bluuebunny/crossref_metadata_2025_split huggingface dataset:
Macro-coherent radiative emission of neutrino pair between parity-even atomic states
Authors: Tashiro M. , Das B. P. , Ekman J. , Jönsson P. , Sasao N. , Yoshimura M. 
Published: November 2019

Abstract
A new scheme to determine the neutrino mass matrix is proposed using atomic de-excitation between two states of a few eV energy spacing. The determination of the smallest neutrino mass of the order of 1 meV and neutrino mass type, Majorana or Dirac, becomes possible, if one can coherently excite more than 1 gram of atoms using two lasers.
ANALYZING THE ASYMMETRIC EFFECTS OF CRUDE OIL PRICE CHANGES ON CHINA’S PETROLEUM PRODUCT PRICES
Authors: LIAO XIANCHUN , BAEK JUNGHO 
Published: November 2019

As the world’s second-largest crude oil consumer, China depends on imports for approximately 60% and domestic production for approximately 40%, of its oil demand. Therefore, it is very interesting to assess the pass-through effects of both domestic and international crude oil prices to gasoline and diesel prices. After the short- and long-run investigations using the nonlinear autoregressive distributed lag (ARDL) methodology of Shin et al. [Shin, Y, BC Yu and M Greenwood-Nimmo (2014). Modelling asymmetric cointegration and dynamic multipliers in a nonlinear ARDL framework” Festschrift in Honor of Peter Schmidt: Econometric Methods and Applications, R Sickels and W Horrace (eds.), pp. 281–314. Springer.], we find overwhelming evidence supporting the asymmetric price transmission mechanism between crude oil prices and gasoline prices in both the short- and long-run. In the case of diesel prices, on the other hand, the asymmetry effects seem likely to be a long-run phenomenon.
CD8+ T cells regulate liver injury in obesity-related nonalcoholic fatty liver disease
Authors: Breuer Denitra A. , Pacheco Maria Cristina , Washington M. Kay , Montgomery Stephanie A. , Hasty Alyssa H. , Kennedy Arion J. 
Published: November 2019

Nonalcoholic steatohepatitis (NASH) has increased in Western countries due to the prevalence of obesity. Current interests are aimed at identifying the type and function of immune cells that infiltrate the liver and key factors responsible for mediating their recruitment and activation in NASH. We investigated the function and phenotype of CD8+ T cells under obese and nonobese NASH conditions. We found an elevation in CD8 staining in livers from obese human subjects with NASH and cirrhosis that positively correlated with α-smooth muscle actin, a marker of hepatic stellate cell (HSC) activation. CD8+ T cells were elevated 3.5-fold in the livers of obese and hyperlipidemic NASH mice compared with obese hepatic steatosis mice. Isolated hepatic CD8+ T cells from these mice expressed a cytotoxic IL-10-expressing phenotype, and depletion of CD8+ T cells led to significant reductions in hepatic inflammation, HSC activation, and macrophage accumulation. Furthermore, hepatic CD8+ T cells from obese and hyperlipidemic NASH mice activated HSCs in vitro and in vivo. Interestingly, in the lean NASH mouse model, depletion and knockdown of CD8+ T cells did not impact liver inflammation or HSC activation. We demonstrated that under obese/hyperlipidemia conditions, CD8+ T cell are key regulators of the progression of NASH, while under nonobese conditions they play a minimal role in driving the disease. Thus, therapies targeting CD8+ T cells may be a novel approach for treatment of obesity-associated NASH. NEW & NOTEWORTHY Our study demonstrates that CD8+ T cells are the primary hepatic T cell population, are elevated in obese models of NASH, and directly activate hepatic stellate cells. In contrast, we find CD8+ T cells from lean NASH models do not regulate NASH-associated inflammation or stellate cell activation. Thus, for the first time to our knowledge, we demonstrate that hepatic CD8+ T cells are key players in obesity-associated NASH.
A new role for heat shock factor 27 in the pathophysiology of Clostridium difficile toxin B
Authors: Yanda Murali K. , Guggino William B. , Cebotaru Liudmila 
Published: November 2019

Clostridium difficile (CD) is a common pathogen that causes severe gastrointestinal inflammatory diarrhea in patients undergoing antibiotic therapy. Its virulence derives from two toxins, toxin CD, A and B (TcdA and TcdB) (Borriello et al. Rev Infect Dis 12, Suppl 2: S185-191, 1990). Among the prime candidates for CD colonization are patients with cystic fibrosis (CF), who are routinely treated with antibiotics and frequently hospitalized. Indeed, ~50% of patients with CF are colonized with virulent forms of CD but do not exhibit diarrhea (Bauer et al. Clin Microbiol Infect 20: O446–O449, 2014; Binkovitz et al. Am J Roentgenol 172: 517–521, 199; Zemljic et al. Anaerobe 16: 527–532, 2010). We found that TcdB has global effects on colonic cells, including reducing the steady-state levels of sodium-proton exchange regulatory factors, reducing the levels of heat shock protein (Hsp) 27, and increasing the fraction of total Hsp27 bound to the cystic fibrosis transmembrane conductance regulator (CFTR). Also, since some mutations in CFTR seem to be protective, we asked whether CFTR is a target of TcdB. We show here that TcdB increases the maturation of CFTR and transiently increases its function. These combined effects promote increased surface expression of CFTR, resulting in a transient increase in Cl− secretion. This increase is followed by a precipitous decline in both CFTR-dependent Cl− secretion and transepithelial resistance (TER), suggesting a breakdown in the epithelial cells’ tight junctions. We also found that overexpressing Hsp27 reverses some of the deleterious effects of TcdB, in particular preserving TER and therefore likely the maintenance of barrier function. Thus, our data suggest that Hsp27 plays a role in the diarrhea generated by CD infection and is a potential therapeutic target for treating this diarrhea. NEW & NOTEWORTHY Clostridium difficile (CD) is a common pathogen that causes severe gastrointestinal inflammatory diarrhea in patients undergoing antibiotic therapy. We provide new evidence that heat shock protein (Hsp) 27 is one of the key players in CD pathology and that increasing Hsp27 can prevent the decrease in transepithelial resistance induced by toxin CD B, pointing the way for pharmacologic therapies for patients with chronic CD infection that can increase Hsp27 as a means to mitigate the effects of CD on gastrointestinal pathology.
Effects of Polygonatum sibiricum Polysaccharides (PSP) on Human Esophageal Squamous Cell Carcinoma (ESCC) via NF-κB Signaling Pathway
Authors: Zhou Weizheng , Hong Jiang , Zhu Ji , Wang Xiaowei 
Published: November 2019

Objective. To explore the effects of different concentrations of Polygonatum sibiricum polysaccharides (PSP) on human esophageal squamous cell carcinoma (ESCC) cell line Eca109 and explore the new approach for the treatment of ESCC. Methods. Eca109 cells were divided into 5 groups, including one control group and 4 experimental groups where the concentrations of PSP used were 50, 100, 200, and 400 μg/mL. The proliferation rate of Eca109 cells in each group was measured with the CCK8 assay, and the apoptosis rate in each group was analyzed by flow cytometry; the in vitro scratch assay was used to determine the migration ability of Eca109 cells after PSP treatment; the expression levels of IL-1, IL-6, IL-10, TNF-α, and TGF-β were measured by RT-PCR, and the expression levels of TLR4 and proteins that are related to NF-κB signaling pathways were determined by Western blot. Results. PSP significantly inhibited the proliferation of Eca109 cells (p<0.05) on a time- and dose-dependent manner; the apoptosis rates of Eca109 cells in experimental groups were significantly increased after 48 h of culture (p<0.05); PSP significantly reduced the migration and invasion ability of Eca109 cells (p<0.05); RT-PCR results showed that the expression of IL-10 in Eca109 cells increased significantly after treatment with PSP (p<0.05), while the expression of IL-1, IL-6, TNF-α, and TGF-β decreased significantly (p<0.05). Compared with the control group, the expression level of TLR4, NF-κB/p50, and NF-κB/p65 protein in each experimental group was significantly lower than that in the control group (p<0.05). Conclusions. PSP significantly inhibited the proliferation, invasion, and migration of Eca109 cells and promoted cell apoptosis. These observed effects were probably due to the PSP’s inhibition on the NF-κB signaling pathway in Eca109 cells via the regulation of the TLR4 expression.
ДИСЛІПІДЕМІЧНІ ЗМІНИ ЯК ПРЕДИКТОРИ ПРОГРЕСУВАННЯ ЗОВНІШНЬОСЕКРЕТОРНОЇ НЕДОСТАТНОСТІ ПІДШЛУНКОВОЇ ЗАЛОЗИ У ХВОРИХ НА ХРОНІЧНИЙ ПАНКРЕАТИТ
Authors: Arkhij E. J. , Prylypko L. B. , Moskal O. M. 
Published: November 2019

Хронічний панкреатит (ХП) відноситься до нозологій, показники захворюваності яких мають тенденцію до загальносвітового зростання. Визначено ряд причин, які сприяють появі та прогресуванню хронічного запального процесу на рівні підшлункової залози (ПЗ). Одними із таких є дисліпопротеїнемії.
Мета дослідження: проаналізувати особливості ліпідного метаболізму у пацієнтів, які страждають на ХП із екзокринною недостатністю.
Матеріали та методи: нами обстежено 79 пацієнтів з ознаками ХП, які знаходилися на стаціонарному лікуванні у Хустській РЛ протягом 2017-2018 років. Відповідно до отриманих результатів було сформовано три досліджувані групи. Першу складали пацієнти на ХП із легкою зовнішньосекреторною недостатністю ПЗ (ЗНПЗ) (n = 50), другу ‒ із помірною ЗНПЗ (n = 29), до третьої включили практично здорових людей (n = 23). Для оцінки екзокринної функції ПЗ визначали рівень еластази-1 у калі. Ліпідний гомеостаз оцінювали за наступними показниками: загальний холестерол (ЗХС), тригліцерол (ТГ), холестерол ліпопротеїнів низької щільності (ХС ЛПНЩ), холестерол ліпопротеїнів дуже низької щільності (ХС ЛПДНЩ), холестерол ліпопротеїнів високої щільності (ХС ЛПВЩ) та індекс атерогенності (ІА). Крім того, провели кореляційний аналіз впливу дисліпідемічних розладів на виразність ЗНПЗ.
Результати досліджень вказують на наявність у хворих на ХП “ліпідного дистрес-синдрому”, що проявлявся у вигляді гіперхолестеролемії, гіпертригліцеролемії, підвищення концентрації ХС ЛПНЩ, ХС ЛПДНЩ та зниження вмісту ХС ЛПВЩ. Встановлено залежність екзокринної недостатності від вираженості дисліпідемічних розладів.
Висновки: у хворих на ХП виявлено ознаки порушень ліпідного метаболізму та доведено вплив останніх на екзокринну функцію ПЗ. Тому вважаємо необхідним ретельне дослідження ліпідограми у всіх пацієнтів із ознаками хронічного ураження ПЗ.
ОСТЕОІНДУКТИВНІ ПРЕПАРАТИ ДЛЯ ЗАМІЩЕННЯ КІСТКОВИХ ДЕФЕКТІВ У СТОМАТОЛОГІЇ
Authors: Duda K. M. , Klishch I. M. 
Published: November 2019

В статті вивчено проблему дефіциту кісткової тканини альвеолярного гребеня як ускладнення стоматологічних захворювань, що утруднює подальшу імплантацію. Висвітлено загальні дані про матеріали, які застосовують для заміщення дефектів кісткової тканини в щелепно-лицевій ділянці. Обґрунтовано репаративні властивості матеріалів, що пришвидшують остеоінтеграцію. Проаналізовано позитивні властивості та недоліки препаратів кожної з існуючих груп залежно від походження.
Мета – проаналізувати літературні дані щодо остеоіндуктивних препаратів, які застосовують у стоматології.
Висновок. На сьогоднішній день ще не існує кісткового матеріалу, який би відповідав усім вимогам. Необхідний пошук нових, безпечних, доступних і легких в експлуатації штучних матеріалів, які повинні мати велику амортизаційну здатність, високу витривалість, антимікробну дію і резистентність до інфекції, пористу структуру та інертність до біологічних тканин і не викликати запальних, алергічних і токсичних реакцій.
ВПЛИВ РЕЗЕКЦІЇ РІЗНИХ ОБ’ЄМІВ ПАРЕНХІМИ ПЕЧІНКИ НА ЇЇ ЖОВЧОУТВОРЮВАЛЬНУ ФУНКЦІЮ
Authors: Hnatjuk M. S. , Monastyrska N. Ya. , Tatarchuk L. V. 
Published: November 2019

Вступ. На сьогодні в клініках широко виконують резекцію печінки. Видалення великих її об’ємів призводить до розвитку різних пострезекційних ускладнень та змін жовчоутворення.
Мета дослідження – вивчити особливості жовчоутворювальної функції печінки при резекції різних об’ємів її паренхіми.
Методи дослідження. Дослідження проведено на 45 лабораторних статевозрілих білих щурах-самцях, яких поділили на 3 групи: 1-ша нараховувала 15 інтактних тварин; 2-га – 15 щурів після резекції 31,5 % паренхіми печінки; 3-тя – 15 тварин, у яких було видалено 58,1 % об’єму печінки. Через місяць від початку досліду за умов тіопенталового наркозу катетеризували спільну жовчну протоку і проводили забір жовчі протягом 1 год. При цьому розраховували інтенсивність секреції жовчі, в якій визначали концентрацію жовчних кислот: таурохолевої, глікохолевої, холевої, хенодезоксихолевої+дезоксихолевої, вміст фосфоліпідів, вільних жирних кислот, триацилгліцеролів і протеїнів. Евтаназію тварин здійснювали шляхом кровопускання за умов тіопенталового наркозу через місяць від початку експерименту. Гістологічні мікропрепарати печінки досліджували світлооптично. Кількісні показники обробляли статистично.
Результати й обговорення. Резекція 58,1 % паренхіми печінки призводила до пострезекційної портальної гіпертензії, яка характеризувалася розширенням ворітної печінкової вени, повнокров’ям з дилатацією брижових вен, венозного русла тонкої і товстої кишок, асцитом, спленомегалією. Інтенсивність секреції жовчі за досліджуваних умов експерименту знизилася на 28,9 % порівняно з контролем, концентрація таурохолевої кислоти – на 21,5 %, глікохолевої – на 15,56 %, холевої – на 18,6 %, а хенодезоксихолевої+дезоксихолевої – на 16,2 %, концентрація фосфоліпідів – на 11,0 %, вільних жирних кислот – на 10,4 %, триацилгліцеролів – на 19,8 %, протеїнів – на 8,02 %. Світлооптично в мікропрепаратах печінки тварин 3-ї групи спостереження відмічали повнокров’я венозних судин, осередки гіпертрофії, дистрофії гепатоцитів, появу лімфоїдно-гістіоцитарних інфільтратів та збільшення стромальних структур.
Висновок. Резекція лівої і правої бокових часток печінки призводить до пострезекційної портальної гіпертензії та змін жовчоутворення і жовчовиділення, що характеризується зниженням інтенсивності секреції жовчі, концентрації жовчних кислот, фосфоліпідів, вільних жирних кислот, триацилгліцеролів та протеїнів.
Spontaneous Atrial Fibrillation in Transgenic Goats With TGF (Transforming Growth Factor)-β1 Induced Atrial Myopathy With Endurance Exercise
Authors: Regouski Misha , Galenko Oxana , Doleac Jason , Olsen Aaron L. , Jacobs Victoria , Liechty Dustin , White Kenneth L. , Bunch T. Jared , Lee Pamela M. , Rutigliano Heloisa M. , Polejaeva Irina A. , Cutler Michael J. 
Published: November 2019

Background:
There is increasing evidence that endurance exercise is associated with increased risk of atrial fibrillation (AF). However, it is unknown if the relationship between endurance exercise and AF is dependent on an atrial myopathy.

Methods:
Six cardiac-specific TGF (transforming growth factor)-β1 transgenic and 6 wild-type (WT) goats were utilized for these studies. Pacemakers were implanted in all animals for continuous arrhythmia monitoring and AF inducibility. AF inducibility was evaluated using 5 separate 10 s bursts of atrial pacing (160–200 ms). Three months of progressive endurance exercise (up to 90 minutes at 4.5 mph) was performed. Quantitative assessment of circulating microRNAs and inflammatory biomarkers was performed.

Results:

Sustained AF (≥30 s) was induced with 10 s of atrial pacing in 4 out of 6 transgenic goats compared with 0 out of 6 WT controls at baseline (
P
<0.05). No spontaneous AF was observed at baseline. Interestingly, between 2 and 3 months of exercise 3 out of 6 transgenic animals developed self-terminating spontaneous AF compared with 0 out of 6 WT animals (
P
<0.05). There was an increase in AF inducibility in both transgenic and WT animals during the first 2 months of exercise with partial normalization at 3 months (transgenic 67%; 100%; 83% versus WT 0%; 67%; 17%). These changes in AF susceptibility were associated with a decrease in circulating microRNA-21 and microRNA-29 during the first 2 months of exercise with partial normalization at 3 months in both transgenic and WT animals. Finally, MMP9 (matrix metallopeptidase 9) was increased during the second and third months of exercise training.

Conclusions:
This study demonstrates a novel transgenic goat model of cardiac fibrosis (TGF-β1 overexpression) to demonstrate that endurance exercise in the setting of an underlying atrial myopathy increases the incidence of spontaneous AF. Furthermore, endurance exercise seems to increase inducible AF secondary to altered expression of key profibrotic biomarkers that is independent of the presence of an atrial myopathy.
Application of Hybrid Matrix Metalloproteinase-Targeted and Dynamic
201
Tl Single-Photon Emission Computed Tomography/Computed Tomography Imaging for Evaluation of Early Post-Myocardial Infarction Remodeling
Authors: Thorn Stephanie L. , Barlow Shayne C. , Feher Attila , Stacy Mitchel R. , Doviak Heather , Jacobs Julia , Zellars Kia , Renaud Jennifer M. , Klein Ran , deKemp Robert A. , Khakoo Aarif Y. , Lee TaeWeon , Spinale Francis G. , Sinusas Albert J. 
Published: November 2019

Background:

The induction of matrix metalloproteinases (MMPs) and reduction in tissue inhibitors of MMPs (TIMPs) plays a role in ischemia/reperfusion (I/R) injury post-myocardial infarction (MI) and subsequent left ventricular remodeling. We developed a hybrid dual isotope single-photon emission computed tomography/computed tomography approach for noninvasive evaluation of regional myocardial MMP activation with
99m
Tc-RP805 and dynamic
201
Tl for determination of myocardial blood flow, to quantify the effects of intracoronary delivery of recombinant TIMP-3 (rTIMP-3) on I/R injury.

Methods:

Studies were performed in control pigs (n=5) and pigs following 90-minute balloon occlusion–induced ischemia/reperfusion (I/R) of left anterior descending artery (n=9). Before reperfusion, pigs with I/R were randomly assigned to intracoronary infusion of rTIMP-3 (1.0 mg/kg; n=5) or saline (n=4). Three days post-I/R, dual isotope imaging was performed with
99m
Tc-RP805 and
201
Tl along with contrast cineCT to assess left ventricular function.

Results:

The ischemic to nonischemic ratio of
99m
Tc-RP805 was significantly increased following I/R in saline group (4.03±1.40), and this ratio was significantly reduced with rTIMP-3 treatment (2.22±0.57;
P
=0.03). This reduction in MMP activity in the MI-rTIMP-3 treatment group was associated with an improvement in relative MI region myocardial blood flow compared with the MI-saline group and improved myocardial strain in the MI region.

Conclusions:
We have established a novel hybrid single-photon emission computed tomography/computed tomography imaging approach for the quantitative assessment of regional MMP activation, myocardial blood flow, and cardiac function post-I/R that can be used to evaluate therapeutic interventions such as intracoronary delivery of rTIMP-3 for reduction of I/R injury in the early phases of post-MI remodeling.
Intravascular Lithotripsy in Calcified Coronary Lesions
Authors: Aksoy Adem , Salazar Carlos , Becher Marc Ulrich , Tiyerili Vedat , Weber Marcel , Jansen Felix , Sedaghat Alexander , Zimmer Sebastian , Leick Jürgen , Grube Eberhard , Gonzalo Nieves , Sinning Jan-Malte , Escaned Javier , Nickenig Georg , Werner Nikos 
Published: November 2019

Background:
Optimal plaque preparation of calcified coronary lesions is key to prevent stent failure. The purpose of this study was to determine the strategy success and safety of intravascular lithotripsy (IVL) in calcified lesions of an all-comers cohort.

Methods:
Patients with calcified coronary lesions were screened in 3 centers. Seventy-one patients were eligible for IVL. Patients were assigned to (group A) primary IVL therapy for patients with calcified de-novo lesions (n=39 lesions), (group B) secondary IVL therapy for patients with calcified lesions in which noncompliant balloon dilatation failed (n=22 lesions), and (group C) tertiary IVL therapy in patients with stent underexpansion after previous stenting (n=17 lesions). Primary end point was strategy success (stent expansion with <20% in-stent residual stenosis) and safety outcomes (procedural complications, in-hospital major adverse cardiovascular event).

Results:

Seventy-eight calcified lesions were treated using the Shockwave C
2
balloon. Mean diameter stenosis of calcified lesions was 71.8±13.1% at baseline, decreased to 45.1±17.4% immediately after IVL, and to 17.5±15.2% after stenting. Mean minimal lumen diameter was 1.01±0.49 mm at baseline and increased to 1.90±0.61 after IVL, and to 2.88±0.56 mm after stenting. The primary end point of strategy success was reached in 84.6% (group A), 77.3% (group B), and 64.7% (group C). Device delivery and IVL treatment were possible in all lesions. Four type b dissections were observed without further sequelae. No patient suffered from in-hospital major adverse cardiovascular event. Seven Shockwave balloons ruptured during treatment without any sequelae.

Conclusions:
IVL provides a valid strategy for lesion preparation in severely calcified coronary lesions with high success rate, low procedural complications, and low major adverse cardiovascular event rates.
Alirocumab Reduces Total Hospitalizations and Increases Days Alive and Out of Hospital in the ODYSSEY OUTCOMES Trial
Authors: Szarek Michael , Steg Ph. Gabriel , DiCenso Dina , Bhatt Deepak L. , Bittner Vera A. , Budaj Andrzej , Diaz Rafael , Goodman Shaun G. , Gotcheva Nina , Jukema J. Wouter , Pordy Robert , Roe Matthew T. , Sourdille Timothée , White Harvey D. , Xavier Denis , Zeiher Andreas M. , Schwartz Gregory G. ,   for the ODYSSEY OUTCOMES Committees and Investigators*
Published: November 2019

Background:
In ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab), alirocumab was compared with placebo, added to high-intensity or maximum tolerated statin treatment after acute coronary syndrome in 18 924 patients. Alirocumab reduced first occurrence of the primary composite end point—coronary heart disease death, nonfatal myocardial infarction, fatal or nonfatal ischemic stroke, or hospitalization for unstable angina—as well as total nonfatal cardiovascular events and all-cause deaths. The present analysis determined whether alirocumab reduced total (first and subsequent) hospitalizations and death and increased days alive and out of hospital (DAOH) and percent DAOH in ODYSSEY OUTCOMES.

Methods and Results:

In prespecified analyses, hazard functions for total hospitalizations and death were jointly estimated by a semiparametric model, while in post hoc analyses, DAOH and percent DAOH were compared between treatment groups with Poisson regression and one-inflated beta regression, respectively. With 16 629 total hospitalizations and 726 deaths, 331 fewer hospitalizations, and 58 fewer deaths were observed with alirocumab compared with placebo, translating to 15.6 total hospitalizations or deaths avoided with alirocumab per 1000 patient-years of assigned treatment. Alirocumab reduced total hospitalizations (hazard ratio, 0.96 [95% CI, 0.92–1.00];
P
=0.04) and increased DAOH relative to placebo (rate ratio, 1.003 [95% CI, 1.000–1.007];
P
=0.05), primarily through a reduction in days dead (rate ratio, 0.847 [95% CI, 0.728–0.986];
P
=0.03). Patients randomized to alirocumab were also more likely to survive to the end of the study without hospitalization (odds ratio, 1.06 [95% CI, 1.00–1.13];
P
=0.03).

Conclusions:
Alirocumab reduced total hospitalizations with corresponding small increases in DAOH and percent DAOH. These outcomes provide alternative patient-centered metrics to capture the totality of alirocumab clinical efficacy after acute coronary syndrome.

Clinical Trial Registration:

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT01663402.