bluuebunny/crossref_metadata_2025_split huggingface dataset:
Early wasting in India: a public health challenge
Authors: Young Melissa Fox , Martorell Reynaldo 
Published: June 2021

A new pattern of wasting by age emerged with the use of the WHO growth curves in India. The highest rates of wasting (30%) are in the first six months and decrease thereafter. This represents a public health challenge as both the determinants and solutions are unclear. Traditional food‐based supplements are not appropriate for this population. Data from the 2005–2006 National Family Health Survey 3 was used to examine the determinants of early wasting in India with a focus on potentially modifiable factors (poor condition of mothers/breastfeeding practices). The results (odds ratios; 95%CI) of an unadjusted model predicting wasting in infants < 6 mo were the following: maternal variables [BMI < 18.5 k/m2 (1.31;1.07–1.61), height < 150 cm (1.11;0.92–1.35), age ≤18 years at first birth (0.94; 0.76–1.16), anemic (1.24;1.00–1.53)], breastfeeding within 1 hr of birth (0.71;0.55–0.93), receiving prelacteal feed (1.07;0.86–1.32), and exclusive breastfeeding (0.90;0.73–1.11). After adjusting for covariates (child age/sex/birth‐order, residence, maternal education/occupation, marital status, wealth, caste and religion), having a thin mother (1.31; 1.05–1.63) and early breastfeeding (0.68; 0.52–0.90) remained significant predictors. Priority areas for preventing the onset of early wasting should include improving the mother's nutrition before and during pregnancy and promotion of breastfeeding.Grant Funding Source : Funding support provided by a BMGF grant through a subcontract with CARE‐India
Long‐term Dietary patterns in China, 1991–2009
Authors: Batis Carolina , Zhang Bing , Popkin Barry 
Published: June 2021

Little is known about dietary patterns over time in transitional societies. Using the China Health and Nutrition Survey, we followed 3012 adults aged 18 y or older in 1991 with complete dietary data in each of 7 waves (1991, 1993, 1997, 2000, 2004, 2006 and 2009). Diet was measured by a combination of a household food inventory (detailed weighing of changes in household food) and 3 consecutive days of 24‐h recall. Dietary intake was grouped into 42 food groups. A factor analysis (STATA 12), followed by a varimax orthogonal rotation was performed at each wave. Factors with eigenvalues >1 were retained.Two clear patterns emerge over time. One was linked with a diet high in rice, vegetables, high‐fat red meat and fish, and inversely associated with wheat and corn intake. This pattern remained relatively similar in all waves. A second pattern was associated with high animal products intake (red and organ meats, poultry, eggs, fish and sea products) in all waves. During the series of surveys, other food groups began to be linked with this same dietary pattern: alcohol (beginning in 1993), pastries, cookies, deep‐fried cereals and fruits (beginning in 1997), fast‐food (in 2006), and sweetened dairy (in 2009).These results provide insights into the dynamic shifts in a major unhealthy eating pattern in China as the economy shifted and new products were introduced into the food distribution system.Grant Funding Source : CONACYT (grant 212018), NIH (R01‐HD30880), the Fogarty International Center (D43‐TW009077)
Wnt/β‐catenin pathway is activated by thyroid hormone and is required for its hepatomitogenic activity
Authors: Fanti Maura , Perra Andrea , Pibiri Monica , Schwartz Michael , Monga Satdarshan P. , Ledda-Columbano GM , Columbano Amedeo 
Published: June 2021

Thyroid hormones regulate cell growth, cell differentiation, and metabolic functions via their interaction with the thyroid hormone nuclear receptors (TRs). Recently, it was shown that intestinal epithelial cell proliferation is controlled by triiodothyronine (T3), and that TR‐β directly controls transcription of the β‐catenin gene. However, whether T3 has any effect on the activation of the Wnt pathway and β‐catenin in the liver, is unknown. Here we show by immunohistochemistry that livers from T3‐treated rats exhibited a strong increase in β‐catenin protein with its accumulation in the cytoplasm and an overall increase in the number of β‐catenin‐positive hepatocytes. The increased expression of β‐catenin was associated with increased glutamine synthetase, and an enhancement in nuclear accumulation of cyclin D1, both known targets of β‐catenin. Moreover, while T3 induced hepatocyte proliferation in wt mice, no proliferative response was observed in Ctnnb1−/− mice. T3 treatment also caused enhanced levels of Cyp2E1 mRNA, another gene known to be up‐regulated by β‐catenin. The increased expression of Cyp2E1 was associated with liver injury and mortality induced by a single administration of acetaminophen.ConclusionOur results indicate that T3 induces Ctnnb1 transcription and that high levels of this hormone may be responsible, through activation of β‐catenin, of increased hepatocyte proliferation and an enhanced susceptibility to drug‐induced liver injury. AIRC and PRIN, Italy.
Proinflammatory macrophage ablation in CD11b‐diphtheria toxin receptor (DTR) transgenic mice impairs skeletal muscle regeneration
Authors: WANG HANZHOU , Porter Laurel , Sarwar Zaheer , McManus Linda M. , Shireman Paula K. 
Published: June 2021

Macrophages can be beneficial or detrimental to regeneration following muscle injury and macrophage polarization states are not well‐defined during this process. We previously demonstrated that macrophage ablation with diphtheria toxin (DT) given at day 1 after cardiotoxin injury increased residual necrotic myofibers and resulted in smaller regenerated myofibers in DTR mice compared to control mice that received mutant DT while mice receiving DT at day 4 were similar to controls. We used flow cytometry to evaluate the kinetics of macrophage surface markers to investigate the role of macrophage subtypes in muscle regeneration. In control mice, the majority of macrophages (CD11b+/F480+) were Ly6C+7/4+proinflammatory macrophages at day 1–2 after injury and switched to Ly6C−7/4−macrophages at day 4 after injury. M2 markers CD206+ or CD301+ were present on a small percentage of cells. Interestingly, the predominate macrophage population present from day 3–6 was negative for all 4 markers (Ly6C, 7/4, CD206 and CD301). Administration of DT at day 1 in DTR mice resulted in macrophage ablation at day 2–3 after injury with an increase in macrophages at day 4. Thus, the early recruitment of proinflammatory macrophages was critical for muscle regeneration; further studies are needed to define markers present on macrophages in the later stages of the regenerative process.Funding: Veterans Administration and NIH HL07423
A role for Galectin‐9 in neutrophil trafficking
Authors: Cooper Dianne , Iqbal Asif J , Niki Toshiro , Hirashima Mitsuomi , Perretti Mauro 
Published: June 2021

Galectin‐9 (Gal‐9) was initially characterized as a potent eosinophil chemoattractant but has subsequently been found to have immunosuppressive effects in models of collagen‐ induced arthritis and carageenan paw oedema. Its effects on neutrophil recruitment and behavior during inflammation have not been thoroughly investigated. Here we show that Gal‐9 binds readily to the surface of freshly isolated PMN and binding is not augmented upon activation with PAF but is sensitive to lactose addition. Gal‐9 binding to endothelial cells is low in comparison to PMN and is not modulated by endothelial activation by TNFα. Neutrophils were found to transmigrate to Gal‐9 under static conditions with peak recruitment observed at 10nM. This concentration was not however found to be directly chemotactic for neutrophils in a Boyden chamber assay. Pre‐incubation of PMN with Gal‐9 significantly increased neutrophil transmigration whilst pre‐incubation of HUVEC with Gal‐9 was without effect. At concentrations active in the flow chamber, Gal‐9 did not significantly alter PMN or endothelial adhesion molecule expression (active CD11b, L‐selectin shedding, E‐selectin, VCAM‐1, ICAM‐1). In conclusion, these data indicate that neutrophils rather than endothelial cells are target cells for Gal‐9 and that Gal‐9 promotes neutrophil transmigration during acute inflammation indicating a novel role for this protein.This work was supported by a Non‐Clinical Career Development Fellowship from Arthritis Research‐UK (18103).
EFFECTS OF GROWTH HORMONE ADMINISTRATION ON CARDIAC REMODELING PROCESS IN RATS WITH AORTIC STENOSIS‐INDUCED HEART FAILURE
Authors: Lima Aline Regina Ruiz , Damatto Ricardo , Campos Dijon , Martinez Paula , Guizoni Daniele , Bonomo Camila , Cézar Marcelo , Silva Frederico , Zanati Silméia , Campana Alvaro , Okoshi Katashi , Okoshi Marina 
Published: June 2021

ObjectiveTo evaluate the growth hormone (GH) administration influence on cardiac structures and function in aortic stenosis‐induced chronic heart failure rats.MethodsMale wistar rats were submitted to surgery to induce aortic stenosis. After heart failure findings detection, rats cardiac structures and ventricular function were assessed by transthoracic echocardiogram. Aortic stenosis group (EAo) animals were randomly subdivided in two groups, EAo GH treated group (EAo‐GH, n=10) and EAo without treatment group (EAo, n=15). Sham group was also constituted(n=18). After the treatment period, all animals were yet submitted to echocardiogram.ResultsGH administration preserved body weight (BW) (Sham 484±42; EAo 415±31; EAo‐GH 476±58 g; p<0.05 EAo vs Sham and EAo‐GH). Left ventricular diastolic diameter/BW was higher in EAo group than Sham; EAo‐GH and Sham groups were similar (Sham 15.5±1.5; EAo18.5±3.2; EAo‐GH 16.5±3.6 mm/kg; p<0.05 EAo vs. Sham). Left ventricular posterior wall thickness was higher in both EAo groups than Sham (Sham 1.43±0.09; EAo2.25±0.25; EAo‐GH 2.41±0.37 mm; p<0.05 EAo and EAo‐GH vs. Sham). Fractional shortening was smaller in EAo group than other groups (Sham 59.1±5.6; EAo 49.8±14.7; EAo‐GH 59.8±12.1 %; p<0.05 EAo vs. Sham and EAo‐GH).ConclusionGrowth hormone administration attenuates cardiac remodeling process in aortic stenosis‐induced heart failured rats.
Adiponectin Deficiency Accentuates High Fat Diet‐Induced Cardiac Hypertrophy and Contractile Dysfunction through Regulation of Autophagy
Authors: Guo Rui , Ren Jun 
Published: June 2021

ObjectivesAdiponectin (APN), an adipose‐derived adipokine, offers cardioprotective effects although the precise mechanism behind APN‐exerted beneficial action is unclear. The aim of this study was to examine if autophagy plays a role in APN‐exerted cardiac effects in high fat diet‐induced obesity.MethodsAdult C57BL/6 wild‐type and APN deficient mice were fed a low (10% calorie from fat) or high fat (45% calorie from fat) diet for 22 weeks. Cardiomyocyte contractile and Ca2+ transient properties were evaluated, including peak shortening (PS), duration and maximal velocity of shortening/relengthening (TPS/TR90, ± dL/dt), electrically stimulated change in fura‐fluorescence intensity (ΔFFI), and intracellular Ca2+ decay rate. Myocardial function was evaluated using echocardiography. DEXA was used to evaluate adiposity. Lipid deposition was examined using myocardial histology. Energy expenditure, oxygen consumption and physical activity were monitored by metabolic cages system. Glucose tolerance test and protein markers of autophagy pathway including LC3, p62 and Beclin‐1 were also performed.ResultsHigh fat diet induced obesity, glucose intolerance, cardiac hypertrophy, dampened metabolic ability, and cardiac dysfunction, the effects of which were accentuated by APN deficiency. Furthermore, ANP deficiency augmented fat diet‐induced increased in LC3II, ratio of LC3II to LC3I and the autophagy adaptor p62, as well as decrease in Beclin‐1.ConclusionsOur results revealed that APN deficiency aggravates high fat diet‐induced obesity, glucose intolerance, metabolic ability and cardiac dysfunction through decreased autophagosome formation and fusion.The research is supported by Wyoming INBRE (P20RR016474)
Fibroblast growth factor‐2 exerts protective effects on cardiac mitochondria
Authors: Srisakuldee Wattamon , Nickel Barbara E , Kardami Elissavet 
Published: June 2021

Fibroblast growth factor‐2 (FGF‐2) is a potent cardioprotective agent, by a mechanism linked to connexin43 (Cx43) phosphorylation at protein kinase C (PKC) target serines such as S262. Here we have examined the effects of FGF‐2 on mitochondrial resistance to calcium‐ induced opening of the permeability transition pore (swelling), in relation to cardiac mitochondrial Cx43 levels and phosphorylation.Subsarcolemmal mitochondria isolated from FGF‐2‐treated hearts: (a) showed 1.5–2 fold increase in total Cx43, PKCε, TOM20 translocase, and a over 30‐fold increase in phospho‐S262‐Cx43, compared to control mitochondria obtained from untreated hearts; (b) were more resistant to calcium‐induced swelling and cytochrome C release; (c) were resistant to calcium‐induced mitochondrial Cx43 degradation. Calpeptin, a potent inhibitor of the calcium activated protease calpain, prevented Cx43 degradation in control mitochondria. Stimulation of control mitochondria with the phorbol‐ester PMA, or FGF‐2, increased both mitochondrial Cx43 phosphorylation at S262 and resistance to calcium‐induced swelling / cytochrome c release.Our data imply that FGF‐2 cardioprotection is mediated by increasing mitochondrial resistance to calcium damage, via Cx43 translocation to mitochondria and mitochondrial Cx43 phosphorylation.This work is supported by Heart and Stroke Foundation of Canada and St. Boniface Hospital Research Foundation.
Central sympathoinhibition improves left ventricular function and survival during the transition from hypertrophy to heart failure in Dahl salt‐sensitive rats
Authors: Honda Nobuhiro , Hirooka Yoshitaka , Matsukawa Ryuichi , Itou Koji , Sunagawa Kenji 
Published: June 2021

BackgroundSympathetic hyperactivity is cardinal manifestation in heart failure (HF). Enhanced central sympathetic drive leads to poor prognosis in HF. Moxonidine is a sympathoinhibitory antihypertensive drug acting on the imidazoline receptors in the central nervous system. Therefore, we hypothesized that moxonidine improves hypertension induced cardiac remodeling, function, and survival in Dahl‐salt sensitive hypertensive rats.Methods and ResultsDahl salt‐sensitive rats fed 8% NaCl diet from age 7 weeks served as hypertension‐induced HF and followed until 20 week‐old. Salt loading increases blood pressure, left ventricle hypertrophy, and progressive urinary norepinephrine excretion (uNE). Fractional shortening (%FS) was gradually reduced overtime. Intracerebroventricular infusion of moxonidine or vehicle was performed from 14 to 20 week‐old. Moxonidine tended to lower heart rate and blood pressure. Moxonidine attenuated the reduction of %FS (37±1.3 vs. 43±0.9%, n=7, n=4, p<0.05) and lowered uNE (3.0±0.2 vs. 0.6±0.2μg/day, n=7, n=4, p<0.001). Furthermore, moxonidine improved the survival rate (50 vs. 80%, 20 week‐old, n=10, n=5 p<0.05).ConclusionMoxonidine acting on the central nervous system improves the cardiac function and prognosis in this rats model of hypertension associated with sympathoinhibition.
Three‐dimensional reconstruction and measurement of cervical vertebral CT images: Anatomical bases for cervical anterior transpedicular screw fixation
Authors: Ouyang Jun , Chen Chun , Wu Changfu , Wu Peidong 
Published: June 2021

ObjectiveTo study the morphometric characteristics of Chinese lower cervical vertebrae in order to investigate the feasibility of cervical anterior transpedicular screw (ATPS) fixation and provide anatomical data.MethodsCervical CT images from 50 healthy volunteers (35 male and 15 female) were collected. All the images from C3–C7 were reconstructed by Mimics 13.0 software. We measured the dimensions of the vertebral bodies and pedicles from images of multiplanar reconstruction, as well as the parameters related to ATPS technology.ResultsSome of the vertebrae parameters has a statistic differences between the male and female groups (P<0.05). And the sagittal Pedicle Angles increased with the number of cervical vertebrae in all specimens (P<0.05).ConclusionsThis study provides the cervical spine morphological parameters from Chinese population, which provides the basis for ATPS research for osteoporosis patients.
Adenosine A2A receptor activation attenuates Th1 and Th17 polarization in the airway
Authors: Pei Hong , Ken Ruey , Huynh Nhut , Linden Joel 
Published: June 2021

ObjectiveTo determine the role of A2A receptor activation on the appearance of Th1 and Th17 cells in mouse lung following exposure to LPS and allergens, and on the production of cytokines by established Th1 or Th17 cells upon allergen challenge.Methods and ResultsTh1 and Th17 asthma mouse models were established by airway sensitization with LPS and allergens followed by rechallenge with allergens alone. A2A receptor activation with CGS28160 during sensitization strongly inhibited the development of Th1 and Th17 cells; increased CD4 Foxp3 positive cells; and reduced pulmonary inflammation, vascular permeability and airway hyperresponsiveness (AHR). In contrast, the application of CGS28160 only before allergen rechallenge only moderately reduced IFN‐γ production and neutrophil infiltration into lung; had no effects on IL‐17A production, vascular permeability and AHR.Conclusionsthe results indicate that A2A receptor activation plays an important role in controlling the polarization of naïve T cells to Th1 and Th17, but fails to inhibit the release of IL‐17A from Th17 cells. The results suggest that A2AR activation may be more effective at inhibiting allergen sensitization that the response to allergens in sensitized lungs.
Hyperoxia‐induced Retinal Microvasculopathy Correlates with Lung Injury and Inflammation in Neonatal Mice
Authors: Mezu-Ndubuisi Olachi Joy , Reddy Narsa M , Wanek Justin , Teng Pang-yu , Shahidi Mahnaz , Reddy Sekhar P 
Published: June 2021

ObjectivePremature infants with respiratory failure require oxygen supplementation, which can destroy developing lungs and lead to acute lung injury (ALI). Continued oxygen use also damages retinal tissue by disrupting normal angiogenesis, leading to retinopathy of prematurity (ROP). Using a mouse model of oxygen‐induced retinopathy (OIR) and ALI, we assessed the correlation between retinal microvascular abnormalities in vivo and lung tissue injury ex vivo.MethodsNeonatal C57BL6/J mice were exposed to 75% oxygen from postnatal day 7 (P7) to P12 and then exposed to room air until P17. Fluorescein angiography (FA) images of the retinal vasculature were acquired in vivo. Bronchoalveolar lavage (BAL) was performed on the mice lung tissue ex vivo, followed by cytometry and protein estimation of the BAL fluid. The total cell count was used as a measure of lung inflammation; while total protein estimation was used to assess lung injury.ResultsIn vivo FA imaging of retinal vasculature revealed aberrant neovascularization and regions of capillary network loss in mice exposed to hyperoxia compared to room air exposed controls (Figure 1A). There was a 4‐fold increase in total inflammatory cells (Figure 1B) and a 3‐fold increase in protein levels in BAL fluids of hyperoxia‐exposed mice compared to room air controls.ConclusionsOur findings demonstrate a correlation between retinal microvasculopathy and lung tissue injury and inflammation in neonates, suggesting in vivo imaging of retinal microvasculature could be a potential biomarker for lung injury.Source of Research Support: R01 HL66109, R01 ES011863 and R01 EY017918
Protective Effect of Perilla Leaf Extract and its Constituents on t‐BHP‐induced Oxidative Stress in Liver
Authors: Yang Sung-Yong , Hong Chung-Oui , Koo Yun-Chang , Nam Mi-Hyun , Lee Kwang-Won 
Published: June 2021

Perilla frutescens are popular plant in East Asia, and the leaves of perilla were known for antioxidant, anti‐allergic, anti‐inflammatory and anti‐tumor effect. According to our previous study, P. frutescens included two major polyphenolic compounds, caffeic acid and rosmarinic acid. Previous our study showed protective effect of P. frutescens extract (PLE) on oxidative hepatotoxicity. Our group isolated of caffeic acid from P. frutescens and it enhanced γ‐glutamylcysteine synthetase activity and glutathione level. Based on high performance liquid chromatography analysis data, PLE have 1.32 μg caffeic acid/mg dry material (DM) and 26.84 μg rosmarinic acid/mg DM. And in vitro study showed that PLE and its constituents have protective effect on t‐BHP‐induced oxidative stress in HepG2 cells. Also, in vivo study showed pretreatment with PLE (1000 mg/kg b.w.), caffeic acid (1.32 mg/kg b.w.) and rosmarinic acid (26.84 mg/kg b.w.) for 5 days before a single dose of t‐BHP (i.p. 0.5 mmol/kg b.w.) lowered lipid peroxidation level and increased the reduced form of glutathione. And mixed caffeic acid and rosmarinic acid has more protective effect than single dose of compound on oxidative stress. Therefore, we conclude that caffeic acid and rosmarinic acid from Perilla frutescens has synergistic protective effect on oxidative stress in vitro and in vivo.Grant Funding Source : Ministry of Education, Science and Technology. Korea
Nano‐fibrous microspheres with sustained growth factor delivery for bone regeneration
Authors: Liu Xiaohua 
Published: June 2021

In this study, we developed a unique scaffolding system in which the biodegradable nano‐fibrous microspheres (NF‐MS) serve both as an injectable scaffold and as a growth factor carrier for bone regeneration. The NF‐MS were fabricated by a novel approach, which integrated an emulsification and a thermally induced phase separation technique. The NF‐MS mimicked the architecture of natural collagen fibers at a nanometer scale and had many unique properties including extraordinarily high surface area and extremely low density. Growth factors were effectively encapsulated (>90%) into the NF‐PLLA microspheres through a simple process without using any organic solvent. In vitro release kinetics indicated that the encapsulated recombinant human bone morphogenetic protein 7 (rhBMP‐7) in the NF‐MS were released in a temporal controlled manner. When used as an injectable scaffold for repairing the rat critical‐size calvarial defects, the rhBMP‐7‐loaded NF‐MS induced a much more significant amount of new bone formation than the rhBMP‐7‐free NF‐MS control. We conclude that the nano‐fibrous architecture combined with the sustained release of bioactive rhBMP‐7 from the NF‐MS are excellent cell carrier for bone regeneration. Support: NIH5P30DE20742Grant Funding Source: NIH 5P30DE20742
Early Events in DNA Replication
Authors: Diffley John F.X. 
Published: June 2021

The eukaryotic cell cycle coordinates the accurate duplication and segregation of the genome during proliferation. The large genomes of eukaryotic cells are replicated from multiple replication origins during S phase. These origins are not activated synchronously at the beginning of S phase, but instead fire throughout S phase according to a pre‐determined, cell type specific program. Only after the entire genome is completely replicated do cells proceed into mitosis.Ensuring that each origin is efficiently activated once and only once during each S phase is crucial for maintaining the integrity of the genome. This is achieved by a two‐step mechanism. The first step, known as licensing, involves the loading of the Mcm2–7 proteins into pre‐replicative complexes (pre‐RCs) at origins. We have recently reconstituted this reaction with purified proteins (Remus et al. Cell 2009 139: 719–30). In this reaction, Mcm2–7 are loaded as a head‐to‐head double hexamer around double stranded DNA. Mcm2–7 loading requires the Origin Recognition Complex (ORC) as well as Cdc6 and Cdt1. I will describe recent experiments showing that individual Mcm subunits play distinct roles during pre‐RC assembly by interacting with different assembly factors. I will also show that the role of cyclin dependent kinases in promoting initiation has been conserved, at least in part, between yeast and humans.