bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Colour of Your Inside: Anatomical Body Painting
Authors: Finn Gabrielle Maria 
Published: June 2021

Medical students still primarily learn anatomy from studying preserved human cadavers. These are monochrome due to the preservation process, unlike the inside of the living body.In an effort to overcome some of the surprise at dealing with 'living colour' and introduce living anatomy, we have adopted a number of approaches. These include projection of images on the surface of the living body, using medical students as the 'canvas', and body painting of detailed renditions of anatomical features on the skin. These serve a number of purposes, most importantly it helps students to achieve greater anatomical knowledge, specifically of surface anatomy. It is often the bold use of colour that aids students recall the anatomy projected. Students' learning transfers from surface to deep through the act of being the painter (doing) and the painted (reading instructions and observing).Students engage in concurrent peer‐physical examination. Students develop an understanding of what it feels like to undress and be examined, developing greater body awareness, potentially developing more empathetic physicians.Students enjoy painting as an adjunct to didactic lectures.Research internally supported.Grant Funding SourceDurham University
Preventing HIV in Developing Countries: Status of Biomedical Interventions
Authors: Vermund Sten H 
Published: June 2021

Insights have emerged as to ongoing HIV prevention challenges.VaccinesThe "STEP" study of a multivalent adenovirus‐vectored prime with a DNA boost did not prevent HIV; in fact, persons with prior adenovirus (+) status were infected with HIV more often than were adenovirus (‐) persons.MicrobicidesBoth cellulose sulfate and Carraguard failed to prevent HIV.BarriersThe female diaphragm was not successful in preventing HIV in Zimbabwe.Behavior changeA meta‐analysis (Cochrane review) suggested no efficacy of abstinence‐only based behavior change (BMJ 2007).Risk reduction for injection drug useHIV seroincidence has declined substantially where needle exchange programs and drug addiction treatment are available.Male circumcisionRandomized clinical trials in South Africa, Kenya, and Uganda indicated &approx;50% reduction in seroincidence among circumcised men.Control of sexually transmitted infectionsThe suppression of HSV‐2 with chronic acyclovir did not reduce HIV seroconversions.Prevention of mother to child transmissionUse of 2‐3 drugs in pregnant women and use of post‐partum prophylaxis in breastfeeding infants can reduce HIV drug resistance and also can increase efficacy (PEPI study). Early therapy of HIV(+) infants is more effective than later therapy (CHER study).Work in progressWe will highlight recent findings in the HIV Prevention Trials Network.
Effects of dietary resistant starch on body fat in three different types of mice
Authors: Zhou Jun , Martin Roy J , Tulley Richard T , Raggio Anne M , Shen Li , Lissy Elizabeth , McCutcheon Kathleen L , Keenan Michael J 
Published: June 2021

Resistant starch (RS) is a dietary fermentable fiber, which decreases dietary energy density and causes fermentation in the lower gut. We previously showed dietary RS decreases body fat in rats. The current studies examined the effects in lean and obese mice. In a 12 week study, the effect of RS on body fat was compared in C57Bl/6J (lean) mice to two control diets: regular control diet or the control diet that had equal energy density as the RS diet (EC). All test diets had 7% (wt/wt) dietary fat. In a 16 week study, the effect of RS on body fat was compared with EC in lean mice and two obese mouse models. All mice were fed control or RS diet for 6 weeks with 7% dietary fat. At week 7, the dietary fat was increased to 11% for half of the mice. The pH of cecal contents was measured as an indicator of RS fermentation.ResultsCompared with EC, RS decreased body fat and improved glucose tolerance in lean mice, but not in obese mice. RS decreased RER in both lean and obese mice. Dietary fat did not interfere with these results. The pH of cecal contents in RS fed mice was decreased for lean mice but not for obese mice, implying the impaired RS fermentation in obese mice.Conclusion1) decreased body fat by RS is not simply due to dietary energy dilution in lean mice, and 2) along with their inability to ferment RS, RS fed obese mice did not show decreased body fat. Supported by the NIH.
Comparison of the satiety effect of protein, fat and carbohydrate preloads with the same energy, volume and palatability.
Authors: Tomé Daniel , Potier Mylène , Fromentin Gilles , Lesdema Aurélie , Benamouzig Robert , Martin‐Rouas Christine , Marsset‐Baglieri Agnès 
Published: June 2021

Numerous studies have shown that a protein proload more efficiently induces satiety than fat and carbohydrate. However, there are still some contradictions because of the diversity of designs employed: energy density, volume, palatability, texture of the preloads and the fact that they are common foods or not. The aim of this study was to compare the effect on satiety of different liquid preloads constituted only by protein, fat or carbohydrate in very controlled conditions.56 subjects have participated to 4 randomised test days, one day per macronutrient and a control day. In each test day, they had to consume the preload entirely (245kcal; 250mL) and their food intake was mesured during the next meals. The volunteers were separed in two groups: the first one (T0) consumed the preload immediatly before lunch and the second one (T1) one hour before.Whatever the delay, no difference was found on food intake at lunch between the 3 different preloads. In the 2 groups, energy intake of preload and lunch was higher after lipid preload than in the control conditions. In the T0 group, the same result was observed with the protein preload.Our results do not confirm the higher satiety effect of proteins, may be because we used non common foods as preloads. According to the concept of learned satiety, the results could not be the same if the subjects were previously familiarised to the uncommon tested preloads.
Iron fortified milk distributed by a Mexican National program improves the intellectual performance in a cohort of children when consumed 12‐24 mo of age. An effectiveness study.
Authors: Villalpando Salvador , Shamah‐Levy Teresa , Cuevas‐Nasú Lucía , Mundo‐Rosas Verónica , Salazar Coronel Aracelí A. 
Published: June 2021

ObjectiveTo evaluate the intellectual performance of a cohort of children consuming iron fortified milk distributed by federal program LICONSA at 7 years of age.Methods586 infants 12‐24 mo of age were randomly assigned to receive 400 mL/d, for 1 year, containing either 5.3 (FM) or 0.2 (NFM) mg of iron. A control group never received milk from the program (C). Iron status indicators were superior in FM at 6 and 12 mo follow‐up. When children were 7 years of age, 82% of the original sample was recovered and intellectual performance was evaluated using WISC test.ResultsGlobal (100 p), execution (111p) and verbal (89p) scales were significantly greater in FM than in NFM (95.7, 107, 84 pp) and than in C (95, 107, 82.8 pp) respectively (p range 0.01‐0.001).ConclusionsEffectiveness of the program for intellectual improvement is benefited 5 million beneficiaries.Supported by Liconsa, and Ministry of Social Development SEDESOL.
Assessing the roles of various retinoid‐metabolizing CYP enzymes in liver disease
Authors: D'Ambrosio Diana N. , Kluwe Johannes , Yang Jian Zhang , Jacobs Matt , Schwabe Robert F. , Blaner William S. 
Published: June 2021

Development of liver disease (LD) is associated with progressive depletion of hepatic stellate cell (HSC) retinoid‐storing lipid droplets. It is not clear whether this loss is the result of increased hepatic mobilization of retinol or increased retinoid catabolism by hepatic cytochrome P450 (CYP) enzymes. Wild type (WT) mice were treated with CCl4 as a model of experimentally induced hepatic fibrosis (EIHF). We did not observe any alterations in the expression of genes encoding proteins involved in retinoid transport in the livers of WT mice in response to CCl4. However, we did find that EIHF is accompanied by an approximate 4‐fold elevation in CYP26A1 and CYP2S1 mRNA levels. Because retinol uptake and storage in the liver involves both hepatocytes and HSCs, we were interested in understanding how each cell type may contribute to the progression of LD. We isolated hepatocytes and HSCs from the livers of WT mice and generated CYP expression profiles for each cell type. HSCs have approximately 50‐fold higher levels of CYP2S1 mRNA relative to hepatocytes, whereas CYP26A1 is highly expressed in hepatocytes. The high expression of CYP2S1 in HSCs and its induction in EIHF provides evidence for a role of this cytochrome in the progression of LD. Thus, the loss of HSC lipid droplets in LD may arise from increased CYP‐mediated retinoid catabolism and not increased retinol mobilization from the liver.Grant Funding SourceR01 DK079221
Effects of cytosolic RIP140 in adipocyte glucose uptake
Authors: Lin Yi‐Wei , Ho Ping‐Chih , Gupta Pawan , Tsui Yao‐Chen , Ha Sung Gil , Tsai Nien‐Pei , Wei Li‐Na 
Published: June 2021

Receptor interacting protein 140 (RIP140) is a versatile transcriptional co‐repressor and plays roles in metabolic processes. Our previous studies showed that protein kinase C epsilon (PKC epsilon) could trigger RIP140 export to the cytoplasm through coordination of phosphorylation and arginine‐methylation. Here, we found that the expression of cytosolic RIP140 decreased basal and insulin‐stimulated glucose uptake in 3T3‐L1 adipocyte. Targeting PKC epsilon by siRNA or specific inhibitor, a trigger inhibiting RIP140 translocation to cytoplasm, also improves glucose uptake. In RIP140 null adipocyte, re‐expression of RIP140 mutant mimicking PKC epsilon stimulated phosphorylation decreased insulin‐stimulated glucose uptake. Re‐expressing RIP140 mutant deficient in PKC epsilon stimulated phosphorylation had no effects on insulin‐stimulated glucose uptake. These results indicate nuclear PKC epsilon activation promotes RIP140 export from nucleus to cytoplasm, and the cytosolic RIP140 exerts a novel activity in the cytoplasm to regulate glucose uptake and insulin sensitivity in adipocyte.This work was supported by DA11190, DA11806, DK54733, DK60521, K02‐DA13926 to L.‐N. W.
Prenatal Exposure to Disrupted Methyl Metabolism Affects Expression & Allele‐Specific Methylation of H19/Igf2 in Brain
Authors: Wade Rachel E , Boersma Heather , Devlin Angela M 
Published: June 2021

Epigenetic processes may play a role in the metabolic programming associated with prenatal nutrition. We studied the effect of prenatal exposure to disrupted maternal methyl metabolism on expression and allele‐specific methylation of H19/Igf2 in brain. H19/Igf2 expression is regulated by a differentially methylated domain (DMD). We studied F1 hybrid offspring from male Cast/EiJ mice and female C57BL6/J mice [with (Cbs+/‐) and without (Cbs+/+) heterozygous disruption of the cystathionine‐ß ‐synthase gene] fed a control or high methionine/low folate (HH) diet during pregnancy. The F1 hybrid offspring were then fed the control or HH diet from weaning for 6 weeks. Independent of prenatal diet, Cbs+/‐ x Cast mice fed the post‐weaning HH diet had higher (P<0.001) plasma homocysteine than Cbs+/+ x Cast mice fed the control diet. This was accompanied by higher (P<0.05) S‐adenosylhomocysteine (SAH), lower (P<0.01) S‐adenosylmethionine/SAH ratios, and lower (P<0.01) Igf2 mRNA in brain. Mice exposed to the prenatal and post‐weaning HH diet had higher (P=0.05) H19 mRNA, lower H19/Igf2 mRNA ratios, and higher (P<0.05) paternal and maternal allele DMD methylation in brain than mice not exposed to the prenatal HH diet. These findings show that prenatal exposure to disrupted maternal methyl metabolism is associated with differential methylation and expression of H19/Igf2 and suggests a role for methyl metabolism in metabolic programming.Grant Funding SourceCIHR/Sick Kids Foundation, Heart & Stroke Foundation
Metabolic syndrome risk is associated with higher CRP levels in young adults
Authors: Morrell Jesse Stabile , Burke Joanne D , Lofgren Ingrid E , Reilly Ruth A 
Published: June 2021

Research related to chronic disease risk prevalence in young adults is lacking. The Young Adult Health Risk Screening Initiative, begun in 2005, is an ongoing cross‐sectional investigation of chronic disease risk in college‐age adults (18‐24) at the University of New Hampshire. Metabolic syndrome (MetS) in relation to C‐reactive protein (CRP) levels was examined in a subset of 88 college‐age men. Fasting glucose, triglycerides, HDL‐C and CRP were measured by fingerstick (Cholestech® LDX). Blood pressure, height, weight, and waist circumference were measured according to standard protocols. MetS criteria include abdominal obesity (waist circum. = 40 in), hypertrigylceridemia (= 150 mg/dl), low HDL‐C (< 40 mg/dl), hypertension (= 130 mm Hg systolic or = 85 mm Hg systolic), and elevated glucose (= 100 mg/dl). Mean CRP levels were 1.3 ± 0.2 mg/L; mean number of MetS criteria was 1.4 ± 0.1. CRP levels were higher among young men with BMI = 25 as compared to those with BMI < 25 (1.6 vs. 0.8 mg/L, p < 0.05). CRP levels were higher among participants with abdominal obesity (1.9 vs. 1.1 mg/L, p < 0.01) and elevated glucose (2.4 vs. 0.8 mg/dl, p < 0.01). After controlling for BMI, recent cold symptoms, and family history of heart disease, CRP levels were positively related to the number of MetS criteria (r2=0.27, p < 0.05). Findings suggest that the inflammatory marker CRP is associated with MetS criteria in young, college‐age men.Supported in part by the UNH Dietetic Internship.Grant Funding SourceNone
Rapid reversal of human intestinal ischemia‐reperfusion induced damage by shedding of injured enterocytes and reepithelialisation
Authors: Grootjans Joep , Derikx Joep PM , Matthijsen Robert A , Thuijls Geertje , de Bruïne Adriaan P , van Bijnen Annemarie A , van Dam Ronald M , Buurman Wim A , Dejong Cornelis HC 
Published: June 2021

Intestinal ischemia reperfusion (I‐IR) has primarily been studied in animal models whereas human data on I‐IR are scarce. We developed a harmless human experimental model aiming to unravel the sequelae of human small I‐IR.In this model, an isolated part of jejunum, to be removed for surgical reasons, was subjected in vivo to various ischemic periods by vascular clamping, followed by reperfusion. Damage to the intestinal barrier was objectified with immunohistochemistry for morphology (H/E), tight junction proteins (TJ) ZO‐1 and Claudin‐3, apoptosis marker M30, cytokines and neutrophil activation products. To assess epithelial cell damage, arteriovenous (V‐A) concentration differences of Intestinal‐Fatty Acid Binding Protein (I‐FABP) were measured.Jejunal histology revealed the appearance of subepithelial spaces after 30 minutes ischemia (fig 1B, normal tissue: fig 1A) with loss of TJ. Mean (SEM) I‐FABP release significantly increased immediately upon reperfusion (fig 2: 290 (46) to 3997 (554) pg/ml, p<0.001). After 25 minutes reperfusion massive apoptosis and shedding of damaged enterocytes into the lumen was seen (fig 1C). Within 60 minutes of reperfusion the epithelial barrier was fully restored, while debris of apoptotic, shedded enterocytes was found in the lumen (fig 1D). This study revealed a unique gut‐specific mechanism of the reversal of IR‐induced intestinal damage.
Type III Transforming Growth Factor‐ β Receptor regulates proliferation and apoptosis in epicardial cells
Authors: Sanchez Nora Sylvia , Austin Anita F , Compton Leigh A , Love Joey D , Barnett Joey V 
Published: June 2021

Epicardial cells transform into the myocardium and form coronary vessels. The Type III Transforming Growth Factor‐ β Receptor (Tgfbr3) is required for coronary vessel development. Tgfbr3‐/‐ embryos have an irregular epicardium, few coronary vessels, and die at E14.5. To explore TGF βR3 signaling we made immortalized epicardial cell lines from E11.5 embryos. Tgfbr3+/+, +/‐, and ‐/‐ cells form a tight epithelium. TGF β1 or TGF β2 (250 pM) caused transformation and induced the smooth muscle marker, SM22α. Circular wounds were made in cell monolayers and the percent wound closure calculated. Tgfbr3 +/+ and +/‐ cells closed the wound by 48h. Tgfbr3‐/‐ cells required 72h (p<0.05). Tgfbr3 +/+ and +/‐ cells gave similar proliferation rates when measured by BrdU, peaking at 48h (33.1% and 33.93%) and returning to basal levels (19.9% and 20.85%) by 72h. Tgfbr3‐/‐ cells sustained a basal proliferation rate 13% lower at 48h (p=0.001). As a second measure of proliferation, we used the in vivo reduction of MTS tetrazolium. Tgfbr3‐/‐ cells had a rate of proliferation 2‐fold lower at 48h and 2.6 fold lower at 72h (p<0.05). Apoptosis was determined by Apo‐One Caspase 3/7 Homogenous assay. The apoptosis rate in Tgfbr3‐/‐ cells was 1.8, 3.3 and 5.9‐ fold higher than Tgfbr3+/+ cells at 24, 48, 72h, respectively (p<0.05). In summary, TGFβR3 is not required for transformation in epicardial cells, but does regulate proliferation and apoptosis.Source: HL085708, HL076133 (AFA), AHA0655129 (JVB), GM007628 (NSS), & GM07347 (LAC).
Chase‐ing regeneration: engineering chondroitinase for mammalian expression
Authors: Curinga Gabrielle Mercedes , Jin Ying , Zhang Chen , Mashburn Charles , Snow Diane M , Smith George M 
Published: June 2021

Neurons fail to regenerate following spinal cord injury partly due to the up‐regulation of chondroitin sulfate proteoglycans (CSPGs). Animal models of neuronal injury show enhanced regeneration when treated with chondroitinase, a bacterial enzyme that degrades inhibitory CSPG glycosaminoglycan (GAG) side chains. Unfortunately, this treatment paradigm is limited by the lack of a non‐invasive, sustained delivery method. This study aims to increase the therapeutic potential of chondroitinase by "engineering" the bacterial chondroitinase gene for maximum sustained expression in mammals and by using a lentiviral gene therapy approach for delivery. Injection of "engineered" chondroitinase lentivirus resulted in sustained activity as detected by digestion of GAG chains two weeks post‐injection. Transplantation of primary astrocytes and Schwann cells that were previously transduced with chondroitinase lentivirus also resulted in GAG chain degradation at the two week time point. Lack of macrophage immunoreactivity following both methods of chondroitinase delivery suggests minimal host immune response and supports the non‐invasive nature of our approach. Finally, in contrast to control neurons, preliminary data suggests that chondroitinase transduced neurons extend axons through regions of CSPG in vitro. These data significantly advance the clinical therapeutic potential for chondroitinase. Supported by NIH‐NIDA 1T32 DA022738, NIH‐NINDS 1 P30 NS051220‐01, and KSCHIRT #6‐13.Grant Funding SourceNIH
Lycopene‐accumulating E. coli transformed with human CMO II as a lycopene metabolism model
Authors: Lu Chi‐Hua , Gong Xiaoming , Marisiddaiah Raju , Rubin Lewis P. , Erdman John W. 
Published: June 2021

Mouse and ferret CMO II have been reported to asymmetrically cleave beta‐carotene or lycopene at the 9', 10' double bond and form apo‐10′‐carotenal or apo‐10′‐lycopenal. To investigate the ability of human CMO II to cleave lycopene, four E. coli strains were prepared: control, lycopene‐accumulating (LYC), lycopene‐accumulating transformed with human CMO II (Lyc‐CMO II), and lycopene‐accumulating transformed with an enzymatic site mutated human CMO II (Lyc‐mtCMO II). E coli were extracted with acetone by sonication, and lycopene metabolic products (lycopenoids) were determined by HPLC. PCR and western blot confirmed that the CMO II gene was successfully expressed in E. coli cells. Among the strains tested, Lyc‐mtCMO II accumulated the highest lycopene content, followed by LYC, Lyc‐CMO II, and control, while the lycopenoids, apo‐8′‐lycopenal, apo‐10′‐lycopenal, apo‐12′‐lycopenal, apo‐10′‐lycopenoic acid, and apo‐15′‐lycopenoic acid, were below limits of detection. (Supported by CA125384A, HD42174, and RR18728)Grant Funding SourceCA125384A
Overweight, Obesity and television viewing in adolescents of Public School from Mexico
Authors: Morales‐Ruán Ma. del Carmen , Gómez Luz María , Shamah‐Levy Teresa 
Published: June 2021

ObjectiveTo determine whether time spent in television (TV) viewing is related to overweight and obesity in adolescents from Public Schools.Materials and MethodsCross sectional design. Adolescents aged 10 to 19 were included in the National Health Survey in Scholar Population (ENSE 2008). Weight and Height were measured and BMI was calculated. TV watching time was also measured and finally the time dedicated to moderated and vigorous physical activity was recorded. A logistic regression model was created to estimate the relationship between the overweight and obesity and time spent watching TV, physical activity, age, gender, and school level (elementary or junior high school).ResultsA total sample of 39,653 adolescents was studied. Overweight and obesity prevalence were of 33.3% and 30.9% in men and women respectively. A positive relation between hours spent viewing TV and overweight and obesity was found. Adolescents who spent watching TV from 7 to 13 hr/week increase the chance of suffer overweight or obesity (OR 1.20, p < 0.05), watch TV from 14 to 20 hr/week increase 29% the probability of to develop these conditions and watching TV more than 21 h/week increases the same risk in 32% (OR 1.32, p<0.05) in comparison with those adolescents who dedicate less than 7 h/week to watch TV.ConclusionA positive association exists between the spent time in front of TV and the overweight and obesity.
Hepatic synthesis of palmitate and oleate during the postprandial period is suppressed in response to low fat/high carbohydrate intake in subjects with type 2 diabetes
Authors: Wilke Michaelann , French Margaret A , Goh Yeow K , Ryan Edmond A , Clandinin Michael T 
Published: June 2021

The objective of this research was to determine whether diabetes and/or low fat intake would increase postprandial de novo lipogenesis of saturated fatty acids (FAs), negatively affecting VLDL‐triglyceride composition. It was hypothesized that low fat/high carbohydrate intake, particularly in diabetes, would result in higher hepatic synthesis of total and saturated FAs. A short‐term low glycemic/low fat diet was compared to a high oleate/high fat diet in seven subjects with type 2 diabetes mellitus and 7 matched non‐diabetic control subjects in a blinded randomized crossover design. For the first time in humans, de novo synthesis of myristate, palmitate, palmitoleate and oleate was estimated using deuterium incorporation techniques. The synthesis of all FAs increased significantly during the postprandial period, but there was large variation in synthetic rates. Myristate exhibited the highest rate of synthesis, whereas palmitate was the major net de novo FA synthesized. The lower fat diet acutely stimulated FA synthesis in control but not diabetic subjects. These results indicate a lack of short term lipogenic response to dietary carbohydrate in diabetes subjects. Funded by the CDA and CIHR.Nutrition & MetabolismBiochemistry of Vitamins and Minerals (400‐ASN)Energy and Nutrient Metabolism (401‐ASN)Human and Clinical Nutrition (402‐ASN)Metabolic and Disease Processes (403‐ASN)Late Breaking Category ‐ Nutrition & Metabolism400‐ASN Biochemistry of Vitamins and Minerals401‐ASN Energy and Nutrient Metabolism402‐ASN Human and Clinical Nutrition403‐ASN Metabolic and Disease ProcessesAbstract 870Grant Funding SourceCanadian Diabetes Association