bluuebunny/crossref_metadata_2025_split huggingface dataset:
Feline Ureteral Strictures: 10 Cases (2007–2009)
Authors: Zaid M.S. , Berent A.C. , Weisse C. , Caceres A. 
Published: February 2011

Background: Feline ureteral obstructions have emerged as a common problem. Ureteral strictures rarely are reported as a cause and the predisposing factors and clinical course of this condition have not been described.Objectives: Evaluate cases of feline ureteral strictures and characterize historical features, clinical signs, diagnostic imaging, surgical and endoscopic findings, histopathology, treatment modalities, and short‐ and long‐term outcomes.Animals: Ten cats diagnosed with ureteral strictures based on compatible findings from at least 2 of the following: ultrasonography, ureteropyelography, surgical exploration, or histopathology.Methods: Retrospective study.Results: Median age, serum creatinine concentration, and size of the renal pelvis were 12 years, 3.7 mg/dL, and 11.75 mm, respectively. Six of 10 cats had hyperechoic periureteral tissue on ultrasound examination at the stricture site. Four cats had evidence of a circumcaval ureter at surgery. Eight cats had an intervention including ureteral stent placement (n = 6) and traditional surgery (n = 2). Seven of 8 cats had decreases in serum creatinine concentration and renal pelvic parameters preceding discharge and 6 had persistently improved results at their last examination. All patients survived to discharge. Median survival time was >294 days (range, 14 to >858 days) with 6/10 cats still alive.Conclusions and Clinical Importance: Ureteral strictures may occur in cats secondary to ureteral surgery, inflammation, a circumcaval ureter, impacted ureterolithiasis, or for unknown causes. With appropriate and timely intervention, the prognosis for long‐term survival is good. In addition to ureteral reimplantation or ureteronephrectomy, ureteral stenting or SC ureteral bypass may be considered as future therapeutic options.
Cardiac Troponin I Concentrations in Ponies Challenged with Equine Influenza Virus
Authors: Durando M.M. , Birks E.K. , Hussey S.B. , Lunn D.P. 
Published: February 2011

Background: Myocarditis is thought to occur secondary to equine influenza virus (EIV) infections in horses, but there is a lack of published evidence.Hypothesis/Objectives: We proposed that EIV challenge infection in ponies would cause myocardial damage, detectable by increases in plasma cardiac troponin I (cTnI) concentrations.Animals: Twenty‐nine influenza‐naïve yearling ponies: 23 were part of an influenza vaccine study (11 unvaccinated and 12 vaccinated), and were challenged with 108 EID50 EIV A/eq/Kentucky/91 6 months after vaccination. Six age‐matched healthy and unvaccinated ponies concurrently housed in a separate facility not exposed to influenza served as controls.Methods: Heparinized blood was collected before and over 28 days after infection and cTnI determined. Repeated measures analysis of variance, chi‐square, or clustered regression analyses were used to identify relationships between each group and cTnI.Results: All EIV‐infected ponies developed clinical signs and viral shedding, with the unvaccinated group displaying severe signs. One vaccinated pony and 2 unvaccinated ponies had cTnI greater than the reference range at 1 time point. At all other times, cTnI was <0.05 ng/mL. All control ponies had normal cTnI. There were no significant associations between cTnI and either clinical signs or experimental groups. When separated into abnormal versus normal cTnI, there were no significant differences among groups.Conclusions and Clinical Importance: This study demonstrated no evidence of severe myocardial necrosis secondary to EIV challenge with 108 EID50 EIV A/eq/Kentucky/91 in these sedentary ponies, but transient increases in cTnI suggest that mild myocardial damage may occur.
Effects of the Insulin‐Sensitizing Drug Pioglitazone and Lipopolysaccharide Administration on Insulin Sensitivity in Horses
Authors: Suagee J.K. , Corl B.A. , Wearn J.G. , Crisman M.V. , Hulver M.W. , Geor R.J. , McCutcheon L.J. 
Published: February 2011

Background: Obesity and insulin resistance increase the risk of laminitis in horses. Pioglitazone (PG) is an insulin‐sensitizing drug used in humans that is absorbed after oral administration to horses.Hypothesis: PG treatment will increase insulin sensitivity and transcript abundance of glucose and lipid transporters in adipose and skeletal muscle tissues.Animals: Sixteen lean, healthy horses.Methods: Eight horses were administered PG (1 mg/kg bodyweight PO) for 12 days before induction of insulin resistance through IV administration of lipopolysaccharide (LPS). Treated and untreated controls (CN; n = 8) were subjected to testing of peripheral insulin sensitivity and biopsies of both subcutaneous (nuchal ligament) adipose tissue and skeletal muscle before and after treatment, and 24 hours after LPS administration.Results: PG treatment did not improve basal insulin sensitivity (CNs: 1.4 ± 0.3, PG‐treated: 1.9 ± 1.3; P > .4) or mitigate LPS‐induced insulin resistance (CNs: 0.4 ± 0.3, PG‐treated: 0.4 ± 0.3); however, transcript abundance of glucose and lipid transporters was altered in both skeletal muscle and subcutaneous adipose tissue.Conclusions and Clinical Importance: Either a higher dose or longer treatment period might be required for physiological effects to be observed. PG is a novel therapeutic agent requiring further investigation in horses in order to determine treatment efficacy.
Repetitive Stimulation of the Common Peroneal Nerve as a Diagnostic Aid for Botulism in Foals
Authors: Aleman M. , Williams D.C. , Jorge N.E. , Magdesian K.G. , Brosnan R.J. , Feary D.J. , Hilton H.G. , Kozikowski T.A. , Higgins J.K. , Madigan J.E. , LeCouteur R.A. 
Published: February 2011

Background: Botulism is a potentially fatal paralytic disorder for which definitive diagnosis is difficult.Objectives: To determine if repetitive stimulation of the common peroneal nerve will aid in the diagnosis of botulism in foals.Animals: Four control and 3 affected foals.Methods: Validation of the test in healthy foals for its comparison in foals with suspected botulism. Controls were anesthetized and affected foals were sedated to avoid risks of anesthesia. The common peroneal nerve was chosen for its superficial location and easy access. Stimulating electrodes were placed along the common peroneal nerve. For recording, the active and reference electrodes were positioned over the midpoint and distal end of the extensor digitorum longus muscle, respectively. Repeated supramaximal stimulation of the nerve was performed utilizing a range of frequencies (1–50 Hz). Data analysis consisted of measuring the amplitude and area under the curve for each M wave and converting these values into percentages of decrement or increment based on the comparison of subsequent potentials to the initial one (baseline) within each set.Results: A decremental response was seen at all frequencies in control foals. Decremental responses also were observed in affected foals at low frequencies. An incremental response was seen in all affected foals at 50 Hz.Conclusions and Clinical Importance: Decreased baseline M wave amplitudes with incremental responses at high rates are supportive of botulism. Repetitive nerve stimulation is a safe, simple, fast, and noninvasive technique that can aid in the diagnosis of suspected botulism in foals.
Hypercoagulability in Dogs with Protein‐Losing Enteropathy
Authors: Goodwin L.V. , Goggs R. , Chan D.L. , Allenspach K. 
Published: February 2011

Background: Dogs with protein‐losing enteropathy (PLE) have previously been reported to present with thromboembolism; however, the prevalence and pathogenesis of hypercoagulability in dogs with PLE have not been investigated so far.Hypothesis: Dogs with PLE are hypercoagulable compared with healthy control dogs.Animals: Fifteen dogs with PLE. Thirty healthy dogs served as controls (HC).Methods: A prospective study was performed including 15 dogs with PLE. All dogs were scored using the canine chronic enteropathy activity index (CCECAI). Thromboelastography (TEG) and other measures of coagulation were evaluated. Recalcified, unactivated TEG was performed and reaction time (R), kinetic time (K), alpha angle (α), and maximum amplitude (MA) values were recorded. Nine dogs were reassessed after initiation of immunosuppressive treatment.Results: All dogs with PLE in the study were hypercoagulable with decreased R (PLE: median 7.8, range [2.4–11.2]; HC: 14.1 [9.1–20.3]), decreased K (PLE: 2.5 [0.8–5.2]; HC: 8.25 [4.3–13.1]), increased α (PLE: 56.7 [38.5–78.3]; HC: 25.6 [17–42.4]), and increased MA (PLE: 68.2 [54.1–76.7]; HC: 44.1, [33.5–49]) (all P < .001). Median antithrombin (AT) concentration was borderline low in PLE dogs; however, mean serum albumin concentration was severely decreased (mean 1.67 g/dL ± 5.1, reference range 2.8–3.5 g/dL). Despite a significant improvement in serum albumin and CCECAI, all 9 dogs with PLE were hypercoagulable at re‐examination.Conclusions and Clinical Importance: The hypercoagulable state in dogs with PLE cannot be solely attributed to loss of AT. Despite good clinical response to treatment, dogs remained hypercoagulable and could therefore be predisposed to thromboembolic complications.
Reflections on a decade of research by ASEAN dental faculties: analysis of publications from ISI‐WOS databases from 2000 to 2009
Authors: Sirisinha Stitaya , Koontongkaew Sittichai , Phantumvanit Prathip , Wittayawuttikul Ruchareka 
Published: February 2011

AbstractThis communication analyzed research publications in dentistry in the Institute of Scientific Information Web of Science databases of 10 dental faculties in the Association of South‐East Asian Nations (ASEAN) from 2000 to 2009. The term used for the “all‐document types” search was “Faculty of Dentistry/College of Dentistry.” Abstracts presented at regional meetings were also included in the analysis. The Times Higher Education System QS World University Rankings showed that universities in the region fare poorly in world university rankings. Only the National University of Singapore and Nanyang Technological University appeared in the top 100 in 2009; 19 universities in the region, including Indonesia, Malaysia, the Philippines, Singapore, and Thailand, appeared in the top 500. Data from the databases showed that research publications by dental institutes in the region fall short of their Asian counterparts. Singapore and Thailand are the most active in dental research of the ASEAN countries.
The role of work ability in the relationship between aerobic capacity and sick leave: a mediation analysis
Authors: Strijk Jorien E , Proper Karin I , van Stralen Maartje M , Wijngaard Peter , van Mechelen Willem , van der Beek Allard J 
Published: February 2011

ObjectivesTo examine: (1) the relationships between aerobic capacity, work ability and sick leave; (2) the potential mediating effect of work ability in the relationship between aerobic capacity and sick leave; and (3) the influence of age on these relationships.MethodsInformation on aerobic capacity (predicted VO2max), age, gender, type of work, cardiovascular risk and body mass index was collected from 580 workers at baseline. Work ability was assessed with the Work Ability Index at first follow-up (mean 3.4±1.3 years after baseline). The second follow-up period was defined as the time between completing the Work Ability Index and the first registered sick leave episode. Mediation analyses were performed using linear and Cox regression models.ResultsA lower aerobic capacity was found to be significantly related to sick leave (HR=0.98; τ=−0.018; 95% CI 0.970 to 0.994). There was a significant positive relationship between aerobic capacity and work ability (α=0.165; 95% CI 0.122 to 0.208). Also, lower work ability was significantly related to sick leave after controlling for aerobic capacity (HR=0.97; β=−0.033; 95% CI 0.949 to 0.987). The mediating effect of work ability in the relationship between aerobic capacity and sick leave was −0.005 (SE=0.002), and mediated 27.8% (95% CI 10.4 to 45.2) of the total effect of aerobic capacity on sick leave. Age did not influence the relationship between aerobic capacity and sick leave.ConclusionsFit workers had better work ability, and both fit workers and workers with higher work ability were at lower risk of starting an episode of sick leave.
MicroRNA-205 Inhibits Src-Mediated Oncogenic Pathways in Renal Cancer
Authors: Majid Shahana , Saini Sharanjot , Dar Altaf A. , Hirata Hiroshi , Shahryari Varahram , Tanaka Yuichiro , Yamamura Soichiro , Ueno Koji , Zaman Mohd Saif , Singh Kamaldeep , Chang Inik , Deng Guoren , Dahiya Rajvir 
Published: February 2011

Abstract
The Src family of protein kinases (SFK) plays key roles in regulating fundamental cellular processes, including cell growth, differentiation, cell shape, migration, and survival, and specialized cell signals in various malignancies. The pleiotropic functions of SFKs in cancer make them promising targets for intervention. Here, we sought to investigate the role of microRNA-205 (miR-205) in inhibition of Src-mediated oncogenic pathways in renal cancer. We report that expression of miR-205 was significantly suppressed in renal cancer cell lines and tumors when compared with normal tissues and a nonmalignant cell line and is correlated inversely with the expression of SFKs. miR-205 significantly suppressed the luciferase activity of reporter plasmids containing the 3′-UTR (untranslated region) sequences complementary to either Src, Lyn, or Yes, which was abolished by mutations in these 3′-UTR regions. Overexpression of miR-205 in A498 cells reduced Src, Lyn, and Yes expression, both at mRNA and protein levels. Proliferation of renal cancer cells was suppressed by miR-205, mediated by the phospho-Src–regulated ERK1/2 pathway. Cell motility factor FAK (focal adhesion kinase) and STAT3 activation were also inhibited by miR-205. Transient and stable overexpression of miR-205 in A498 cells resulted in induction of G0/G1 cell-cycle arrest and apoptosis, as indicated by decreased levels of cyclin D1 and c-Myc, suppressed cell proliferation, colony formation, migration, and invasion in renal cancer cells. miR-205 also inhibited tumor cell growth in vivo. This is the first study showing that miR-205 inhibits proto-oncogenic SFKs, indicating a therapeutic potential of miR-205 in the treatment of renal cancer. Cancer Res; 71(7); 2611–21. ©2011 AACR.
Cyclophilin A Promotes Cardiac Hypertrophy in Apolipoprotein E–Deficient Mice
Authors: Satoh Kimio , Nigro Patrizia , Zeidan Asad , Soe Nwe Nwe , Jaffré Fabrice , Oikawa Masayoshi , O'Dell Michael R. , Cui Zhaoqiang , Menon Prashanthi , Lu Yan , Mohan Amy , Yan Chen , Blaxall Burns C. , Berk Bradford C. 
Published: February 2011

Objective—

Cyclophilin A (CyPA, encoded by
Ppia
) is a proinflammatory protein secreted in response to oxidative stress in mice and humans. We recently demonstrated that CyPA increased angiotensin II (Ang II)–induced reactive oxygen species (ROS) production in the aortas of apolipoprotein E (
Apoe
)
−/−
mice. In this study, we sought to evaluate the role of CyPA in Ang II–induced cardiac hypertrophy.

Methods and Results—

Cardiac hypertrophy was not significantly different between
Ppia
+/+
and
Ppia
−/−
mice infused with Ang II (1000 ng/min per kg for 4 weeks). Therefore, we investigated the effect of CyPA under conditions of high ROS and inflammation using the
Apoe
−/−
mice. In contrast to
Apoe
−/−
mice,
Apoe
−/−
Ppia
−/−
mice exhibited significantly less Ang II–induced cardiac hypertrophy. Bone marrow cell transplantation showed that CyPA in cells intrinsic to the heart plays an important role in the cardiac hypertrophic response. Ang II–induced ROS production, cardiac fibroblast proliferation, and cardiac fibroblast migration were markedly decreased in
Apoe
−/−
Ppia
−/−
cardiac fibroblasts. Furthermore, CyPA directly induced the hypertrophy of cultured neonatal cardiac myocytes.

Conclusion—
CyPA is required for Ang II–mediated cardiac hypertrophy by directly potentiating ROS production, stimulating the proliferation and migration of cardiac fibroblasts, and promoting cardiac myocyte hypertrophy.
Lipid-Free Apolipoprotein A-I and Discoidal Reconstituted High-Density Lipoproteins Differentially Inhibit Glucose-Induced Oxidative Stress in Human Macrophages
Authors: Tabet Fatiha , Lambert Gilles , Cuesta Torres Luisa F. , Hou Liming , Sotirchos Irene , Touyz Rhian M. , Jenkins Alicia J. , Barter Philip J. , Rye Kerry-Anne 
Published: February 2011

Objective—
The goal of this study was to investigate the mechanisms by which apolipoprotein (apo) A-I, in the lipid-free form or as a constituent of discoidal reconstituted high-density lipoproteins ([A-I]rHDL), inhibits high-glucose–induced redox signaling in human monocyte-derived macrophages (HMDM).

Methods and Results—

HMDM were incubated under normal (5.8 mmol/L) or high-glucose (25 mmol/L) conditions with native high-density lipoproteins (HDL) lipid-free apoA-I from normal subjects and from subjects with type 2 diabetes (T2D) or (A-I)rHDL. Superoxide (O
2
−
) production was measured using dihydroethidium fluorescence. NADPH oxidase activity was assessed using lucigenin-derived chemiluminescence and a cyotochrome
c
assay. p47phox translocation to the plasma membrane, Nox2, superoxide dismutase 1 (SOD1), and SOD2 mRNA and protein levels were determined by real-time polymerase chain reaction and Western blotting. Native HDL induced a time-dependent inhibition of O
2
−
generation in HMDM incubated with 25 mmol/L glucose. Lipid-free apoA-I and (A-I)rHDL increased SOD1 and SOD2 levels and attenuated 25 mmol/L glucose-mediated increases in cellular O
2
−
, NADPH oxidase activity, p47 translocation, and Nox2 expression. Lipid-free apoA-I mediated its effects on Nox2, SOD1, and SOD2 via ABCA1. (A-I)rHDL-mediated effects were via ABCG1 and scavenger receptor BI. Lipid-free apoA-I from subjects with T2D inhibited reactive oxygen species generation less efficiently than normal apoA-I.

Conclusion—
Native HDL, lipid-free apoA-I and (A-I)rHDL inhibit high-glucose–induced redox signaling in HMDM. The antioxidant properties of apoA-I are attenuated in T2D.
C/EBP Homologous Protein Deficiency Attenuates Myocardial Reperfusion Injury by Inhibiting Myocardial Apoptosis and Inflammation
Authors: Miyazaki Yuji , Kaikita Koichi , Endo Motoyoshi , Horio Eiji , Miura Mitsutoshi , Tsujita Kenichi , Hokimoto Seiji , Yamamuro Megumi , Iwawaki Takao , Gotoh Tomomi , Ogawa Hisao , Oike Yuichi 
Published: February 2011

Objective—
To investigate whether and how the endoplasmic reticulum (ER) stress–induced, CCAAT/enhancer-binding protein-homologous protein (CHOP)-mediated pathway regulates myocardial ischemia/reperfusion injury.

Methods and Results—

Wild-type and
chop
-deficient mice underwent 50 minutes of left coronary artery occlusion followed by reperfusion. Expression of
chop
and spliced
x-box binding protein-
1 (
sxbp1
) mRNA was rapidly and significantly increased in reperfused myocardium of wild-type mice.
chop
-deficient mice exhibited markedly reduced injury size after reperfusion compared with wild-type mice, accompanied by a decreasing number of terminal deoxynucleotidyl transferase dUTP nick-end labeling–positive cardiomyocytes. Interestingly, myocardial inflammation, as assessed by expression of inflammatory cytokines and chemokines and numbers of infiltrated inflammatory cells, was also attenuated in
chop
-deficient mice. Moreover, expression of
interleukin-6
mRNA in response to lipopolysaccharide was enhanced by simultaneous stimulation with thapsigargin, a potent ER stressor, in wild-type cardiomyocytes but not in
chop
-deficient cardiomyocytes. Finally, we found that superoxide was produced in reperfused myocardium and that intravenous administration of edaravone, a free radical scavenger, immediately before reperfusion significantly suppressed the superoxide overproduction and subsequent expression of
sxbp1
and
chop
mRNA, followed by reduced injury size in wild-type mice.

Conclusion—
The ER stress–induced, CHOP-mediated pathway, which is activated in part by superoxide overproduction after reperfusion, exacerbates myocardial ischemia/reperfusion injury by inducing cardiomyocyte apoptosis and myocardial inflammation.
Glucocorticoid Insensitivity at the Hypoxic Blood–Brain Barrier Can Be Reversed by Inhibition of the Proteasome
Authors: Kleinschnitz Christoph , Blecharz Kinga , Kahles Timo , Schwarz Tobias , Kraft Peter , Göbel Kerstin , Meuth Sven G. , Burek Malgorzata , Thum Thomas , Stoll Guido , Förster Carola 
Published: February 2011

Background and Purpose—
Glucocorticoids potently stabilize the blood–brain barrier and ameliorate tissue edema in certain neoplastic and inflammatory disorders of the central nervous system, but they are largely ineffective in patients with acute ischemic stroke. The reasons for this discrepancy are unresolved.

Methods—

To address the molecular basis for the paradox unresponsiveness of the blood–brain barrier during hypoxia, we used murine brain microvascular endothelial cells exposed to O
2
/glucose deprivation as an in vitro model. In an in vivo approach, mice were subjected to transient middle cerebral artery occlusion to induce brain infarctions. Blood–brain barrier damage and edema formation were chosen as surrogate markers of glucocorticoid sensitivity in the presence or absence of proteasome inhibitors.

Results—

O
2
/glucose deprivation reduced the expression of tight junction proteins and transendothelial resistance in murine brain microvascular endothelial cells in vitro. Dexamethasone treatment failed to reverse these effects during hypoxia. Proteasome-dependent degradation of the glucocorticoid receptor impaired glucocorticoid receptor transactivation thereby preventing physiological glucocorticoid activity. Inhibition of the proteasome, however, fully restored the blood–brain barrier stabilizing properties of glucocorticoid during O
2
/glucose deprivation. Importantly, mice treated with the proteasome inhibitor Bortezomib in combination with steroids several hours after stroke developed significantly less brain edema and functional deficits, whereas respective monotherapies were ineffective.

Conclusions—
We for the first time show that inhibition of the proteasome can overcome glucocorticoid resistance at the hypoxic blood–brain barrier. Hence, combined treatment strategies may help to combat stroke-induced brain edema formation in the future and prevent secondary clinical deterioration.