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Physical parameterizations in global atmospheric and ocean models typically include free parameters that are not theoretically or empirically constrained. New methods are required to determine the optimal parameter combinations for such models in an objective, exhaustive, yet computationally feasible manner. Here we propose to apply computationally inexpensive radial basis function (RBF) surrogate models to minimize a "cost," or error, function of an atmospheric model or a physical parameterization. The RBF is iteratively updated as more input‐output pairs are obtained during the optimization. The approach is used to optimize the eddy‐diffusivity/mass‐flux boundary‐layer parameterization of the convective boundary‐layer in a single‐column model framework. The optimization based on surrogate models is able to identify parameter combinations that reduce the error of the untuned default setting by 41%. The probability to detect a low‐error solution increases rapidly especially over the first tens of single‐column model evaluations. In comparison, a quadratic polynomial model only yields an error reduction of 17% since (a) high‐order parameter interactions are not accounted for and (b) the construction of the polynomial is not based on an iterative sampling approach. The RBF surrogate models achieve this 17% error reduction for 40% of the polynomial model's cost. Interestingly, one of the emerging optimal settings describes a pure mass flux parameterization without eddy‐diffusivity component. A second optimal solution is characterized by a plume fractional area of 20–30% and an eddy‐mixing time scale of ∼700 s. Key Points: Radial basis function (RBF) surrogate models provide an efficient framework to optimize physics parameterizations such as EDMFThe RBF surrogate models detect solutions much better than those provided by a commonly used quadratic polynomial model and are less costlyA multiplume model without eddy‐diffusivity flux emerges as one of the optimal settings for the cloud‐free and cloud‐topped convective PBL [ABSTRACT FROM AUTHOR]

The central nervous system (CNS) constantly monitors nutrient availability in the body and, in particular, in the gastrointestinal (GI) tract to regulate nutrient and energy homeostasis. Extrinsic parasympathetic and sympathetic nerves are crucial for CNS nutrient sensing in the GI tract. These extrinsic afferent nerves detect the nature and amount of nutrients present in the GI tract and relay the information to the brain, which controls energy intake and expenditure accordingly. Dietary fat and fatty acids are sensed through various direct and indirect mechanisms. These sensing processes involve the binding of fatty acids to specific G protein-coupled receptors expressed either on the afferent nerve fibres or on the surface of enteroendocrine cells that release gut peptides, which themselves can modulate afferent nerve activity through their cognate receptors or have endocrine effects directly on the brain. Further dietary fat sensing mechanisms that are related to enterocyte fat handling and metabolism involve the release of several possible chemical mediators such as fatty acid ethanolamides or apolipoprotein A-IV. We here present evidence for yet another mechanism that may be based on ketone bodies resulting from enterocyte oxidation of dietary fat-derived fatty acids. The presently available evidence suggests that sympathetic rather than vagal afferents are involved, but further experiments are necessary to critically examine this concept. [ABSTRACT FROM AUTHOR]

Summary Many new substances are currently being investigated for their usefulness in the pharmacotherapy of obesity. Most drugs interfere with monoamine neurotransmitter (serotonin, noradrenalin, dopamine and histamine) effects and act as an appetite suppressant. Other approaches are to primarily increase thermogenesis (e.g. β[sub 3] -adrenoceptor agonists), or to decrease fat absorption by inhibiting the pancreatic lipase (orlistat). New promising agents are substances that increase the effect of corticotropin releasing factor (CRF) or urocortin in the brain (CRF-binding protein ligand inhibitor) and a neuropeptide Y (NPY) Y[sub 5] receptor antagonist. The clinical relevance of leptin in the therapy of obesity is probably limited, but can not be fully evaluated at the moment. As obesity has a multifactorial basis, all these substances have in common the fact that they can not cure obesity. They should only be used as an adjunct to classical strategies like diet and exercise in severe obesity. For developing new, perhaps even more specific pharmacological agents, further research is needed to understand the individually different genetic and physiological basis of obesity. [ABSTRACT FROM AUTHOR]

Presents information on a study that investigated the extrinsic gut neural mediation of the suppression of food intake in male Sprague-Dawley rats. Roles of subdiaphragmatic vagal and nonvagal visceral afferents in the suppression of food intake; What the results indicate; Contribution of intact vagus to behavioral and neural effects of interleukin-1beta.

Studies the role of tumor necrosis factor (TNF)-alpha in bacterial lipopolysaccharide-induced hypophagia. Acute bacterial infections as host defense reaction; Effect of lipopolysaccharides (LPS) hypophagia in the body; Mechanism of LPS tolerance.

Presents a study of reduced food intake in bacterially infected rats. Role played by the vagal or nonvagal nerves from the upper gut in the reduction of food; Methodology of the study; Infection of the rats with lipopolysaccharide and miramyl dipeptide.

Presents information on the TNF-... tolerance blocks lipopolysaccharide (LPS)-induced hypophagia. What the acute bacterial infections serves as; Observation of anorexia.

Chronic exposure to a diet rich in fats changes the gastrointestinal milieu and alters responses to several signals involved in the control of food intake. Oleoylethanolamide (OEA) is a gut-derived satiety signal released from enterocytes upon the ingestion of dietary fats. The anorexigenic effect of OEA, which requires intestinal PPAR-alpha receptors and is supposedly mediated by vagal afferents, is associated with the induction of c-fos in several brain areas involved in the control of food intake, such as the nucleus of the solitary tract (NST) and the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON). In the present study we investigated whether the exposure to a high fat diet (HFD) alters the hindbrain and hypothalamic responses to OEA. To this purpose we evaluated the effects of OEA at a dose that reliably inhibits eating (10 mg/kg i.p.) on the induction of c-fos in the NST, area postrema (AP), PVN and SON in rats maintained either on standard chow or a HFD. We performed a detailed analysis of the different NST subnuclei activated by i.p. OEA and found that peripheral OEA strongly activates c-fos expression in the AP, NST and in the hypothalamus of both chow and HFD fed rats. The extent of c-fos expression was, however, markedly different between the two groups of rats, with a weaker activation of selected NST subnuclei and stronger activation of the PVN in HFD-fed than in chow-fed rats. HFD-fed rats were also more sensitive to the immediate hypophagic action of OEA than chow-fed rats. These effects may be due to a decreased sensitivity of vagal afferent fibers that might mediate OEA's actions on the brain and/or an altered sensitivity of brain structures to OEA. [ABSTRACT FROM AUTHOR]

Glucagon-like peptide-1 receptor ( GLP-1R) agonists such as exendin-4 ( Ex-4) affect eating and metabolism and are potential candidates for treating obesity and type II diabetes. In the present study, we tested whether vagal afferents mediate the eating-inhibitory and avoidance-inducing effects of Ex-4. Subdiaphragmatic vagal deafferentation ( SDA) blunted the short-term (< 1 h) but not long-term eating-inhibitory effect of i.p.-infused Ex-4 (0.1 μg/kg) in rats. A dose of 1 μg/kg Ex-4 reduced 0.5, 1, 2 and 4 h cumulative food intake in SDA and sham-operated rats to a similar extent. Paradoxically, SDA but not sham rats developed a conditioned flavour avoidance ( CFA) after i.p. Ex-4 (0.1 μg/kg). SDA completely blunted the induction of c- Fos expression by Ex-4 in the hypothalamic paraventricular nucleus. Ex-4, however, increased the number of c- Fos expressing cells, independent of intact vagal afferents, in the nucleus accumbens and in the central nucleus of the amygdala, the lateral external parabrachial nucleus, the caudal ventrolateral medulla and the dorsal vagal complex. These data suggest that intact vagal afferents are only necessary for the full expression of the early satiating effect of Ex-4 but not for later eating-inhibitory actions, when circulating Ex-4 might reach the brain via the circulation. Our data also dissociate the satiating and avoidance-inducing effects of the low Ex-4 dose tested under our conditions and suggest that vagal afferent signalling may protect against the development of CFA. Taken together, these findings reveal a complex role of vagal afferents in mediating the effects of GLP-1 R activation on ingestive behaviour. [ABSTRACT FROM AUTHOR]

LPS, a potent activator of the innate immune system, is commonly used to investigate the acute phase response to infection, including anorexia. We investigated the association between the intensity of LPS anorexia and (1) the activation of brain sites initially responding to LPS, measured with c-Fos expression, and (2) co-localization of c-Fos responses with tyrosine hydroxylase (TH), a marker of catecholaminergic (CA) neurons, in the A1 noradrenergic cells (A1). Male Long-Evans rats received 1ml/kg ip injections of 0, 12.5 or 100μg/kg LPS at dark onset. Food intake was measured in one set of rats, and c-Fos and its co-localization with TH in another, unfed set 90min post-injection. LPS reduced 120min food intake in a significantly dose-related manner. LPS increased c-Fos expression in the A1, RPa, nucleus tractus solitarius, paraventricular nucleus, and CeA. C-Fos expression was dose-related, however, only in the RPa and CeA. LPS induced c-Fos in TH-positive neurons in the A1, but this was not dose-related. These results suggest that the dose-related effect of LPS on food intake (1) may originate in differential neuronal processing of LPS-induced signals in the RPa or CeA and (2) does not originate in CA neurons in the A1. [Copyright &y& Elsevier]

High-fat (HF) feeding and obesity lead to progressive reductions in insulin sensitivity and type 2 diabetes mellitus. The cytokine TNF-α has been shown to contribute to this pathology in overweight HF-fed mice. Here we examined whether genetic deficiency of TNF-α protects against the development of insulin resistance independent of HF-feeding or obesity. Eight-wk old TNF-α KO and wild-type (WT) mice were fed chow (CH) or HF (60% energy from fat) diet. One and 4 week later plasma glucose and insulin levels were measured after 12-h fasts and 3-h re-feeding. Plasma leptin and resistin levels and body adiposity were measured after 4 week. KO mice ate more CH, but not more HF diet, than WT mice. BW and adiposity increased more in HF than CH mice, and TNF-α deficiency had no effect on either, despite the CH intake difference. Fasting glucose was lower after 1 week in KO HF than WT HF mice. Fasting insulin was lower in KO CH than WT CH mice. Fed glucose tended to be increased in KO mice in all tests, but was significantly so only in 4-week CH. Fed insulin was markedly lower in KO mice in all tests. Fasting leptin and resistin were increased by HF, with no genotype effect. Fed leptin (CH and HF) and resistin (HF) were reduced in KO mice. These data suggest that TNF-α deficiency improves insulin sensitivity even in the absence of HF-feeding or obesity, and that the mechanism may involve reduced circulating leptin. [Copyright &y& Elsevier]

We recently reported that brief, remotely controlled intrameal hepatic-portal vein infusions of glucagon-like peptide-1 (GLP-1) reduced spontaneous meal size in rats. To investigate the neurobehavioural correlates of this effect, we equipped male Sprague-Dawley rats with hepatic-portal vein catheters and assessed (i) the effect on eating of remotely triggered infusions of GLP-1 (1 nmol/kg, 5 min) or vehicle during the first nocturnal meal after 3 h of food deprivation and (ii) the effect of identical infusions performed at dark onset on c-Fos expression in several brain areas involved in the control of eating. GLP-1 reduced (P < 0.05) the size of the first nocturnal meal and increased its satiety ratio. Also, GLP-1 increased (P < 0.05) the number of c-Fos-expressing cells in the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala, but not in the arcuate or paraventricular hypothalamic nuclei. These data suggest that the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala play a role in the eating-inhibitory actions of GLP-1 infused into the hepatic-portal vein; it remains to be established whether activation of these brain nuclei reflect satiation, aversion, or both. [ABSTRACT FROM AUTHOR]

OBJECTIVE AND METHODS: Mercaptoacetate (MA) inhibits hepatic fatty acid oxidation (FAO) and stimulates feeding in rats fed fat-rich diets. To test whether the feeding stimulation by MA depends on hepatic FAO, we compared the effects of intraperitoneally injected MA (45.6 mg/kg body weight) with saline in rats fed diets containing 18% predominately long-chain triacylglycerols (LCTs; >/=90% 16 C) or 18% medium-chain triacylglycerols (MCTs; 51% 10-12 C). We hypothesized that, because medium-chain fatty acids reach the liver and are oxidized faster than long-chain fatty acids, if MA's feeding-stimulatory effect depends on hepatic FAO, MA should stimulate feeding more in MCT-fed rats than in LCT-fed rats. RESULTS: Although MA injected in mid-light phase stimulated feeding similarly in MCT- and LCT-fed rats, MA injected at light onset initially stimulated food intake (1 h) only in LCT- and not in MCT-fed rats. To investigate MA's metabolic effects during the initial hour, rats were sacrificed 30 min after light-onset injections. At this time plasma beta-hydroxybutyrate appeared to be higher in MCT- than in LCT-fed rats and to be increased by MA. In a final experiment, MA did not affect fatty acid content in liver and duodenum tissues but increased fatty acids in duodenal tissue mitochondria from 12 h-fasted rats fed chow. CONCLUSION: In light-onset tests, adaptation to the MCT diet increased hepatic FAO but not the feeding-stimulatory effect of MA in comparison with adaptation to the LCT diet, suggesting that at this time MA does not act in the liver to stimulate feeding or that this effect is not due to FAO inhibition. Inhibition of duodenal mitochondrial FAO may be another metabolic process through which MA stimulates feeding. [ABSTRACT FROM AUTHOR]

Abstract: To determine whether Toxoplasma gondii infection could modify biological phenomena associated with brain ischemia, we investigated the effect of permanent middle cerebral artery occlusion (MCAO) on neuronal survival, inflammation and redox state in chronically infected mice. Infected animals showed a 40% to 50% decrease of infarct size compared with non-infected littermates 1, 4 and 14 days after MCAO. The resistance of infected mice may be associated with increased basal levels of anti-inflammatory cytokines and/or a marked reduction of the MCAO-related brain induction of two pro-inflammatory cytokines, tumor necrosis factor-alpha and interferon-gamma (IFNγ). In addition, potential anti-inflammatory/neuroprotective factors such as nerve growth factor, suppressor of cytokine signaling-3, superoxide dismutase activity, uncoupling protein-2 and glutathione (GSH) were upregulated in the brain of infected mice. Consistent with a role of GSH in central cytokine regulation, GSH depletion by diethyl maleate inhibited Toxoplasma gondii lesion resistance by increasing the proinflammatory cytokine IFNγ brain levels. Overall, these findings indicate that chronic toxoplasmosis decisively influences both the inflammatory molecular events and outcome of cerebral ischemia. [Copyright &y& Elsevier]

Abstract: Because of the increasing anthelmintic resistance and the impact of conventional anthelmintics on the environment, it is important to look for alternative strategies against gastrointestinal nematodes. Phytotherapy could be one of the major options to control these pathologies. Extracts or ingredients of six different plant species were tested against exsheathed infective larvae of Haemonchus contortus using a modified methyl-thiazolyl-tetrazolium (MTT) reduction assay. Pyrantel tartrate was used as reference anthelmintic. Bromelain, the enzyme complex of the stem of Ananas comosus (Bromeliaceae), the ethanolic extracts of seeds of Azadirachta indica (Meliaceae), Caesalpinia crista (Caesalpiniaceae) and Vernonia anthelmintica (Asteraceae), and the ethanolic extracts of the whole plant of Fumaria parviflora (Papaveraceae) and of the fruit of Embelia ribes (Myrsinaceae) showed an anthelmintic efficacy of up to 93%, relative to pyrantel tartrate. Based on these results obtained with larval Haemonchus contortus, the modified MTT reduction assay could be a possible method for testing plant products with anthelmintic properties. [Copyright &y& Elsevier]

This study tested the hypothesis that purebred Boran ( Bos indicus) cows and crossbreds of Boran and Holstein respond differently to long-term changes of feeding level in nutrient partitioning to milk and body fat stores. A total of 27 cows of these two genotypes were subjected either to a low or a high feeding level from their first oestrus as heifers until birth of their third calf. Half of the cows of each genotype were then switched to the other feeding level during the third reproduction cycle. If at all, Boran cows responded to a change in the feeding level almost exclusively by a corresponding change in body weight but not milk yield. Crossbred cows kept continuously on the low feeding level had a lower milk yield than those continuously fed the high level, but lost similar amounts of body weight. In crossbred cows, changing the feeding level from high to low was accompanied by a mobilization of body reserves, whereas a change from low to high level resulted mostly in an increase in milk yield. Certain other genotype differences in metabolic response were obvious from differences in body composition and from the metabolic profile either reflected in blood (particularly insulin-like growth factor I) or in adipose tissue (lipoprotein lipase). Reproductive performance differed between genotypes, with shorter lactations associated with earlier occurrences of the first oestrus in the Boran cows. Generally, feeding history appeared to have at least as much influence on energy partitioning as the actual feeding level. In conclusion, purebred Boran cows seem to react to long-term food fluctuations mainly by mobilizing and restoring body fat reserves, whereas cows crossbred with Holstein tend to spend extra energy preferentially for milk production. [ABSTRACT FROM AUTHOR]

Abstract: To investigate the possible involvement of leptin signaling in lipopolysaccharide (LPS) anorexia, we compared the anorectic effect of LPS in genetically obese (fa/fa) Zucker rats and in their lean (Fa/?) counterparts. The effects of interleukin-1β (IL-1β) and muramyl dipeptide (MDP) were also tested. LPS [100 μg/kg body weight (BW)], IL-1β (2 μg/kg BW) and MDP (2.2 mg/kg BW) injected intraperitoneally (i.p.) at lights out reduced food intake similarly in obese and lean rats. LPS injection at 500 or 1000 μg/kg BW (i.p.) also reduced food intake and BW similarly in obese and lean rats, but obese regained BW faster than lean rats. LPS (2.45 μg or 9.8 μg/h/rat) administered chronically with i.p. implanted osmotic pumps reduced food intake similarly on experimental day 1, regardless of the genotype. After day 3, the lean rats'' anorectic response and recovery were dose-dependent, whereas the anorectic response in obese rats was minimally affected by dose (significant dose effect only on day 3). Again, obese rats regained lost BW faster than lean rats. These results do not support a role for leptin as the sole mediator of anorexia induced by bacterial products (LPS and MDP) and IL-1β. [Copyright &y& Elsevier]

The cell surface component CD14 and the toll-like receptors 2 and 4 (TLR2 and TLR4) are important in mediating the immune responses to bacterial products in mammals. Using mice genetically deficient in CD14, TLR2, or TLR4, we studied the role of these molecules in the anorectic effects of LPS and muramyl dipeptide (MDP). CD14 or TLR2 knockout (KO) and TLR4-deficient (TLR4DEF) mice as well as corresponding wild-type (WT) colittermates were injected intraperitoneally at dark onset with LPS (2 µg/mouse), MDP (10 mg/kg), interleukin 1 β (IL- 1β, 150 ng/mouse), or vehicle, and food intake was recorded. LPS and MDP reduced food intake in WT mice of all genotypes tested. The anorectic effect of LPS was attenuated (P < 0.04) in CD14-KO and TLR4-DEF mice but not in TLR2-KO (P > 0.05). The anorectic effect of MDP was blunted in CD14-KO and TLR2-KO (P < 0.02) mice but not in TLR4-DEF mice. IL-1β reduced food intake similarly in all genotypes tested. These results indicate that CD14 is involved in mediating the anorectic effects of both LPS and MDP. Furthermore, TLR4 and TLR2 are specifically involved in mediating the anorectic effects of LPS and MDP, respectively. The results are consistent with the hypothesis that TLR4 functions as the true LPS receptor and that TLR2 is involved in recognition of gram-positive bacterial products. [ABSTRACT FROM AUTHOR]

Forty-eight helminth-free lambs were divided into eight groups (A–H) of six animals. Groups A–G were infected artificially with 10 000 third stage larvae of Haemonchus contortus and 20 000 third stage larvae of Trichostrongylus colubriformis, whereas group H remained uninfected. Thirty days post-infection the lambs were treated orally with a single dosage of one of the following products: group A with 3 mg/kg body weight (BW) of an aqueous ethanol extract (70%, v/v) of the seeds of Azadirachta indica A. Juss syn. Melia azedarach L. (Meliaceae); group B with 1 g/kg BW of a raw powder of the leaves of Ananas comosus (L.) Merr. (Bromeliaceae); group C with 0.3 mg/kg BW of an aqueous ethanol extract of a 1:1 mixture (g/g) of Vernonia anthelmintica (L.) Willd. (Asteraceae) seeds and Embelia ribes Burm (Myrsinaceae) fruits; group D with 183 mg/kg BW of an aqueous ethanol extract of the whole plants of Fumaria parviflora Lam. (Fumariaceae); group E with 28 mg/kg BW of an aqueous ethanol extract of the seeds of Caesalpinia crista L. (Caesalpiniaceae); group F with 25 mg/kg BW of pyrantel tartrate and group G with 50% ethanol. Group H remained untreated. Only the ethanol extract of F. parviflora caused a strong reduction of the faecal egg counts (100%) and a 78.2 and 88.8% reduction of adult H. contortus and T. colubriformis on day 13 post-treatment. The extract was as effective as the reference compound pyrantel tartrate. Therefore, the ethanol extract itself or single constituents of F. parviflora could be a promising alternative source of anthelmintic for the treatment of gastrointestinal trichostrongylids in small ruminants. [Copyright &y& Elsevier]

Examines the role of cyclooxygenase (COX)-2 in lipopolysaccharide (LPS)-induced anorexia in rats. Influence of nonselective SOX inhibition on LPS attenuation; Efficacy of resveratrol in inducing anorexia; Factors mediating the COX-2 anorectic response to peripheral LPS.

Respiratory syncytial virus (RSV) has been reported to induce the production of chemokines in the airway epithelia. Dendritic cells (DC) are the most potent antigen-presenting cells. They are located throughout the body and release chemokines in response to inflammation and infection. We have investigated the chemokine profile of bovine DC in response to exposure to bovine RSV (BRSV). Transcripts for several chemokines were detected by RT-PCR, subsequently cloned and expressed, and the products analysed by western blotting. To test the effect of the recombinant chemokines on RSV-induced T cell proliferation, DC were pulsed with BRSV, irradiated, and added to purified bovine CD4+ T cells from RSV-immune cattle in combination with various concentrations of recombinant chemokines, and the proliferative response of the T cells assessed. Eotaxin was the only chemokine, of those investigated, that specifically enhanced the T cell response to BRSV-pulsed DC. Addition of MIP-1α to control wells or to wells containing BRSV-pulsed DC had similar effects, suggesting non-specific stimulation of T cells. RANTES and MIP-3α did not seem to influence the proliferative response of T cells co-cultured with BRSV-pulsed DC. Thus, although BRSV induced the production of several chemokines by DC, only eotaxin promoted a BRSV specific CD4+ T cell proliferative response. [Copyright &y& Elsevier]

Experiments on the host cell spectrum of bovine leukaemia virus (BLV), a retrovirus closely related to the human T-cell leukaemia virus (HTLV), have yielded conflicting data. Currently, BLV is known to infect B cells, whereas its ability to infect other cell types, e.g. monocytes/macrophages, is doubtful. As monocytes/macrophages may have profound effects on the diversity of the T-cell response, we studied the possibility of in vitro infection, using bovine monocytes and SV40-transformed bovine macrophages. Proviral DNA was detected by nested polymerase chain reaction (PCR) from day 1 until the end of the experiments at either day 5 or day 80, depending on the quantity of virus used for infection. In addition, the infection was associated with morphological changes in infected cells as revealed by electron microscopy. The in vitro infection did not significantly change either the expression of surface antigens (CD11b, CD32, and major histocompatibility complex (MHC) class II) or the amounts of cytokine transcripts (interleukin (IL)-1β, tumour necrosis factor (TNF)-α, IL-6 and IL-12p40) with or without lipopolysaccharide (LPS) stimulation. The data suggest that BLV can infect monocytes, but the infection does not seem to influence the function or the phenotype of these cells. Infected monocytes may, however, play a role as a viral reservoir in vivo. [ABSTRACT FROM AUTHOR]

Summary A 5-week experiment with 24 multiparous early lactating Brown Swiss cows was conducted to investigate the effects of supplementary rumen-protected methionine in conjunction with dietary protein reduction on metabolism and performance after 1 week of control measurement. Three rations containing 175, 150 and 125 g of crude protein/kg feed dry matter were supplemented with methionine. The fourth ration, also only containing 125 g of crude protein/kg dry matter, remained unsupplemented. The four treatment groups had a similar metabolic supply of other essential amino acids, protein and energy, as calculated by various approaches. The two low protein rations were, however, slightly deficient in ruminally degraded protein. Treatment effects remained low on feed intake, forage meal pattern, milk yield and fat as well as lactose content. In contrast, the content and yield of milk protein significantly declined only in the unsupplemented low protein ration relative to the initial value. Compared with this ration, the decline in milk protein yield was clearly delayed in the supplemented low protein ration. Blood plasma methionine tended to be reduced without supplementation and to be increased with additional methionine. Supplementation of methionine reduced other plasma amino acids. Plasma insulin, glucose, lactate, ketone bodies and aspartate amino transferase activity indicated a certain liver stress and a somewhat elevated energy requirement with high and particularly with low protein content (when unsupplemented). Methionine improved metabolic protein utilization, followed by the lowest plasma, urine and milk urea levels in the supplemented low protein diet. In conclusion, no major adverse effects were assessed under the conditions tested. Supplementation of methionine may nevertheless be useful in rations with particularly low protein content fed to early lactating cows in order to prevent negative long-term effects which were only visible here as trends. [ABSTRACT FROM AUTHOR]

Presents information on a study which examined the metabolic effects of adding lysine and methionine to a ration of calculated deficiency in amino acids in Brown Swiss cows. Material and methods; Results and discussion; Conclusions.

Summary Background: Athletes consume arginine and/or aspartate as potential nutritional ergogenics. Their metabolic effects are controversial and there is some evidence that ingestion of large doses of single amino acids can adversely affect the nitrogen balance or induce an amino acid imbalance. Nevertheless, the general metabolic influence of an arginine aspartate supplementation during a prolonged exercise bout has not yet been investigated. Aim of the study: The aim of this study was, therefore, to investigate the general metabolic impact of a chronic supplementation with arginine aspartate in endurancetrained athletes at rest and during a marathon run. Methods: Fourteen endurance-trained runners participated in this field study which was carried out according to a double-blind crossover design. 15 g of arginine aspartate or a carbohydrate-based placebo were supplemented daily for 14 days before a marathon run. Blood samples for analysis of metabolites and hormones were collected shortly before the run, after 31 km, at the end of the run, and alter a recovery period of two hours. Additionally, the respiratory exchange ratio was determined during the run. Results: The plasma level of carbohydrate (glucose, lactate, pyruvate) and fat metabolites (fatty acids, glycerol, &beta-hydroxybutyrate), cortisol, insulin, ammonia, lactate dehydrogenase, and creatine kinase as well as the respiratory exchange ratio were unaffected by the supplementation. In contrast, the plasma level of somatotropic hormone, glucagon, urea, and arginine were significantly increased, and the level of most of the remaining plasma amino acids as well as their sum was significantly reduced. Conclusions: There was no obvious metabolic benefit derived from the chronic supplementation with arginine aspartate. And since furthermore the consequences of a reduction of the total plasma amino acid level are not known, the practice of using single amino acid supplements as potential ergogenics should [ABSTRACT FROM AUTHOR]

An inbreeding program has been carried out with the Swiss sublines of Roman high- and low-avoidance rats since 1993. The present study reports the first experiments conducted with young animals of those inbred strains (RHA-I/Verh and RLA-I/Verh, respectively) from the sixth and seventh inbreeding generations. The results confirmed expected behavioral profiles. Compared to the RHA-I/Verh strain, RLA-I/Verh rats showed decreased entries into the illuminated central arena of an hexagonal tunnel maze, as well as decreased spontaneous locomotor activity and increased defecations, in two independent experiments. Young RLA-I/Verh females explored less than did their RHA-I/Verh counterparts during session 1 of a conditioned-fear experiment preceding shock administration, and in session 2 (conducted 24 h after the application of three footshocks), they showed greater conditioned behavioral inhibition (i.e., reduced amount of rearing), as well as higher defecation scores, than did RHA-I/Verh females. [ABSTRACT FROM AUTHOR]