Effects of aerobic, strength or combined exercise on perceived appetite and appetite-related hormones in inactive middle-aged men

© 2017 Human Kinetics, Inc. Aerobic exercise (AE) and strength exercise (SE) are reported to induce discrete and specific appetite-related responses; however, the effect of combining AE and SE (i.e., combined exercise; CE) remains relatively unknown. Twelve inactive overweight men (age: 48 ± 5 y; BMI: 29.9 ± 1.9 kg·m2) completed four conditions in a random order: 1) nonexercise control (CON) (50 min seated rest); 2) AE (50 min cycling; 75% VO2peak); 3) SE (10 × 8 leg extensions; 75% 1RM); and 4) CE (50% SE + 50% AE). Perceived appetite, and appetiterelated peptides and metabolites were assessed before and up to 2 h postcondition (0P, 30P, 60P, 90P, 120P). Perceived appetite did not differ between trials (p < .05). Acylated ghrelin was lower at 0P in AE compared with CON (p = .039), while pancreatic polypeptide (PP) was elevated following AE compared with CON and CE. Glucose-dependent insulinotropic peptide (GIPtotal) was greater following all exercise conditions compared with CON, as was glucagon, although concentrations were generally highest in AE (p < .05). Glucose was acutely increased with SE and AE (p < .05), while insulin and C-peptide were higher after SE compared with all other conditions (p < .05). In inactive, middle-aged men AE, SE and CE each have their own distinct effects on circulating appetite-related peptides and metabolites. Despite these differential exercise-induced hormone responses, exercise mode appears to have little effect on perceived appetite compared with a resting control in this population

The deleted in brachydactyly B domain of ROR2 is required for receptor activation by recruitment of Src

The transmembrane receptor 'ROR2' resembles members of the receptor tyrosine kinase family of signalling receptors in sequence but its' signal transduction mechanisms remain enigmatic. This problem has particular importance because mutations in ROR2 are associated with two human skeletal dysmorphology syndromes, recessive Robinow Syndrome (RS) and dominant acting Brachydactyly type B (BDB). Here we show, using a constitutive dimerisation approach, that ROR2 exhibits dimerisation-induced tyrosine kinase activity and the ROR2 C-terminal domain, which is deleted in BDB, is required for recruitment and activation of the non-receptor tyrosine kinase Src. Native ROR2 phosphorylation is induced by the ligand Wnt5a and is blocked by pharmacological inhibition of Src kinase activity. Eight sites of Src-mediated ROR2 phosphorylation have been identified by mass spectrometry. Activation via tyrosine phosphorylation of ROR2 receptor leads to its internalisation into Rab5 positive endosomes. These findings show that BDB mutant receptors are defective in kinase activation as a result of failure to recruit Src

Driving Restrictions Advised by Midwestern Cardiologists Implanting Cardioverter Defibrillators: Present Practices, Criteria Utilized, and Compatibility with Existing State Laws

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73175/1/j.1540-8159.1992.tb03115.x.pd

Harmonic publication and citation counting: sharing authorship credit equitably – not equally, geometrically or arithmetically

Bibliometric counting methods need to be validated against perceived notions of authorship credit allocation, and standardized by rejecting methods with poor fit or questionable ethical implications. Harmonic counting meets these concerns by exhibiting a robust fit to previously published empirical data from medicine, psychology and chemistry, and by complying with three basic ethical criteria for the equitable sharing of authorship credit. Harmonic counting can also incorporate additional byline information about equal contribution, or the elevated status of a corresponding last author. By contrast, several previously proposed counting schemes from the bibliometric literature including arithmetic, geometric and fractional counting, do not fit the empirical data as well and do not consistently meet the ethical criteria. In conclusion, harmonic counting would seem to provide unrivalled accuracy, fairness and flexibility to the long overdue task of standardizing bibliometric allocation of publication and citation credit

Protein and folic acid content in the maternal diet determine lipid metabolism and response to high-fat feeding in rat progeny in an age-dependent manner

Maternal diet during gestation can exert a long-term effect on the progeny’s health by programming their developmental scheme and metabolism. The aim of this study is to analyze the influence of maternal diet on lipid metabolism in 10- and 16-week-old rats. Pregnant dams were fed one of four diets: a normal protein and normal folic acid diet (NP-NF), a protein-restricted and normal folic acid diet (PR-NF), a protein-restricted and folic-acid-supplemented diet (PR-FS), or a normal protein and folic-acid-supplemented diet (NP-FS). We also tested whether prenatal nutrition determines the reaction of an organism to a postweaning high-fat diet. Blood biochemistry and biometrical parameters were evaluated. The expression patterns of PPARα, PPARγ, and LXRα in the liver and adipose tissue were examined by real-time PCR. In the 10-week-old, rats folic acid supplementation of the maternal diet was associated with reduced circulating glucose and total cholesterol concentrations (P < 0.01 and P < 0.001, respectively). Neither prenatal diets nor postnatal feeding affected blood insulin concentrations. In the 16-week-old rats, body weight, abdominal fat mass and central adiposity were reduced in the progeny of the folic acid–supplemented dams (P < 0.01, P < 0.001 and P < 0.01, respectively). Maternal protein restriction had no effect on biometry or blood biochemical parameters. Folic acid supplementation of the maternal diet was associated with reduced expression of PPARα, PPARγ, and LXRα in the liver (P < 0.001). Reduced protein content in the maternal diet was associated with increased PPARα mRNA level in the liver (P < 0.001) and reduced LXRα in adipose tissue (P < 0.01). PPARα and PPARγ transcription in the liver, as well as LXRα transcription in adipose tissue, was also dependent on interaction effects between prenatal and postnatal diet compositions. PPARγ transcription in the liver was correlated with the abdominal fat mass, body weight, and calorie intake, while PPARγ transcription in adipose tissue was correlated with reduced body weight and calorie intake. Total serum cholesterol concentration was correlated with LXRα transcription in the liver. Folic acid supplementation of the maternal diet may have favorable effects for lipid metabolism in the progeny, but these effects are modified by the postnatal diet and age. Furthermore, the expression of LXRα, PPARα, and PPARγ in the liver and adipose tissue largely depends on the protein and folic acid content in the maternal diet during gestation. However, the altered transcription profile of these key regulators of lipid metabolism does not straightforwardly explain the observed phenotype

Physical Activity After Surgery for Severe Obesity: The Role of Exercise Cognitions

# The Author(s) 2010. This article is published with open access at Springerlink.com Background Physical activity after bariatric surgery is associated with sustained weight loss and improved quality of life. Some bariatric patients engage insufficiently in physical activity. This may be due to exercise cognitions, i.e., specific beliefs about benefits of and barriers to physical exercise. The aim of this study was to examine whether and to what extent both physical activity and exercise cognitions changed at 1 and 2 years post-surgery and whether exercise cognitions predict physical activity. Methods Forty-two bariatric patients (38 women, 4 men; mean age 38±8 years, mean body mass index prior to surgery 47±6 kg/m 2) filled out self-report instruments to examine physical activity and exercise cognitions pre- and post-surgery

Harmonic Allocation of Authorship Credit: Source-Level Correction of Bibliometric Bias Assures Accurate Publication and Citation Analysis

Authorship credit for multi-authored scientific publications is routinely allocated either by issuing full publication credit repeatedly to all coauthors, or by dividing one credit equally among all coauthors. The ensuing inflationary and equalizing biases distort derived bibliometric measures of merit by systematically benefiting secondary authors at the expense of primary authors. Here I show how harmonic counting, which allocates credit according to authorship rank and the number of coauthors, provides simultaneous source-level correction for both biases as well as accommodating further decoding of byline information. I also demonstrate large and erratic effects of counting bias on the original h-index, and show how the harmonic version of the h-index provides unbiased bibliometric ranking of scientific merit while retaining the original's essential simplicity, transparency and intended fairness. Harmonic decoding of byline information resolves the conundrum of authorship credit allocation by providing a simple recipe for source-level correction of inflationary and equalizing bias. Harmonic counting could also offer unrivalled accuracy in automated assessments of scientific productivity, impact and achievement