Predicting development of sustained unresponsiveness to milk oral immunotherapy using epitope-specific antibody binding profiles

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Inflammatory status modulates plasma lipid and inflammatory marker responses to kiwifruit consumption in hypercholesterolaemic men

Background and aimsKiwifruit has the potential to improve markers of metabolic dysfunction, but the response may be influenced by inflammatory state. We aimed to investigate whether inflammatory state would modulate the effect of consuming two green kiwifruit daily on plasma lipids and markers of inflammation.Methods and resultsEighty-five hypercholesterolaemic men completed a 4-week healthy diet run-in, before randomisation to a controlled cross-over study of two 4-week interventions of two green kiwifruit/day plus healthy diet (intervention) or healthy diet alone (control). Anthropometric measures and fasting blood samples (plasma lipids, serum apolipoproteins A1 and B, high-sensitivity C-reactive protein (hs-CRP) and interleukin (IL)-6, tumour necrosis factor-alpha (TNF-α) and IL-10) were taken at baseline, 4 and 8 weeks. Subjects were divided into low and medium inflammatory groups, using pre-intervention hs-CRP concentrations (hs-CRP <1 and 1–3 mg/L, respectively).In the medium inflammatory group the kiwifruit intervention resulted in significant improvements in plasma high-density lipoprotein cholesterol (HDL-C) (mean difference 0.08 [95% CI: 0.03, 0.12] mmol/L [P < 0.001]), total cholesterol (TC)/HDL-C ratio (−0.29 [−0.45, −0.14] mmol/L [P = 0.001]), plasma hs-CRP (−22.1 [−33.6, −4.97]% [P = 0.01]) and IL-6 (−43.7 [−63.0, −14.1]% [P = 0.01]) compared to control treatment. No effects were seen in the low inflammatory group. There were significant between inflammation group differences for TC/HDL-C (P = 0.02), triglyceride (TG)/HDL-C (P = 0.05), and plasma IL-6 (P = 0.04).ConclusionsInflammatory state modulated responses to the kiwifruit intervention by improving inflammatory markers and lipid profiles in subjects with modestly elevated CRP, suggesting this group may particularly benefit from the regular consumption of green kiwifruit.Registered 16th March 2010, Australian New Zealand Clinical Trials Registry (no. ACTRN12610000213044), www.ANZCTR.org.au.     

The one year exercise and lifestyle intervention program KLAKS: Effects on anthropometric parameters,cardiometabolic risk factors and glycemic control in childhood obesity

Objective

Regular physical exercise within structured lifestyle programs may improve weight status and minimize metabolic risk factors in childhood obesity. The aim of this study was to evaluate the effect of the one-year combined physical exercise/lifestyle program KLAKS on anthropometric and metabolic parameters and glycemic control in childhood obesity.

Materials and Methods

142 overweight/obese (BMI > 90th percentile) candidates (7–18 years) were enrolled, 115 participants completed the program. Anthropometrics and biochemical parameters were obtained at beginning and completion. An oral glucose tolerance test (OGTT) was performed in a subgroup of participants. Course of glucose and insulin levels within OGTT was correlated with several parameters and is reported here for those who completed the program.

Results

The mean standard deviation scores (SDS) decreased significantly for BMI, waist circumference, waist-to-height ratio (WHtR) and percentage body fat (all p ≤ 0.01). Improved metabolic risk markers included mean glucose levels within an OGTT at follow-up compared to baseline (p < 0.0001) and HbA1c (p = 0.05) as well as indications of improvement for gamma-glutamyl-transferase and free fatty acids.

Conclusions

The one-year combined exercise/lifestyle program KLAKS significantly improves markers of obesity and glycemic control. Impaired cardiometabolic risk markers, even subclinical, are also favorably influenced by program participation.     

Pattern of milk feeding and family size as risk factors for iron deficiency anemia among poor Egyptian infants 6 to 24 months old

Infants between 6 and 24 months of age are at the highest risk of development of iron deficiency anemia (IDA) in developing countries. Consuming unmodified cow's milk, delayed introduction of solid foods after 6 months, and high birth order could be predictors of the presence of IDA. Three hundred infants between the ages of 6 and 24 months (mean, 13.94 ± 6.17 months) from Ain Shams University Children's Hospital were enrolled in the study. Data collected included demographic information and dietary assessment including the type of milk feeding, introduction of solid foods, and daily iron intake. The infants were examined, and anthropometric measurements were recorded. Anemic infants (hemoglobin level <11 g/dL) were further evaluated by complete blood count, hemoglobin electrophoresis, and iron profile. Anemia was diagnosed among 198 infants (66%), of whom 129 (43%) had IDA. Red cell distribution width at a cutoff value of 15.8% was 86% sensitive and 74% specific in predicting IDA. The main risk factors for IDA included being between 6 and 18 months of age, of the male sex, birth order above the second order, consuming cow's milk, predominant breast-feeding beyond 6 months of age, and low daily iron intake. We conclude that IDA is the most common cause of anemia among Egyptian infants 6 to 24 months old of low socioeconomic standard. Independent clinical predictors were consuming cow's milk during the first 6 months, delayed introduction of solid foods after 6 months, and birth order beyond the second order.     

4～5周龄D2BF1小鼠的血液学参考值、主要脏器重量及脏器系数的测定

目的测定4~5周龄D2BF1小鼠血液学参考值,且与同龄DBA/2、C57BL小鼠比较,并提供D2BF1小鼠主要脏器重量、脏器系数的参考值。方法随机选取4～5周龄D2BF1小鼠雌雄各10只,分别称重,摘除眼球采血后,颈椎脱臼处死,摘除主要脏器称重,并将测定的血液学值与同龄的C57BL和DBA/2小鼠进行比较分析。结果D2BF1小鼠雌雄之间血液值MCV有显著性差异（P〈0.05）,其余无显著性差异（P〉0.05）。与同龄的C57BL小鼠相比,血液值WBC、Lymph%、Gran%有极显著性差异（P〈0.01）。其余无显著性差异（P〉0.05）。与同龄的DBA/2小鼠相比,WBC、Mid%、RBC、MCH有极显著性差异（P〈0.01）,Mid有显著性差异（P〈0.05）。其余无显著性差异（P〉0.05）。结论D2BF1代小鼠白细胞及分类明显低于C57BL和DBA/2小鼠,值得进一步研究。     

Differential effect of a microsomal deacetylase inhibition on the mutagenicity in Salmonella typhimurium of 2-acetylaminofluorene by liver homogenates of guinea pigs, mice and rats.

The effect of paraoxon, a microsomal deacetylase inhibitor, on the mutant genicity of 2-acetylaminofluorene (AAF) by liver homogenates was compared between the AAF carcinogenesis-resistant guinea pigs and the susceptible mice and rats. The mutagenicity of AAF was mostly abolished by paraoxon, not only in the 3 kinds of untreated animals but also in guinea pigs treated with a combination of phenobarbital and 5,6-benzoflavone, whereas about 50% of the mutagenicity was resistant to paraoxon in treated mice and rats. We suggest that microsomal deacetylase activity is crucially involved in the mutagenic activation of AAF by guinea pig liver homogenates, while the enzyme activity other than the deacetylase activity is also important in the activation by liver homogenates from treated mice or rats.     

Preventive effect of silymarin against taurolithocholate-induced cholestasis in the rat

Increased amounts of monohydroxylated bile salts (BS) have been found in neonatal cholestasis, parenteral nutrition-induced cholestasis and Byler's disease, among others. We analyzed whether the hepatoprotector silymarin (SIL), administered i.p. at the dose of 100mg/kg/day for 5 days, prevents the cholestatic effect induced by a single injection of the model monohydroxylated BS taurolithocholate (TLC, 30 micromol/kg, i.v.) in male Wistar rats. TLC, administered alone, reduced bile flow, total BS output, and biliary output of glutathione and HCO(3)(-) during the peak of cholestasis (-75, -67, -81, and -80%, respectively, P<0.05). SIL prevented partially these alterations, so that the drops of these parameters induced by TLC were of only -41, -25, -60, and -64%, respectively (P<0.05 vs. TLC alone); these differences between control and SIL-treated animals were maintained throughout the whole (120 min) experimental period. Pharmacokinetic studies showed that TLC decreased the intrinsic fractional constant rate for the canalicular transport of both sulfobromophthalein and the radioactive BS [14C]taurocholate by 60 and 68%, respectively (P<0.05), and these decreases were fully and partially prevented by SIL, respectively. SIL increased the hepatic capability to clear out exogenously administered TLC by improving its own biliary excretion (+104%, P<0.01), and by accelerating the formation of its non-cholestatic metabolite, tauromurideoxycholate (+70%, P<0.05). We conclude that SIL counteracts TLC-induced cholestasis by preventing the impairment in both the BS-dependent and -independent fractions of the bile flow. The possible mechanism/s involved in this beneficial effect will be discussed.