A competitive direct enzyme-linked immunosorbent assay for the rapid detection of deoxynivalenol: development and application in agricultural products and feedstuff

A competitive direct enzyme-linked immunosorbent assay (cd-ELISA) was developed for the rapid detection of deoxynivalenol (DON) in food and feedstuff. Polyclonal antibodies against DON were generated by immunizing rabbits with 3-HS-DON-BSA conjugates. In this assay, the sensitivity (measured as IC₅₀) and limit of detection (measured as IC₁₅) were 0.03 and 0.003?mg?kg^?1, respectively. A total of eight sample types (barley, wheat, oat, maize, rice, flour, milk and feedstuff) were chosen to evaluate the cd-ELISA assay performance. The sample could be directly detected after extraction and dilution with double-distilled water. The limit of detection in the samples was in the range of 0.15–0.48?mg?kg^?1. In the end, the spike and recovery results in both cd-ELISA and high-performance liquid chromatography (HPLC) were compared for assay validation. The recovery results ranged between 70% and 100%. A good correlation (R²?=?0.9613) between ELISA and HPLC was obtained.     

A comparison of time-resolved fluoroimmunoassay and ELISA in the detection of casein in foodstuffs

With the aim of lowering the detection limit for casein in foods, three competitive assays are described: direct time-resolved fluoroimmunoassay (TR-FIA), using europium-conjugated antibody, indirect TR-FIA, using biotinylated antibody with europium-conjugated streptavidin and ELISA, using a HRP-conjugated secondary antibody. Food samples (instant potato, flour mix, packet soup, spice-mix) were analysed. Standard curve sensitivities in direct and indirect TR-FIAs did not differ significantly (p=0.097), but both TR-FIAs were considerably less sensitive (both p<0.0001) than ELISA (LOQs 1.3, 1.5 and?<?1.0 mg kg^?1, respectively). The precision and working analyte range was similar in all three methods. Casein content measured in food products was comparable, using the three assays and rocket immunoelectrophoresis. The TR-FIA approach provided no improvement over the ELISA. All three assays allowed quantification of casein in foodstuffs in the order of 1–1.5 mg kg^?1, providing a basis for more rigorous validation and collaborative testing.     

Systemic effects of angiotensin III in conscious dogs during acute double blockade of the renin-angiotensin-aldosterone-system

Aims: The study was designed to determine (i) whether the effects of angiotensin III (AngIII) are similar to those of angiotensin II (AngII) at identical plasma concentrations and (ii) whether AngIII operates solely through AT₁‐ receptors. Methods: Angiotensin II (3 pmol kg^?1 min^?1–3.1 ng kg^?1 min^?1) or AngIII (15 pmol kg^?1 min^?1–14 ng kg^?1 min^?1) was infused i.v. during acute inhibition of angiotensin converting enzyme (enalaprilate; 2 mg kg^?1) and of aldosterone (canrenoate; 6 mg kg^?1 plus 1 mg kg^?1 h^?1). Arterial plasma concentrations of angiotensins were determined by radioimmunoassay using a cross‐reacting antibody to AngII. During ongoing peptide infusion, candesartan (2 mg kg^?1) was administered to block the AT₁‐receptors. Results: Angiotensin immunoactivity in plasma increased to 60 ± 10 pg mL^?1 during infusion of AngII or infusion of AngIII. AngII significantly increased mean arterial blood pressure (+14 ± 4 mmHg) and plasma aldosterone by 79% (+149 ± 17 pg mL^?1) and reduced plasma renin activity and sodium excretion (?41 ± 16 mIU L^?1 and ?46 ± 6 μmol min^?1 respectively). AngIII mimicked these effects and the magnitude of AngIII responses was statistically indistinguishable from those of AngII. All measured effects of both peptides were blocked by candesartan. Conclusion: At the present arterial plasma concentrations, AngIII is equipotent to AngII with regard to effects on blood pressure, aldosterone secretion and renal functions, and these AngIII effects are mediated through AT₁‐ receptors. The metabolic clearance rate of AngIII is five times that of AngII.     

Honey and quercetin reduce ochratoxin A-induced DNA damage in the liver and the kidney through the modulation of intestinal microflora

This study was conducted to evaluate the interactions between the gut microbiota, ochratoxin A and functional food such as honey and quercetin, and the consequences of these interactions on ochratoxin-induced DNA damage in blood, liver and kidney cells. Honey (2?g?kg^?1) or Quercetin (50?mg?kg^?1) was applied to mice by intragastric application every day for 15 days, immediately before ochratoxin treatment (100?µg?kg^?1). We investigated colonic probiotic bacteria count, β-glucuronidase activity, the alkaline comet assay in blood, liver and kidney, the number of cells in the peritoneal cavity, macrophage spreading index and hematological and biochemical parameters. Honey and QU may reduce ochratoxin-induced DNA damage in the liver and kidney, β-glucuronidase activity and inflammation, partly through increasing the colon Bifidobacteria and Lactobacilli counts. The obtained results suggest that honey and QU counteracted the OTA-induced toxicity due to their bifidogenic activity and antigenotoxic activity.     

Development of an antibody-based colloidal gold immunochromatographic lateral flow strip test for natamycin in milk and yoghurt samples

An immunochromatographic lateral flow strip test was developed for the detection of natamycin (Nata) residues in milk and cheese samples. Monoclonal antibody (mAb) against Nata was produced with a half maximal inhibitory concentration of 1.85?μg?L^?1. MAb conjugated with gold nanoparticles was the detection reagent. Nata conjugated with ovalbumin via the 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide/N-hydroxysuccinimide method immobilized on a nitrocellulose membrane was the capture reagent. This semi-quantitative method required only 15?min to complete. The optimum concentrations of coating antigen and mAb were 0.15?µg?mL^?1 and 0.2?µg?mL^?1, respectively. Based on an optical density scanner, the visual limit of detection of Nata was 5?μg?L^?1 and 10?μg?kg^?1 in milk and yoghurt samples, respectively.     

Subchronic administration of nandrolone decanoate in acetylcholinesterase activity in Wistar rats

Health sciences have recently discovered the medical uses of nandrolone decanoate (ND), an androgenic anabolic steroid (AAS), and reported its use in human and animal patients. Clinical evidences suggest that the AAS excess may affect the cholinergic system, which is responsible for several vital functions like learning, memory, and the organization of the movements. Thus, our aim is to research the subchronic effect of ND when administered in varying doses on the acetylcholinesterase (AChE) activity in these brain structures: cerebellum (CE), hippocampus, striatum (ST), and cortex of adult rats. We used 36 male Wistar rats, which were divided into six groups (n?=?6). The groups were divided into: G1—control (physiologic solution), G2—diluents control (only an oleaginous vehicle of vegetal origin—olive oil), G3—0.42?mg?kg^?1 of ND, G4—1.8?mg?kg^?1 of ND, G5—4.6?mg?kg^?1 of ND, and G6—10.0?mg?kg^?1 of ND. We applied the doses once every week during a 3-week period. The values obtained demonstrated a significant increase in the AChE activity (referring to ST and CE for the 4.6 and 10.0?mg?kg^?1 doses of ND). The ND causes increase in AChE activity, which could impair neurotransmission and cholinergic modulation.     

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

β-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05?mg?·?kg^?1 +0.05?mg?·?kg^?1?·?h^?1, n?=?24); (2) naloxone (N, bolus 0.8?mg?·?kg^?1?+?0.4?mg?·?kg^?1, n?=?24); or (3) volume-matched saline (S, n?=?24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22?m?·?min^?1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60?min [5.93 (0.32)?mM] and 90?min [4.16 (0.29)?mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26?mM] and N [4.97 (0.38) and 3.44 (0.25)?mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU?·?ml^?1] at 60 and 90?min compared to S [24.5 (0.5) and 20.6 (0.6)?uIU?·?ml^?1] and N [24.5 (0.4) and 21.6 (0.7)?uIU?· ml^?1] groups. Plasma C-peptide declined to a greater extent at 60 and 90?min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.     

Influence of sympathetic and AT1‐receptor blockade on angiotensin II and adrenergic agonist‐induced renal vasoconstrictions in spontaneously hypertensive rats

Aim: This study investigated the influence of angiotensin II (Ang II) receptor and adrenergic blockade on the renal vasoconstrictions caused by Ang II and adrenergic agonists in spontaneously hypertensive rats (SHR). Methods: Forty‐eight SHR were subjected to 7 days of losartan (10 mg kg^?1 day^?1 p.o.), carvedilol (5 mg kg^?1 day^?1 p.o.) or losartan + carvedilol (10 mg kg^?1 day^?1 + 5 mg kg^?1 day^?1 p.o.). On day 8, the rats were anaesthetized and renal vasoconstrictor experiments performed. One group of rats underwent acute unilateral renal denervation. Results: There were significant (P < 0.05) reductions in the renal vasoconstrictor responses to noradrenaline, phenylephrine, methoxamine and Ang II after losartan and carvedilol treatments compared with that in untreated rats (all P < 0.05). However, in renally denervated SHR treated with carvedilol, the vasoconstrictor responses to all the vasoactive agents were enhanced compared with those in SHR with intact renal nerves treated with carvedilol. Intact SHR given both losartan and carvedilol showed greater renal vasoconstrictor responses to the vasoactive agents than when given either losartan or carvedilol alone (all P < 0.05). Conclusion: Carvedilol reduced the vasoconstrictor response to Ang II and all the adrenergic agonists in the presence of the renal nerves, but, following the removal of renal sympathetic activity, carvedilol enhanced the sensitivity of both renal α₁‐adrenoceptors and AT₁ receptors to the vasoactive agents. Co‐treatment with losartan and carvedilol reduced the renal vasoconstrictor responses to exogenously administered vasoactive agents but to a lesser extent than losartan or carvedilol alone. The results obtained demonstrate an interaction between Ang II receptors and adrenergic neurotransmission in the SHR.     

Body dimensions,exercise capacity and physical activity level of adolescent Nandi boys in western Kenya

The aim of this study was to characterize untrained Nandi boys (mean age 16.6 years) from a town (n = 11) and from a rural area (n = 19) in western Kenya (altitude ?2000 m.a.s.l.) in regard to their body dimensions, oxygen uptake and physical activity level. The town boys had a mean maximal oxygen uptake (VO_2max) of 50 (range: 45–60) mL?kg^?1?min^?1, whereas the village boys reached a value of 55 (37?63)?mL?kg^?1?min^?1 (?p<0.01) in VO_2max. The running economy, determined as the oxygen cost at a given running speed, was 221?mL?kg^?1?km^?1 (597?mL?kg^?0.75?km^?1) for town as well as for village boys. The body mass index (BMI) was very low for town as well as for village boys (18.6 vs 18.4?kg?m^?2). The daily mean time spent working in the field during secondary school and doing sports were significantly higher in village boys compared to town boys (working in the field: 44.2 (0–128) vs 1.3 (0–11)?min, p<0.01; sports: 32.0 (11–72) vs 12.8 (0–35)?min, p<0.01, respectively). A positive correlation between the daily time spent doing sports and VO_2max was found when pooling the data from the town and the village boys (R = 0.55, p<0.01). It is concluded that the body dimensions of adolescent Nandi town and village boys corresponds well with findings in Kenyan elite runners. They are very slender with relatively long legs. In addition, the VO_2max of the village boys was higher than that of the town boys, which is probably due to a higher physical activity level of the village boys during secondary school.     

Integration of Pig-a, micronucleus, chromosome aberration, and Comet assay endpoints in a 28-day rodent toxicity study with 4-nitroquinoline-1-oxide

As part of the Stage III Pig‐a multilaboratory validation trial, we examined the induction of CD59‐negative reticulocytes and total red blood cells (RET^CD59? and RBC^CD59?, respectively) in male Sprague Dawley® rats treated with 4‐nitroquinoline‐1‐oxide (4NQO), for 28 consecutive days by oral gavage, at doses of 1.25, 2.50, 3.75, 5.00, and 7.50 mg kg^?1 day^?1 (the high dose group was sacrificed on Day 15 due to excessive morbidity/mortality). Animals also were evaluated for: micronucleated reticulocytes (mnRET) by flow cytometry; DNA damage in peripheral blood, liver, and stomach using the Comet assay; and chromosome aberrations (CAb) in peripheral blood lymphocytes (PBL). All endpoints were analyzed at two or more timepoints where possible. Mortality, body and organ weights, food consumption, and clinical pathology also were evaluated, and demonstrated that the maximum tolerated dose was achieved at 5.00 mg kg^?1 day^?1. The largest increases observed for the genetic toxicology endpoints (fold‐increase compared to control, where significant; all at 5.00 mg kg^?1 day^?1 on Day 29) were: RET^CD59? (21X), RBC^CD59? (9.0X), and mnRET (2.0X). In contrast, no significant increases were observed for the CAb or Comet response, in any tissue analyzed, at any timepoint. Because 4NQO is a well known mutagen, clastogen, and carcinogen, the lack of response for these latter endpoints was unexpected. These results emphasize the extreme care that must betaken in dose and endpoint selection when incorporating genotoxicity endpoints into routine toxicity studies as has been recommended or is under consideration by various regulatory and industrial bodies. Environ. Mol. Mutagen., 2011. © 2011 Wiley‐Liss, Inc.     

Biphasic intra-thoracic pressure regulation augments cardiac index during porcine peritonitis: a feasibility study

Preservation of cardiac output (CO) and pulmonary artery pressure (PAP) is vital to maintaining tissue oxygenation in sepsis. This feasibility study tested the hypothesis that therapeutic intra-thoracic pressure regulation (tIPR), delivered with a novel device, was designed to non-invasively enhance venous return by creating sub-atmospheric intra-thoracic pressure during the expiratory phase of mechanical ventilation, improves CO without fluid resuscitation in a porcine E. coli peritonitis model of sepsis. Seven pigs were intubated, anaesthetized and instrumented with a Swan-Ganz and femoral artery catheter. After a 30?min basal period, a fibrin clot containing 4–5?×?10⁹ cfu kg^?1 E. coli O111.B4 was implanted in the peritoneum. One hour after clot implantation, tIPR was utilized for 30?min and then removed from the ventilator circuit for 30?min. This tIPR cycle was repeated 4-times. Changes in haemodynamic parameters were calculated by comparing pre-tIPR values to peak values during tIPR administration. Following peritonitis, tIPR significantly increased the peak cardiac index (mean?±?SEM) (14.8?±?2.6 vs 7.9?±?2.3?ml kg^?1) and mean arterial pressure (10.2?±?1.5 vs 4.9?±?1.1?mmHg) and simultaneously decreased PAP (?7.7?±?1.5 vs ?2.7?±?0.8?mmHg). These results support the feasibility of the concept that therapeutic application of negative expiratory pressure may provide a non-invasive and complementary approach to increase cardiac output and organ perfusion in the setting of septic shock.     

Acid-induced increase in duodenal mucosal permeability is augmented by nitric oxide inhibition and vasopressin

The aim of the study was to determine if and by what mechanism(s) nitric oxide inhibition modulates the susceptibility of the duodenum to hydrochloric acid-induced disturbances of mucosal integrity. A second aim was to investigate whether basal permeability is a determinant of epithelial acid barrier function. Using an in situ duodenal perfusion model, mucosal permeability, alkaline secretion and morphology were investigated in anaesthetized rats. Luminal perfusion with 50 mm hydrochloric acid increased duodenal mucosal permeability in the control animals. In animals receiving the nitric oxide synthase inhibitor N-nitro-l -arginine methyl ester (l -NAME 3 mg kg^?1 and 1 mg kg^?1 h^?1) and in those receiving vasopressin (1 IU kg^?1 h^?1), however, the mean increase in permeability in response to acid was markedly higher. In rats treated with either hexamethonium (20 mg kg^?1) or atropine (0.5 mg kg^?1) l -NAME failed to augment the acid-induced increase in permeability. Perfusion with hypotonic saline (25 mm ) increased basal permeability but did not influence the response to acid. Exposure of the duodenum to hydrochloric acid caused very subtle changes of duodenal morphology. It is concluded that both inhibition of endogenous nitric oxide synthesis and vasopressin treatment augment the acid-induced increase in mucosal permeability. The mechanisms involved may be related to changes of Starling forces in the microcirculatory bed. Endogenous nitric oxide may protect the duodenal mucosa by regulating vascular permeability and interstitial fluid pressure.     

Exercise training reduces oxidative stress in people living with HIV/AIDS: a pilot study

Background: Exercise training has been shown to be an effective strategy to balance oxidative stress status; however, this is underexplored in people living with HIV/AIDS (PLWHA).

Objective: To evaluate the effects of exercise training on oxidative stress in PLWHA receiving antiretroviral therapy.

Methods: Patients performed 24 sessions (3 times per week, 8 weeks) of either aerobic (AT), resistance (RT), or concurrent training (CT). Glutathione disulphide to glutathione ratio (GSSG/GSH) in circulating erythrocytes and thiobarbituric acid–reactive substances (TBARS) in plasma samples were assessed as oxidative stress markers. Eight PLWAH completed the training protocol (AT =3, RT =3, CT =2). The GSSG/GSH and TBARS values were logarithmically transformed to approximate a normal distribution. A paired t-test was used to determine the differences between baseline and post-training values.

Results: Data-pooled analysis showed a decrease in GSSG/GSH and TBARS after the training period: log GSSG/GSH= –1.26?±?0.57 versus –1.54?±?0.65, p?=?.01 and log TBARS =0.73?±?0.35 versus 0.43?±?0.21, p?=?.01. This was paralleled by a rise in peak oxygen uptake (VO_2peak?=?29.14?±?5.34 versus 32.48?±?5.75?ml kg^?1 min^?1, p?=?.04). All the subjects who performed resistance exercises showed an average gain of 37?±?8% in muscle strength with no difference between performing single or multiple sets in terms of muscle strength gain. The results reinforce the clinical importance of exercise as a rehabilitation intervention for PLWHA and emphasizes the safety of exercise at the physiological level with the potential to mediate health outcomes.     

An alternative method to determine maximal accumulated O2 deficit in runners

An accepted measure of anaerobic capacity is the maximal O₂ deficit. But it is not feasible to use O₂ deficit if ≥10 submaximal runs are needed to extrapolate the O₂ demand of high velocity running (Medbø et al. 1988). Recently, an alternative method to determine O₂ deficit was proposed (Hill 1996) using only results of supramaximal cycle ergometer tests. The purpose of this study was to evaluate this alternative method with data from treadmill tests. Twenty-six runners ran at 95%, 100%, 105%, and 110% of their velocity at VO₂max. Times to exhaustion, velocity, and accumulated oxygen uptake (VO₂) from each individual's four tests were fit to the following equation using iterative nonlinear regression: The mean values derived for O₂ demand and O₂ deficit were 0.198?±?0.031?ml?·?kg^?1?·?m^?1 and 42?±?22?ml?· kg^?1. SEE for the parameters were 0.007?±?0.007?ml?· kg^?1?·?m^?1 and 8?±?10?ml?·?kg^?1, respectively. Mean R² was 0.998?±?0.003. It was concluded that O₂ deficit can be determined from all-out treadmill tests without the need to perform submaximal tests.     

Heme oxygenase-1/biliverdin/carbon monoxide pathway downregulates hypernociception in rats by a mechanism dependent on cGMP/ATP-sensitive K<Superscript>+</Superscript> channels

Objective and design

To investigate the role of heme oxygenase-1 (HO-1), carbon monoxide (CO), and biliverdin (BVD) in the zymosan-induced TMJ arthritis in rats.

Materials and Methods

Mechanical threshold was assessed before and 4 h after TMJ arthritis induction in rats. Cell influx, myeloperoxidase activity, and histological changes were measured in the TMJ lavages and tissues. Trigeminal ganglion and periarticular tissues were used for HO-1, TNF-α, and IL-1β mRNA time course expression and immunohistochemical analyses. Hemin (0.1, 0.3, or 1 mg kg^?1), DMDC (0.025, 0.25, or 2.5 µmol kg^?1), biliverdin (1, 3, or 10 mg kg^?1), or ZnPP-IX (1, 3 or 9 mg kg^?1) were injected (s.c.) 60 min before zymosan. ODQ (12.5 µmol kg^?1; s.c.) or glibenclamide (10 mg kg^?1; i.p.) was administered 1 h and 30 min prior to DMDC (2.5 µmol kg^?1; s.c), respectively.

Results

Hemin (1 mg kg^?1), DMDC (2.5 µmol kg^?1), and BVD (10 mg kg^?1) reduced hypernociception and leukocyte migration, which ZnPP (3 mg kg^?1) enhanced. The effects of DMDC were counteracted by ODQ and glibenclamide. The HO-1, TNF-α, and IL-1β mRNA expression and immunolabelling increased.

Conclusions

HO-1/BVD/CO pathway activation provides anti-nociceptive and anti-inflammatory effects on the zymosan-induced TMJ hypernociception in rats.

     

IgE antibodies to omega-5 gliadin associate with immediate symptoms on oral wheat challenge in Japanese children

Background: Gliadins have been implicated in immunoglobulin E (IgE)‐mediated allergy to ingested wheat and ω‐5‐gliadin is known to represent a major allergen in wheat‐dependent exercise‐induced anaphylaxis. Less known is whether ω‐5‐gliadin is a clinically relevant allergen in children with immediate allergy to ingested wheat. This study investigates whether specific IgE antibodies to ω‐5‐gliadin (sIgE‐ω‐5‐gliadin‐ab) could be used as a marker for oral wheat challenge outcome in wheat‐sensitized children. A secondary objective was to study whether the level of sIgE‐ω‐5‐gliadin was related to symptom severity in children with a positive challenge test. Methods: Serum samples from 88 children sensitized to wheat, of whom 35 underwent wheat challenge, were collected consecutively. sIgE‐ω‐5‐gliadin‐ab was related to a physician’s diagnosis of wheat allergy and challenge symptoms. Results: The mean concentration of sIgE‐ω‐5‐gliadin‐ab was 7.25 kU_A/l in patients with wheat allergy and 1.08 kU_A/l in patients with no wheat allergy (P < 0.01). sIgE‐ω‐5‐gliadin‐ab was only detected in 12 of the non‐wheat allergic children and 11 of them had a specific IgE to wheat below 1.30 kU_A/l. Children reacting with severe symptoms upon challenge (n = 8) had increased levels of sIgE‐ω‐5‐gliadin‐ab compared to children with moderate, mild or no symptoms (P < 0.001). Conclusions: The presence of sIgE‐ω‐5‐gliadin‐ab is related to the reaction level to wheat challenge outcome in wheat‐sensitized children. The sIgE‐ω‐5‐gliadin‐ab was found to be associated with a strong convincing history of wheat allergy also in those cases when oral food challenge was avoided. The sIgE‐ω‐5‐gliadin‐ab level may serve as a marker for clinical reactivity in wheat‐sensitized individuals.     

Physical activity, cardio-respiratory fitness, and metabolic traits in rural Mexican Tarahumara

Objectives: To study the association between physical activity energy expenditure (PAEE) and cardio‐respiratory fitness (CRF) with key metabolic traits and anthropometric measures in the Tarahumara of Mexico. Methods: A cross‐sectional study was carried out in five rural communities in Chihuahua, México including 64 adult Tarahumara, mean (SD) age 40.7 (12.9) years. Using a combined accelerometer and heart rate sensor, PAEE was measured over three consecutive days and nights and a sub‐maximal step test was carried out in order to (1) calibrate heart rate at the individual level and (2) to estimate CRF. Random blood glucose level and resting blood pressure (BP) were measured with standard anthropometrics. Results: Mean (SD) PAEE was 71.2 (30.3) kJ kg^?1 day^?1 and CRF was 36.6 (6.5) mlO₂ min^?1 kg^?1. Mean (SD) glucose was 127.9 (32.4) mg/dl, with 3.3% having diabetes. Mean (SD) systolic and diastolic BP was 122 (20.8) and 82 (14.8) mm Hg, respectively, with 28.1% having hypertension. Mean body mass index was 27.5 (4.2) kg m^?2, with 71.9% being overweight. Following adjustment for age and sex, weak inverse associations were observed between PAEE and systolic BP (β = ?0.20, P = 0.27) and diastolic BP (β = ?0.16, P = 0.23); and between CRF and systolic BP (β = ?0.51, P = 0.14) and diastolic BP (β = ?0.53, P = 0.06). The inverse associations with glucose were also weak and not statistically significant for neither PAEE (β = ?0.01, P = 0.63) nor CRF (β = ?0.05, P = 0.27). Conclusions: This study suggests high levels of overweight and hypertension in the Tarahumara, and points to fitness and physical activity as potential intervention targets although findings should be confirmed in larger samples. Am. J. Hum. Biol. 2012. © 2012 Wiley Periodicals, Inc.     

Short-term pharmacologically induced growth study of ontogenetic allometry of oxygen uptake in children

Background: A range of allometric coefficients have been proposed in describing the maximal oxygen uptake (VO_2max): body mass relation in children using weight-bearing ergometry. However, a wide deviation in the allometric coefficients for VO_2max may be apparent when selected pediatric cohorts are studied in conjunction with clinical intervention for growth abnormalities.

Aim: The purpose of this study was to determine the allometric coefficients for VO_2max after short-term pharmacologically induced growth in pre- and early pubescent children.

Subjects and methods: The treatment group consisted of nine subjects with non-growth hormone (GH)-deficient short stature and one with GH-deficient short stature (mean age: 13.7?±?1.7 years). Ten pre- and early pubescent children matched for age, height, weight, VO_2max and body mass index (BMI) were controls. The treatment group were evaluated before (Pre-GH) and after (Post-GH) 4 months of subcutaneous GH therapy (0.05?mg?kg^?1day^?1?×?6 days week^?1).

Results: The mean ontogenetic coefficient for the treatment group was 1.50?±?0.20 and for the control group was 0.77?±?0.34. The mean allometric coefficient for body mass relative to VO_2max was significantly higher in the treatment group compared with the control group (p<0.05). Height, weight, fat free mass (FFM), VO_2max indexed to body mass (mL?kg^?1?min^?1) and FFM (mL?kgFFM^?1?min^?1) increased (p<0.05) with GH therapy. GH therapy also increased insulin-like growth factor-I (IGF-I) and served as a biochemical marker of GH therapy (p<0.05). The control group had no significant differences in all the variables tested (p<0.05).

Conclusion: The scaling for oxygen uptake (VO₂) for body mass varies with GH treatment and the increase in VO_2max that commonly occurs in conjunction with physical growth in the pre-and early pubescent individual may be linked to an increase in FFM and linear size.

Résumé. Arrière plan: Une gamme de coefficients d’allométrie a été proposée pour décrire la relation entre consommation d’énergie maximum (VO_2max) et masse corporelle, chez des enfants examinés par ergométrie avec charge pondérale. On observe cependant qu’une large déviation des coefficients d’allométrie pour le VO_2max peut apparaître lorsque des cohortes pédiatriques sont étudiées pour les anomalies de la croissance, en conjonction avec une intervention clinique.

But: Le but de cette étude est de déterminer les coefficients d’allométrie pour le VO_2max à la suite d’une courte poussée de croissance induite par pharmacologie chez des enfants prépubères ou de puberté récente.

Sujets et méthodes: Le groupe sous traitement consiste en neuf sujets de stature courte sans déficience d’hormone de croissance (HC) et d’un sujet de stature courte suite suite à une déficience de l’hormone de croissance (âge moyen?: 13,7?±?1,7?ans). On a pris comme contrôles, dix enfants prépubères et de puberté récente appariés pour l’âge, la stature, le poids, le VO_2max et l’IMC. Le groupe en traitement a été évalué avant (Pré-HC) et après (post-HC) quatre mois d’injections d’HC sous cutanée (0,05?mg?kg^?1?jour^?1?×?6?jours semaine^?1).

Résultats: Le coefficient ontogénique moyen pour le groupe sous traitement est de 1,50?±?0,20 et pour le groupe de contrôle 0,77?±?0,34. Le coefficient allométrique moyen pour la masse corporelle en rapport avec VO_2max est significativement plus élevé dans le groupe traité que dans le groupe contrôle (p<0,05). La stature, le poids, la masse maigre, le VO_2max rapporté à la masse corporelle (mL?kg^?1?min^?1) et à la masse maigre (mL?kg^?1?min^?1) s’accroissent avec la thérapie par HC (p?<?0,05). La thérapie HC accroît également le facteur I de croissance insulino mimétique, lequel sert de marqueur biochimique de la thérapie HC (p?<?0,05). Le groupe de contrôle ne présente pas de différence significative pour toutes les variables examinées (p?<?0,05).

Conclusion: L’échelle de VO₂ en fonction de la masse corporelle, varie avec les traitement par HC et l’augmentation en VO_2max qui se produit en général en conjonction avec la croissance physique chez l’individu prépubère ou pubère récent, peut être liée à l’accroissement de la masse maigre et de la taille linéaire.

Zusammenfassung. Hintergrund: Eine Vielzahl allometrischer Koeffizienten ist vorgeschlagen worden, um die Relation von maximaler Sauerstoffaufnahme (VO_2max) zu Körpermasse im Kindesalter unter Verwendung von gewichtsbezogener Ergometrie zu beschreiben. Allerdings wird eine weite Abweichung allometrischer Koeffizienten für VO_2max offensichtlich, wenn ausgewählte pädiatrische Stichproben in Verbindung mit klinischen Interventionen bei Wachstumsstörungen untersucht werden.

Ziel: Sinn dieser Studie war die Bestimmung von allometrischen Koeffizienten für VO_2max nach kurzzeitigem medikamenteninduzierten Wachstum bei präpubertären Kindern und Kindern in der frühen Pubertät.

Probanden und Methoden: Die Behandlungsgruppe bestand aus neun Probanden mit nicht-wachstumshormonbedingtem Kleinwuchs und einem Patienten mit Kleinwuchs aufgrund eines Wachstumshormonmangels (mittleres Alter: 13,7?±?1,7?Jahre). Die Kontrollgruppe bestand aus zehn gleichaltrigen präpubertären Kindern und Kindern in der frühen Pubertät von vergleichbarer Körperhöhe und vergleichbarem Gewicht, VO_2max und BMI. Die Behandlungsgruppe wurde vor (prä-GH) und nach (post-GH) 4-monatiger subkutaner Wachstumshormontherapie (0,05?mg?kg^?1?Tage^–1?×?6?Tage Woche^?1) untersucht.

Ergebnisse: Der mittlere ontogenetische Koeffizient für die Behandlungsgruppe war 1,50?±?0,20 und für die Kontrollgrupp.,77?±?0,34. Der mittlere allometrische Koeffizient für Körpermasse relativ zu VO_2max war in der Behandlungsgruppe signifikant höher als in der Kontrollgruppe (p?<?0,05). Körperhöhe, Gewicht, fettfreie Masse (FFM), VO_2max in Bezug zu Körpermasse (mL?kg^?1?min^?1) und FFM (mL?kg?FFM^?1?min^?1) stiegen mit Wachstumshormontherapie (p?<?0,05). Die Wachstumshormontherapie führte auch zu einem Anstieg des Insulin-like Growth Factor-I (IGF-I) und diente als biochemischer Marker der Wachstumshormontherapie (p?<?0,05). Die Kontrollgruppe zeigte keine signifikanten Unterschiede bei den getesteten Variablen (p?<?0,05).

Zusammenfassung: Die Anpassung von VO₂ an Körpermasse variiert mit der Wachstumshormontherapie, und der Anstieg von VO_2max, der üblicherweise in Verbindung mit körperlichem Wachstum vor und zu Beginn der Pubertät auftritt, könnte mit einer Vermehrung von FFM und Körperlänge verknüpft sein.

Resumen. Antecedentes: Se ha propuesto un rango de coeficientes alométricos para describir la relación entre el consumo máximo de oxígeno (VO_2max) y la masa corporal en niños, utilizando la prueba de esfuerzo (ergometría “weight-bearing”). Sin embargo, puede ponerse de manifiesto una amplia desviación de los coeficientes alométricos para el VO_2max cuando se estudian las cohortes pediátricas seleccionadas junto con la intervención clínica para las anomalías del crecimiento.

Objetivo: El objetivo de este estudio fue determinar los coeficientes alométricos para el VO_2max tras un crecimiento a corto plazo inducido farmacológicamente en niños pre-puberales y con pubertad temprana.

Sujetos y métodos: El grupo de tratamiento consistió en nueve individuos con baja estatura no deficientes de hormona de crecimiento (GH) y uno con baja estatura y deficiente para la GH (edad media: 13,7?±?1,7 años). Diez niños pre-puberales y con pubertad temprana de la misma edad, estatura, peso, VO_2max e IMC fueron los controles. El grupo de tratamiento fue evaluado antes (Pre-GH) y después (Post-GH) de 4 meses de terapia subcutánea con GH (0,05?mg?kg^?1?día^–1?×?6?días por semana^?1).

Resultados: El coeficientes ontogénico medio para el grupo de tratamiento fue de 1,50?±?0,20 y para el grupo de control de 0,77?±?0,34. El coeficiente alométrico medio para la masa corporal respecto al VO_2max fue significativamente mayor en el grupo que recibía tratamiento que en el grupo control (p?<?0,05). La estatura, el peso, la masa libre de grasa (FFM), el VO_2max indexado para la masa corporal (mL?kg^?1?min^?1) y la FFM (mL?kg?FFM^?1?min^?1) aumentaban (p?<?0,05) con la terapia con GH. Esta terapia también incrementaba el factor de crecimiento semejante a la insulina tipo I (IGF-I) y sirvió como un marcador bioquímico de la terapia con GH (p?<?0,05). El grupo de control no mostró diferencias significativas en ninguna de las variables testadas (p?<?0,05).

Conclusión: la escala del VO_2max para la masa corporal varía con el tratamiento con GH; el incremento en el VO_2max que ocurre habitualmente junto con el crecimiento físico en los individuos pre-puberales y de pubertad temprana puede estar asociado con un incremento de la FFM y del tamaño lineal.     

Effect of intense interval workouts on running economy using three recovery durations

The purposes of this study were to determine whether running economy (RE) is adversely affected following intense interval bouts of 10?×?400-m running, and whether there is an interaction effect between RE and recovery duration during the workouts. Twelve highly trained male endurance athletes [maximal oxygen consumption; V˙O_{2 max} =72.5 (4.3) ml·kg^?1·min^?1; mean (SD)] performed three interval running workouts of 10?×?400 m with a minimum of 4 days between runs. Recovery duration between the repetitions was randomly assigned at 60, 120 or 180 s. The velocity for each 400-m run was determined from a treadmill V˙O_{2 max} test. The average running velocity was 357.9 (9.0) m?·?min^?1. Following the workout, the rating of perceived exertion (RPE) increased significantly (P??1. Changes in RE from pre- to post-workout, as well as heart rate (HR) and respiratory exchange ratio (R) were similar for the three recovery conditions. When averaged across conditions, oxygen consumption (V˙O₂) increased significantly (P??1?·?min^?1 at 200?m?·?min^?1, and from 53.1 to 54.5?ml?·?kg^?1?·?min^?1 at 268 m?·?min^?1, respectively). HR increased (from 124 to 138, and from 151 to 157 beats?·?min^?1 respectively) and R decreased (from 0.90 to 0.78, and from 0.93 to 0.89, respectively) at 200 and 268 m?·?min^?1, respectively (P?V˙O₂, HR and R were independent of the recovery duration between the repetitions.     

Purification and bioactivity of a sulphated polysaccharide conjugate from viscera of abalone Haliotis discus hannai Ino

A sulphated polysaccharide conjugate ACP I was purified from the viscera of abalone Haliotis discus hannai Ino, and its immunostimulatory and anti-tumour activities were studied in vivo. Effect of ACP I on immune function was investigated in normal and cyclophosphamide-induced immunosuppressive mice. The anti-tumour effect was investigated by growth inhibition of tumour. Dose-dependent increase in spleen and thymus relative weight, lymphocyte proliferation, phagocytosis of macrophage, natural killer cell activity and antibody production was observed in all the tested mice administered with 10, 20 and 40 mg kg^?1 body weight of ACP I. Significant increase of the above function was observed especially in immunosuppressive mice at dose of 40 mg kg^?1. A significant inhibition of tumour growth was observed in 10, 20 and 40 mg kg^?1 ACP I groups, with inhibitory rates of 40.24, 41.91 and 46.43%, respectively. Results suggested that ACP I might have immunomodulating and anti-tumour potential deserving application in functional food industry.