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Summary Proximate composition, fatty acids profiles and other nutritional values were evaluated for fillets of Limanda aspera (yellowfin sole), Lepidopsetta bilineata (southern rock sole) and Lepidopsetta polyxystra (northern rock sole) and compared to North Sea plaice (Pleuronectes platessa). Additional information is given on the composition of fillets from arrowtooth flounder (Atheresthes stomias). Plaice (0.8% lipid) and Alaska soles (1.0–1.2% lipid) can be classified as lean species, resulting in low 0.3–0.5 g ∑EPA+DHA/100 g muscle, although the fatty acid profiles of the extracted lipids were characterised by high amount of n-3 fatty acids (33.2–47.3%). Arrowtooth flounder belong to the medium-fat species (4.3%). Taurine was the most prevalent free amino acid; mean values ranging between 221 mg100 g−1 and 247 mg100 g−1 wet weight. The selenium content varied between 130 and 310 μg kg−1 ww. Sensory attributes of Southern and Northern rock sole were comparable to plaice.

In the presented study the effect of different iodine (I) levels and sources in hen feed on the iodine concentration of different tissues, blood serum, and eggs of laying hens was studied. For this purpose, two experiments were conducted with 30 laying hens each. In these experiments feed was enriched with KI and Ca(IO(3))(2), respectively, at 0 (Control), 0.25, 0.5, 2.5 and 5 mg I/kg feed, resulting a analysed iodine level from 0.44 to 4.20 mg/kg feed. After four weeks experimental feeding the iodine concentrations of thyroid glands, blood, meat, liver, abdominal fat and eggs were measured with inductively coupled plasma mass spectrometry. The experimental treatment did not affect hen performance. The iodine supplementation significantly increased the iodine concentration of eggs (144-1304 μg/kg), thyroid glands (3367-5975 μg/g), blood serum (16-67 μg/kg) and liver (13-43 μg/kg). Meat (about 14 μg I/kg) and abdominal fat (about 12 μg I/kg) were not significantly affected by iodine treatment. Comparative regression analyses showed that at a similar iodine intake, the supply via KI resulted in significantly higher iodine deposition into eggs than Ca(IO(3))(2). Due to the high carry-over of iodine into eggs, eggs may considerably contribute to the iodine supply of the consumers.

Since the Second World War the consumer behaviour in developed countries changed drastically. Primarily there existed the demand for sufficient food after a period of starvation, afterwards the desire for higher quality was arising, whereas today most people ask for safe and healthy food with high quality. Therefore a united approach comprising consistent standards, sound science and robust controls is required to ensure consumers' health and to maintain consumers' confidence and satisfaction. Chemical analysis along the whole food chain downstream (tracking) from primary production to the consumer and upstream (tracing) from the consumer to primary production is an important prerequisite to ensure food safety and quality. In this frame the focus of the following paper is the "chemical safety of meat and meat products" taking into account inorganic as well as organic residues and contaminants, the use of nitrite in meat products, the incidence of veterinary drugs, as well as a Failure Mode and Effect Analysis (FMEA) system assessing (prioritizing) vulnerable food chain steps to decrease or eliminate vulnerability.

Die Spanne zwischen dem Wert der empfohlenen Aufnahme des Spurenelements Iod und dem oberen Grenzwert ist klein. Um herauszufinden, wie sich Iodzusatze im Tierfutter sowie Iodsalz in Wurst und Schinken auf die Iodversorgung auswirken, wurden Futterungsversuche durchgefuhrt und Fleischerzeugnisse aus dem Handel untersucht. Solche Studien erfordern eine flexible Iodanalytik.

Supplementation of animal feed with iodine influences the iodine content of milk and therefore, in addition to salt iodination, provides another possibility for improving the human iodine supply. On the other hand, excessive iodine intake by humans through drinking milk must be avoided. Furthermore, the iodine content of milk varies, depending on the presence of iodine antagonists in feed (e.g., glucosinolates in rapeseed) and the applied iodine species. This study evaluated the impact of various feed iodine supplementation levels up to the permitted maximum level, the effect of applying rapeseed compared with a glucosinolate-free ration, and the impact of 2 different iodine species on the iodine content of milk. A total of 32 dairy cows were divided into 4 groups with 8 animals each. Two groups received distillers dried grains with solubles (DDGS) as the protein source, and the others received rapeseed meal (RSM, 16.5% of total diet). In each case, half the animals received feed supplemented with iodine in the form of potassium iodide, and the other half received feed supplemented with iodine in the form of calcium iodate. Iodine supplementation levels of 0, 0.5, 1, 2, 3, 4, and 5 mg/kg of dry matter (DM) were tested in consecutive periods of 21 d each. The milk iodine concentration increased with increasing iodine supplementation of the feed. Rapeseed meal in the ration (0.58 mmol of glucosinolates/kg of diet DM) diminished the milk iodine concentration by up to one-half to one-third of the concentration achieved by DDGS. At iodine supplementation levels of 2 mg/kg of DM and higher, the differences were significant. The application of iodate predominantly resulted in higher milk iodine concentrations compared with iodide, but not significantly in any period. At the highest tested iodine supplementation (5 mg/kg of DM), the milk iodine concentration increased up to 1,464 (iodide) and 1,578 microg/kg (iodate) when feeding DDGS and up to 718 (iodide) and 620 microg/kg (iodate) in the RSM groups. The carry over of iodine from feed into milk amounted to 30 to 56% when using DDGS, and 11 to 25% when using RSM. The maximum level of iodine currently allowed in the feed of dairy cows in Europe could lead to high milk iodine concentrations. As a result, the Tolerable Upper Intake Level in human nutrition could be exceeded. Therefore, this maximum level needs to be reevaluated. In addition to iodine supplementation, the application of RSM in the ration must be considered when estimating the iodine content of milk.

Na+ loading without Cl− fails to increase blood pressure in the DOCA model. We compared the changes in the total body (TB) effective Na+, K+, Cl−, and water (TBW) content as well as in intracellular (ICV) or extracellular (ECV) volume in rats receiving DOCA-NaCl, DOCA-NaHCO3, or DOCA-KHCO3. We divided 42 male rats into 5 groups. Group 1 was untreated, group 2 received 1% NaCl, and groups 3, 4, and 5 were treated with DOCA and received 1% NaCl, 1.44% NaHCO3, or 1.7% KHCO3 to drink. We measured mean arterial blood pressure (MAP) directly after 3 wk. Tissue electrolyte and water content was measured by chemical analysis. Compared with control rats, DOCA-NaCl increased MAP while DOCA-NaHCO3 and DOCA-KHCO3 did not. DOCA-NaCl increased TBNa+ 26% but only moderately increased TBW. DOCA-NaHCO3 led to similar TBNa+ excess, while TBW and ICV, but not ECV, were increased more than in DOCA-NaCl rats. DOCA-KHCO3 did not affect TBNa+ or volume. At a given TB(Na++K+) and TBW, MAP in DOCA-NaCl rats was higher than in control, DOCA-NaHCO3, and DOCA-KHCO3 rats, indicating that hypertension in DOCA-NaCl rats was not dependent on TB(Na++K+) and water mass balance. Skin volume retention was hypertonic compared with serum and paralleled hypertension in DOCA-NaCl rats. These rats had higher TB(Na++K+)-to-TBW ratio in accumulated fluid than DOCA-NaHCO3 rats. DOCA-NaCl rats also had increased intracellular Cl− concentrations in skeletal muscle. We conclude that excessive cellular electrolyte redistribution and/or intracellular Na+ or Cl− accumulation may play an important role in the pathogenesis of salt-sensitive hypertension.

The skin interstitium sequesters excess Na+ and Cl- in salt-sensitive hypertension. Mononuclear phagocyte system (MPS) cells are recruited to the skin, sense the hypertonic electrolyte accumulation in skin, and activate the tonicity-responsive enhancer-binding protein (TONEBP, also known as NFAT5) to initiate expression and secretion of VEGFC, which enhances electrolyte clearance via cutaneous lymph vessels and increases eNOS expression in blood vessels. It is unclear whether this local MPS response to osmotic stress is important to systemic blood pressure control. Herein, we show that deletion of TonEBP in mouse MPS cells prevents the VEGFC response to a high-salt diet (HSD) and increases blood pressure. Additionally, an antibody that blocks the lymph-endothelial VEGFC receptor, VEGFR3, selectively inhibited MPS-driven increases in cutaneous lymphatic capillary density, led to skin Cl- accumulation, and induced salt-sensitive hypertension. Mice overexpressing soluble VEGFR3 in epidermal keratinocytes exhibited hypoplastic cutaneous lymph capillaries and increased Na+, Cl-, and water retention in skin and salt-sensitive hypertension. Further, we found that HSD elevated skin osmolality above plasma levels. These results suggest that the skin contains a hypertonic interstitial fluid compartment in which MPS cells exert homeostatic and blood pressure-regulatory control by local organization of interstitial electrolyte clearance via TONEBP and VEGFC/VEGFR3-mediated modification of cutaneous lymphatic capillary function.

1. The objective of this study was to determine the influence of iodine (I) supplementation of feed, within the range of the European guidelines, on the performance of broiler chickens and I transfer into different organs and tissues, especially meat. The main emphasis was to assess whether broiler meat could be enriched and used as an I source in human nutrition. 2. Two experiments were performed, one with KI and the other with Ca(IO(3))(2). For each experiment, 288 d-old broiler chicks were divided into 4 groups (72 birds/group) and fed on diets with supplementations between 0 and 5 mg I/kg feed. The birds were reared to 35 d of age under standard conditions. Six birds per group were slaughtered at 35 d and samples of blood, thyroid gland, liver, pectoral and thigh meat taken. 3. Iodine treatment did not significantly affect the growth and slaughter performance of the broiler chickens. In all investigated parameters, I concentrations increased significantly with increasing I intake of the animals. The lowest I concentrations were measured in the meat, but they were considerably higher in blood serum, liver and thyroid gland. Since the I content of meat was still low in the highest supplemented group (highest median concentration: 67·8 µg I/kg thigh meat), there is no evidence that this could substantially improve I supply in human nutrition.

We showed recently that mononuclear phagocyte system (MPS) cells provide a buffering mechanism for salt-sensitive hypertension by driving interstitial lymphangiogenesis, modulating interstitial Na + clearance, and increasing endothelial NO synthase protein expression in response to very high dietary salt via a tonicity-responsive enhancer binding protein/vascular endothelial growth factor C regulatory mechanism. We now tested whether isotonic saline and deoxycorticosterone acetate (DOCA)-salt treatment leads to a similar regulatory response in Sprague-Dawley rats. Male rats were fed a low-salt diet and received tap water (low-salt diet LSD), 1.0% saline (high-salt diet HSD), or DOCA+1.0% saline (DOCA-HSD). To test the regulatory role of interstitial MPS cells, we further depleted MPS cells with clodronate liposomes. HSD and DOCA-HSD led to Na + accumulation in the skin, MPS-driven tonicity-responsive enhancer binding protein/vascular endothelial growth factor C–mediated hyperplasia of interstitial lymph capillaries, and increased endothelial NO synthase protein expression in skin interstitium. Clodronate liposome MPS cell depletion blocked MPS infiltration in the skin interstitium, resulting in unchanged tonicity-responsive enhance binding protein/vascular endothelial growth factor C levels and absent hyperplasia of the lymph capillary network. Moreover, no increased skin endothelial NO synthase protein expression occurred in either clodronate liposome–treated HSD or DOCA-salt rats. Thus, absence of the MPS-cell regulatory response converted a salt-resistant blood-pressure state to a salt-sensitive state in HSD rats. Furthermore, salt-sensitive hypertension in DOCA-salt rats was aggravated. We conclude that MPS cells act as onsite controllers of interstitial volume and blood pressure homeostasis, providing a local regulatory salt-sensitive tonicity-responsive enhancer binding protein/vascular endothelial growth factor C–mediated mechanism in the skin to maintain normal blood pressure in states of interstitial Na + and Cl − accumulation. Failure of this physiological extrarenal regulatory mechanism leads to a salt-sensitive blood pressure response.

Catheter-based renal sympathetic denervation for resistant hypertension: A multicenter safety and proof-of-principle cohort study. Lancet 373: 1275–1281, 2009 {#article-title-2} 1886 1888 Upon the initiative of Smithwick and Thompson (1) of the Massachusetts General Hospital, resection of the splanchnic nerves through a posterior infradiaphragmatic approach plus removal of the sympathetic chain from the level of the eighth dorsal ganglion to the second lumbar ganglion had been used with relative frequency in cases of desperate hypertension at the time when antihypertensive medication was not yet available. In the hands of other investigators, the results were spectacular in a minority of patients but not quite satisfactory in many patients (2,3). Despite improvement of headache, reversal of papilledema in malignant hypertension, etc. , the long-term reduction of BP was quite variable and the 5-yr mortality remained approximately 40% (2). A 10-yr follow-up compared 100 patients who were subjected to thoracolumbar sympathectomy with 1500 patients who received symptomatic therapy. Lasting BP reduction was seen only in one third of the patients (4). Whereas the average BP levels were reduced, occasional BP spikes were not. The average difference of preoperative to postoperative systolic BP values was 21 mmHg. The authors saw reduction of cerebrovascular accidents and less progression of proteinuria and renal dysfunction, but 10-yr mortality was still 41%. Against this background, once effective antihypertensive medication was available, this relatively crude procedure fell out of favor and remained a sleeping beauty. With today's better insight into the role of sympathetic activity in the genesis of hypertension and particularly the role of the kidney in sympathetic activation, there has been a renaissance in the interest of the renal sympathetic nervous system, including its role in primary hypertension—apart from its undoubted role in the hypertension of chronic kidney disease (5–10). Renal disease and, in animal experiments, even minor renal tissue damage such as injection of minute volumes of phenol, trigger afferent signals that ascend via …

The idea that an osmotically inactive Na+ storage pool exists that can be varied to accommodate states of Na+ retention and/or Na+ loss is controversial. We speculated that considerable amounts of osmotically inactive Na+ are lost with growth and that additional dietary salt excess or salt deficit alters the polyanionic character of extracellular glycosaminoglycans in osmotically inactive Na+ reservoirs. Six-week-old Sprague-Dawley rats were fed low-salt (0.1%; LS) or high-salt (8%; HS) diets for 1 or 4 wk. At their death, we separated the tissues and determined their Na+, K+, and water content. Three weeks of growth reduced the total body Na+ content relative to dry weight (rTBNa+) by 23%. This “growth-programmed” Na+ loss originated from the bone and the completely skinned and bone-removed carcasses. The Na+ loss was osmotically inactive (45–50%) or osmotically active (50–55%). In rats aged 10 wk, compared with HS, 4 wk of LS reduced rTBNa+ by 9%. This dietary-induced Na+ loss was osmotically inactive (≈50%) and originated largely from the skin, while ≈50% was osmotically active. LS for 1 wk did not reduce skin Na+ content. The mobilization of osmotically inactive skin Na+ with long-term salt deprivation was associated with decreased negatively charged skin glycosaminoglycan content and thereby a decreased water-free Na+ binding capacity in the extracellular matrix. Our data not only serve to explain discrepant results in salt balance studies but also show that glycosaminoglycans may provide an actively regulated interstitial cation exchange mechanism that participates in volume and blood pressure homeostasis.

Water-free Na + storage may buffer extracellular volume and mean arterial pressure (MAP) in spite of Na + retention. We studied the relationship among internal Na + , K + , water balance, and MAP in Sprague-Dawley rats, with or without deoxycorticosterone-acetate (DOCA) salt, with or without ovariectomy (OVX). The rats were fed a low-salt (0.1% NaCl) or high-salt (8% NaCl) diet for 5 weeks. DOCA salt increased MAP (161±14 versus 123±4 mm Hg; P P + by &40% to 45%; however, water-free Na + retention by osmotically inactive Na + storage and by osmotically neutral Na + /K + exchange allowed the rats to maintain the extracellular volume close to normal. DOCA-OVX salt rats showed similar Na + retention. However, their osmotically inactive Na + storage capacity was greatly reduced and only partially compensated by neutral Na + /K + exchange, resulting in greater volume retention despite similar Na + retention. For every 1% wet weight total body water gain, MAP increased by 2.3±0.2 mm Hg in DOCA salt rats and 2.5±0.3 mm Hg in DOCA-OVX salt rats. Because water-free Na + retention buffered total body water content by 8% to 11% wet weight, we conclude that this internal Na + escape buffered MAP. Extrarenal Na + and volume balance seem to play an important role in long-term volume and MAP control.

The crystal structure of the monoclinic η5-C5H5RU(CO)2(CONH2) has been determined by X-ray diffraction (space group P1̄ with Z - 4 and a = 1248,3 pm, b = 963,3 pm, c = 845,2 pm, α= 97,35°, β= 106,11°, and γ= 99,32°). The Ru is pseudo-octahedrally coordinated to the η5-C5H5 ring, the two CO groups and the CONH2 ligand with a planar RuC(O)N-moiety. Dimers are formed by N-H···O hydrogen bonds connecting the carbamoyl ligands of two molecules. Further hydrogen bonds link these dimers to form a helical chain.