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Objective: The age of menarche is usually considered to be affected by nutritional, health-related, social, and economic factors and has significantly decreased since the mid-19th century. The present study was performed to investigate whether the timing of menarche paralleled the general acceleration of physical development, or whether this pattern differed.
Study Design: In all, 30 German studies on menarcheal age (n = > 200) since 1848 were collected. Frequency distributions were analyzed.
Results: During the second half of the 19th and the early 20th century, mean menarcheal age decreased from 18 to 12-13 years in Europe. Yet, the data fail to support the conventional hypothesis that menarcheal age mainly depends on nutritional, health, and economic factors.
Conclusions: We suggest that later than usual menarche may not necessarily be regarded as a physical illness, but in view of the apparently physiological delay of menarche in the 19th century, may be viewed as "collective social amenorrhea."
Target Audience: Obstetricians & Gynecologists and Family Physicians.
Learning Objectives: After participating in this CME activity, physicians should be better able to evaluate menarche as an indicator of developmental tempo in both historical and modern settings, compare menarche in healthy mid-19th century girls with menarche in average modern girls, and assess the marked sensitivity of full pubertal development to environmental circumstances.
Sphingosine-1-phosphate lyase (SPL) is the only known enzyme that irreversibly cleaves sphingosine-1-phosphate (S1P) into phosphoethanolamine and (2E)-hexadecenal during the final step of sphingolipid catabolism. Because S1P is involved in a wide range of physiological and diseased processes, determining the activity of the degrading enzyme is of great interest. Therefore, we developed two procedures based on liquid chromatography (LC) for analysing (2E)-hexadecenal, which is one of the two S1P degradation products. After separation, two different quantification methods were performed, tandem mass spectrometry (MS) and fluorescence detection. However, (2E)-hexadecenal as a long-chain aldehyde is not ionisable by electrospray ionisation (ESI) for MS quantification and has an insufficient number of corresponding double bonds for fluorescence detection. Therefore, we investigated 2-diphenylacetyl-1,3-indandione-1-hydrazone (DAIH) as a derivatisation reagent. DAIH transforms the aldehyde into an ionisable and fluorescent analogue for quantitative analysis. Our conditions were optimised to obtain the outstanding limit of detection (LOD) of 1 fmol per sample (30 mu L) for LC-MS/MS and 0.75 pmol per sample (200 mu l) for LC determination with fluorescence detection. We developed an extraction procedure to separate and concentrate (2E)-hexadecenal from biological samples for these measurements. To confirm our new methods, we analysed the (2E)-hexadecenal level of different cell lines and human plasma for the first time ever. Furthermore, we treated HT-29 cells with different concentrations of 4-deoxypyridoxine (DOP), which competitively inhibits pyridoxal-5-phosphate (P5P), an essential cofactor for SPL activity, and observed a significant decrease in (2E)-hexadecenal relative to the untreated cells.
During aging, intracranial volume remains unchanged and represents maximally attained brain size, while various interacting biological phenomena lead to brain volume loss. Consequently, intracranial volume and brain volume in late life reflect different genetic influences. Our genome-wide association study (GWAS) in 8,175 community-dwelling elderly persons did not reveal any associations at genome-wide significance (P < 5 x 10(-8)) for brain volume. In contrast, intracranial volume was significantly associated with two loci: rs4273712 (P = 3.4 x 10(-11)), a known height-associated locus on chromosome 6q22, and rs9915547 (P = 1.5 x 10(-12)), localized to the inversion on chromosome 17q21. We replicated the associations of these loci with intracranial volume in a separate sample of 1,752 elderly persons (P = 1.1 x 10(-3) for 6q22 and 1.2 x 10(-3) for 17q21). Furthermore, we also found suggestive associations of the 17q21 locus with head circumference in 10,768 children (mean age of 14.5 months). Our data identify two loci associated with head size, with the inversion at 17q21 also likely to be involved in attaining maximal brain size.
Ultrasound evaluation of the patellar tendon cross-sectional area and its relation to maximum force
(2012)
Test-retest-reliability of metabolic and cardiovascular load during isokinetic strength testing
(2012)
Background: Environmental alternations leading to fetal programming of cardiovascular diseases in later life have been attributed to maternal factors. However, animal studies showed that paternal obesity may program cardio-metabolic diseases in the offspring. In the current study we tested the hypothesis that paternal BMI may be associated with fetal growth.
Methods and Results: We analyzed the relationship between paternal body mass index (BMI) and birth weight, ultrasound parameters describing the newborn's body shape as well as parameters describing the newborns endocrine system such as cortisol, aldosterone, renin activity and fetal glycated serum protein in a birth cohort of 899 father/mother/child triplets. Since fetal programming is an offspring sex specific process, male and female offspring were analyzed separately. Multivariable regression analyses considering maternal BMI, paternal and maternal age, hypertension during pregnancy, maternal total glycated serum protein, parity and either gestational age (for birth weight) or time of ultrasound investigation (for ultrasound parameters) as confounding showed that paternal BMI is associated with growth of the male but not female offspring. Paternal BMI correlated with birth parameters of male offspring only: birth weight; biparietal diameter, head circumference; abdominal diameter, abdominal circumference; and pectoral diameter. Cortisol was likewise significantly correlated with paternal BMI in male newborns only.
Conclusions: Paternal BMI affects growth of the male but not female offspring. Paternal BMI may thus represent a risk factor for cardiovascular diseases of male offspring in later life. It remains to be demonstrated whether this is linked to an offspring sex specific paternal programming of cortisol secretion.
In this study, effects of oral beta-carotene supplementation to mares (beta-carotene group: 1000 mg/day, n = 15; control group: n = 15) from 2 weeks before foaling until 6 weeks thereafter on concentrations of beta-carotene, vitamin A and a-tocopherol in plasma, colostrum and milk and plasma of their foals were determined. In addition, effects on fertility were studied. Beta-carotene concentrations increased in plasma and colostrum of beta-carotene-supplemented mares compared to control mares (p < 0.05). In mares of both groups, beta-carotene concentrations were higher in colostrum than in milk (p < 0.05). In foals, beta-carotene concentrations increased with colostrum uptake and were higher in foals born to supplemented mares (p < 0.05; control group: 0.0003 +/- 0.0002 mu g/ml on day 0, 0.008 +/- 0.0023 mu g/ml on day 1; beta-carotene group: 0.0005 +/- 0.0003 mu g/ml on day 0, 0.048 +/- 0.018 mu g/ml on day 1). Concentrations of vitamin A and a-tocopherol were higher in colostrum than in milk (p < 0.05) but did not differ between groups. Concentration of a-tocopherol in plasma of mares decreased over time and in foals, increased markedly within 4 days after birth. All but one mare (control group) showed oestrus within 2 weeks post-partum. Occurrence of oestrus did not differ between groups. More mares of the control group (7/7 vs. 5/12 in the beta-carotene group) became pregnant after being bred in first post-partum oestrus (p < 0.05). In conclusion, beta-carotene supplementation to mares increased beta-carotene concentrations in plasma, colostrum and milk of mares and plasma of their foals but had no positive effects on fertility.
Micronutrient deficiencies are widespread in developing countries, particularly in remote communities such as mobile pastoralists. The nutritional and vitamin A status of this population is not well-documented in Chad. This study assessed serum retinol levels among women and children under five-year-old in nomadic and semi-nomadic pastoralist and rural-settled communities, who are similarly exposed to risk factors such as gastrointestinal parasitic infection, anaemia and emaciation. The novel method of portable fluorometry was used for the first time to measure beta-carotene and retinol levels in a pastoral nomadic area. Moderate level blood retinol deficiency (< 0.7 mu mol/L) was observed in 5% (CI 1-11) of nomadic, 29% (CI 13-45) of semi-nomadic and 22% (CI 8-35) of sedentary women. In children, 1% (CI 0.1-4), 17% (CI 9-25) and 28% (CI 18-39), respectively, had moderate level blood retinol deficiency. In nomadic communities, women and children had blood retinol levels close to normal. Deficiency of retinol was strongly linked with lifestyle (nomadic, semi-nomadic and settled) among women and lifestyle and age among children. The results support an ecological linkage between human retinol levels and livestock milk retinol. This study shows the feasibility of portable retinol and beta-carotene measurement in human blood as well as human and animal milk under remote field conditions, but the approach requires further validation.
Tagetes spp. belongs to the Asteraceae family. It is recognized as a major source of lutein ester (lutein esterified with fatty acids such as lauric, myristic and palmitic acids), a natural colorant belonging to the xanthophylls or oxygenated carotenoids. Four species of Tagetes flower (Tagetes tenuifolia, Tagetes erecta, Tagetes patula, and Tagetes lucida) were used to extract lutein and lutein esters with three different methods. The results showed that T. erecta, type "orangeprinz", is the richest source of lutein esters (14.4 +/- 0.234 mg/g) in comparison to other Tagetes spp. No significant differences between extractions of lutein esters with medium-chain triacylglycerols (MCT) oil, orange oil or solvent (hexane/isopropanol) could be observed. MCT oil also improved stability of lutein esters at 100 degrees C for 40 min. Emulsification of MCT oil improved the stability of lutein ester extract against UV light at 365 nm for 72 h. Finally, an emulsion was prepared under food processing conditions, spray dried and its bioavailability investigated in a preliminary human intervention study. The results show a lower resorption, but further data suggest improvements in implementation of such supplements. (c) 2012 Elsevier Ltd. All rights reserved.
Oxidation of PTH at methionine residues results in loss of biological activity. PTH may be oxidized in patients with renal disease. The aim of this study was to develop an assay considering oxidation of PTH. Oxidized hPTH was analyzed by high resolution nano-liquid chromatography coupled to ESI-FTT tandem mass spectrometry (nanoLC-ESI-FT-MS/MS) directly and after proteolytic cleavage. The oxidized hPTH(1-84) sample shows TIC-peaks at 18-20 min and several mass peaks due to mass shifts caused by oxidations. No significant signal for oxidized hPTH(1-84) species after removal of oxidized PTH molecules by a specific column with monoclonal antibodies (MAB) raised against the oxidized hPTH was detectable. By using this column in samples from 18 patients on dialysis we could demonstrate that measured PTH concentrations were substantially lower when considering oxidized forms of PTH. The relationship between PTH concentrations determined directly and those concentrations measured after removal of the oxidized PTH forms varies substantially. In some patients only 7% of traditionally measured PTH was free of oxidation, whereas in other patients 34% of the traditionally measured PTH was real intact PTH. In conclusion, a huge but not constant proportion of PTH molecules are oxidized in patients requiring dialysis. Since oxidized PTH is biologically inactive, the currently used methods to detect PTH in daily clinical practice may not adequately reflect PTH-related bone and cardiovascular abnormalities in patients on dialysis.
Plant oxylipins are an important class of signaling molecules in plants. The cyclic adducts of epinephrine or norepinephrine with the naturally occurring oxylipin (12Z,15Z)-9-hydroxy-10-oxo-octadeca-12,15-dienoic acid (KODA, 1) or its synthetic analogues (2-6) have been reported to possess flower-inducing activity toward Lemna paucicostata. By in vivo and in vitro experiments with seedlings of Pharbitis nil cv. Violet carbonyl groups of the alpha-ketols (1 and 3) and the ketones (7 and 9) were enantio-selectively reduced to give their corresponding vicinal diols (2 and 4) and alcohols (8 and 10). The stereochemistry at the oxymethine carbon was determined based on the long range C H coupling constants and the modified Mosher's method. Orientation of the adjacent hydroxyl group in (1 and 3) did not affect the enantio-selectivity, whereas the conversion was slightly affected and higher yields were obtained with the R-enantiomers of the alpha-ketols.
Hypomagnesemia affects insulin resistance and is a risk factor for diabetes mellitus type 2 (DM2) and gestational diabetes mellitus (GDM). Two single nucleotide polymorphisms (SNPs) in the epithelial magnesium channel TRPM6 ((VI)-I-1393, (KE)-E-1584) were predicted to confer susceptibility for DM2. Here, we show using patch clamp analysis and total internal reflection fluorescence microscopy, that insulin stimulates TRPM6 activity via a phosphoinositide 3-kinase and Rac1-mediated elevation of cell surface expression of TRPM6. Interestingly, insulin failed to activate the genetic variants TRPM6 ((VI)-I-1393) and TRPM6((KE)-E-1584), which is likely due to the inability of the insulin signaling pathway to phosphorylate TRPM6(T-1391) and TRPM6(S-1583). Moreover, by measuring total glycosylated hemoglobin (TGH) in 997 pregnant women as a measure of glucose control, we demonstrate that TRPM6((VI)-I-1393) and TRPM6((KE)-E-1584) are associated with higher TGH and confer a higher likelihood of developing GDM. The impaired response of TRPM6((VI)-I-1393) and TRPM6((KE)-E-1584) to insulin represents a unique molecular pathway leading to GDM where the defect is located in TRPM6.
Objectives: In an experimental heart failure model, we tested the hypothesis that furosemide causes excess mortality.
Background: Post-hoc analysis of large clinical heart failure trails revealed that furosemide treatment might be associated with worsening of morbidity and even mortality in heart failure patients.
Methods and results: Myocardial infarction was induced in 7 +/- 1 week old male Wistar rats by ligation of the left coronary artery. In study 1, animals were randomly assigned to treatment with furosemide (10 mg/kg/d via drinking water, n = 33) or placebo (n = 33) starting 18 days after surgery. In study 2, animals received furosemide from day 18 and were then randomized to ongoing treatment with either furosemide only (n = 38) or furosemide plus ACE-inhibitor Ramipril (1 mg/kg/d, n = 38) starting on day 42. In study 1 survival rate in the furosemide group was lower than in the placebo group (hazard ratio {HR} 3.39, 95% confidence interval {CI} 1.14 to 10.09, p = 0.028). The furosemide group had a lower body weight (-6%, p = 0.028) at the end of the study and a higher sclerosis index of the glomeruli (+9%, p=0.026) than the placebo group. Wet lung weight, infarct size, and cardiac function were similar between the groups. In study 2, the furosemide group had a higher mortality rate than the furosemide + ramipril group (HR 4.55, 95% CI 2.0 to 10.0, p = 0.0003).
Conclusion: In our rat model of heart failure furosemide, provided at a standard dose, was associated with increased mortality. This increased mortality could be prevented by additional administration of an ACE-inhibitor.