bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diabetes Self‐Management Cuban Americans
Authors: Vaccaro Joan A , Huffman Fatma G , Zarini Gustavo , Nath Subrata 
Published: June 2021

ObjectivesWe investigated the relationship among factors predicting inadequate glucose control among 182 Cuban‐Americans (Females=110, Males=72) (CA) with type 2 diabetes mellitus (T2DM).MethodsCross‐sectional study CA adults self‐reported with type 2 diabetes (T2D) from a randomized mailing list in three counties of South Florida. Participants were screened by trained interviewers for heritage and diabetes status and participants signed informed consent form. Statistical analyses used SPSS and included descriptive statistic, multiple logistic and ordinal logistic regression models.ResultsOnly 54% reported having a diet prescribed/told to schedule meals. Those told to schedule meals were 3.62 more likely to schedule (CI 1.81, 7.26) p<0.001. Age, WC, BMI and gender were not significant predictors of HbA1c. We found, by ordinal logistic regression of 5‐scale Likert, that participants with inadequate glucose control (HbA1c> 8.5) were more than four‐fold likely to never follow a meal plan , OR 5.39 (1.40, 20.7).ConclusionsNearly half CA are not given dietary guidance, yet our results indicate CA may improve glycemic control by receiving dietary instructions.Grant Funding SourceAmerican Diabetes Association
Socioeconomic factors associated with obesity in adolescents in Guadalajara, Mexico
Authors: Romero‐Velarde Enrique , Martínez‐Gloria Esther Alicia , Vásquez‐Garibay Edgar Manuel , Troyo‐Sanromán Rogelio 
Published: June 2021

ObjectiveTo identify differences in socioeconomic factors associated with obesity in adolescents from different social classes.Methods and materialsIn a cross sectional study 328 adolescents from three junior high schools were included; 131 from low, 106 from middle and 91 from high social class. Socioeconomic information was obtained; the body mass index (kg /m2) was used to evaluate the presence of obesity (BMI >95 percentile) or healthy weight (BMI percentile 5‐85). The association between the presence of obesity and socioeconomic characteristics was measured with the odds ratio (OR) and x2 test.ResultsThe prevalence of obesity was higher in middle (24.5%) than low (18.3%) or high class schools (19.8%). There was an association between the presence of obesity in adolescents and mother's obesity in schools of low (OR = 2.77) and middle (OR = 3.0) social classes and with father's obesity in schools of middle (OR = 2.81) and high (OR = 3.62) social classes. The practice of physical activities was a protection factor for obesity in adolescents from low social class (OR = 0.28 [0.10‐0.76]).ConclusionsThe prevalence of obesity was higher in adolescents of middle social class; probably, the highest prevalence is moving from higher to lower social classes in Mexico. Adolescents from low social class might have less oportunities to practice physical activities and look for health attention.
Energy expenditure in chow‐fed female non‐human primates of various weights
Authors: Rising Russell 
Published: June 2021

ObjectiveIn this study daily energy expenditures (EE) and respiratory quotients (RQ) in female monkeys of various body weights were determined.Methods16 socially reared Bonnet Macaque female monkeys [5.5 ± 1.4 kg body weight, modified BMI (length measurement from head to base of the tail) = 28.8 ± 6.7 kg/crown‐rump length, m2 and 11.7 ± 4.6 years] were placed in the primate Enhanced Metabolic Testing Activity Chamber (Model 3000a, EMTAC Inc. Fort Lee, NJ) for 22‐hour measurements of EE (kcal/kg) and RQ (VCO2/VO2). All were fed monkey chow (4.03 kcal/g) ad‐libitum under a 12/12 hour light/dark cycle. Metabolic data were corrected for differences in body weight. Results were divided into day (8‐hours), dark (12 hours) and morning (2‐hours) periods. Data analysis was conducted utilizing SPSS (Version 13).ResultsModified BMI negatively correlated with 22‐hour energy expenditure in all monkeys (r=‐0.64, p<0.01). The large variability of daily energy intake (4.5 to 102.0 kcal/kg) necessitated division into two groups, non‐eaters (<13 kcal/kg) and eaters (>23 kcal/kg). There were also reductions (p<0.05) in both 22‐hour and dark period RQs in the "non‐eaters" in comparison to those who were "eaters". Monkeys were also classified as "lean" (modified BMI < 25) or "obese" (modified BMI > 30). The obese group had lower EE (p<0.05) during each time period and over the entire 22‐hours (p<0.05), in comparison to their lean counterparts.ConclusionThere is an association between a reduction of energy expenditure and a gain in body weight.
Prevention of DNA damage by polyphenol‐rich food
Authors: Briviba Karlis , Bub Achim , Watzl Bernhard , Rechkemmer Gerhard , Barth Stephan W 
Published: June 2021

Epidemiological and experimental data suggest that an increased intake of plant food rich in polyphenols can reduce the risk of cancers. DNA damage is an important step in the initiation of carcinogenesis. Here we report data on the effect of polyphenol rich food such as apples and apple juice on DNA damage in colon epithelial cells from animal studies and in peripheral blood lymphocytes (PBL) from human intervention studies.1,2‐Dimethylhydrazine‐induced DNA strand breaks in colon epithelial cells in rats were significantly inhibited by consumption of cloudy and clear apple juice. In a human intervention study, consumption of 1 kg apples caused no changes in endogenous DNA strand breaks, in Fpg‐sensitive sites (oxidative purine damage) or in the capacity to protect DNA against damage induced by hydrogen peroxide in PBL. But, a statistically significant decrease in the levels of endonuclease III sensitive sites (oxidative pyrimidine damage) and an increase in capacity to protect DNA against strand breaks induced by iron chloride were identified. In contrast to the effects of apples, a human intervention with 2, 5 or 8 servings of fruit and vegetables/day had no effect on DNA damage in PBL. Thus, we have identified apples as another fruit to add to the already known types of fruit (kiwi) and vegetables (tomato) with antigenotoxic properties and partly characterized their antigenotoxic mechanism in humans.Supported by the Deutsche Forschungsgemeinschaft and the Federal Ministry of Research and Education, Germany
The role of MMP2 in persistent inflammation in Chronic Obstructive Pulmonary Disease (COPD)
Authors: Gosselink John , Hayashi Shizu , Elliott W Mark , Xing Li , Chan Becky , Wright Claire , Pare Peter , Sin Don , Pierce John , Pierce Richard , Patterson Alex , Cooper Joel , Hogg James 
Published: June 2021

RationaleMMP2 modifies chemokines in ways that allow them to continue to bind to their receptors but fail to activate them (Science. 2000, 289:1202‐6).ObjectiveTo investigate the role of MMP2 expression and activity in the development of the persistent inflammatory process associated with progression of COPD.MethodsThe expression of MMP2 was measured by Taqman quantitative PCR in 136 paired samples of small bronchioles and surrounding lung tissue separated by laser capture microdissection from 63 patients in all 4 categories of COPD severity. MMP2 mRNA expression was compared to forced expiratory volume in one second (FEV1) by linear regression analysis. As well, MMP2 activity was measured in 11 of these COPD patients' lungs by gelatin zymography.ResultsMMP2 expression and activity decreased in both the small airways and surrounding lung tissue with disease progression in COPD.ConclusionsThis sharp reduction of MMP2 expression and activity may contribute to the persistence of the inflammatory process in COPD by reducing the proteolytic modification of chemokines that normally blocks chemokine receptors to reduce the inflammatory response.Supported by grants NIH‐HL‐P50 084922 and CIHR MOP‐82815
Metformin Improves Endothelial Function in Obese Rats
Authors: Lobato Nubia Souza , Akamine Eliana Hiromi , Filgueira Fernando Paranaiba , Tostes Rita de Cássia , Carvalho Maria Helena Catelli , Fortes Zuleica Bruno 
Published: June 2021

AimObesity is associated with insulin resistance and vascular alterations. Since metformin (MET) improves insulin sensitivity and vascular dysfunction in diabetes, we evaluated the effects of MET on vascular reactivity in monosodium glutamate (MSG) obese rats. Methods andResultsWistar rats received MSG from day 2 to day 6 after birth for obesity induction. MSG rats (18 weeks) presented higher Lee index, fat accumulation, dyslipidemia and insulin resistance. MET (300mg/kg/day, 15 days) had beneficial effects on these parameters. In the mesenteric arteriolar bed the response to norepinephrine, enhanced in MSG rats, was corrected by MET. This correction was reverted by L‐NAME and tetraethylammonium (TEA), but not by indomethacin. The response to acetylcholine (ACh), reduced in MSG rats, was corrected by MET. L‐NAME, indomethacin or TEA did not alter this correction. The vasodilation to sodium nitroprusside was enhanced by MET. Althought MET did not alter the reduced nitric oxide (NO) production, it reverted the reduced PGI2/TXA2 release and the enhanced reactive oxygen species (ROS) generation in MSG rats.ConclusionMET restores vascular dysfunction in MSG rats by reducing ROS generation, modulating membrane hyperpolarizating and reestablishing the balanced release of prostanoids. The hyperresponsiveness of the smooth muscle to NO with MET treatment might contribute to its beneficial effects. FAPESP
Reference moist smokeless tobacco‐induced oxidative stress in human oral keratinocyte cell lines leads to cell death via JNK and p38 MAPK signaling
Authors: Mitchell Clint , Piper John , Joyce Andrew , Fariss Marc , McKallip Robert 
Published: June 2021

The use of moist smokeless tobacco products is associated with acute oral injuries such as leukoplakia. Unfortunately, there is a limited understanding of the mechanisms and signaling pathways associated with these injuries. The present studies investigate the effects of a Reference 1S3 moist smokeless tobacco extract (STE) on oral injury, oxidative stress and MAPK signaling in multiple human oral keratinocyte cell lines utilizing cytospin slide analysis to observe alterations in cell morphology, DCF‐DA fluorescence, and western blotting techniques. STE caused dose‐dependent keratinocyte cell death within 30 minutes to 3 h of exposure. STE enhanced the activity of ERK1/2, JNK1/2, p38 MAPK and ASK1, an upstream activator of JNK1/2 and p38 MAPK. Inhibition of JNK1/2 or p38 MAPK, but not ERK1/2, suppressed STE‐induced cell death. STE promoted the generation of reactive oxygen species (ROS). The anti‐oxidants, Trolox and L‐ascorbic acid, suppressed ROS production, ASK1, JNK1/2 and p38 MAPK activation, and reduced cell death after STE exposure. Thus, reference STE leads to cell death in human oral keratinocyte cell lines in part through oxidative stress via activation of ASK1 and the JNK1/2 and p38 MAPK pathways.Research supported by Altria Client Services, 601 East Jackson St. Richmond, VA 23219 U.S.A.
Flow‐induced remodeling: interplay of local inflammation and vascular tone
Authors: Matlung Hanke , Bakker Erik N.T.P. , Bonta Peter , de Vries Carlie J , vanBavel Ed 
Published: June 2021

We hypothesize that small artery remodeling is facilitated by inflammation but that smooth muscle cell tone sets its inward or outward direction.MethodsMouse mesenteric arcade arteries were ligated, resulting in low flow and high flow vessels. Immediate effects on tone were determined by in vivo microscopy. Structural remodeling was quantified after two days.ResultsVessels exposed to high blood flow dilated, followed by outward remodeling. Low flow vessels constricted, followed by inward remodeling. Macrophage numbers increased 5‐fold in both groups, and remodeling was absent after macrophages depletion. Yet, the pattern of pro‐ and anti‐inflammatory cytokine expression was similar in high and low flow vessels. Low flow vessels under subsequent full dilation showed increased outward remodeling, as tested by a sequence of 1 day in vivo and 1 day in vitro study in a cannulation setup (13 ± 3% in inflamed arteries versus 6 ± 1% in control, n=5, p<0.05).ConclusionAltered blood flow is associated with an inflammatory response that facilitates remodeling; the direction is determined by vascular tone. Supported by the Netherlands Heart Foundation (NHS 2001T038).
Differential Regulation of Ubiquitin ligases Atrogin‐1 and MuRF‐1 in Angiotensin II‐Mediated Skeletal Muscle Atrophy
Authors: Yoshida Tadashi , Semprun‐Prieto Laura , Sukhanov Sergiy , Delafontaine Patrick 
Published: June 2021

Advanced congestive heart failure is associated with activation of the renin‐angiotensin system and skeletal muscle atrophy. Angiotensin II (Ang II) infusion in mice produces cachexia secondarily to increase of muscle proteolysis mediated by two E3 ubiquitin ligase Atrogin‐1 and MuRF‐1, and also decreased levels of circulating and skeletal muscle IGF‐1.To determine mechanisms linking ubiquitin ligase expression and IGF‐1 signaling, time‐course dependent expression of Atrogin‐1, MuRF‐1, IGF‐1 and IGF‐1 receptor (IGF1R) was analyzed in skeletal muscles of Ang II infused mice. Expression of Atrogin‐1, MuRF‐1 and IGF1R were elevated one day after the initiation of Ang II‐infusion and were gradually decreased on day 4 and day 7. On the other hand, the expression of IGF‐1 was reduced on day 7. In skeletal muscles of mice overexpressing IGF‐1 specifically in skeletal muscle (MLC‐IGF‐1 mice), no significant reduction of skeletal muscle weight was observed after Ang II infusion and the basal and Ang II‐induced expression of Atrogin‐1 was significantly repressed. On the other hand, basal and Ang II‐induced expression of MuRF‐1 in skeletal muscles of MLC‐IGF‐1 mice was not different from WT animals.These data demonstrate that the IGF‐1 prevention of Ang II induced skeletal muscle atrophy is mediated via the ability of IGF‐1 to repress Atrogin‐1 expression, rather than MuRF‐1 expression.This work was supported by NIH Grant HL080682
The effects of sleep on the cardiovascular and the thermoregulatory systems – possible role for hypocretin
Authors: Schwimmer Hagit , Zeitzer Jamie M , Yanagisawa Masashi , Nishino Seiji , Stauss Herald M , Abboud Francois M , Mignot Emmanuel 
Published: June 2021

The hypocretin neuropeptides modulate sleep and are anatomically connected to brain structures important for both sleep regulation and autonomic activity. We examined the role of hypocretins in autonomic regulation using a rat model in which hypocretin neurons are ablated. We simultaneously monitored core (Tc) and tail (Tt) temperatures, blood pressure (BP), ECG and locomotor activity. We analyzed the daily patterns, relative contribution of sleep and circadian components, transitional changes, baroreceptor reflex, and heart rate (HR) and BP variability.Tc and HR are affected by both sleep and time of day, but BP is exclusively affected by sleep. BP and HR both have specific, reproducible patterns of change during state transitions. Tt preceded the actual transitions, implying peripheral early starting of the transition. The loss of hypocretin neurons caused a sleep state‐dependent decrease in BP. The relative contributions of sleep and time‐of‐day effects were differential based on the specific variable being examined. Hypocretins appear to be involved in mediating the effects of sleep on BP and vasoconstriction of skin blood vessels.
Assessment of heart rate variability during different sleep stages in rats: analysis of non‐stationarities
Authors: Tobaldini Eleonora , Magagnin Valentina , Porta Alberto , Montano Nicola , Kocsis Bernat 
Published: June 2021

An increasing interest has been focused on the assessment of autonomic regulation during sleep by means of heart rate variability (HRV) analysis. The common tools to analyze HRV require signal stationarity, but no studies addressed this problem during sleep. Aim of our study was to evaluate the prevalence of non‐stationarities on HRV series during different sleep stages.We recorded ECG in rats for 8 hours with episodes of wake (W), slow wave sleep (SWS) and REM sleep and evaluated the stationarity of HRV series of lengths ranging from 100 to 300 beats (with steps of 50). For each series, 8 sub‐sequences of 50 samples were randomly selected and checked if mean and variance remained constant over all the patterns by means of analysis of variance (F‐test) and Bartlett test respectively.We found increasing percentages of non‐stationarity (from 60 to 100%) with series length increasing from 100 to 200 beats, while all the series longer than 200 were totally non‐stationary. The percentage of non‐stationarity were similar between W, SWS and REM. In conclusion, our data suggest to use time series shorter than 200 beats to reduce non stationarities when assessing HRV during sleep in rats. Moreover, the sources on non‐stationarity may be different in different sleep‐wake stages, being prevalently related to motor activity during W and SWS and more dependent upon sympathetic‐parasympathetic shifts during REM sleep.
Bumetanide and HOE642 administered after initiation of rat middle cerebral artery occlusion effectively reduce rat brain Na uptake and infarct
Authors: Chen Yi‐Je , Anderson Steven E. , O'Donnell Martha E. 
Published: June 2021

Increased brain Na uptake across an intact blood‐brain barrier (BBB) contributes to cerebral edema formation in the early hours of ischemic stroke. We have shown previously that a luminal BBB Na‐K‐Cl cotransporter and Na/H exchanger are stimulated by ischemic factors and that both edema and infarct induced by middle cerebral artery occlusion (MCAO) are reduced by i.v. bumetanide or HOE642, inhibitors of the cotransporter and exchanger, respectively. The present study was conducted to determine whether bumetanide and HOE642 reduce the brain Na uptake that underlies edema in ischemic stroke and further, whether they are effective when given after the onset of ischemia. Rats were given bumetanide (30 mg/kg), HOE642 (30 mg/kg) or vehicle i.v. 20 min before, or 1 or 2 hr after initiation of left MCAO. Localized 23Na magnetic resonance spectroscopy with the shift reagent DyTTHA was used to assess total and extravascular brain [Na] in selected regions of interest during up to 5 hr of MCAO. The ipsilateral/contralateral brain ratios of both total [Na] and extravascular [Na] increased linearly following induction of ischemia. Bumetanide and HOE642 significantly reduced brain Na uptake and infarct when given before or after the start of MCAO. Our findings suggest that inhibition of the Na‐K‐Cl cotransporter and Na/H exchanger, even 2 hr after the start of ischemia, effectively reduces brain Na uptake and infarct.Supported by NINDS
Role of Mitochondria in SR Calcium Buffering in Human Airway Smooth Muscle
Authors: Yang Binxia , Thompson Michael , Prakash Y S , Pabelick Christina 
Published: June 2021

Sarcoplasmic reticulum (SR) Ca2+ release and reuptake are important mechanisms in airway smooth muscle (ASM) intracellular Ca2+ [Ca2+]i regulation. In other tissues, there is increasing evidence for a role of mitochondria in [Ca2+]i buffering, especially following SR Ca2+ release. Mitochondrial buffering may also influence Ca2+ influx. The purpose of the present study was to examine the role of mitochondria in [Ca2+]i buffering in human ASM. Cells were loaded with fura‐2 and exposed to 10 µM histamine in "0" Ca2+ HBSS containing 1mM lanthanum and 1µM nifedipine (to block Ca2+ influx/efflux) and in the additional presence of 1µM RU360 (mitochondrial Ca2+ uniporter inhibitor) or 1µM CGP37157 (CGP; mitochondrial Na+/Ca2+ exchange inhibitor). Compared to controls, peak [Ca2+]i levels were increased by 30% in the presence of CGP, while RU360 had not effect. Both CGP and RU360 significantly increased store‐operated Ca2+ entry. In cells co‐loaded with fura‐2 and rhod‐2 (mitochondrial Ca2+ indicator), exposure to 5 µM caffeine showed instantaneous SR Ca2+ release followed by an increase in [Ca2+]mito. Exposure to 1 µM ACh resulted in ACh‐induced [Ca2+]i oscillations that were reflected by mitochondria (but with a time delay). In ASM cells co‐labeled for mitochondria (MitoTracker) and SR (fluorescent ryanodine) migration of mitochondria towards SR was observed upon exposure to ACh or cyclopiazonic acid. This migration was completely inhibited by phalloidin (actin inhibitor). These data demonstrate an important role of mitochondria in [Ca2+]i buffering in ASM.Supported by NIH grant RR024150, and the Flight Attendants Medical Research Institute (FAMRI). Additional funding from the Department of Anesthesiology, Mayo Clinic.
Role of γ‐glutamyl transpeptidase in redox regulation of K+ channel remodeling in heart failure
Authors: Zheng Ming‐Qi , Tang Kang , Xie Bin , Zimmerman Matthew C , Rozanski George J 
Published: June 2021

γ‐Glutamyl transpeptidase (γGT) regulates cellular GSH levels in response to extracellular GSH (GSHo). The objective of this study was to identify the role of γGT in reversing K+ channel remodeling in heart failure, which was induced in rats by chronic myocardial infarction (MI). Assays of tissue extracts from MI hearts showed marked increases in γGT activity, protein and mRNA in left ventricle and septum compared with sham hearts. Voltage‐clamp studies of ventricular myocytes from MI hearts showed that down‐regulation of transient outward K+ current (Ito) was reversed after 4‐5 h by 10 mM GSHo or N‐acetylcysteine (NACo). The effect of GSHo but not NACo was blocked by γGT inhibitors acivicin or S‐hexyl‐GSH. Inhibition of GSH synthesis by buthionine sulfoximine did not prevent up‐regulation of Ito by GSHo, but an SOD mimetic (MnTPyP) and catalase blocked recovery of Ito by GSHo. Confocal microscopy using the fluorogenic dye DCFH showed that GSHo increased ROS generation by MI myocytes and to a lesser extent in sham myocytes. Moreover, up‐regulation of Ito by GSHo was blocked by inhibitors of tyrosine kinase (genistein, lavendustin A, AG1024) or thioredoxin reductase (auranofin, 13‐cis‐retinoic acid). These data suggest that GSHo elicits γGT‐ and ROS‐dependent transactivation of tyrosine kinase signaling which up‐regulates K+ channel activity/expression via redox mechanisms.Supported by NIH grant HL066446.
Increase of myogenic tone in the cerebral arteries of dyslipidemic mice is not due to a vessel wall remodelling
Authors: Bolduc Virginie , Drouin Annick , Robillard Isabelle F. , Des Rosiers Christine , Thorin Éric 
Published: June 2021

The role of dyslipidemia in mediating changes in vascular structure, mechanic and function is poorly understood. Isolated pressurized cerebral arteries of LDLr‐/‐hApoB+/+ (ATX) mice showed an increase of myogenic tone (MT) compared to WT at 3‐mo‐old (22 ± 2 % vs 14 ±1 % at 80 mmHg, p<0.05). We hypothesized that the increased MT was associated with vessel wall remodelling. Cerebral compliance, measured as pressure‐induced dilatation in the presence of potassium cyanide (7.7 mM), showed no difference between ATX and WT mice. Because ATX mice present a 7 fold increase in circulating cholesterol and triglyceride, we studied the phospholipids (PL) bilayer composition. There was no variation between groups in the amounts of C16:0, C18:0, C18:1n9, C18:1n7, C18:2, C20:4 and C22:6 contained in the PL and free fatty acids fractions extracted from total brain vessels. A quantitation kit measured similar level of free cholesterol in brain vessel between groups. Western blot showed no difference in collagen III deposition in the vessel wall. In conclusion, our data suggest that increase in MT in cerebral arteries of ATX mice is not due to a vessel wall remodelling.This work is financed by the Canadian Institutes of Health Research.