bluuebunny/crossref_metadata_2025_split huggingface dataset:
Draft Genome Sequence of Pannonibacter indicus Strain HT23
T
(DSM 23407
T
), a Highly Arsenate-Tolerant Bacterium Isolated from a Hot Spring in India
Authors: Bandyopadhyay Saumya , Whitman William B. , Das Subrata K. 
Published: May 2017

ABSTRACT

Pannonibacter indicus
strain HT23
T
, a highly arsenate-tolerant bacterium, was isolated from a tropical hot spring. The estimated genome is 4.2 Mb with 3,818 protein-coding sequences containing putative genes, some of which are involved in arsenate resistance.
Draft Whole-Genome Sequences of Multidrug-Resistant Escherichia coli O157:H7 Strains Isolated from Feedlot Cattle Treated with Growth-Promoting Agents
Authors: Rehman Muhammad A. , Carrillo Catherine , Malouin François , Diarra Moussa S. 
Published: May 2017

ABSTRACT

Enterohemorrhagic
Escherichia coli
serotype O157:H7 is a major cause of foodborne outbreaks and hemolytic-uremic syndrome. Here, we report the draft genome sequences of three antibiotic-resistant
E. coli
O157:H7 strains isolated from feedlot cattle. These draft genome sequences will aid in the development of sequence-based tools for the detection of virulence and antimicrobial resistance genotypes.
Draft Genome Sequence of Gardnerella vaginalis Strain ATCC 49145 Associated with Bacterial Vaginosis
Authors: Kidane Destaalem T. , Arivett Brock A. , Crigler Jacob , Vick Eric J. , Farone Anthony L. , Farone Mary B. 
Published: May 2017

ABSTRACT

Gardnerella vaginalis
is a Gram-variable bacterium associated with bacterial vaginosis, a common vaginal inflammation in women of reproductive age. This study reports the whole-genome sequencing for the clinical isolate strain ATCC 49145. The draft genome is composed of 21 contigs containing 1,325 protein-coding sequences, 45 tRNAs and a single tmRNA (SsrA).
Randomised controlled trial evaluating the short-term analgesic effect of topical diclofenac on chronic Achilles tendon pain: a pilot study
Authors: Bussin Erin Rebecca , Cairns Brian , Bovard Jim , Scott Alexander 
Published: May 2017

ObjectivesTo determine if a topically applied non-steroidal anti-inflammatory drug (diclofenac) can provide short-term pain relief for chronic Achilles tendinopathy (CAT), in order to inform the development of a new rehabilitation protocol.Design and settingPilot double-blind, cross-over randomised controlled trial providing participants with tertiary care. The study was conducted at a single research centre in Vancouver, BC.ParticipantsSixteen adults with unilateral CAT and three adults with bilateral CAT participated.InterventionsParticipants received two successive treatments (10% diclofenac gel or placebo gel) in random order over a 3-day period. There was a 1-week washout period between the treatments. Allocation was by simple randomisation, and the participants as well as the assessing/treating researcher were blinded to treatment allocation.Outcome measuresThe primary outcome measure was pain level (0–10) during tendon loading (hopping). Secondary outcome measures included pain at rest, pressure pain threshold of the Achilles tendon and symptom improvement.ResultsNineteen adults participated in the study, and all were included in the analysis. Diclofenac gel significantly reduced the average pain during tendon loading (p<0.001) and at rest (p=0.031). The average baseline hopping pain was 4.8/10 (95% CI 3.92 to 5.68) and was reduced to 3.1/10 (2.35–3.85) by diclofenac. Pain at rest was decreased and pressure pain threshold increased with diclofenac treatment, but not with placebo gel. There were no observed or reported side effects of either treatment.ConclusionsIn this small, short-term study, diclofenac was able to improve symptoms and reduce pain during tendon loading in participants with CAT, whereas placebo gel was not. A future study of diclofenac as a supplement to rehabilitation, with longer follow-up and powered to detect a difference between diclofenac and placebo, is indicated.Trial registrationISRCTN60151284,http://www.isrctn.com/ISRCTN60151284EthicsUBC Clinical Research Ethics Board approval was obtained for this research. The certificate number of the ethics certificate of approval to conduct research is H15-00999.
V̇o2 kinetics associated with moderate-intensity exercise in heart failure: impact of intrathecal fentanyl inhibition of group III/IV locomotor muscle afferents
Authors: Van Iterson Erik H. , Johnson Bruce D. , Joyner Michael J. , Curry Timothy B. , Olson Thomas P. 
Published: May 2017

Heart failure (HF) patients demonstrate impaired pulmonary, circulatory, and nervous system responses to exercise. While HF demonstrates prolonged [time constant (τ)] pulmonary O2 uptake (V̇o2) on-kinetics, contributing to exercise intolerance, it is unknown whether abnormal V̇o2 kinetics couple with ventilatory and circulatory dysfunction secondary to impaired group III/IV afferents in HF. Because lower lumbar intrathecal fentanyl inhibits locomotor muscle afferents, resulting in improved exercise ventilation and hemodynamics, we tested these hypotheses: HF will demonstrate 1) rapid V̇o2 on-kinetics and 2) attenuated steady-state V̇o2 amplitude and O2 deficit (O2def) during exercise with fentanyl versus placebo. On separate visits (randomized), breath-by-breath V̇o2 was measured in HF (ejection fraction: 27 ± 6%, New York Heart Association class I–III) and age- and sex-matched controls (both n = 9, ages: 60 ± 6 vs. 63 ± 8 yr, P = 0.37) during cycling transitions at 65% peak workload (78 ± 24 vs. 115 ± 39 W, P < 0.01) with intrathecal fentanyl or placebo. Regardless of group or condition, optimal phase II (primary component) curve fits reflected a phase I period equal to 35 s (limb-to-lung timing) via single-exponential functions. Condition did not affect steady-state V̇o2, the phase II τ of V̇o2, or O2def within controls ( P > 0.05). Without differences in steady-state V̇o2, reduced O2def in fentanyl versus placebo within HF (13 ± 4 vs. 22 ± 15 ml/W, P = 0.04) was accounted for by a rapid phase II τ of V̇o2 in fentanyl versus placebo within HF (45 ± 11 vs. 57 ± 14 s, P = 0.04), respectively. In an integrative manner, these data demonstrate important effects of abnormal locomotor muscle afferents coupled to pulmonary and circulatory dysfunction in determining impaired exercise V̇o2 in HF. Effects of abnormal muscle afferents on impaired exercise V̇o2 and hence exercise intolerance may not be discernable by independently assessing steady-state V̇o2 in HF. NEW & NOTEWORTHY Inhibition of locomotor muscle afferents results in rapid primary-component O2 uptake (V̇o2) on-kinetics accounting for the decreased O2 deficit in heart failure (HF). This study revealed that abnormal musculoskeletal–neural afferents couple with pulmonary and circulatory dysfunction to provoke impaired exercise V̇o2 in HF. Steady-state V̇o2 cannot properly phenotype abnormal muscle afferent contributions to impaired exercise V̇o2 in HF.
Ten days of repeated local forearm heating does not affect cutaneous vascular function
Authors: Francisco Michael A. , Brunt Vienna E. , Jensen Krista Nicole , Lorenzo Santiago , Minson Christopher T. 
Published: May 2017

The aim of the present study was to determine whether 10 days of repeated local heating could induce peripheral adaptations in the cutaneous vasculature and to investigate potential mechanisms of adaptation. We also assessed maximal forearm blood flow to determine whether repeated local heating affects maximal dilator capacity. Before and after 10 days of heat training consisting of 1-h exposures of the forearm to 42°C water or 32°C water (control) in the contralateral arm (randomized and counterbalanced), we assessed hyperemia to rapid local heating of the skin ( n = 14 recreationally active young subjects). In addition, sequential doses of acetylcholine (ACh, 1 and 10 mM) were infused in a subset of subjects ( n = 7) via microdialysis to study potential nonthermal microvascular adaptations following 10 days of repeated forearm heat training. Skin blood flow was assessed using laser-Doppler flowmetry, and cutaneous vascular conductance (CVC) was calculated as laser-Doppler red blood cell flux divided by mean arterial pressure. Maximal cutaneous vasodilation was achieved by heating the arm in a water-spray device for 45 min and assessed using venous occlusion plethysmography. Forearm vascular conductance (FVC) was calculated as forearm blood flow divided by mean arterial pressure. Repeated forearm heating did not increase plateau percent maximal CVC (CVCmax) responses to local heating (89 ± 3 vs. 89 ± 2% CVCmax, P = 0.19), 1 mM ACh (43 ± 9 vs. 53 ± 7% CVCmax, P = 0.76), or 10 mM ACh (61 ± 9 vs. 85 ± 7% CVCmax, P = 0.37, by 2-way repeated-measures ANOVA). There was a main effect of time at 10 mM ACh ( P = 0.03). Maximal FVC remained unchanged (0.12 ± 0.02 vs. 0.14 ± 0.02 FVC, P = 0.30). No differences were observed in the control arm. Ten days of repeated forearm heating in recreationally active young adults did not improve the microvascular responsiveness to ACh or local heating. NEW & NOTEWORTHY We show for the first time that 10 days of repeated forearm heating is not sufficient to improve cutaneous vascular responsiveness in recreationally active young adults. In addition, this is the first study to investigate cutaneous cholinergic sensitivity and forearm blood flow following repeated local heat exposure. Our data add to the limited studies regarding repeated local heating of the cutaneous vasculature.
4-1BB–Enhanced Expansion of CD8+ TIL from Triple-Negative Breast Cancer Unveils Mutation-Specific CD8+ T Cells
Authors: Harao Michiko , Forget Marie-Andrée , Roszik Jason , Gao Hui , Babiera Gildy V. , Krishnamurthy Savitri , Chacon Jessica A. , Li Shumin , Mittendorf Elizabeth A. , DeSnyder Sarah M. , Rockwood Korrene F. , Bernatchez Chantale , Ueno Naoto T. , Radvanyi Laszlo G. , Vence Luis , Haymaker Cara , Reuben James M. 
Published: May 2017

Abstract
Triple-negative breast cancer (TNBC) highly infiltrated with CD8+ tumor-infiltrating lymphocytes (TIL) has been associated with improved prognosis. This observation led us to hypothesize that CD8+ TIL could be utilized in autologous adoptive cell therapy for TNBC, although this concept has proven to be challenging, given the difficulty in expanding CD8+ TILs in solid cancers other than in melanoma. To overcome this obstacle, we used an agonistic antibody (urelumab) to a TNFR family member, 4-1BB/CD137, which is expressed by recently activated CD8+ T cells. This approach was first utilized in melanoma and, in this study, led to advantageous growth of TILs for the majority of TNBC tumors tested. The agonistic antibody was only added in the initial setting of the culture and yet favored the propagation of CD8+ TILs from TNBC tumors. These expanded CD8+ TILs were capable of cytotoxic functions and were successfully utilized to demonstrate the presence of immunogenic mutations in autologous TNBC tumor tissue without recognition of the wild-type counterpart. Our findings open the way for a successful adoptive immunotherapy for TNBC. Cancer Immunol Res; 5(6); 439–45. ©2017 AACR.
Janus Kinase 3, a Novel Regulator for Smooth Muscle Proliferation and Vascular Remodeling
Authors: Wang Yung-Chun , Cui Xiao-Bing , Chuang Ya-Hui , Chen Shi-You 
Published: May 2017

Objective—
Vascular remodeling because of smooth muscle cell (SMC) proliferation is a common process occurring in several vascular diseases, such as atherosclerosis, aortic aneurysm, post-transplant vasculopathy, restenosis after angioplasty, etc. The molecular mechanism underlying SMC proliferation, however, is not completely understood. The objective of this study is to determine the role and mechanism of Janus kinase 3 (JAK3) in vascular remodeling and SMC proliferation.

Approach and Results—
Platelet-derived growth factor-BB, an SMC mitogen, induces JAK3 expression and phosphorylation while stimulating SMC proliferation. Janex-1, a specific inhibitor of JAK3, or knockdown of JAK3 by short hairpin RNA, inhibits the SMC proliferation. Conversely, ectopic expression of JAK3 promotes SMC proliferation. Mechanistically, JAK3 promotes the phosphorylation of signal transducer and activator of transcription 3 and c-Jun N-terminal kinase in SMC, 2 signaling pathways known to be critical for SMC proliferation and vascular remodeling. Blockade of these 2 signaling pathways by their inhibitors impeded the JAK3-mediated SMC proliferation. In vivo, knockdown of JAK3 attenuates injury-induced neointima formation with attenuated neointimal SMC proliferation. Knockdown of JAK3 also induces neointimal SMC apoptosis in rat carotid artery balloon injury model.

Conclusions—
Our results demonstrate that JAK3 mediates SMC proliferation and survival during injury-induced vascular remodeling, which provides a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases.
Serotonin Signaling Through the 5-HT
1B
Receptor and NADPH Oxidase 1 in Pulmonary Arterial Hypertension
Authors: Hood Katie Y. , Mair Kirsty M. , Harvey Adam P. , Montezano Augusto C. , Touyz Rhian M. , MacLean Margaret R. 
Published: May 2017

Objective—
Serotonin can induce human pulmonary artery smooth muscle cell (hPASMC) proliferation through reactive oxygen species (ROS), influencing the development of pulmonary arterial hypertension (PAH). We hypothesize that in PASMCs, serotonin induces oxidative stress through NADPH-oxidase–derived ROS generation and reduced Nrf-2 (nuclear factor [erythroid-derived 2]-like 2) antioxidant systems, promoting vascular injury.

Approach and Results—

HPASMCs from controls and PAH patients, and PASMCs from Nox1
−/−
mice, were stimulated with serotonin in the absence/presence of inhibitors of Src kinase, the 5-HT
1B
receptor, and NADPH oxidase 1 (Nox1). Markers of fibrosis were also determined. The pathophysiological significance of our findings was examined in vivo in serotonin transporter overexpressing female mice, a model of pulmonary hypertension. We confirmed thatserotonin increased superoxide and hydrogen peroxide production in these cells. For the first time, we show that serotonin increased oxidized protein tyrosine phosphatases and hyperoxidized peroxiredoxin and decreased Nrf-2 and catalase activity in hPASMCs. ROS generation was exaggerated and dependent on cellular Src-related kinase, 5-HT
1B
receptor, and the serotonin transporter in human pulmonary artery smooth muscle cells from PAH subjects. Proliferation and extracellular matrix remodeling were exaggerated in human pulmonary artery smooth muscle cells from PAH subjects and dependent on 5-HT
1B
receptor signaling and Nox1, confirmed in PASMCs from Nox1
−/−
mice. In serotonin transporter overexpressing mice, SB216641, a 5-HT
1B
receptor antagonist, prevented development of pulmonary hypertension in a ROS-dependent manner.

Conclusions—

Serotonin can induce cellular Src-related kinase–regulated Nox1-induced ROS and Nrf-2 dysregulation, contributing to increased post-translational oxidative modification of proteins and activation of redox-sensitive signaling pathways in hPASMCs, associated with mitogenic responses. 5-HT
1B
receptors contribute to experimental pulmonary hypertension by inducing lung ROS production. Our results suggest that 5-HT
1B
receptor–dependent cellular Src-related kinase-Nox1-pathways contribute to vascular remodeling in PAH.
Relationship of Autoantibodies to MDA-LDL and ApoB-Immune Complexes to Sex, Ethnicity, Subclinical Atherosclerosis, and Cardiovascular Events
Authors: Prasad Anand , Clopton Paul , Ayers Colby , Khera Amit , de Lemos James A. , Witztum Joseph L. , Tsimikas Sotirios 
Published: May 2017

Objective—
Modifications of lipid constituents within atherosclerotic lesions generate neoepitopes that activate innate and adaptive immune responses. We aimed to define the prevalence, distribution, and relationship of autoantibody titers of oxidized lipoproteins to subclinical atherosclerosis and major adverse cardiovascular events (MACE) in different ethnic groups.

Approach and Results—

IgG and IgM autoantibodies to malondialdehyde-modified low-density lipoprotein (MDA-LDL) and apolipoprotein B-100-immune complexes were measured in 3509 individuals (1814 blacks, 1031 whites, 589 Hispanics, and 85 no race identifier) from the Dallas Heart Study with median 10.5-year follow-up. Coronary artery calcium score, abdominal aortic plaque by magnetic resonance imaging, and MACE were quantified. IgG MDA-LDL and IgG and IgM apolipoprotein B-100-immune complexes were significantly different between groups, with blacks having the highest levels of IgG MDA-LDL and IgG apolipoprotein B-100-immune complexes and Hispanics having the highest levels of IgM apolipoprotein B-100-immune complexes (
P
<0.001 for all). IgGs tended to be higher and IgMs lower with age for all markers. In multivariable-adjusted binary logistic regression analysis, a doubling of IgG MDA-LDL levels was associated with prevalent coronary artery calcium score >10 Agatston units (odds ratio [95% confidence interval], 1.21 [1.07–1.36];
P
=0.002). Multivariable-adjusted Cox regression analysis revealed that IgG MDA-LDL was independently associated with time to incident MACE in the entire group (hazard ratio [95% confidence interval], 1.76 [1.16–2.72];
P
=0.009 for fourth versus first quartile). This effect was particularly prominent in black subjects (hazard ratio [95% confidence interval], 2.52 [1.39–4.57];
P
=0.002).

Conclusions—
Autoantibodies to oxidized lipoproteins and immune complexes with apoB-100 lipoproteins vary significantly by sex, age, and ethnicity. Higher baseline IgG MDA-LDL titers independently associate with new MACE. These findings may contribute to the understanding of differences in ethnic-specific MACE events.
Festuca galiciensis, a new species of the F. valesiaca group (Poaceae) from Ukraine
Authors: BEDNARSKA IRYNA , BRAZAUSKAS GINTARAS 
Published: May 2017

Festuca galiciensis, a new endemic species from Western Ukraine is described. Its ecology, distribution, morphology and leaf anatomy are discussed. The taxonomic relationship of the new species with F. rupicola, with which it grows in mixed populations, and its delimitation with respect to other species of the F. valesiaca group, are also discussed.
HLA-DRB1*04:05 allele is associated with intracortical lesions on three-dimensional double inversion recovery images in Japanese patients with multiple sclerosis
Authors: Shinoda Koji , Matsushita Takuya , Nakamura Yuri , Masaki Katsuhisa , Yamasaki Ryo , Yamaguchi Hiroo , Togao Osamu , Hiwatashi Akio , Kira Jun-ichi 
Published: May 2017

Background: Cortical lesions (CLs) frequently observed in Caucasian patients with multiple sclerosis (MS) contribute to disability. However, it remains unclear whether CLs are associated with clinical features and genetic risk factors, such as HLA-DRB1*15:01 and -DRB1*04:05 in Asian MS patients. Objective: To elucidate the frequency of CLs and their association with HLA-DRB1 and DPB1 alleles in Japanese MS patients. Methods: Three-dimensional double inversion recovery imaging and clinical information were retrospectively obtained from 92 Japanese MS patients. Results: CLs of any type, intracortical lesions (ICLs), and leukocortical lesions (LCLs) were detected in 39.1%, 26.1%, and 28.3% of patients, respectively. MS patients with ICLs had a significantly higher frequency of secondary progression and greater Expanded Disability Status Scale (EDSS) scores than those without ICLs. Similar trends were observed with CLs and LCLs. The number of all three lesion types positively correlated with EDSS scores. The frequency and number of ICLs were significantly higher in HLA-DRB1*15:01 carriers than in HLA-DRB1*15:01 non-carriers, but significantly lower in HLA-DRB1*04:05 carriers than in HLA-DRB1*04:05 non-carriers. Multivariate logistic regression analysis revealed a negative association of HLA-DRB1*04:05 with ICLs. Conclusion: ICLs are associated with greater disease severity in Japanese MS patients and are partly suppressed by the HLA-DRB1*04:05 allele.
A study to evaluate the prevalence of impaired awareness of hypoglycaemia in adults with type 2 diabetes in outpatient clinic in a tertiary care centre in Singapore
Authors: Zhu Ling , Ang Li Chang , Tan Wee Boon , Xin Xiaohui , Bee Yong Mong , Goh Su-Yen , Teh Ming Ming 
Published: May 2017

Background: Impaired awareness of hypoglycaemia (IAH) predisposes affected patients to severe hypoglycaemia. There are few data on prevalence of IAH in adults with insulin-treated type 2 diabetes in Asia. We aim to ascertain the prevalence of IAH among insulin-treated patients with type 2 diabetes in an outpatient clinic in a tertiary care centre in Singapore. Methods: A total of 374 patients with insulin-treated type 2 diabetes attending the outpatient diabetes clinic in a tertiary referral centre in Singapore were recruited over a 4-month period. Participants completed a questionnaire to document baseline characteristics and assess their hypoglycaemia awareness status, using a combination of the Clarke, Gold and Pedersen-Bjergaard methods. Results: Using the Clarke, Gold and Pedersen-Bjergaard methods, prevalence of IAH in our cohort was 9.6%, 13.4% and 33.2% respectively. Overall, 7.2% of participants suffered from severe hypoglycaemia in the preceding year. The IAH group had more episodes of severe hypoglycaemia across all three methods, compared with the normal awareness group ( p < 0.01). There were no significant differences in mean HbA1c, duration of diabetes and insulin treatment between the IAH and normal awareness groups. Conclusions: IAH is prevalent in adults with insulin-treated type 2 diabetes in Asia, and is associated with significantly increased risk of severe hypoglycaemia.
Ethnicity of Patients With Germline GCM2-Activating Variants and Primary Hyperparathyroidism
Authors: Guan Bin , Welch James M. , Vemulapalli Meghana , Li Yulong , Ling Hua , Kebebew Electron , Simonds William F. , Marx Stephen J. , Agarwal Sunita K. 
Published: May 2017

Abstract

Context:
Germline gain-of-function variants in the transcription factor GCM2 were found in 18% of kindreds with familial isolated hyperparathyroidism (FIHP). These variants [c.1136T&gt;A (p.Leu379Gln) and c.1181A&gt;C (p.Tyr394Ser)] were located in a 17-amino acid transcriptional inhibitory domain named C-terminal conserved inhibitory domain (CCID).

Objective:
We investigated the ethnicity of individuals with germline variants in the GCM2 CCID in our primary hyperparathyroidism (PHPT) patient samples and in the Genome Aggregation Database.

Design:
Ethnicity information was obtained from an in-house clinical database and genetic counseling. Sanger sequencing of blood DNA was used to determine the genotype of the GCM2 CCID region. Luciferase reporter assays were performed to determine the functional impact of GCM2 variants.

Setting and Patients:
National Institute of Diabetes and Digestive and Kidney Diseases endocrine clinic is a service that accepts PHPT referral patients.

Results:
The GCM2 p.Tyr394Ser variant was found in 41% [95% confidence interval (CI), 22% to 64%] of Ashkenazi Jewish (AJ) kindreds with FIHP and in 27% (95% CI, 17% to 40%) of AJ patients with sporadic PHPT. The p.Tyr394Ser variant was also found in sporadic PHPT patients of European ancestry, but at a lower prevalence. The p.Leu379Gln variant was found in 8% (95% CI, 1% to 26%) of European kindreds with FIHP and 0.5% (95% CI, 0% to 3.0%) of sporadic PHPT cases of European ancestry. The sporadic PHPT patients with GCM2-activating variants often had multigland involvement or postoperative recurrent or persistent disease.

Conclusions:
Specific GCM2-activating variants enriched among various ethnic backgrounds could contribute to a large number of cases with FIHP or sporadic PHPT.