bluuebunny/crossref_metadata_2025_split huggingface dataset:
Factors Associated with Fast Food Consumption at Global Fast Food Restaurant in the Tokyo Region
Authors: Yoshizawa Kazuko K 
Published: June 2021

BackgroundFast food consumption has increased in Japan. Even though t is speculated that younger people eat fast food more often than older people do, it is not well known which factors associated with the increased level. Objective of this study is to find what factors are associated with the fast food intake.MethodA questionnaire was disseminated to 1464 residents aged 10s – 60s in Tokyo and its suburbs by use of internet in Sept. 2011. The questionnaire includes questions about preference of fast food restaurants, its reasons, etc. Logistic regression was used for statistical analyses. Results were statistically significant if p‐value was less than 0.05.ResultsThe most frequently visited fast food restaurant by all age groups was McDonald. The proportion of the category of housewife who visits McDonald was 84% and that of businessman was 25%. Logistic regression analysis showed that location (OR 2.52, 95% CI 1.84–3.42) and tastiness (OR 2.40, 95% CI 1.78–3.26) were associated with fast food consumption adjusting for convenience, serving size, and price.ConclusionThe important factors associated with increased levels of fast food consumption are location and tastiness while portion size, convenience and price were not important factors.
Effect of lactation on antioxidant indices and bone mineral density in adult women
Authors: Kamp Fernanda , Gomes Vivianne Magalhães , Silva Danúbia Incutto , Bezerra Flávia Fioruci , Torres Alexandre Guedes 
Published: June 2021

The aims of this study were to compare indices of antioxidant status and bone mineral density (BMD) during lactation and to investigate the relationship of those indices with BMD. Lactating women (30.8 ± 4.8 y) with low calcium intake (≈600 mg/d), participated in the study at 2–4 (early lactation, EL; n= 14) and at 12–14 (middle lactation, ML; n= 11) wk postpartum. Indices of antioxidant status [ferric‐reducing ability of plasma (FRAP); erythrocyte aminolevulinic acid dehydratase activity (d‐ALAD); in vitro zinc‐d‐ALAD activation (Zn‐d‐ALAD%)] and measures of BMD [at total body (TBMD) and at lumbar spine (L2–L4)] were evaluated. When compared to EL, FRAP did not change, but Zn‐d‐ALAD% increased (P < 0.01), and d‐ALAD (P ≤ 0.05), TBMD (P ≤ 0.02) and L2–L4 (P ≤ 0.01) decreased, at ML. d‐ALAD was negatively associated with Zn‐d‐ALAD% (r= −0.63; p < 0.02), and tented to be positively associated with L2–L4 (r = 0.49; P = 0.07). No associations between FRAP and bone measurements were observed. Our results suggest that the decrease in d‐ALAD during lactation appears to be related to an impairment on zinc status, that could further contribute to accentuate bone loss during lactation, mainly in low calcium intake.Financial support: CNPq (Brazil)
Korean pine nut oil decreases the amount of white adipose tissue by affecting lipid metabolism in C57BL/6 mice
Authors: Shin Sunhye , Park Soyoung , Lim Yeseo , Han Sung Nim 
Published: June 2021

Korean pine nut oil (PNO) has been reported to reduce weight gain and the amount of white adipose tissue. Effects of PNO on lipid metabolism were investigated to understand the mechanisms of decrease in amount of white adipose tissue. Five‐wk‐old C57BL/6 mice were fed control diets containing 10% kcal fat from PNO or soybean oil (SBO) (PC or SC) or high‐fat diets containing 35% kcal fat from lard and 10% kcal fat from PNO or SBO (PHF or SHF) for 12 weeks. Expression levels of jejunal Cd36, Ifabp, Dgat2, and Apoa4, and epididymal Lpl, Plin1, Ucp2, Adrb3, Pparg, Ppargc1a, and Ppard were determined by Real‐time PCR. There was no difference in daily food intake between SBO‐ and PNO‐fed mice. Overall, PNO‐fed mice gained less weight (P = 0.014) and had less white adipose tissue (P = 0.004). PC and PHF groups had significantly less amount of white adipose tissue compared with SC group (30% less, P = 0.046) and SHF group (18% less, P = 0.033), respectively. Overall, PNO downregulated the mRNA expression of Cd36 (P = 0.025) and Lpl (P = 0.020). PC group had significantly lower Lpl mRNA expression (0.62‐fold, P = 0.035) than SC group. Overall, PNO tended to downregulate the Apoa4 mRNA expression (P = 0.068) and upregulate Adrb3 mRNA expression (P = 0.081). These results indicate that PNO is less efficiently absorbed, utilized, and stored in the body than SBO, which leads to less accumulation of fat mass in C57BL/6 mice.Supported by the Korea Research Foundation grant funded by the Korea government (KRF‐2010–0024878)
Acute lipids response to fructose beverage in adolescents with NAFLD
Authors: Jin Ran , Le Ngoc‐Anh , Vos Miriam 
Published: June 2021

ObjectiveDyslipidemia and insulin resistance are commonly reported in nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the acute lipid response to fructose in adolescents with NAFLD (hepatic fat >; 5% by MRS), and examined the difference as compared to similar overweight adolescents with normal hepatic fat (< 5%, non‐NAFLD).MethodsWe recruited overweight Hispanic adolescents that self‐reported high consumption of sugar beverages (≥24 oz per day) as this is known to be a high risk population for NAFLD. 50 recruited subjects underwent a fructose tolerance test, and their blood samples were collected at fasting and 30, 60, 90 min after oral fructose load (50 grams).ResultsOver 70% of study population had NAFLD, and they had higher ALT (p=0.003), AST (p<0.001), fasting TG (p=0.003), insulin (p=0.005), HOMA‐IR (p=0.01), and adipose IR (p<0.001), as compared to non‐NAFLD. With fructose load, plasma glucose response was not different between the two groups; however, NAFLD subjects had high AUC of insulin (40.6 ± 6.1 vs. 17.2 ± 3.1, p=0.001) and less FFA suppress (AUC: 0.19 ± 0.07 vs. 0.46 ± 0.09, p=0.05).ConclusionOverweight Hispanic adolescents with increased hepatic steatosis are more insulin resistant compared to similar non‐NAFLD overweight adolescents. This insulin resistance results in decreased tolerance of an oral fructose bolus as demonstrated by failure of NEFA suppression.
Interlukin‐18, An Indicator of Insulin Resistance?
Authors: Mabrouk Randa Reda , Ghareeb Hala , Elkabarity RANIA Hamdy 
Published: June 2021

Adipose tissue expression of IL‐18 is increased in obesity but is not affected by weight loss, indicating that its plasma changes is related to insulin resistance rather than obesity. The study was designed to detect the level of IL‐18 and to determine its correlation with insulin resistance and inflammation in both morbidly obese and normal subjects.Quantitative analysis of hs‐CRP, IL‐18, Homeostasis Model Assessment ‐ Insulin Resistance Index (HOMA‐IR), and fasting insulin was performed in 35 morbidly obese individuals with fasting blood glucose>;100mg/dl and in matched healthy control group.IL‐18 was significantly higher in patients than in the control group. There was also a statistically significant correlation between IL‐18 and hs‐CRP (P<0.05) and a statistically significant correlation between IL‐18 and insulin and HOMA (P<0.05). Receiver‐operating characteristic (ROC) curve analysis was applied to assess the performance of IL‐18 as predictor of insulin resistance. The area under curve (AUC) was 0.890, and the optimum cut‐off level was 171pg/ml. This had a diagnostic sensitivity 100%, specificity 71.9%, negative predictive value (NPV) 100%, positive predictive value (PPV) 80.9%, and diagnostic efficacy of 87.1%.In conclusion, we have shown that high levels of IL‐18 are associated with an increased risk of insulin resistance, and that this is independent of obesity, hs‐CRP, triglycerides and cholesterol.
A Role for Palmitoleate in Regulating Macrophage Activation
Authors: Xu Hang , Guo Xin , Li Honggui , Woo Shih‐lung , Wu Chaodong 
Published: June 2021

Increased macrophage proinflammatory activation contributes to atherosclerotic problems. We investigated the effects of palmitoleate treatment on the inflammatory status of bone marrow‐derived macrophages (BMDM). After differentiation, wild‐type BMDM were treated with palmitoleate (50 μM) for 48 h in the presence of lipopolysaccharides (LPS, 100 ng/ml) for the last 30 min to stimulate macrophage proinflammatory signaling or interleukin‐4 (IL‐4, 10 ng/ml) for 48 h to inhibit macrophage proinflammatory activation. LPS stimulation caused an increase in the phosphorylation of JNK1/2 and NF‐κB p65 in BMDM. This stimulatory effect of LPS was partially blunted by treatment with palmitoleate. On the other hand, IL‐4 displayed a weak effect on decreasing the phosphorylation of JNK1/2 and NF‐κB p65 in BMDM. However, in palmitoleate‐treated BMDM, the inhibitory effect of IL‐4 was much more potent, evidenced by the fact that the combined treatment with IL‐4 and palmitoleate nearly abolished the phosphorylation of JNK1/2 and significantly decreased the phosphorylation of NF‐κB p65. Together, these data suggest that palmitoleate is anti‐inflammatory bioactive lipid which may be useful for prevention of cardiovascular disease.Grant Funding Source: American Diabetes Association, American Heart Association
IT Telehealth Center for Telecytopathology
Authors: Markovic Olivera , Markovic Nenad 
Published: June 2021

Since 2004, when for the first time, we presented our MarkPap® biomarker‐based platform technology, we followed‐up on subsequent EB meetings with the results of our translational research from manual to semi‐automated procedures, from diagnosis at the Point‐of‐Care (POC) to diagnosis at distance (digital and wireless), from its primary application in detecting abnormal cells on cervical specimens to other applications, including self‐collection of specimens at home.This presentation is the most recent development: The IT Telehealth Center as a prototype design for an architecture (application software and hardware) of a local center implemented with a proprietary communication network to a global networking system, connected with a unique medical diagnostic protocol to enable automatic exchange of secure digital image (high resolution, still, metadata) files between humans on both sides of the networking system (POC and medical centers). The automation makes this center a low‐cost device for mass cancer screening.We acknowledge the support of Dr. Oleg Panashchenko, Mr. Stephen McJonathan, and Ricca Chemical Company, USA.
Long‐term physiologic T3 supplementation as an adjunct therapy in hypertensive heart disease
Authors: Pol Christine Jantina , Weltman Nathan Y , Zhang Youhua , Koder Adrienne , Raza Sarah , Plummer Maria , Gerdes A Martin 
Published: June 2021

Re‐expression of the fetal gene phenotype in hypothyroidism and hypertension suggest low cardiac thyroid hormone (TH) levels during hypertension. Short‐term TH treatment in Spontaneously Hypertensive Heart Failure (SHHF) rats near heart failure is known to promote beneficial remodeling. The current study examined the effects of long‐term T3 treatment in SHHF rats. SHHF rats were treated with a physiological oral T3 dosage (4ìg/kg/day) from 12–24 months of age. SHHF rats had a decline in serum free TH levels and cardiac tissue T3 levels, cardiac dysfunction, and elevated LV collagen content compared to normotensive controls. Normalization of serum and cardiac tissue TH levels in T3 treated rats normalized heart rate, LV end‐systolic diameter, fractional shortening, systolic wall stress, and LV collagen levels. Improvements in LV end‐systolic pressure, maximal rate of pressure development and decline, and time constant of isovolumic relaxation trended toward improvement but did not reach statistical significance.In conclusion, hypertension in rat leads to chronic low serum and cardiac tissue TH levels. Long long‐term treatment with T3 is safe. In the absence of anti‐hypertensive treatment, cardiac dysfunction could not be completely prevented. But, results suggest that T3 treatment of patients with hypertension might serve as a helpful adjunct to existing therapy. Supported by the NIH RO1 HL103671‐01A1.
Resveratrol optimizes the pharmacotherapy of captopril in renal hypertensive rats
Authors: Garcia Arthur F. E. , Restini Carolina B.A. 
Published: June 2021

We evaluate the probable cardiac benefit by the antioxidant Resveratrol (RESV) treatment and Captopril (CPT). It was measured Cardiac and Ventricular Hypertrophy Indexes (CHI; VHI) and Systolic Blood Pressure (SBP). Male Wistar rats (180g) had undergone surgery for implantation of a silver clip in the left renal artery. Control rats were undergone fictitious laparotomy (2K). Six weeks after surgery, 2K‐1C (SBP >; 160 mmHg) and 2K rats were submitted to different treatments by gavage, 3 times/week: RESV (20mg/kg); vehicle; CPT (6 or 12 mg/kg) and the association of the CPT doses + RESV (20mg/kg). 3 weeks after, SBP, CHI and VHI were measured. CHI was reduced in RESV 2K (3.0 ± 0.05, n=9) when compared to RESV 2K‐1C (3.4±0.1, n=18) and 2K‐1C (3.4 ±0.2, n=9) or 2K (3.2 ± 0.3, n=6) untreated. CPT equalized to the other groups CHI values to the RESV 2K.VHI also was reduced in RESV 2K (2.2 ± 0.05, n = 9) compared to RESV 2K‐1C (2.7 ± 0.1, n = 18) and 2K‐1C (2.9 ± 0.2, n = 9) or 2K (2.7 ± 0.2, n = 6) untreated. CPT presented the same effects on VHI and CHI values. Untreated 2K‐1C, CHI and VHI, was increased compared to the 2K‐1C RESV or RESV + CPT (VHI: 2.2 ± 0.1; CHI: 2.9 ± 0.1, n = 4) treated. RESV effectively reduced the SBP in 2K‐1C (99.0 ± 4.1, n = 10) when compared to RESV 2K (100.0 ± 10.4, n=8) and 2K (105.0 ± 5.0, n=8) or 2K‐1C (170.0 ± 10.8 n = 4) untreated. In the 2K‐1C, SBP reduction by CPT (140.0 ± 4.5, n=4) was less effective than by RESV or CPT + RESV (154.0 ± 13.7, n=5). RESV has potential to reduce SBP on 2K‐1C. CPT or RESV had effectively reduced the CHI and VHI in 2K‐1C and 2K rats, suggesting both treatments are acting in the same via to attenuate the hypertrophy.Support: PIBIC‐CNPq (02–2012). Ethics Committee approval: 007/2010.
Regulation of AT1‐Receptors by ARAP1 is involved in vasodilatation during sepsis‐induced hypotension
Authors: Mederle Katharina , Doblinger Elisabeth , Kattler Veronika , Höcherl Klaus , Schweda Frank , Castrop Hayo 
Published: June 2021

Hypotension in septic patients results from hypovolemia, vasodilatation and hyporeactivity to vasoconstrictors. Altered expression of angiotensin receptors might contribute to reduced vascular tone during sepsis. The AT1 receptor‐associated protein 1 (ARAP1) is expressed in vascular smooth muscle cells and increases the surface expression of the AT1‐receptor. Here we assessed the role of ARAP1 in sepsis‐induced hypotension.Mean arterial blood pressure (MAP) (102±2 vs.103±2 mmHg; n=6; p=.66) and glomerular filtration rate (296±20 vs. 315±30 μl/min; n=10; p=.61) were similar in ARAP1−/− and WT mice. Plasma renin concentration was increased in ARAP1−/− mice compared to WT mice (66±6 vs. 41±4 ng AngI/ml/h; n=23; p=.001). Dose‐dependent changes in vascular resistance were right‐shifted in isolated perfused kidneys from Arap1−/− mice. LPS‐treatment (3mg/kg) induced a marked downregulation of ARAP1 expression in different organs. Following LPS, MAP (84±2 vs. 90±1 mmHg; n=10; p=.03) and heart rate (446±13 vs. 492±10 bpm; n=10; p=.01) decreased to lower levels in ARAP1−/− mice compared to WT mice.Under baseline conditions, ARAP1−/− mice seem to normalize blood pressure by compensatory activation of the RAS. However, sepsis‐induced hypotension is enhanced in ARAP1−/− mice. Downregulation of ARAP1 expression during sepsis may contribute to hypotension by causing reduced vascular sensitivity to Ang II.
HIF‐1alpha and AMPK interactions regulate cellular hypoxia adaptation in the subtotal nephrectomy model of CKD
Authors: Singh Prabhleen , Satriano Joseph , Li Hui , Hallows Kenneth 
Published: June 2021

HIF‐1α activation in subtotal nephrectomy (STN) ameliorates hypoxia and improves GFR. The AMPK pathway facilitates adaptation to hypoxia, and there is significant overlap between the actions and targets of HIF‐1α and AMPK. Here we investigate the effects of HIF‐1α activation on cellular physiology and the interaction between HIF‐1α and AMPK in early STN kidney.Kidneys harvested from control, 1‐week STN, and STN treated with DMOG (HIF‐1α inducer) were examined by Western blotting. The expression of molecular markers for hypertophy (p70S6k) and apoptosis (cleaved caspase‐3) were elevated in STN, while a marker for autophagy (LC3II/LC3I) was reduced. HIF‐1α induction completely reversed these processes. The activated AMPK (pAMPK) to total AMPK ratio was low in STN and increased by HIF‐1α activation. All results were significant at p<0.05.Interactions between HIF‐1α and AMPK in HK2 and MDCK with AMPK knockdown (KD) cell lines were investigated. Consistent with the in vivo data, DMOG treatment increased pAMPK levels, increased LC3II/LC3I and lowered p70S6k in HK2 cells. These effects were reversed by HIF‐1α inhibition by YC‐1, with a dramatic increase in cleaved caspase3. AMPK activation by AICAR blocked the increase in cleaved caspase3 induced by YC‐1, and this was reversed in the AMPK KD cells. Inhibition of LC3II/LC3I by YC‐1 was AMPK‐independent. Finally, both AMPK and HIF‐1α activation inhibited p70S6K.We propose that HIF‐1α activation in the STN kidney facilitates hypoxic adaptation and cell survival by inhibiting hypertrophy and apoptosis and activating autophagy and the AMPK pathway. These novel findings suggest that HIF‐1α and AMPK closely interact with each other to mount a coordinated cellular response to hypoxic stress.
Quercetin Flavonoid Has In Vivo Antioxidant Properties By Increasing Hepatic Expression Of Gpx And Hepatic Gpx Enzyme Activity In Old Rats
Authors: Nassef Noha , Louka Manal , Habib Haidy 
Published: June 2021

BackgroundQuercetin, one of the major flavonoids present in the human diet, has been associated with a wide range of biological properties, including antioxidant, anti‐inflammatory and anticarcinogenic actions. The antioxidant action is considered as the most likely mechanism for the beneficial effects of quercetin. However, little is known on its activity in vivo. Therefore, the present study aimed to investigate the in vivo effects of quercetin on mRNA and activity levels of hepatic GSTa2 in aged rats. This study was carried out on 28 male Wistar albino rats of 24‐months age. Rats were allocated into 2 groups: 1‐Quercetin treated group (14 rats): Received Quercetin (50 mg/kg by gavage for 7 days). 2‐Control group (14 rats): Received 1 ml/kg distilled water by gavage for 7 days.ResultsQuercetin treatment resulted in significant increase in relative hepatic mRNA levels for glutathione peroxidase (GPx) and liver GPx enzyme activity (1.67 ± 0.78 versus 1 ± 0.05, p< 0.01 and 375.92±27.84 versus 242.78 ±19.79 mU/mg protein, p<0.01 respectively). On the other hand, it significantly decreased relative hepatic mRNA levels for Gsta2, hepatic GST enzyme activity and hepatic glutathione concentrations (0.45 ± 0.16 versus 1 ± 0.04, p< 0.01, 127.78±12.9 versus 181.85±17.23 mU/mg protein, p<0.01 and 19.55 ±3.96 versus 23.78 ± 3.28, p<0.01 respectively). No significant difference was found in BMI or in plasma concentration of ox‐LDL between the two groups of aged rats.ConclusionOur results indicate that quercetin flavonoid has in vivo antioxidant properties by increasing hepatic expression of GPx and hepatic GPx enzyme activity in old rats.
Altered activation of a different type of nitric oxide synthase over the course of repeated hepatic ischemia/reperfusion in rats
Authors: Miyake Takashi , Yokoyama Yukihiro , Kokuryo Toshio , Mizutani Tetsushi , Imamura Atsushi , Nagino Masato 
Published: June 2021

ObjectiveThe aim of this study was to determine the intrahepatic kinetics of nitric oxide synthase during ischemia/reperfusion (I/R).MethodsIntrahepatic nitric oxide (NO) levels were measured using a selective NO sensor. Changes in hepatic microcirculation were investigated using intravital microscopy. Hepatic expression of endothelial nitric oxide synthase (eNOS), phospho‐eNOS, and inducible NOS (iNOS) were evaluated by western blot, reverse transcription polymerase chain reaction (RT‐PCR), and immunohistochemical analysis.ResultsIntrahepatic NO levels gradually increased and then reached a plateau approximately 15 min after starting ischemia. The sinusoids after reperfusion were dilated compared with the sinusoids before ischemia. The expression of phospho‐eNOS during I/R markedly increased during the first ischemia, and then the levels attenuated during the subsequent repeating I/R cycles; however, the expression of iNOS gradually increased, as observed by western blot, RT‐PCR, and immunohistochemical analysis.ConclusionOur results indicate that eNOS, through activation of the phospho‐eNOS system, promptly responds to ischemic stress in the super‐acute phase of ischemia. Subsequently, repeating I/R stress induces iNOS gene expression, although it may take at least an hour to upregulate the iNOS protein.
Chromatin Replication and Epigenome Maintenance
Authors: Alabert Constance , Groth Anja 
Published: June 2021

In dividing cells, faithful duplication of the genome must be accompanied by reproduction of the chromatin landscape on new DNA. Our research focuses on how human cells replicate chromatin and ensure transmission of genetic and epigenetic information during cell division.Recently, we have developed an explorative proteomic approach, Nascent Chromatin Capture (NCC), to profile chromatin replication in human cells. NCC relies on biotin‐dUTP labeling of replicating DNA and cross‐linking, followed by affinity‐purification of tagged chromatin and quantitative proteomics. By comparing nascent newly synthesized chromatin with mature post‐replicative chromatin, we provide association dynamics for 3995 proteins. Highly enriched in nascent chromatin, we find the complete human replisome followed by central players in chromatin assembly and cohesion establishment. In contrast, a large set of chromatin proteins including histone H1 show delayed association. By combining NCC enrichment with experimentally derived chromatin probabilities, we also use the data set to identify new replication factors. Together, this provides an extensive resource to understand genome and epigenome maintenance. In addition, this proteomic instrument provides opportunity to address transmission of histone marks and replication stress responses.
RNA‐seq analysis identifies novel gene signatures common to SHP knockout mice and human steatosis, fibrosis, NASH and cirrhosis
Authors: Smalling Rana , Delker Don , Zhang Yuxia , McGuiness Michael , Liu Shuanghu , Hagedorn Curt , Wang Li 
Published: June 2021

Chronic hepatitis C virus and non‐alcoholic fatty liver disease are major causes of cirrhosis and hepatocellular carcinoma. It is vital to identify genetic changes fueling liver disease progression in order to better prevent, diagnose and treat chronic liver disease. Nuclear receptor small heterodimer partner (Shp) null mice are an attractive model as they have altered hepatic lipid and bile acid metabolism and develop spontaneous hepatoma. Using next generation RNA sequencing, we identified common genes that were significantly differentially expressed in Shp−/− mice, hepatitis C cirrhosis, and non‐alcoholic steatohepatitis (NASH). Novel gene signatures and their functional significance were validated in human steatosis, fibrosis, NASH, alcohol and hepatitis C cirrhosis as well as in Shp−/− and SHP transgenic mice, liver fibrosis, inflammation and bile acid injury models. The novel genes include peptidoglycan recognition protein 2 (PGLYRP2), monooxygenase, DBH‐like 1 (MOXD1), dual specific phosphatase‐4 (DUSP4), thrombospondin 1 (THBS1), tetraspanin 4 (TSPAN4), SPARC‐related modular calcium binding protein‐2 (SMOC‐2), latent transforming growth factor‐beta binding protein 4 (LTBP4), and family with sequence similarity 198a (FAM198A).ConclusionOur study has identified novel genes implicated in chronic human liver diseases using RNA sequencing and Shp−/− mice as our primary model.This study was supported by the NIH DK080440 (LW) and CA148068 (CHH).