bluuebunny/crossref_metadata_2025_split huggingface dataset:
Perception of Teaching and Assessing Technical Proficiency in American College of Veterinary Surgeons Small Animal Surgery Residency Programs
Authors: Kim Stanley E. , Case J. Brad , Lewis Daniel D. , Ellison Gary W. 
Published: June 2015

ObjectiveTo determine how American College of Veterinary Surgeons (ACVS) small animal surgery residency programs are teaching and assessing technical skills, and ascertain the perceived value of those methods.Study DesignInternet‐based survey.Sample PopulationResidents and Diplomate supervisors of ACVS small animal residency programs.MethodsResidents and supervisors were surveyed on their experience of surgery instruction, use of different resources for teaching, type and frequency of feedback, and perceived effectiveness of their programs in imparting technical proficiency.ResultsA total of 130 residents (62%) and 119 supervisors (44%) participated. Both residents and supervisors estimated the resident was the primary surgeon for a mean of 64% of cases, although this proportion varied widely between participants. The majority of residents and supervisors considered that direct intraoperative guidance was the most effective way for residents to develop technical skills. Verbal interactions between supervisor and resident occurred frequently and were highly valued. Regular wet laboratories and access to simulation models were uncommon. Despite over 90% of all participants reporting that a sufficient level of technical aptitude would be attained, only 58% of residents were satisfied with their technical skills training.ConclusionResidents relied on direct interaction with supervisors to develop technical skills. The traditional mode of instruction for veterinary residents is the apprenticeship model, which is partly driven by ACVS requirements of supervisory support. Exposure to other teaching and assessment methods was variable. The current structure of residency programs is successful in imparting technical competency as perceived by supervisors and residents. However, consideration of a more formal method of residency training with structured assessment of technical skills as in human medicine should not be dismissed.
Effect of Intramedullary Rod Diameter on a String of Pearls Plate‐Rod Construct in Mediolateral Bending: An In Vitro Mechanical Study
Authors: Rutherford Scott , Demianiuk Ryan M. , Benamou Jérôme , Beckett Clifford , Ness Malcolm G. , Déjardin Loïc M. 
Published: June 2015

ObjectiveTo evaluate the effect of intramedullary rod (IMR) diameter on the mechanical behavior of string of pearls (SOP) plate‐rod constructs.Study DesignIn vitro mechanical study.Sample populationSynthetic bone models (n = 24).MethodsLocking 3.5 mm SOP plates were fixed to a tibial bone model with a 50 mm fracture gap. Four experimental groups (n = 4) were tested: monocortical SOP construct alone and monocortical SOP constructs augmented with a 2.4, 3.2, or 4.0 mm IMR corresponding to 24, 32, or 40% filling of the medullary cavity diameter (SOP‐24, SOP‐32, SOP‐40). Control groups (n = 4) were stabilized with either a bicortical SOP plate (SOP‐B) or a 3.5 mm limited contact dynamic compression plate (LC‐DCP) with a 4.0 mm IMR filling 40% of the medullary cavity diameter (LC‐DCP‐40). Specimens were tested in mediolateral bending. Construct compliance (CC) and angular deformation (AD) were compared between construct types (P < .05).ResultsCC and AD incrementally decreased with increasing IMR diameter (P < .001). There were no statistical differences between SOP‐24 and SOP‐B (P = .806) or between SOP‐32 and LC‐DCP‐40 (P = .773), which was also the least compliant of all constructs (P < .001). AD followed an identical pattern of significance.ConclusionsBiological osteosynthesis often relies on more compliant bridging constructs to promote beneficial micromotion at the fracture. Our study suggests use of a smaller diameter IMR (SOP‐32) is comparable to a conventional plate‐rod construct (LC‐DCP‐40). Should greater compliance be desired, an even smaller diameter IMR (SOP‐24) may prove beneficial while as stable as an accepted bicortical construct (SOP‐B).
Spontaneously hypertensive rats have more orexin neurons in the hypothalamus and enhanced orexinergic input and orexin 2 receptor‐associated nitric oxide signalling in the rostral ventrolateral medulla
Authors: Lee Yen‐Hsien , Tsai Min‐Chien , Li Tzu‐Ling , Dai Yu‐Wen E. , Huang Shang‐Cheng , Hwang Ling‐Ling 
Published: June 2015

New Findings

What is the central question of this study?
Our previous study demonstrates that elevated orexin 2 receptor (OX2R) activity within the rostral ventrolateral medulla (RVLM) contributes to hypertension in spontaneously hypertensive rats (SHRs), and a lower OX2R protein level was detected in their RVLM. The present study aims to explore the mechanisms underlying elevated orexinergic activity in the RVLM of SHRs, compared with their normotensive counterparts, Wistar‐Kyoto rats.

What is the main finding and its importance?
Increased orexinergic input into the RVLM and enhanced OX2R responsiveness in the RVLM, which was mainly mediated by augmented OX2R–neuronal nitric oxide synthase signalling, may underlie the elevated OX2R activity within the RVLM of SHRs.

Our previous study showed that elevated orexin 2 receptor (OX2R) activity within the rostral ventrolateral medulla (RVLM) contributes to hypertension in spontaneously hypertensive rats (SHRs). Herein, we investigated the mechanism(s) underlying the elevated OX2R activity. The following results were found. (i) More hypothalamic orexin A‐immunoreactive (OXA‐IR) cells existed in SHRs than in Wistar‐Kyoto (WKY) rats at either 4 (2217 ± 43 versus 1809 ± 69) or 16 weeks of age (1829 ± 59 versus 1230 ± 84). The number of OXA‐IR cells that project to the RVLM was higher in 16‐week‐old SHRs than in WKY rats (91 ± 11 versus 52 ± 11). (ii) Higher numbers of OXA‐IR and RVLM‐projecting OXA‐IR cells were found in the dorsomedial and perifornical hypothalamus of 16‐week‐old SHRs. (iii) Spontaneously hypertensive rats had higher levels of orexin A and B in the hypothalamus and higher levels of orexin A in the RVLM than did WKY rats. (iv) Unilateral intra‐RVLM application of OX2R agonist, orexin A or [Ala11,d‐Leu15]‐orexin B (50 pmol) induced a larger pressor response in SHRs than in WKY rats. (v) Intra‐RVLM pretreatment with a neuronal nitric oxide synthase (NOS) inhibitor, 7‐nitro‐indazole (2.5 pmol), or a soluble guanylate cyclase inhibitor, methylene blue (250 pmol), reducedthe intra‐RVLM [Ala11,d‐Leu15]‐orexin B‐induced pressor response in both WKY rats and SHRs. In contrast, an inducible NOS inhibitor, aminoguanidine (100 pmol), was ineffective. (vi) Neuronal NOS was co‐expressed with OX2R in RVLM neurons. In conclusion, increased orexinergic input and enhanced OX2R–neuronal NOS signalling may underlie elevated OX2R activity in the RVLM and contribute to the pathophysiology of hypertension in SHRs.
A novel method for determining human ex vivo submaximal skeletal muscle mitochondrial function
Authors: Hey‐Mogensen Martin , Gram Martin , Jensen Martin Borch , Lund Michael Taulo , Hansen Christina Neigaard , Scheibye‐Knudsen Morten , Bohr Vilhelm A. , Dela Flemming 
Published: June 2015

Key points
The present study utilized a novel method aiming to investigate mitochondrial function in human skeletal muscle at submaximal levels and at a predefined membrane potential.
The effect of age and training status was investigated using a cross‐sectional design.
Ageing was found to be related to decreased leak regardless of training status.
Increased training status was associated with increased mitochondrial hydrogen peroxide emission.
AbstractDespite numerous studies, there is no consensus about whether mitochondrial function is altered with increased age. The novelty of the present study is the determination of mitochondrial function at submaximal activity rates, which is more physiologically relevant than the ex vivo functionality protocols used previously. Muscle biopsies were taken from 64 old or young male subjects (aged 60–70 or 20–30 years). Aged subjects were recruited as trained or untrained. Muscle biopsies were used for the isolation of mitochondria and subsequent measurements of DNA repair, anti‐oxidant capacity and mitochondrial protein levels (complexes I–V). Mitochondrial function was determined by simultaneous measurement of oxygen consumption, membrane potential and hydrogen peroxide emission using pyruvate + malate (PM) or succinate + rotenone (SR) as substrates. Proton leak was lower in aged subjects when determined at the same membrane potential and was unaffected by training status. State 3 respiration was lower in aged untrained subjects. This effect, however, was alleviated in aged trained subjects. H2O2 emission with PM was higher in aged subjects, and was exacerbated by training, although it was not changed when using SR. However, with a higher manganese superoxide dismuthase content, the trained aged subjects may actually have lower or similar mitochondrial superoxide emission compared to the untrained subjects. We conclude that ageing and the physical activity level in aged subjects are both related to changes in the intrinsic functionality of the mitochondrion in skeletal muscle. Both of these changes could be important factors in determining the metabolic health of the aged skeletal muscle cell.
Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men
Authors: Gram Martin , Vigelsø Andreas , Yokota Takashi , Helge Jørn Wulff , Dela Flemming , Hey‐Mogensen Martin 
Published: June 2015

Key points
Currently, it is not known whether impaired mitochondrial function contributes to human ageing or whether potential impairments in mitochondrial function with age are secondary to physical inactivity.
The present study investigated mitochondrial respiratory function and reactive oxygen species emission at a predefined membrane potential in young and older men subjected to 2 weeks of one‐leg immobilization followed by 6 weeks of aerobic cycle training.
Immobilization increased reactive oxygen species emission and decreased ATP generating respiration. Subsequent aerobic training reversed these effects.
By contrast, age had no effect on the measured variables.
The results of the present study support the notion that increased mitochondrial reactive oxygen species production mediates the detrimental effects seen after physical inactivity and that ageing per se does not cause mitochondrial dysfunction.
AbstractMitochondrial dysfunction, defined as increased oxidative stress and lower capacity for energy production, may be seen with ageing and may cause frailty, or it could be that it is secondary to physical inactivity. We studied the effect of 2 weeks of one‐leg immobilization followed by 6 weeks of supervised cycle training on mitochondrial function in 17 young (mean ± SEM: 23 ± 1 years) and 15 older (68 ± 1 years) healthy men. Submaximal H2O2 emission and respiration were measured simultaneously at a predefined membrane potential in isolated mitochondria from skeletal muscle using two protocols: pyruvate + malate (PM) and succinate + rotenone (SR). This allowed measurement of leak and ATP generating respiration from which the coupling efficiency can be calculated. The protein content of the anti‐oxidants manganese superoxide dismuthase (MnSOD), CuZn superoxide dismuthase, catalase and gluthathione peroxidase 1 was measured by western blotting. Immobilization decreased ATP generating respiration using PM and increased H2O2 emission using both PM and SR similarly in young and older men. Both were restored to baseline after the training period. Furthermore, MnSOD and catalase content increased with endurance training. The young men had a higher leak respiration at inclusion using PM and a higher membrane potential in State 3 using both substrate combinations. Collectively, the findings of the present study support the notion that increased mitochondrial reactive oxygen species mediates the detrimental effects seen after physical inactivity. Age, on the other hand, was not associated with impairments in anti‐oxidant protein levels, mitochondrial respiration or H2O2 emission using either protocol.
ClC‐1 mutations in myotonia congenita patients: insights into molecular gating mechanisms and genotype–phenotype correlation
Authors: Imbrici P. , Maggi L. , Mangiatordi G. F. , Dinardo M. M. , Altamura C. , Brugnoni R. , Alberga D. , Pinter G. Lauria , Ricci G. , Siciliano G. , Micheli R. , Annicchiarico G. , Lattanzi G. , Nicolotti O. , Morandi L. , Bernasconi P. , Desaphy J.‐F. , Mantegazza R. , Camerino D. Conte 
Published: June 2015

Key points
Loss‐of‐function mutations of the skeletal muscle ClC‐1 channel cause myotonia congenita with variable phenotypes.
Using patch clamp we show that F484L, located in the conducting pore, probably induces mild dominant myotonia by right‐shifting the slow gating of ClC‐1 channel, without exerting a dominant‐negative effect on the wild‐type (WT) subunit.
Molecular dynamics simulations suggest that F484L affects the slow gate by increasing the frequency and the stability of H‐bond formation between E232 in helix F and Y578 in helix R.
Three other myotonic ClC‐1 mutations are shown to produce distinct effects on channel function: L198P shifts the slow gate to positive potentials, V640G reduces channel activity, while L628P displays a WT‐like behaviour (electrophysiology data only).
Our results provide novel insight into the molecular mechanisms underlying normal and altered ClC‐1 function.
AbstractMyotonia congenita is an inherited disease caused by loss‐of‐function mutations of the skeletal muscle ClC‐1 chloride channel, characterized by impaired muscle relaxation after contraction and stiffness. In the present study, we provided an in‐depth characterization of F484L, a mutation previously identified in dominant myotonia, in order to define the genotype–phenotype correlation, and to elucidate the contribution of this pore residue to the mechanisms of ClC‐1 gating. Patch‐clamp recordings showed that F484L reduced chloride currents at every tested potential and dramatically right‐shifted the voltage dependence of slow gating, thus contributing to the mild clinical phenotype of affected heterozygote carriers. Unlike dominant mutations located at the dimer interface, no dominant‐negative effect was observed when F484L mutant subunits were co‐expressed with wild type. Molecular dynamics simulations further revealed that F484L affected the slow gate by increasing the frequency and stability of the H‐bond formation between the pore residue E232 and the R helix residue Y578. In addition, using patch‐clamp electrophysiology, we characterized three other myotonic ClC‐1 mutations. We proved that the dominant L198P mutation in the channel pore also right‐shifted the voltage dependence of slow gating, recapitulating mild myotonia. The recessive V640G mutant drastically reduced channel function, which probably accounts for myotonia. In contrast, the recessive L628P mutant produced currents very similar to wild type, suggesting that the occurrence of the compound truncating mutation (Q812X) or other muscle‐specific mechanisms accounted for the severe symptoms observed in this family. Our results provide novel insight into the molecular mechanisms underlying normal and altered ClC‐1 function.
Neuroendocrine factors regulate retinoic acid receptors in normal and hypoplastic lung development
Authors: Pereira‐Terra Patrícia , Moura Rute S. , Nogueira‐Silva Cristina , Correia‐Pinto Jorge 
Published: June 2015

Key points
Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associated with the RA signalling pathway in this animal model.
In this study, the interaction between neuroendocrine factors and RA was explored in the CDH rat model.
The authors found that normal fetal lung explants treated with RA, bombesin and ghrelin showed an increase in lung growth. Hypoplastic lungs presented higher expression levels of the RA receptors α and γ. Moreover bombesin and ghrelin supplementation, in vitro, to normal lungs increased RA receptor α/γ expression whereas administration of bombesin and ghrelin antagonists to normal and hypoplastic lungs decreased it.
These data reveal for the first time that there is a link between neuroendocrine factors and RA, and that neuroendocrine factors sensitise the lung to the RA action through RA receptor modulation.
AbstractCongenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague–Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) α, β and γ expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post‐conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RARα/γ expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RARα/γ expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RARα/γ expression levels, whereas the bombesin and ghrelin antagonists decreased RARα/γ expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up‐regulation of RARα and RARγ.
Cortical actin regulation modulates vascular contractility and compliance in veins
Authors: Saphirstein Robert J. , Gao Yuan Z. , Lin Qian Qian , Morgan Kathleen G. 
Published: June 2015

Key points
Most cardiovascular research focuses on arterial mechanisms of disease, largely ignoring venous mechanisms.
Here we examine ex vivo venous stiffness, spanning tissue to molecular levels, using biomechanics and magnetic microneedle technology, and show for the first time that venous stiffness is regulated by a molecular actin switch within the vascular smooth muscle cell in the wall of the vein.
This switch connects the contractile apparatus within the cell to adhesion structures and facilitates stiffening of the vessel wall, regulating blood flow return to the heart.
These studies also demonstrate that passive stiffness, the component of total stiffness not attributable to vascular smooth muscle activation, is severalfold lower in venous tissue than in arterial tissue.
We show here that the activity of the smooth muscle cells plays a dominant role in determining total venous stiffness and regulating venous return.
AbstractThe literature on arterial mechanics is extensive, but far less is known about mechanisms controlling mechanical properties of veins. We use here a multi‐scale approach to identify subcellular sources of venous stiffness. Portal vein tissue displays a severalfold decrease in passive stiffness compared to aortic tissues. The α‐adrenergic agonist phenylephrine (PE) increased tissue stress and stiffness, both attenuated by cytochalasin D (CytoD) and PP2, inhibitors of actin polymerization and Src activity, respectively. We quantify, for the first time, cortical cellular stiffness in freshly isolated contractile vascular smooth muscle cells using magnetic microneedle technology. Cortical stiffness is significantly increased by PE and CytoD inhibits this increase but, surprisingly, PP2 does not. No detectable change in focal adhesion size, measured by immunofluorescence of FAK and zyxin, accompanies the PE‐induced changes in cortical stiffness. Probing with phospho‐specific antibodies confirmed activation of FAK/Src and ERK pathways and caldesmon phosphorylation. Thus, venous tissue stiffness is regulated both at the level of the smooth muscle cell cortex, via cortical actin polymerization, and by downstream smooth muscle effectors of Src/ERK signalling pathways. These findings identify novel potential molecular targets for the modulation of venous capacitance and venous return in health and disease.
Complete Genome Sequence of Escherichia coli O145:NM Bacteriophage vB_EcoM_AYO145A, a New Member of O1-Like Phages
Authors: Wang Jiaying , Niu Yan D. , Chen Jinding , McAllister Tim A. , Stanford Kim 
Published: June 2015

ABSTRACT

Previously, bacteriophage vB_EcoM_AYO145A, which lyses Shiga toxin-producing
Escherichia coli
O145:NM, was classified as an O1-like virus of the
Myoviridae
family. Here, we report the complete genome sequence of this phage and a comparative genomic analysis with other known O1-like phages.
Genome Sequence of Mycobacteriophage Phayonce
Authors: Pope Welkin H. , Jacobetz Emily , Johnson Courtney A. , Kihle Brooke L. , Sobeski Margaret A. , Werner Madison B. , Adkins Nancy L. , Kramer Zachary J. , Montgomery Matthew T. , Grubb Sarah R. , Warner Marcie H. , Bowman Charles A. , Russell Daniel A. , Hatfull Graham F. 
Published: June 2015

ABSTRACT

Mycobacteriophage Phayonce is a newly isolated phage recovered from a soil sample in Pittsburgh, PA, using
Mycobacterium smegmatis
mc
2
155 as a host. Phayonce's genome is 49,203 bp long and contains 77 protein-coding genes, 23 of them having predicted functions. Phayonce shares a strong similarity in nucleotide sequence with phages of cluster P.
Draft Genome Sequence of
Comamonas
sp. Strain E6 (NBRC 107749), a Degrader of Phthalate Isomers through the Protocatechuate 4,5-Cleavage Pathway
Authors: Shimodaira Jun , Kamimura Naofumi , Hosoyama Akira , Yamazoe Atsushi , Fujita Nobuyuki , Masai Eiji 
Published: June 2015

ABSTRACT

Comamonas
sp. strain E6 can degrade
o
-phthalate, terephthalate, and isophthalate via the protocatechuate 4,5-cleavage pathway. Here, we report the draft genome sequence of E6 in order to provide insights into its mechanisms in
o
-phthalate catabolism and its potential use for biotechnological applications.
Draft Genome Sequences of Marine RNA Viruses SF-1, SF-2, and SF-3 Recovered from San Francisco Wastewater
Authors: Greninger Alexander L. , DeRisi Joseph L. 
Published: June 2015

ABSTRACT
We report the draft genome sequences of marine RNA viruses SF-1, SF-2, and SF-3, which were assembled from metagenomic sequencing of organisms in San Francisco wastewater. These viruses were most closely related to marine RNA virus JP-B and algae viruses.
Draft Genome Sequence of the Putrescine-Producing Strain Lactococcus lactis subsp.
lactis
1AA59
Authors: Ladero Victor , del Rio Beatriz , Linares Daniel M. , Fernandez María , Mayo Baltasar , Martín M. Cruz , Alvarez Miguel A. 
Published: June 2015

ABSTRACT

We report here the 2,576,542-bp genome annotated draft assembly sequence of
Lactococcus lactis
subsp.
lactis
1AA59. This strain—isolated from a traditional cheese—produces putrescine, one of the most frequently biogenic amines found in dairy products.