bluuebunny/crossref_metadata_2025_split huggingface dataset:
Proximal injuries of the accessory ligament of the deep digital flexor tendon in forelimbs and hindlimbs: 12 horses (2006–2010)
Authors: Dyson S. 
Published: September 2011

SummaryThere have been no detailed ultrasonographic descriptions of injuries of the accessory ligament of the deep digital flexor tendon (ALDDFT) in the carpal and proximal metacarpal and tarsal and proximal metatarsal regions. The aims of this study were to describe the: 1) normal ultrasonographic appearance of the proximal aspect of the ALDDFT in fore‐ and hindlimbs and 2) clinical and ultrasonographic features of proximal injuries of the ALDDFT in both fore‐ and hindlimbs. The proximal aspects of the ALDDFT of both fore‐ and hindlimbs of 10 horses free from lameness were examined ultrasonographically. Clinical records of 12 horses examined between January 2006 and December 2010 with proximal injuries of the ALDDFT were reviewed. All 4 horses with proximal lesions of the ALDDFT in a forelimb had no localising clinical signs and diagnostic analgesia was required to localise the source of pain. Eight horses with recent onset hindlimb lameness had oedematous swelling in the proximoplantaromedial aspect of the metatarsal region (n = 7) or more generalised thickening in the region of the proximal aspect of the ALDDFT (n = 1). Diagnosis was confirmed ultrasonographically in all horses. One horse was retired for unrelated reasons. One of 3 horses with forelimb lameness returned to full athletic function. Four of 6 horses with hindlimb lameness returned to work; the remaining 2 horses resumed work, but experienced recurrent injury of the ALDDFT. Proximal injuries of the ALDDFT should be considered as a cause of either fore‐ or hindlimb lameness, even in the absence of gross palpable abnormalities.
Comparison of Performance of the Novel Chromogenic Spectra VRE Agar to That of Bile Esculin Azide and Campylobacter Agars for Detection of Vancomycin-Resistant Enterococci in Fecal Samples
Authors: Jenkins S. G. , Raskoshina L. , Schuetz A. N. 
Published: September 2011

ABSTRACT

A total of 142 stool specimens were evaluated for vancomycin-resistant enterococcus (VRE). Twenty-four-hour sensitivities and specificities, respectively, were 98% and 95% for Spectra VRE chromogenic agar (Remel, Lenexa, KS), 86% and 92% for bile esculin azide with vancomycin (BEAV; Remel), and 96.5% and 92% for
Campylobacter
agar (CAMPY; Remel). Spectra VRE and CAMPY are significantly more sensitive at 24 h than BEAV.
Canada's First Case of a Multidrug-Resistant Corynebacterium diphtheriae Strain, Isolated from a Skin Abscess
Authors: Mina Neil V. , Burdz Tamara , Wiebe Deborah , Rai Jagtar S. , Rahim Tazim , Shing Fern , Hoang Linda , Bernard Kathryn 
Published: September 2011

ABSTRACTA toxigenicCorynebacterium diphtheriaebiovar mitis sequence type 136 (ST136) strain was recovered from a toe infection of an unvaccinated patient recently returned from India. The isolate was resistant to clindamycin, erythromycin (ermXpositive), tetracycline, and trimethoprim-sulfamethoxazole, intermediate to ceftriaxone and cefotaxime, and had high MICs for telithromycin and chloramphenicol but was sensitive to other drugs.
The Latency-Associated UL138 Gene Product of Human Cytomegalovirus Sensitizes Cells to Tumor Necrosis Factor Alpha (TNF-α) Signaling by Upregulating TNF-α Receptor 1 Cell Surface Expression
Authors: Montag Christina , Wagner Jutta Annabella , Gruska Iris , Vetter Barbara , Wiebusch Lüder , Hagemeier Christian 
Published: September 2011

ABSTRACTMany viruses antagonize tumor necrosis factor alpha (TNF-α) signaling in order to counteract its antiviral properties. One way viruses achieve this goal is to reduce TNF-α receptor 1 (TNFR1) on the surface of infected cells. Such a mechanism is also employed by human cytomegalovirus (HCMV), as recently reported by others and us. On the other hand, TNF-α has also been shown to foster reactivation of HCMV from latency. By characterizing a new variant of HCMV AD169, we show here that TNFR1 downregulation by HCMV only becomes apparent upon infection of cells with HCMV strains lacking the so-called ULb′ region. This region contains genes involved in regulating viral immune escape, cell tropism, or latency and is typically lost from laboratory strains but present in low-passage strains and clinical isolates. We further show that although ULb′-positive viruses also contain the TNFR1-antagonizing function, this activity is masked by a dominant TNFR1 upregulation mediated by the ULb′ gene product UL138. Isolated expression of UL138 in the absence of viral infection upregulates TNFR1 surface expression and can rescue both TNFR1 reexpression and TNF-α responsiveness of cells infected with an HCMV mutant lacking the UL138-containing transcription unit. Given that the UL138 gene product is one of the few genes recognized to be expressed during HCMV latency and the known positive effects of TNF-α on viral reactivation, we suggest that via upregulating TNFR1 surface expression UL138 may sensitize latently infected cells to TNF-α-mediated reactivation of HCMV.
Bayesian integrated survey-based assessments: an example applied to North Sea herring (Clupea harengus) survey data
Authors: Hillary Richard 
Published: August 2011

Stock assessments that use only fisheries independent data have been developed from a number of different standpoints over the last 15 years. While the ability of such stock assessments to avoid the use of potentially compromised or hard to interpret commercial data or making certain assumptions that are common to traditional assessments has been established, little has been made of their potential for detecting and estimating complex mortality trends over time or their potential utility in survey-based management procedures. Using North Sea herring ( Clupea harengus ) data as an example, a Bayesian survey-based assessment method that is able to estimate all the key population variables is detailed. However, survival probability, and not fishing mortality that is conditional on natural mortality, is the key parameter. Reversible jump Markov chain Monte Carlo routines were developed to explore the range of ages over which survival separates into year and age effects (a common assumption in many stock assessments). Post hoc estimates of natural mortality suggest that changes over years and ages may have occurred in relativity to historic levels. The derivation of reference points based on survival probability and surplus biomass production are detailed as proxies for more common F-based reference points. The potential role for the outputs of such assessments in a management procedure sense is discussed.
Phenotypic plasticity in physiological status at emergence from nests as a response to temperature in Atlantic salmon (Salmo salar)
Authors: Skoglund Helge , Einum Sigurd , Forseth Torbjørn , Barlaup Bjørn Torgeir 
Published: August 2011

Successful transitions from relying on yolk to exogenous feeding may be strongly influenced by temperature conditions experienced both during embryonic development, through effects on juvenile phenotype, and during initiation of feeding. Here we simultaneously assess these two effects of temperature treatments (2, 5, 8, and 12 °C) in Atlantic salmon ( Salmo salar ). Fry emerging from low incubation temperatures were smaller and had metabolized more energy prior to emergence, but had larger yolk sacs and higher mass specific energy levels, than those experiencing higher temperatures. After emergence, activity, feeding, and growth increased significantly with increasing temperature, but fry were able to initiate feeding and maintain positive growth at all four temperatures. Larger energy stores may provide an advantage when emerging at cold temperatures with a low potential for feeding activity, whereas having a large body size, which is primarily of importance in competitive interactions, may be less important owing to cryptic feeding and sheltering at low temperatures. However, the adaptive significance of the observed phenotypic response to incubation temperature remains untested.
A new method to reconstruct fish diet and movement patterns from δ13C values in otolith amino acids
Authors: McMahon Kelton W. , Fogel Marilyn L. , Johnson Beverly J. , Houghton Leah A. , Thorrold Simon R. 
Published: August 2011

Fish ecologists have used geochemical values in otoliths to examine habitat use, migration, and population connectivity for decades. However, it remains difficult to determine an unambiguous dietary δ13C signature from bulk analysis of otolith. Studies to date have focused on the aragonite component of otoliths with less attention paid to the organic fraction. We describe the application of compound-specific stable isotope analysis (SIA) to analyze amino acid (AA) δ13C values from small amounts (<1 mg) of otolith powder. We examined δ13C values of otolith and muscle AAs from a reef-associated snapper (Lutjanus ehrenbergii (Peters, 1869)) collected along a carbon isotope gradient (isoscape) from seagrass beds to coral reefs. Carbon isotope values in otolith and muscle samples were highly correlated within and among coastal habitats. Moreover, δ13C values of otolith AAs provided a purely dietary record that avoided dilution from dissolved inorganic carbon. Otolith AAs served as a robust tracer of δ13C values at the base of the food web, making compound-specific SIA a powerful tool for dietary reconstructions and tracking the movement of fishes across isoscapes.
Application of a method for estimating effective population size and admixture using diagnostic single nucleotide polymorphisms (SNPs): implications for conservation of threatened Paiute cutthroat trout (Oncorhynchus clarkii seleniris) in Silver King Creek, California
Authors: Finger Amanda J. , Anderson Eric C. , Stephens Molly R. , May Bernard P. 
Published: August 2011

The threatened Paiute cutthroat trout ( Oncorhynchus clarkii seleniris , PCT) is endemic to Silver King Creek, California, USA, which was stocked with non-native trout beginning in 1930. Single nucleotide polymorphism (SNP) and microsatellite data reveal that the trout population in Silver King Creek is weakly structured and composed of introgressed California golden trout ( Oncorhynchus mykiss aguabonita , CAGT), hatchery rainbow trout ( Oncorhynchus mykiss , RT), and some native PCT. Two SNP groups were analyzed: (i) one mitochondrial and five autosomal SNPs, diagnostic between Lahontan cutthroat trout ( Oncorhynchus clarkii henshawi ) or PCT and CAGT or RT and (ii) one mitochondrial and five autosomal SNPs nearly diagnostic between CAGT and RT. The five autosomal cutthroat–rainbow SNPs were used to jointly estimate the cutthroat trout mixing proportion in Silver King Creek and effective population size (Ne) of the admixed population, using a coalescent-based maximum likelihood method. Given the stocking history of Silver King Creek, there are two different scenarios that bound the range of expected point estimates for Ne. We obtain point estimates of Ne = 150 and Ne = 750 for Silver King Creek under these two scenarios. This method will be useful in cases with differentiated taxa and in prioritizing conservation and restoration programs where the populations of concern are introgressed.
A Role for Bone Morphogenetic Protein-4 in Lymph Node Vascular Remodeling and Primary Tumor Growth
Authors: Farnsworth Rae H. , Karnezis Tara , Shayan Ramin , Matsumoto Masataka , Nowell Cameron J. , Achen Marc G. , Stacker Steven A. 
Published: August 2011

Abstract
Lymph node metastasis, an early and prognostically important event in the progression of many human cancers, is associated with expression of VEGF-D. Changes to lymph node vasculature that occur during malignant progression may create a metastatic niche capable of attracting and supporting tumor cells. In this study, we sought to characterize molecules expressed in lymph node endothelium that could represent therapeutic or prognostic targets. Differential mRNA expression profiling of endothelial cells from lymph nodes that drained metastatic or nonmetastatic primary tumors revealed genes associated with tumor progression, in particular bone morphogenetic protein-4 (BMP-4). Metastasis driven by VEGF-D was associated with reduced BMP-4 expression in high endothelial venules, where BMP-4 loss could remodel the typical high-walled phenotype to thin-walled vessels. VEGF-D expression was sufficient to suppress proliferation of the more typical BMP-4–expressing high endothelial venules in favor of remodeled vessels, and mechanistic studies indicated that VEGF receptor-2 contributed to high endothelial venule proliferation and remodeling. BMP-4 could regulate high endothelial venule phenotype and cellular function, thereby determining morphology and proliferation responses. Notably, therapeutic administration of BMP-4 suppressed primary tumor growth, acting both at the level of tumor cells and tumor stromal cells. Together, our results show that VEGF-D–driven metastasis induces vascular remodeling in lymph nodes. Furthermore, they implicate BMP-4 as a negative regulator of this process, suggesting its potential utility as a prognostic marker or antitumor agent. Cancer Res; 71(20); 6547–57. ©2011 AACR.
MALT1 Protease: A New Therapeutic Target in B Lymphoma and Beyond?
Authors: McAllister-Lucas Linda M. , Baens Mathijs , Lucas Peter C. 
Published: August 2011

Abstract
The identification of mucosa-associated lymphoid tissue lymphoma translocation 1 (MALT1) as a gene that is perturbed in the B-cell neoplasm MALT lymphoma, already more than a decade ago, was the starting point for an intense area of research. The fascination with MALT1 was fueled further by the observation that it contains a domain homologous to the catalytic domain of caspases and thus, potentially, could function as a protease. Discoveries since then initially revealed that MALT1 is a key adaptor molecule in antigen receptor signaling to the transcription factor NF-κB, which is crucial for lymphocyte function. However, recent discoveries show that this function of MALT1 is not restricted to lymphocytes, witnessed by the ever-increasing list of receptors from cells within and outside of the immune system that require MALT1 for NF-κB activation. Yet, a role for MALT1 protease activity was shown only recently in immune signaling, and its importance was then further strengthened by the dependency of NF-κB–addicted B-cell lymphomas on this proteolytic activity. Therapeutic targeting of MALT1 protease activity might, therefore, become a useful approach for the treatment of these lymphomas and, additionally, an effective strategy for treating other neoplastic and inflammatory disorders associated with deregulated NF-κB signaling. Clin Cancer Res; 17(21); 6623–31. ©2011 AACR.
Calcification in Major Vessel Beds Relates to Vascular Brain Disease
Authors: Bos Daniel , Ikram M. Arfan , Elias-Smale Suzette E. , Krestin Gabriel P. , Hofman Albert , Witteman Jacqueline C.M. , van der Lugt Aad , Vernooij Meike W. 
Published: August 2011

Objective—
Calcification in atherosclerotic plaques is a novel marker of atherosclerosis and is related to cardiovascular disease. However, its relationship with cerebrovascular disease has not been investigated extensively. We investigated the relationship between calcification in various vessel beds outside the brain and imaging markers of vascular brain disease.

Methods and Results—
A total of 885 community-dwelling people (mean age, 66.7 years) underwent computed tomography of the coronary arteries, aortic arch, and extracranial and intracranial carotid arteries to assess arterial calcification. Brain magnetic resonance imaging scans were performed to assess cerebral infarcts, microbleeds, and white matter lesions (WMLs). Calcification in each vessel bed was associated with presence of cerebral infarcts and with larger WML volume. The most prominent associations were found between intracranial carotid calcification and WML volume and between extracranial carotid calcification and infarcts. Adjustment for cardiovascular risk factors or ultrasound carotid plaque scores did not change these results. No associations were found between calcification and cerebral microbleeds.

Conclusion—
Arterial calcification in major vessel beds is associated with vascular brain disease on magnetic resonance imaging. Most notably, larger intracranial carotid calcification load relates to larger WML volumes, and larger extracranial carotid calcification load relates to the presence of cerebral infarcts, independently of ultrasound carotid plaque score. This suggests that calcification of atherosclerotic plaque yields other information in addition to merely the presence of plaques, providing novel insights into the etiology of vascular brain disease.
Slingshot Isoform-Specific Regulation of Cofilin-Mediated Vascular Smooth Muscle Cell Migration and Neointima Formation
Authors: Torres Rebecca A. , Drake Douglas A. , Solodushko Viktoriya , Jadhav Rashmi , Smith Erika , Rocic Petra , Weber David S. 
Published: August 2011

Objective—
We hypothesized that cofilin activation by members of the slingshot (SSH) phosphatase family is a key mechanism regulating vascular smooth muscle cell (VSMC) migration and neoinitima formation following vascular injury.

Methods and Results—
Scratch wound and modified Boyden chamber assays were used to assess VSMC migration following downregulation of the expression of cofilin and each SSH phosphatase isoform (SSH1, SSH2, and SSH3) by small interfering RNA (siRNA), respectively. Cofilin siRNA greatly attenuated the ability of VSMC migration into the “wound,” and platelet-derived growth factor (PDGF)–induced migration was virtually eliminated versus a 3.5-fold increase in nontreated VSMCs, establishing a critical role for cofilin in VSMC migration. Cofilin activation (dephosphorylation) was increased in PDGF-stimulated VSMCs. Thus, we assessed the role of the SSH family of phosphatases on cofilin activation and VSMC migration. Treatment with either SSH1 or SSH2 siRNA attenuated cofilin activation, whereas SSH3 siRNA had no effect. Only SSH1 siRNA significantly reduced wound healing and PDGF-induced VSMC migration. Both SSH1 expression (4.7-fold) and cofilin expression (3.9-fold) were increased in balloon injured versus noninjured carotid arteries, and expression was prevalent in the neointima.

Conclusion—
These studies demonstrate that the regulation of VSMC migration by cofilin is SSH1 dependent and that this mechanism potentially contributes to neointima formation following vascular injury in vivo.
Cerebral Small Vessel Disease and Risk of Death, Ischemic Stroke, and Cardiac Complications in Patients With Atherosclerotic Disease
Authors: Conijn Mandy M.A. , Kloppenborg Raoul P. , Algra Ale , Mali Willem P.Th.M. , Kappelle L. Jaap , Vincken Koen L. , van der Graaf Yolanda , Geerlings Mirjam I. ,   for the SMART Study Group
Published: August 2011

Background and Purpose—
Cerebral small vessel disease may be related to vascular and nonvascular pathology. We assessed whether lacunar infarcts and white matter lesions on MRI increased the risk of vascular and nonvascular death and future vascular events in patients with atherosclerotic disease.

Methods—
Brain MRI was performed in 1309 patients with atherosclerotic disease from the Second Manifestations of ARTerial disease-Magnetic Resonance (SMART-MR) study. Infarcts were scored visually and volumetric assessment of white matter lesion was performed. Patients were followed for a median of 4.5 years (range, 0.2 to 7.1 years) for death, ischemic stroke, and ischemic cardiac complications.

Results—
Cox regression models showed that presence of lacunar infarcts (n=229) increased the risk of vascular (hazard ratio, 2.6; 95% CI, 1.4 to 4.9) and nonvascular death (hazard ratio, 2.7; 95% CI, 1.3 to 5.3), adjusted for age, sex, vascular risk factors, nonlacunar infarcts, and white matter lesion. These risks were similar for patients with silent lacunar infarcts. White matter lesion volume (relative to total intracranial volume) increased the risk of vascular death (hazard ratio per milliliter increase, 1.03; 95% CI, 1.01 to 1.05) and white matter lesions in the upper quintile compared with lower quintiles increased risk of ischemic stroke (hazard ratio, 2.6; 95% CI, 1.3 to 4.9).

Conclusions—
Cerebral small vessel disease, with or without a history of cerebrovascular disease, is associated with increased risk of death and ischemic stroke in patients with atherosclerotic disease.
In-Hospital Medical Complications, Length of Stay, and Mortality Among Stroke Unit Patients
Authors: Ingeman Annette , Andersen Grethe , Hundborg Heidi H. , Svendsen Marie L. , Johnsen Søren P. 
Published: August 2011

Background and Purpose—
The relationship between in-hospital stroke-related medical complications and clinical outcome remains unclear. We examined whether medical complications were associated with length of stay (LOS) and mortality among stroke unit patients.

Methods—
Using population-based Danish medical registries, we performed a follow-up study among all patients with acute stroke admitted to stroke units in 2 counties between 2003 and 2009 (n=13 721). Data regarding in-hospital medical complications, including pneumonia, urinary tract infection, pressure ulcer, falls, deep venous thrombosis, pulmonary embolism, and severe constipation together with LOS and mortality were prospectively registered.

Results—
Overall, 25.2% of patients (n=3453) experienced 1 or more medical complications during hospitalization. The most common complications were urinary tract infection (15.4%), pneumonia (9.0%), and constipation (6.8%). Median LOS was 13 days (25th and 75th quartiles, 5 and 33). All medical complications were associated with longer LOS. The adjusted relative LOS extension ranged from 1.80 (95% CI, 1.54–2.11) for pneumonia to 3.06 (95% CI, 2.67–3.52) for falls. Patients with 1 or more complications had an increased 1-year mortality rate (adjusted mortality rate ratio [MRR], 1.20; 95% CI, 1.04–1.39). The association was mainly because of pneumonia, which was associated with higher mortality both after 30 days (adjusted MRR, 1.59; 95% CI, 1.31–1.93) and 1 year (adjusted MRR, 1.76; 95% CI, 1.45–2.14).

Conclusions—
In-hospital medical complications were associated with longer LOS and some, in particular pneumonia, also with an increased mortality among patients with acute stroke.