except two (0·6%) with H273Y (N1 numbering; H274Y in N2 numbering) substitution, exhibiting reduced susceptibility to oseltamivir and peramivir, and one with previously unreported G140R and N144K substitutions, exhibiting reduced susceptibility to oseltamivir, zanamivir, and peramivir. All influenza A and B viruses were sensitive to laninamivir. It is unknown whether substitutions N325K, G140R, and N144K were present in the virus prior to culturing because clinical specimens were unavailable for testing.ConclusionsThis study summarizes NAI susceptibility of influenza viruses circulating worldwide during the 2011 Southern Hemisphere (SH) season, assessed using the NA‐Fluor™ Kit. Despite low resistance to NAIs among tested influenza viruses, constant surveillance of influenza virus susceptibility to NAIs should be emphasized.
Periodontitis: a host‐mediated disruption of microbial homeostasis. Unlearning learned concepts
Authors: Bartold P. Mark , Van Dyke Thomas E. 
Published: April 2013

AbstractNew concepts evolve when existing ones fail to address known factors adequately or are invalidated by new evidence. For decades periodontitis has been considered to be caused by specific bacteria or groups of bacteria and, accordingly, treatment protocols have largely been based on anti‐infective therapies. However, close inspection of current data leads one to question whether these bacteria are the cause or the result of periodontitis. Good evidence is emerging to suggest that it is indeed the host response to oral bacteria that leads to the tissue changes noted in gingivitis. These changes lead to an altered subgingival environment that favors the emergence of ‘periodontal pathogens’ and the subsequent development of periodontitis if the genetic and external environmental conditions are favorable for disease development. Thus, it seems that it is indeed the initial early host‐inflammatory and immune responses occurring during the development of gingivitis, and not specific bacteria or their so‐called virulence factors, which determine whether periodontitis develops and progresses. In this review we consider these concepts and their potential to change the way in which we view and manage the inflammatory periodontal diseases.
Risk factors for periodontal disease
Authors: Genco Robert J. , Borgnakke Wenche S. 
Published: April 2013

AbstractRisk factors play an important role in an individual’s response to periodontal infection. Identification of these risk factors helps to target patients for prevention and treatment, with modification of risk factors critical to the control of periodontal disease. Shifts in our understanding of periodontal disease prevalence, and advances in scientific methodology and statistical analysis in the last few decades, have allowed identification of several major systemic risk factors for periodontal disease. The first change in our thinking was the understanding that periodontal disease is not universal, but that severe forms are found only in a portion of the adult population who show abnormal susceptibility. Analysis of risk factors and the ability to statistically adjust and stratify populations to eliminate the effects of confounding factors have allowed identification of independent risk factors. These independent but modifiable, risk factors for periodontal disease include lifestyle factors, such as smoking and alcohol consumption. They also include diseases and unhealthy conditions such as diabetes mellitus, obesity, metabolic syndrome, osteoporosis, and low dietary calcium and vitamin D. These risk factors are modifiable and their management is a major component of the contemporary care of many periodontal patients. Genetic factors also play a role in periodontal disease and allow one to target individuals for prevention and early detection. The role of genetic factors in aggressive periodontitis is clear. However, although genetic factors (i.e., specific genes) are strongly suspected to have an association with chronic adult periodontitis, there is as yet no clear evidence for this in the general population. It is important to pursue efforts to identify genetic factors associated with chronic periodontitis because such factors have potential in identifying patients who have a high susceptibility for development of this disease. Many of the systemic risk factors for periodontal disease, such as smoking, diabetes and obesity, and osteoporosis in postmenopausal women, are relatively common and can be expected to affect most patients with periodontal disease seen in clinics and dental practices. Hence, risk factor identification and management has become a key component of care for periodontal patients.
Catheterization During Adrenal Vein Sampling for Primary Aldosteronism: Failure to Use (1–24) ACTH May Increase Apparent Failure Rate
Authors: Kline Gregory A. , So Benny , Dias Valerian C. , Harvey Adrian , Pasieka Janice L. 
Published: April 2013

“Successful” adrenal vein catheterization in primary aldosteronism (PA) is often defined by a ratio of >3:1 of cortisol in the adrenal vein vs the inferior vena cava. Non‐use of corticotropin (ACTH) during sampling may increase the apparent failure rate of adrenal vein catheterization due to lower cortisol levels. A retrospective study was performed on all patients with confirmed unilateral PA between June 2005 and August 2011. Adrenal vein sampling (AVS) included simultaneous bilateral baseline samples with repeat sampling 15 minutes after intravenous infusion of 250 μg of Cortrosyn (ACTH‐S). Successful catheter placement was judged as adrenal cortisol:IVC cortisol of >3:1, applied to both baseline and ACTH‐S samples and lateralization of aldosteronism was judged as normalized aldosterone/cortisol (A/C) ratio >3 times the contralateral A/C ratio. In ACTH‐S samples, 94% of right‐sided catheterizations were biochemically successful with 100% success on the left. Among baseline samples, only 47% of right‐ and 44% of left‐sided samples met the 3:1 cortisol criteria. However, 95% of apparent “failed” baseline cortisol sets still showed lateralization of A/C ratios that matched the ultimate pathology. Non–ACTH‐stimulated samples may be incorrectly judged as failed catheter placement when a 3:1 ratio is used. ACTH‐stimulated sampling is the preferred means to confirm catheterization during AVS.
Association of B2 Receptor Polymorphisms and ACE Activity With ACE Inhibitor–Induced Angioedema in Black and Mixed‐Race South Africans
Authors: Moholisa Retsilisitsoe R. , Rayner Brian R. , Patricia Owen E. , Schwager Sylva L. U. , Stark Joalice S. , Badri Motassim , Cupido Clint L. , Sturrock Edward D. 
Published: April 2013

Angiotensin‐converting enzyme (ACE) inhibitors are first‐line therapy for the treatment of hypertension, congestive heart failure, and diabetic nephropathy. ACE inhibitors are associated with adverse side effects such as persistent dry cough (ACE‐cough) and, rarely, life‐threatening angioedema (ACE‐AE). The authors investigated the influence of ACE I/D polymorphism in combination with serum ACE activity, B2 receptor −9/+9 polymorphism, and B2 receptor C‐58T single nucleotide polymorphism (SNP) on the development of ACE‐AE and ACE‐cough. The frequencies of ACE I/D as well as B2 receptor +9/−9 and C‐58T polymorphisms were compared in patients with ACE‐AE, ACE‐cough, and ACE inhibitor–exposed controls, and serum ACE activity was measured. There were 52 cases of ACE‐AE, 36 cases of ACE‐cough, and 77 controls. The genotyping revealed a significant association between the B2 −9 allele and ACE inhibitor–induced AE (62% vs 38%, P=.008), and ACE inhibitor–induced cough (61% vs 38%, P=.02) when compared with controls. There was no significant association between ACE I/D polymorphism as well as the B2 C‐58T SNP with both ACE‐induced AE and cough. ACE activity was significantly higher in controls compared with patients with ACE‐AE (34.5±1.14 mU/mL vs 17.8±0.86 mU/mL, P=.0001) and ACE‐cough (34.5±1.14 mU/mL vs 23.3±1.88 mU/mL, P=.0001). Thus, our data suggest that the B2 −9 allele and reduced ACE activity are associated with both ACE‐AE and ACE‐cough.
Kir6.2 E23K polymorphism is related to secondary failure of sulfonylureas in non‐obese patients with type 2 diabetes
Authors: Shimajiri Yoshinori , Yamana Akiko , Morita Shuhei , Furuta Hiroto , Furuta Machi , Sanke Tokio 
Published: April 2013

AbstractAims/IntroductionThe Kir6.2 E23K polymorphism was studied with a special reference to secondary sulfonylurea (SU) failure in non‐obese patients with type 2 diabetes.Materials and MethodsWe recruited 278 non‐obese (body mass index ≤30.0 kg/m2) Japanese patients with type 2 diabetes who had a history of SU treatment (for 11.2 ± 6.3 years) and compared the frequency of the secondary SU failure among the genotypes of the polymorphism. Genotyping of the Kir6.2 E23K was carried out by polymerase chain reaction‐restriction fragment length polymorphism.ResultsThe genotype frequencies of the polymorphism were similar to those previously reported in Japanese patients with type 2 diabetes. The frequency with which patients deteriorated into secondary SU failure was significantly higher in those with the KK genotype than those with EE or EK genotypes. Among 214 patients who eventually received insulin therapy because of secondary SU failure, the period of SU treatment in those with the KK genotype was significantly shorter than those with the EE or EK genotype, although the period from diagnosis to the start of SU treatment was not significantly different.ConclusionsThese data suggest that the Kir6.2 E23K polymorphism is related to the acceleration of secondary SU failure in non‐obese Japanese patients with type 2 diabetes.
Increasing achievement of the target goals for glycemic, blood pressure and lipid control for adults with diagnosed diabetes in Korea
Authors: Yu Sung Hoon , Kang Jun Goo , Hwang Yoo‐Cheol , Ahn Kyu Jeung , Yoo Hyung Joon , Ahn Hong Yup , Park Sung Woo , Park Cheol‐Young 
Published: April 2013

AbstractAims/IntroductionWe investigated the prevalence, treatment and control of diagnosed diabetes in Korean adults from 1998 to 2010.Materials and MethodsThe Korean Ministry of Health and Welfare carried out the Korean National Health and Nutrition Examination Survey (KNHANES) in the years 1998 (I), 2001 (II), 2005 (III), 2007–2009 (IV) and 2010 (V). We estimated the prevalence of diagnosed diabetes in Korean adults and the proportions of well‐controlled diabetes, as defined by having glycosylated hemoglobin <7.0%, blood pressure <130/80 mmHg and low density lipoprotein (LDL) cholesterol <100 mg/dL according to the American Diabetes Association.ResultsThe prevalence of diagnosed diabetes increased significantly from 3.2% in 1998 to 6.4% in 2010 (P < 0.0001). The prevalence of adults with diagnosed diabetes achieving blood pressure and LDL cholesterol target levels increased from 23.8% to 54.2% (P < 0.0001), and 25.7% to 47.7% (P<0.0001), respectively. However, the percentage of patients achieving glycemic goals did not increase significantly from 42.5% to 49.1% (P = 0.3034). Furthermore, there were significant increases in the proportions of individuals achieving all three target levels, from 2.7% in 2005 to 8.7% in 2010 (P < 0.0001).ConclusionsThe prevalence of diagnosed diabetes in Korea increased significantly from 1998 to 2010. The percentages of those achieving all recommendations of the American Diabetes Association have increased, but are still not satisfactory.
Transparent cap‐assisted endoscopic management of foreign bodies in the upper esophagus: A randomized, controlled trial
Authors: Zhang Shenghong , Wang Jinhui , Wang Jinping , Zhong Bihui , Chen Minhu , Cui Yi 
Published: April 2013

AbstractObjectivesIngestion of foreign bodies (FBs) in the upper esophagus is common in South China. It is difficult to manage because of limited working space and inadequate visual field in this area. This randomized, controlled study aimed to evaluate the usefulness of a transparent cap in the endoscopic management of FBs in the upper esophagus.MethodsAdult patients suspected of FBs in the upper esophagus based on the history of FBs ingestion, symptoms, and barium contrast examination were screened for the study between March 1, 2009 and December 31, 2010. Seventy patients with endoscopic‐confirmed FBs in the upper esophagus were recruited and were randomly assigned to two groups: transparent cap‐assisted esophagogastroduodenoscopy group (n = 35) or conventional esophagogastroduodenoscopy group (n = 35). The type, size, and location of FBs, the operation time for removing the FBs, and the clearness of visual field were compared between these two groups.ResultsThe type, size, and location of FBs were similar between the two groups (P > 0.05). The average operation time for removing the FBs was significantly shorter in the transparent cap‐assisted group than in the conventional group (2.6 min vs 4.1 min, P = 0.008). Visual field was rated as “clear” in more cases in the transparent cap‐assisted group than in the conventional group (97.1% vs 25.7%, P < 0.0001).ConclusionsTransparent cap‐assisted endoscopy was a safe and effective method in the management of FBs in the upper esophagus, with a shorter operation time and clearer visual field.
Cyclin E facilitates dysplastic hepatocytes to bypass G1/S checkpoint in hepatocarcinogenesis
Authors: Pok Sharon , Wen Victoria , Shackel Nicholas , Alsop Amber , Pyakurel Pawan , Fahrer Aude , Farrell Geoffrey C , Teoh Narci C 
Published: April 2013

AbstractBackground and AimBy array‐comparative genomic hybridization, we demonstrated cyclin E as one of seven genes associated with hepatocellular carcinoma (HCC) development in Ku70 DNA repair‐deficient mice. We therefore explored the hypothesis that during hepatocarcinogenesis, cyclin E kinase can overcome the inhibitory effects of p53 and establish whether abnormal miRNA(mi‐R)‐34, a co‐regulator of cyclin E and p53, can account for their interactions as “drivers” of HCC.MethodsDysplastic hepatocytes (DNs) and HCCs were generated from diethylnitrosamine (DEN)‐injected C57BL/6 male mice at 3–12 months.ResultsCyclin E/cdk2 was barely expressed in normal liver, but was readily detected in dysplastic hepatocytes, localizing to glutathione‐S transferase pi‐form positive cells dissected by laser‐dissection. Cyclin E kinase activity preceded cyclin D1, proliferating cell nuclear antigen expression in DNs and HCCs despite maximal p53 and p21 expression. We confirmed that cyclin E, rather than cyclin D1, is the proliferative driver in hepatocarcinogenesis by immunoprecipitation experiments demonstrating preferential binding of p21 to cyclin D1, allowing cyclin E‐mediated “escape” from G1/S checkpoint. We then showed cyclin E was responsible for regulating wild‐type p53 by knockdown experiments in primary HCC cells; cyclin E‐knockdown increased p53 and p21, diminished anti‐apoptotic Bcl‐XL and reduced cell viability. Conversely, blocking p53 augmented cyclin E, Bcl‐XL expression and increased proliferation. Physiological interactions between cyclin E/p53/p21 were confirmed in primary hepatocytes. miR‐34a,c were upregulated in dysplastic murine, human liver and HCCs compared with normal liver, and appeared to be linked to cyclin E/p53.ConclusionUpregulation of functionally active cyclin E via miR34 with loss of p53 function is associated with cell‐cycle checkpoint failure increasing proliferative drive that favors hepatocarcinogenesis.
Protecting Minority Homeowners: Race, Foreclosure Counseling and Mortgage Modifications
Authors: COLLINS J. MICHAEL , SCHMEISER MAXIMILIAN D. , URBAN CARLY 
Published: April 2013

AbstractMillions of minority homeowners are at risk of losing their homes as a result of the housing crisis due to mortgage foreclosure and home repossession. One consumer‐oriented policy response to this crisis is mortgage default counseling for borrowers. This study examines the rate at which minority borrowers seek default counseling and the resulting correlation between counseling and the probability that a borrower obtains a modification of his/her original mortgage contract terms. The results suggest that African Americans are more likely to be counseled, relative to Whites. However, Latinos or other non‐White groups are no more or less likely to be counseled. The probability of loan modifications among counseled African Americans is also higher than other counseled borrowers. These results suggest that counseling policies and the public subsidy of default counseling may be one approach for promoting consumer financial well‐being of these households, but also suggest counseling efforts might be better designed for other minority groups. These results also have implications for the application of counseling to other mortgage decisions, such as refinance.
A SURVEY OF THE ECONOMICS OF PATENT SYSTEMS AND PROCEDURES
Authors: Eckert Andrew , Langinier Corinne 
Published: April 2013

AbstractThe last several decades have seen increases in patenting activity worldwide, as well as growing issues related to patent quality. In response to these quality issues a recent patent literature has emerged, that investigates the behavior and incentives of patent examiners, applicants, and third parties. In this paper, we provide an overview of patent procedures, patent systems and a survey of the new economic literature on patent systems. Both theoretical and empirical papers are considered. Policy implications coming from this literature are presented.