bluuebunny/crossref_metadata_2025_split huggingface dataset:
Peri-procedural stroke or death in stenting of symptomatic severe intracranial stenosis
Authors: Yaghi Shadi , Khatri Pooja , de Havenon Adam , Yeatts Sharon , Chang Andrew D , Cutting Shawna , Mac Grory Brian , Burton Tina , Jayaraman Mahesh V , McTaggart Ryan A , Fiorella David , Derdeyn Colin , Zaidat Osama O , Dehkharghani Seena , Amin-Hanjani Sepideh , Furie Karen , Prahbakaran Shyam , Liebeskind David 
Published: September 2019

Background and purposeThere are limited data on predictors of 30-day stroke or death in patients with symptomatic intracranial atherosclerosis (sICAS) undergoing stenting. We aim to determine the factors associated with stroke or death at 30 days in the stenting arm of the SAMMPRIS trial.MethodsThis is a post-hoc analysis of the SAMMPRIS trial including patients who underwent angioplasty/stenting. We compared patient-specific variables, lesion-specific variables, procedure-specific variables, and FDA-approved indications between patients with and without the primary outcome (stroke or death at 30 days). Logistic regression analyses were performed to evaluate associations with the primary outcome.ResultsWe identified 213 patients, 30 of whom (14.1%) met the primary outcome. Smoking status and lesion length were associated with the primary outcome: the odds of stroke or death for non-smokers versus smokers (adjusted OR 4.46, 95% CI 1.79 to 11.1, p=0.001) and for increasing lesion length in millimeters (adjusted OR 1.20, 95% CI 1.02 to 1.39, p=0.029). These had a modest predictive value: absence of smoking history (sensitivity 66.7%, specificity 65.4%) and lesion length (area under curve 0.606). Furthermore, event rates were not significantly different between patients with and without the FDA-approved indication for stenting (15.9% vs 12%, p=0.437).ConclusionIn SAMMPRIS patients who underwent angioplasty/stenting, neither clinical and neuroimaging variables nor the FDA indication for stenting reliably predicted the primary outcome. Further work in identifying reliable biomarkers of stroke/death in patients with sICAS is needed before considering new clinical trials of stenting.Trial registration numberSAMMPRISNCT00576693; Results.
Secukinumab does not impair the immunogenic response to the influenza vaccine in patients
Authors: Richi Patricia , Martín María Dolores , de Ory Fernando , Gutiérrez-Larraya Rosa , Casas Inmaculada , Jiménez-Díaz Ana María , Cava Fernando , Muñoz-Fernandez Santiago 
Published: September 2019

ObjectiveTo evaluate whether immunological response to influenza vaccination is impaired in patients who are receiving secukinumab.Patients and methodsSubjects suffering from psoriatic arthritis or ankylosing spondylitis who were receiving treatment with secukinumab and healthy volunteers were included.All participants received seasonal inactivated trivalent influenza vaccine recommended by the WHO in the 2017–2018 northern hemisphere influenza season, which contained an A/Michigan/45/2015 (H1N1)pdm09-like virus, an A/Hong Kong/4801/2014 (H3N2)-like virus and a B/Brisbane/60/2008-like virus.Haemagglutination inhibition was used to evaluate basal antibody (Ab) titres against the three inﬂuenza vaccine virus strains just before vaccination and at least 4 weeks after the vaccine administration. Response to vaccine was considered as >4-fold increases in Ab titre.ResultsThirty subjects, 17 patients and 13 healthy controls, with a follow-up duration of 33±8 days, were analysed. There were no demographic differences between groups. Patients and controls achieved a median of 4.6-fold and 4.0-fold increases, respectively, for anti H1N1 and almost 4.0 (3.7) for patients and 5.3 for controls for anti-B Ab. Both groups presented a poor response against H3N2, with <1.5-fold increase. Seroconversion rates were similar in both groups. Secukinumab did not influence the response to the influenza vaccine (relative risk: 1.09 (95% CI 0.58 to 2.07) for H1N1, RR: 1.53 (95% CI 0.15 to 15.0) for H3N2 and RR: 0.72 (95% CI 0.32 to 1.83) for B strain).ConclusionIn our study, secukinumab has no effect on the immunogenic response to the influenza vaccine.
Clinical spirocercosis in a dog in the UK
Authors: McKenna Myles , Bristow Poppy Charlotte , Suarez‐Bonnet Alejandro , Fox Mark T , Glanemann Barbara 
Published: September 2019

A 2‐year‐old female neutered crossbreed dog was presented for evaluation of a 3‐day history of haematemesis, melaena and hyporexia. The dog had been imported from a rescue centre in Hungary 4 months prior to presentation. Abdominal CT revealed the presence of a 3 cm×3 cm×4 cm diameter heterogenous intraluminal mass lesion in the gastric cardia, surrounding the ostium of the cardia and continuous with the distal oesophagus. The mass lesion was subsequently surgically resected. Histopathology of the gastric mass lesion was consistent with a Spirocerca lupi granuloma. The patient unfortunately developed a pyothorax and suffered cardiopulmonary arrest resulting in death 2 days postoperatively. To the authors’ knowledge, this is the first reported case of clinical spirocercosis reported in a dog in the UK.
LONG-TERM MECHANICAL COMPATIBILITY OF POLYPROPYLENE SURGICAL MESHES
Authors: KIRILOVA-DONEVA MIGLENA , PASHKOULEVA DESSISLAVA 
Published: September 2019

The properties of meshes: Surgimesh®, Technomesh[Formula: see text] and SurgiproTMaged for up to four years were assessed using tensile tests. We discovered that the elasticity of Technomesh[Formula: see text] increased in both directions, Surgimesh[Formula: see text] became more elastic in the longitudinal direction while the elastic properties of SurgiproTMremained unchanged. The mesh samples did not significantly change their strength and deformability with age. Samples from umbilical and inguinal area of the abdominal wall were isolated from 14 donors. The investigation included 90 specimens divided into three age subgroups — A (up to 60 years), B (61–80 years) and C (over 80 years). The long-term mechanical compatibility of human fascia and meshes was compared. The elastic properties of the meshes are closer to the elastic properties of the fascia in the direction parallel to fibers if the donors’ age is up to 60 years.
Dissociating effects of error size, training duration, and amount of adaptation on the ability to retain motor memories
Authors: Alhussein Laith , Hosseini Eghbal A. , Nguyen Katrina P. , Smith Maurice A. , Joiner Wilsaan M. 
Published: September 2019

Extensive computational and neurobiological work has focused on how the training schedule, i.e., the duration and rate at which an environmental disturbance is presented, shapes the formation of motor memories. If long-lasting benefits are to be derived from motor training, however, retention of the performance improvements gained during practice is essential. Thus a better understanding of mechanisms that promote retention could lead to the design of more effective training procedures. The few studies that have investigated how retention depends on the training schedule have suggested that the gradual exposure of a perturbation leads to improved retention of motor memory compared with an abrupt exposure. However, several of these previous studies showed small effects, and although some controlled the training duration and others the level of learning, none have controlled both. In the present study we disambiguated both of these effects from exposure rate by systematically varying the duration of training, type of trained dynamics, and exposure rate for these dynamics in human force-field adaptation. After controlling for both training duration and the amount of learning, we found essentially identical retention when comparing gradual and abrupt training for two different types of force-field dynamics. By contrast, we found that retention was markedly higher for long-duration compared with short-duration training for both types of dynamics. These results demonstrate that the duration of training has a far greater effect on the retention of motor memory than the exposure rate during training. We show that a multirate learning model provides a computational mechanism for these findings. NEW & NOTEWORTHY Previous studies have suggested that a gradual, incremental introduction of a novel environment is helpful for improving retention. However, we used experimental and computational approaches to demonstrate that previously reported improvements in retention associated with gradual introductions fail to persist when other factors, including the duration of training and the degree of initial learning, are accounted for.
Eradication of Hepatocellular Carcinoma by NKG2D-Based CAR-T Cells
Authors: Sun Bin , Yang Dong , Dai Hongjiu , Liu Xiuyun , Jia Ru , Cui Xiaoyue , Li Wenxuan , Cai Changchun , Xu Jianming , Zhao Xudong 
Published: September 2019

Abstract
Despite the great success of chimeric antigen receptor T (CAR-T)–cell therapy in the treatment of hematologic malignancies, CAR-T–cell therapy is limited in solid tumors, including hepatocellular carcinoma (HCC). NK group 2 member D (NKG2D) ligands (NKG2DL) are generally absent on the surface of normal cells but are overexpressed on malignant cells, offering good targets for CAR-T therapy. Indeed, analysis of The Cancer Genome Atlas and HCC tumor samples showed that the expression of most NKG2DLs was elevated in tumors compared with normal tissues. Thus, we designed a novel NKG2D-based CAR comprising the extracellular domain of human NKG2D, 4-1BB, and CD3ζ signaling domains (BBz). NKG2D-BBz CAR-T cells efficiently killed the HCC cell lines SMMC-7721 and MHCC97H in vitro, which express high levels of NKG2DLs, whereas they less efficiently killed NKG2DL-silenced SMMC-7721 cells or NKG2DL-negative Hep3B cells. Overexpression of MICA or ULBP2 in Hep3B improved the killing capacity of NKG2D-BBz CAR-T cells. T cells expressing the NKG2D-BBz CAR effectively eradicated SMMC-7721 HCC xenografts. Collectively, these results suggested that NKG2D-BBz CAR-T cells could potently eliminate NKG2DL-high HCC cells both in vitro and in vivo, thereby providing a promising therapeutic intervention for patients with NKG2DL-positive HCC.
Abstract 119: Ccl18 as a Potential Mediator of the Pro-Fibrotic Actions of M2 Macrophages in the Vessel Wall During Hypertension
Authors: Zhu Mingyu , Lewis Caitlin V , Finemore Meghan J , Lieu Maggie , Widdop Robert E , Samuel Chrishan S , Drummond Grant R , Kemp-Harper Barbara K 
Published: September 2019

M2 macrophages contribute to vascular fibrosis and stiffening in hypertension and may mediate these actions via release of the pro-fibrotic chemokine, CCL18, which they release to a greater extent than TGF-β1. The role of CCL18 and its cognate receptor, CCR8 in hypertension and vascular fibrosis has not been investigated. This study aimed to identify vascular targets of CCL18 and explore its ability to promote fibrosis.

Blood pressure (BP) of saline or angiotensin II (0.7 mg/kg/day, 28 days;
s.c.
)-treated male C57BL/6J mice was measured by tail cuff. Localisation and expression of CCR8 and the murine functional analogue of CCL18, CCL8, were assessed in the thoracic aorta by immunohistochemistry and qRT-PCR, respectively. Human aortic adventitial fibroblasts (AoAFs) and endothelial cells were treated with the pro-fibrotic agent TGF-β1 (10 ng/ml) or CCL18 (3-300 ng/ml) for 3-72h or 7d, respectively. In human AoAFs, expression of pro-collagen I, mature collagen I and α-SMA and were measured (qRT-PCR, Western blotting). Endothelial-mesenchymal transition was measured via VE-cadherin and α-SMA protein expression.

Angiotensin II infusion significantly elevated systolic BP (151±5 mmHg, p<0.05) as compared to saline treated mice (111±5 mmHg, n=8). In aortas from hypertensive mice, mRNA expression of CCL8 was elevated 3-fold (p<0.05, n=4-8), and CCL8 expression in the aortic wall was co-localised with the M2 macrophage marker CD206. CCR8 expression was evident in the endothelium, adventitia and perivascular fat. In human AoAFs, TGF-β1 caused a 2-fold increase in protein expression of collagen I (24h, p<0.01) and α-SMA (24-72h, p<0.05). CCL18 (300 ng/ml) did not change α-SMA expression, but increased the protein expression of pro-collagen I by 2-fold (24h; p<0.01), and elevated mature collagen I by 3.6-fold (72h; p<0.05). In human aortic endothelial cells, CCL18 (10 ng/ml) induced a trend towards reduced VE-cadherin, while increasing α-SMA expression (1.5-fold, p<0.05).
CCL18 stimulates collagen synthesis from human AoAFs and may promote endothelial-to-mesenchymal cell transition. Expression of its receptor in the vascular wall suggests that the CCL18-CCR8 axis may serve as a potential target for the treatment of vascular fibrosis during hypertension.
Abstract P102: A Vegan Approach for Gestational Hypertension in African Americans
Authors: Moreno Laura 
Published: September 2019

The mortality rates in the African American infant population are higher than average. Non-Hispanic black infants died 11.4 to 1000 live births in 2016. The majority of complications stem from uncontrolled gestational hypertension. The purpose of this paper is to introduce the vegan diet with supplemental prenatal vitamins as a solution to a national crisis of infant mortality in the African American communities that would decrease gestational hypertension and its complications thereby improving maternal and fetal outcomes.The purpose of this paper is to introduce a research review that would strengthen the Vegan concept to prevent gestational hypertension and its complications in African Americans thus improving maternal and fetal outcomes.
Perhaps the ancestors of African Americans, who originally lived in hot, arid climates wherein sodium conservation was important for survival, evolved the physiologic machinery which protected them in their original habitat but makes it difficult for them to handle the excessive sodium they ingest when they migrate. African Americans tend to have higher blood volume, lower plasma renin activity as compared to white population (Langford, 1981). If gestational hypertension is genetic to all Africa, we would expect to see poor outcomes for black women
everywhere, but studies have found that foreign-born black women living in the United States have birth outcomes almost identical to white American women’s. Only descendants of the slave trade carry the hypertension gene and it has been shown to also exist in Western African countries, where Americans collected slaves. In the United States the Western diet consisting of a high content of sugars, fats and oils have pulled many triggers in our body’s responses, one of them being hypertension. Dietary fat reduction is critical in reducing insulin resistance which leads to hypertension. By educating the African American population on how a vegan diet can decrease both the maternal and neonatal mortalities, a significant improvement in mortality can be achieved.
Abstract P2032: Differential Response To Angiotensin II Depends On Microbial Colonization
Authors: Avery Ellen G , Bartolomaeus Hendrik , Kraeker Kristin , Balogh András , Müller Dominik N , Wilck Nicola 
Published: September 2019

The gut microbiome is suspected to play a role in hypertension and target organ damage. In the present study, we used the germ-free mice (GF), which are devoid of bacteria, to investigate if bacterial colonization modulates the response to a hypertensive stimulus.
GF C57BL/6 littermates were separated at 4 weeks and randomized to remain GF or receive bacterial colonization (COL). Angiotensin (Ang) II minipumps were implanted at 12 weeks (+AngII) to induce hypertension, sham-infused mice served as non-hypertensive controls. At 14 weeks, all mice were sacrificed, and inflammation and target organ damage were assessed.
AngII induced a comparable cardiac hypertrophic response in both groups, as measured by left ventricular mass/tibia length. However, accounting for the low basal heart weight in non-hypertensive GF, the hypertrophic response was greater in GF than COL (in mg/cm; GF: 47.2, GF+AngII: 70.17, fold change: 1.5 and COL: 57.9, COL+AngII: 76.09, fold change: 1.3). Similarly, the increase in cardiac perivascular fibrosis in response to AngII was greater in GF than COL (fibrotic/medial area; GF: 3.8, GF+AngII: 5.8 and COL: 3.9, COL+AngII: 5). Inflammation of the cardiac tissue, as evidenced by relative mRNA expression of MCP-1 and TNFa, increased significantly in GF and not in COL. Using flow cytometry, we found that innate anti-inflammatory immune subsets (myeloid derived suppressor cells) are notably missing in GF, and the adaptive immune response to AngII (e.g. Th17 (in % of CD4+: GF: 0.26; GF+AngII: 0.5 and COL: 0.28; COL+AngII: 0.39)) was exacerbated. Kidney damage was also evident in AngII-infused GF and COL. However, genes indicative of tubular damage (KIM-1: GF: 0.3, GF+AngII: 3.3, fold change: 11.0 and COL: 0.2, COL+AngII: 1.5, fold change: 7.5 ), inflammation (TNFa, MCP-1, ICAM), and fibrosis (Col3a1, Col1a2) increased significantly in GF and were only mildly implicated in COL.
Bacterial colonization sizably impacts the response to AngII and hypertensive target organ damage. The magnitude of the pathogenic response to AngII in GF compared to COL mice demonstrates the importance of the gut microbiota in modulating target-organ damage.
Abstract P3026: Impact of Dietary Electrolytes on Post-Nephrectomy Blood Pressure, Proteinuria and Renal Function
Authors: McDonough Alicia A , Lei Hillmin , Priver Taylor S , McFarlin Brandon E , Smith Scotti D , Pastor-Soler Nuria , Ralph Donna L 
Published: September 2019

When chronic kidney disease progresses to end stage renal disease, the optimal treatment is living kidney donation (LKD). A 10 yr prospective study of 1214 donors (PMID 27006347), reported that LKD increased risk of hypertension (HTN), by 3.64-fold, as well as HTN induced albuminuria.
Our objective
was to test whether a DASH-style diet (DD: 0.74% NaCl, 3%K with 1% each: Cl
-
, citrate, HCO
3
-
) would blunt hypertension and albuminuria following UNX vs. a western style diet (WD: 2% NaCl, 1%KCl). Uninephrectomized (UNX) male SD rats (n=5/group) preequilibrated on diets were analyzed 12-14 wks post-UNX.

Systolic BP (SBP, mmHg) was similar pre-UNX in DD (126 ± 8) and WD (132 ± 8); SBP increased post-UNX by 7 ± 2 (DD) and 21 ± 5 (WD) mmHg, p=0.04. Urine injury markers (albumin, angiotensinogen, KIM-1 and plasminogen) increased in both DD and WD (all p<0.01). Kidney weight increased similarly from 1.5 ± 2 (pre-UNX) to 2.3 ± 0.2 g (post-UNX) in pooled DD, WD. By IHC, glomeruli diameters increased 1.6-fold pre-vs. post-UNX.
Transporter profiles were generated from both pre-and post-UNX kidneys. Pre-UNX, DD (vs. WD) exhibited lower abundance of proximal tubule (PT) NHE3, NaPi2 and NHERF1, and higher abundance of NKA α1, NCC, NCCp, claudin 7, SPAK, ENaC subunits and AQP2 (all p < 0.01). Post-UNX (vs. pre-UNX) abundance, normalized to equivalent protein, exhibited lower claudin2, megalin, AQP1 and AQP2 in both DD and WD (all p < 0.01), and, specifically to DD post-UNX: 1.4-fold increases in NCCp, SPAKp and 0.7-fold decreases in cleaved α and γ ENaC (all p<0.05). By IHC, NHE3 localized within the apical microvilli in DD and WD pre- and post-UNX. Lithium clearance (CLi, ml/min/Kg BW) increased post-UNX in DD (p=0.006) not WD; post UNX CLi was higher in DD (0.075 ± 0.013) vs WD (0.042 ± 0.009), p=0.036.

In conclusion, the phenotype of HTN and proteinuria observed following LKD in humans is evident in this pilot SD rat study. Compared to the 2% NaCl/1% KCl “Western style” diet, the 3% K
+
and alkali rich “DASH style diet” lowered baseline PT transporter levels, increased CLi (indicator of flow out of PT), elevated distal Na
+
transporters (likely due to flow from PT) and blunted the rise in BP post-UNX. The findings suggest that DASH style dietary electrolytes may improve outcomes following LKD.
Abstract P3059: ACE S: A NOVEL ANGIOTENSIN BASED MARKER FOR MONITORING PHARMACOLOGIC ACTIVITY OF ACE INHIBITORS IN HYPERTENSIVE PATIENTS
Authors: Domenig Oliver , Ahmed Ashraf H , Guo Zeng , Stoller Andrea , Burkard Thilo , Haschke Manuel , Stowasser Michael , Poglitsch Marko 
Published: September 2019

Angiotensin-converting-enzyme-inhibitors (ACEi) are widely used for treating hypertension and cardiovascular diseases and block Angiotensin-II (Ang-II) formation from Angiotensin-I (Ang-I). The therapeutic response to ACE inhibition critically depends on
in vivo
pharmacologic efficacy and affected by dosing, patient compliance and patient specific compensatory mechanisms, all being relevant topics for the clinical management of hypertension.

Samples were collected from 19 hypertensive patients and 7 confirmed primary aldosteronism (PA) patients. Hypertensive patients were investigated at baseline and after 4 weeks on therapy with a single daily dose of perindopril. PA patients were sampled before and after 14 day administration of ramipril. All samples were analysed by LC-MS/MS based RAAS Triple-A testing which involves the calculation of ACE-S, the ratio between plasma equilibrium levels of Ang-II and Ang-I as a novel marker for circulating ACE activity. ACE activity was further measured by analyzing the time dependent conversion of spiked Ang-I (LC-MS/MS) and by performing a clinical colorimetric ACE assay. Treatment adherence was confirmed by quantification of plasma drug levels.
ACE-S was significantly lower in all patients on perindopril or ramipril therapy compared to baseline (MEDIANS: 0.35 vs. 2.75 pM/pM, p<0.001). While eqAng-II levels were increased up to 5-fold compared to baseline levels in a subset of patients due to renin up-regulation, ACE-S stayed significantly suppressed in all samples investigated. In contrast, ACE inhibition appeared to be less effective using classical enzymatic approaches assessing ACE activity.
The novel angiotensin based marker ACE-S can be used to monitor pharmacologic efficacy of ACE inhibitors independent of their chemical structure. As part of the RAAS Triple-A test that is currently validated in screening for secondary forms of hypertension, ACE-S has the potential to support the clinical management of first-line non-responders in terms of optimizing ACEi dosing and visualizing patient specific compensatory mechanisms, thereby improving the overall control rates in hypertension.
Christological Punctuation
Authors: Calhoun Robert Matthew 
Published: September 2019

AbstractThe 26th edition of the Nestle-Aland Novum Testamentum Graece, followed by the 27th and 28th editions, deleted a punctuation variant in Phil 2:7 noted in the 25th, which drew attention to a syntactical ambiguity in the construal of three successive participial phrases (7b–d). Resolutions of this ambiguity have significant consequences for the passage’s christological perspective. Future editions should revise and restore this variant.
Romans 7 and the Resurrection of Lament in Christ
Authors: Timmins Will N. 
Published: September 2019

AbstractRelatively little attention has been paid to biblical parallels to the wretched “I” of Rom 7:14–25. A few scholars have observed features shared with the psalms of lament, but these studies have been limited in scope and have proved inconclusive in identifying the “I.” A comparison between Romans 7 and one of the psalms of lament, namely Psalm 119, reveals a number of significant verbal and conceptual correspondences, which throw fresh light onto previously unclear aspects of the “I”’s monologue. In addition, Paul’s wretched “I” is revealed as inhabiting the same symbolic world as the Christ-believers in Rome, experiencing with them the resurrection of lament in Christ.