A novel behavioral model of the pasture-based dairy cow from GPS data using data mining and machine learning techniques.

A better understanding of the behavior of individual grazing dairy cattle will assist in improving productivity and welfare. Global positioning systems (GPS) applied to cows could provide a means of monitoring grazing herds while overcoming the substantial efforts required for manual observation. Any model of behavioral prediction using GPS needs to be accurate and robust by accounting for inter-cow variation as well as atmospheric effects. We evaluated the performance using a series of machine learning algorithms on GPS data collected from 40 pasture-based dairy cows over 4 mo. A feature extraction step was performed on the collected raw GPS data, which resulted in 43 different attributes. The evaluated behaviors were grazing, resting, and walking. Classifier learners were built using 10 times 10-fold cross validation and tested on an independent test set. Results were evaluated using a variety of statistical significance tests across all parameters. We found that final model selection depended upon level of performance and model complexity. The classifier learner deemed most suitable for this particular problem was JRip, a rule-based learner (classification accuracy=0.85; false positive rate=0.10; F-measure=0.76; area under the receiver operating curve=0.87). This model will be used in further studies to assess the behavior and welfare of pasture-based dairy cows.

Myostatin alters glucose transporter-4 (GLUT4) expression in bovine skeletal muscles and myoblasts isolated from double-muscled (DM) and normal-muscled (NM) Japanese shorthorn cattle.

The purpose of this study was to determine whether myostatin alters glucose transporter-4 (GLUT4) expression in bovine skeletal muscles and myoblasts isolated from double-muscled (DM) and normal-muscled (NM) Japanese Shorthorn cattle. Plasma concentrations of glucose were lower in DM cattle than in NM cattle (P < 0.01). The expression of GLUT4 messenger RNA (mRNA) in the skeletal muscle ex vivo and in myoblasts at 72 h after differentiation in vitro was higher in DM cattle than in NM cattle (P < 0.01). In contrast, the NM and DM cattle did not differ with respect to skeletal muscle expression of GLUT1 and myocyte enhancer factor-2c (MEF2c), a transcription factor of GLUT4. In differentiated myoblasts, the expression of GLUT1, GLUT4, and MEF2c mRNAs was greater in DM cattle than in NM cattle (P < 0.01). In the presence and absence of insulin, glucose uptake in myoblasts was increased in DM cattle relative to that of NM cattle (P < 0.01). The addition of myostatin decreased the expression of GLUT4 and MEF2c mRNAs in DM myoblasts (P < 0.05). Results of the present study suggest that myostatin inhibits the expression of GLUT4 mRNA possibly via MEF2c and that the greater ability of the DM cattle to produce muscle relative to the NM cattle may be due to their greater sensitivity to insulin and greater use of glucose.

Proliferating bovine intramuscular preadipocyte cells synthesize leptin.

Leptin is thought to be not only a satiety factor but also a stimulator of angiogenesis. We examined leptin, PPARγ2, and vascular endothelial growth factor (VEGF) expression in bovine intramuscular preadipocyte (BIP) cells during proliferation. The cells were seeded at 0.85 × 10(4) cells/cm(2) and collected every day until the fifth day after passage. Leptin mRNA was present in the cells between days 2 and 4, as indicated by RT-PCR analysis. Western blot analysis showed a band for leptin at approximately 16 kDa on all of the days during growth, and the cytoplasmic concentration of leptin was highest on day 2 and decreased gradually thereafter. A PPARγ2 band at approximately 54 kDa was also observed on all days. The concentration was highest on day 2 and decreased thereafter, which is similar to the expression pattern of leptin. In constant, the expression level of VEGF protein did not change while in culture. We have demonstrated that BIP cells can synthesize both leptin and PPARγ2, with maximal synthesis occurring during maximal proliferation. Given the role of leptin in angiogenesis, we speculate that leptin is involved in the neovascularization of adipose tissue, because new organization of adipose tissue requires the growth of new blood vessels.

Enhancing phosphorus and zinc acquisition efficiency in rice: a critical review of root traits and their potential utility in rice breeding.

BACKGROUND: Rice is the world's most important cereal crop and phosphorus (P) and zinc (Zn) deficiency are major constraints to its production. Where fertilizer is applied to overcome these nutritional constraints it comes at substantial cost to farmers and the efficiency of fertilizer use is low. Breeding crops that are efficient at acquiring P and Zn from native soil reserves or fertilizer sources has been advocated as a cost-effective solution, but would benefit from knowledge of genes and mechanisms that confer enhanced uptake of these nutrients by roots. SCOPE: This review discusses root traits that have been linked to P and Zn uptake in rice, including traits that increase mobilization of P/Zn from soils, increase the volume of soil explored by roots or root surface area to recapture solubilized nutrients, enhance the rate of P/Zn uptake across the root membrane, and whole-plant traits that affect root growth and nutrient capture. In particular, this review focuses on the potential for these traits to be exploited through breeding programmes to produce nutrient-efficient crop cultivars. CONCLUSIONS: Few root traits have so far been used successfully in plant breeding for enhanced P and Zn uptake in rice or any other crop. Insufficient genotypic variation for traits or the failure to enhance nutrient uptake under realistic field conditions are likely reasons for the limited success. More emphasis is needed on field studies in mapping populations or association panels to identify those traits and underlying genes that are able to enhance nutrient acquisition beyond the level already present in most cultivars.

Platelet-derived growth factor acts via both the Rho-kinase and p38 signaling enzymes to stimulate contraction in an in vitro model of equine wound healing.

Horses are more prone to complications in the wound healing process than other species, and problems such as chronic inflammation, delayed epithelialization, poor wound contraction, and exuberant granulation tissue are commonly seen, particularly in wounds on the distal limbs. In comparison, wounds of the oral mucosa heal rapidly in a scarless fashion with a high degree of wound contraction. The effect of platelet-derived growth factor BB (PDGF), insulin-like growth factor (IGF)-1, and transforming growth factor beta1 (TGFbeta1) on the contraction of a fibroblast-populated collagen matrix (FPCM) as a model of equine wound contraction was investigated using equine oral fibroblasts. The fibroblasts were embedded into floating FPCM and treated with PDGF, IGF-1, and TGFbeta1. The surface areas of the FPCM were determined daily for 5 d. Platelet-derived growth factor significantly stimulated the contraction of the FPCM at an optimal concentration of 10 ng/mL (P=0.025). Insulin-like growth factor-1 and TGFbeta1 did not significantly affect the contraction of the FPCM relative to the control. To elucidate the mechanisms by which PDGF stimulated contraction of FPCM, the Rho-kinase and p38 cell signaling pathways were blocked, resulting in a significant inhibition (P<0.001) of PDGF-stimulated contraction. Platelet-derived growth factor BB is a potent stimulator of fibroblast migration, and hence the FPCM contraction generated here is probably a result of its effects on cell migration. The results of the present experiment suggest that this effect is stimulated via both the Rho-kinase and p38 signaling pathways in equine oral fibroblasts.

Relationship between the milk yield response to short-term bovine somatotropin treatment and the lipolytic response to adrenaline in dairy cows.

The aim of this experiment was to determine if the milk yield response of dairy cows to short-term treatment with bovine somatotropin (bST) was correlated with the non-esterified fatty-acid (NEFA) response to an adrenaline challenge. Twenty-six multiparous Holstein cows (58+/-5.4 days postpartum) received daily sub-cutaneous injections of saline for 7 days followed by sub-cutaneous injections of 20mg/day of bST for 14 days. On day 7 of the saline treatment and day 14 of the bST treatment the cows were given an intravenous injection of adrenaline (1.4 microg/kg body weight). Blood samples were taken before and after the adrenaline challenge. The difference in milk yield between the saline and the second week of bST treatment (MYR) varied considerably between animals (from -0.4 to +8.0 kg/day). MYR was positively correlated with the change in the basal concentration of NEFA between the saline and second week of bST treatment, as well as with the change in the area under the profile of NEFA above basal values following the adrenaline challenge. It remains to be established whether the greater lipolytic responses to adrenaline of the cows with the greater MYR reflects the deeper negative energy that these animals also experienced or a fundamental difference in the physiology of their adipose tissue.

Correlation of blood and milk components with the milk yield response to bovine somatotropin in dairy cows.

Our aim was to correlate the individual variation in the milk yield response (MYR) of Holstein dairy cows to bovine somatotropin (bST), with changes in milk plasmin and plasminogen activities as well as with plasma hormone and metabolite levels. Thirty-two housed multiparous Holstein cows (90 +/- 3.8 days post partum) received daily subcutaneous injections of saline for 1 week followed by subcutaneous injections of 20 mg/day of bST for 2 weeks. Blood samples were taken at approximately 4h intervals over 24 h at the end of the saline and bST treatment periods. Milk samples were also taken at the end of the saline and bST treatment periods. The difference in milk yield between the saline and the second week of bST treatment (MYR) varied considerably between animals (from -0.2 to +8.6 kg/day, relative to the saline treatment week). Low milk yield before bST treatment was associated with a high MYR. The plasma growth hormone response to treatment was negatively correlated with MYR. Plasma insulin-like growth factor-1 response to treatment was positively correlated with MYR. Furthermore, a high MYR to bST was associated with a lower milk plasminogen level before treatment and a greater reduction in the level of plasminogen in milk following treatment.

Individual variation in the milk yield response to bovine somatotropin in dairy cows.

The objective was to relate the short-term milk yield response (MYR) following use of exogenous bovine somatotropin (bST) to changes in plasma concentrations of metabolites and hormones. Twenty-four Holstein cows (52 +/- 4.1 d postpartum) received daily subcutaneous injections of saline for 1 wk followed by subcutaneous injections of 33 mg/d of bST for 2 wk (Trial 1). The difference in milk yield between wk 1 and 3 for each cow was used to determine the 5 cows with the highest (HR) and 5 with the lowest responses (LR) to bST. These 10 cows were then used in 3 further trials of the same design (Trials 2, 3, and 4, conducted at 122, 181, and 237 +/- 7.6 d postpartum, respectively). Blood samples were taken 2 h after the administration of bST on d 1, 3, 5, 15, 17, and 19 of each trial. The HR group had consistently greater MYR to bST than the LR group throughout their lactation. The LR group had a higher milk yield and lower plasma insulin like growth factor-I (IGF-I) concentrations during the saline treatment in all trials. The increase in plasma somatotropin concentrations following injections of bST was greater for the LR group, whereas the difference in plasma IGF-I level between wk 1 and 3 was greater for the HR group. The HR group had lower levels of 3-hydroxy-butyrate and nonesterified fatty acids before bST treatment. Low short-term response to bST was associated with plasma concentrations of hormones and metabolites that indicate negative energy balance, although other factors may be involved.

Effects of heat exposure on adrenergic modulation of insulin and glucagon secretion in sheep.

The effects of heat exposure on the adrenergic modulation of pancreatic secretion were investigated. Five ewes fed at maintenance level (ME base) were housed in thermoneutral (TN; 20 degrees C) and hot (30 degrees C) environments. Heat exposure caused an increase in respiration rate and a slightly higher rectal temperature, and decreases in basal insulin and glucose concentrations. Infusions of saline plus epinephrine caused increases in glucagon and glucose concentrations, and no significant change in insulin secretion. Phentolamine (an adrenergic alpha-antagonist) plus epinephrine augmented insulin secretion; however, this insulin secretory response was inhibited by heat exposure. Propranolol (a beta-antagonist) plus epinephrine produced a slight decrease in insulin secretion in the TN environment, whereas no effect was observed during heat exposure. While glucagon secretion through alpha-adrenergic stimulation was not affected by heat exposure, homeostatic signals controlling insulin release seemed to be affected during heat exposure. We thus hypothesised that insulin concentration is decreased in sheep fed at maintenance level in hot environments, and that this response is mediated in part by a modulation of beta-adrenergic function.

Effect of alpha 1-acidic glycoprotein in the ascitic fluid of cancer patients on human NK cells: selective suppression of interferon-induced NK activation.

The in vitro effect of C-AGP (pure alpha1-acid glycoprotein from the ascitic fluid of cancer patients) on NK cell cytotoxicity was tested using normal healthy human PBMC. C-AGP had no inhibitory effect on basal NK cell activity. C-AGP selectively suppressed the augmentation of NK cell activity by rIFNalphaA and rIFNgamma, but C-AGP did not prevent the NK activation by rIL-2. NK cells in PBMC treated with C-AGP for 12 h and then washed just once, to remove the C-AGP, fully recovered the ability to respond to rIFNalphaA. However, after the treatment of PBMC with C-AGP for 5 or 6 days, NK cells failed to respond to rIFNalphaA, in spite of washing to remove C-AGP from the cultures. Monocytes were necessary for the suppressive effect of C-AGP on rIFNalphaA activation of NK cells. Indomethacin restored the ability of NK cells to respond to rIFNalphaA in C-AGP-treated PBMC. These results suggest that monocytes are able to selectively suppress the response of NK cells to IFNs in the presence of, or following treatment with C-AGP.

A 63 kDa tumor necrosis factor inhibitor released from a human monocytic leukemia cell line, THP-1.

A human monocytic cell line, THP-1-S, was cultured in a serum-free medium. The effect of the culture supernatant of THP-1-S on the cytotoxicity of rTNF-alpha to three kinds of cell lines and the binding of rTNF to its receptor were tested. The supernatant inhibited the cytotoxicity of rTNF-alpha when tested by the neutral red uptake method. In addition, the supernatant blocked the binding of 125I-rTNF-alpha to its receptor. Furthermore, following precipitation with PEG we detected complexes between rTNF-alpha and the inhibitory factor which formed during incubation with the culture supernatant from THP-1-S cells. However, the supernatant did not bind to or down-regulate the receptor for TNF-alpha on the cell surface of L-M-2d6 cells. This factor eluted with an apparent molecular mass of 63,000 Da by gel filtration and did not react with antibodies against p55 and p75 TNF receptors. These data suggest that human monocytic cells are capable of releasing an inhibitory factor against rTNF-alpha in serum-free culture conditions.

Heat influences on plasma insulin and glucagon in response to secretogogues in non-lactating dairy cows.

Four non-lactating cows were offered a maintenance diet of hay wafer and a commercial concentrate. They were housed in a thermoneutral (TN; 20 degrees C) and then a hot (30 degrees C) environment in an artificial climate chamber. Glucose, arginine, butyrate, and insulin were administered through one jugular catheter, and from a catheter on the other side venous blood was collected. The peak increments in plasma insulin after the glucose and butyrate administrations were lower during heat exposure. The response of insulin after arginine injection was smaller in the hot compared with the thermoneutral environment; however, arginine injection resulted in a significantly higher secretion of glucagon in the hot environment. The response area of insulin after the insulin injection was smaller in the hot environment; however, insulin clearance rate was not changed. It is concluded that in non-lactating cows, insulin release is probably lower during heat exposure. With respect to plasma glucose during heat exposure, the lower basal values, lower concentrations after the end of the glucose infusion, and delayed recovery to basal values after the butyrate and insulin administrations observed, may indicate lower gluconeogenesis and glycogenolysis in the hot environment.

Effect of glucose-dependent insulinotropic polypeptide on whole-body glucose utilization in sheep.

Four adult Corriedale sheep were used in an experiment divided into three parts. In part 1 a primed continuous infusion of [6, 6-2H2]glucose was infused for 7 h. The first 3 h was the control period, from 3 to 7 h glucose-dependent insulinotropic polypeptide (GIP) was infused, and from 5 to 7 h somatostatin was infused. Part 2 of the experiment was the same as for part 1 except that insulin was infused between 3 h and 7 h and GIP was infused between 5 and 7 h. Coincident with the insulin infusion, normal glucose was also infused at a variable rate in order to keep the plasma glucose at basal levels. In part 3 of the experiment [6,6-2H2]glucose was infused for 5 h and somatostatin was infused between 3 and 5 h. Measurements of glucose turnover were made in the last 40 min of the control, GIP only, insulin only, somatostatin only, GIP plus somatostatin and GIP plus insulin infusion periods. Plasma insulin levels were reduced to the limit of detection by the somatostatin infusion; under such conditions whole-body glucose uptake should be entirely non-insulin-mediated (NIMGU). Expressing glucose disposal as glucose metabolic clearance rate demonstrated that elevated, but still physiological GIP levels had no effect on NIMGU but significantly increased insulin-mediated glucose uptake when plasma insulin levels were similar to levels typically observed after a meal. These results indicate that in sheep, GIP may enhance insulin action with respect to glucose disposal following a meal, but has no effect on glucose disposal pathways not responsive to insulin.

Insulin and glucagon secretion in lactating cows during heat exposure.

Heat stress affects endocrine systems in cows. This study investigated changes in insulin and glucagon secretion between thermoneutral (TN; 18 degrees C, relative humidity [RH] 60%) and hot (28 degrees C, RH 60%) environments in lactating cows. Glucose, arginine, and butyrate were administered i.v. to four cows (mean, at 83 d postpartum) in each environment. Blood was collected via a jugular catheter at regular intervals. Heat exposure resulted in a marked increase in respiration rate and rectal temperature. A decrease in milk yield was also observed during heat exposure. Basal insulin concentrations were elevated, and basal glucose concentrations tended to be lower in the hot environment. Peak values of insulin and glucagon following the arginine injection were significantly higher in the hot than in the TN environment. The insulin peak value in response to the butyrate infusion was also higher during the heat exposure. However, insulin and glucagon responses to the glucose load were not affected by heat stress. The increase in plasma glucose concentration following arginine injection was inhibited by the heat exposure. In conclusion, heat stress resulted in a higher insulin secretion in lactating cows. Glucagon secretion in response to the arginine injection was enhanced, but the rise in plasma glucose was inhibited by heat exposure. These changes would be related to a reduction in milk yield during heat stress.

Insulin-independent glucose uptake in growth hormone treated dairy cows.

Our aim was to determine the effect of growth hormone on non-insulin-mediated glucose disposal in lactating dairy cows. Following 5 d of subcutaneous injections of either saline or growth hormone, insulin, somatostatin or insulin plus somatostatin were infused for 2 h each, in a series of experiments. Coincident with this, unlabelled glucose was infused at a variable rate to maintain a constant plasma glucose concentration. Glucose, doubly labelled with deuterium, was also infused for the calculations of glucose turnover. Plasma insulin levels were reduced to nearly zero by the infusion of somatostatin; under such conditions whole body glucose disposal should be non-insulin-mediated. Dairy cows treated with growth hormone, which had significantly increased milk yields on the day before the experimental infusions, did not have different levels of whole body non-insulin-mediated glucose disposal when expressed in absolute terms. Growth hormone did not affect non-mammary non-insulin-mediated glucose uptake estimated by calculation. Growth hormone significantly inhibited insulin-mediated glucose uptake when plasma insulin levels were elevated. Glucose uptake during insulin plus somatostatin infusion was not significantly different from that of the insulin only infusion.

Effects of heat exposure on plasma insulin, glucagon and metabolites in response to nutrient injection in heifers.

Effects of heat exposure on plasma insulin, glucagon, and metabolite responses following injection of various nutrients were investigated in heifers. Four heifers, fed hay wafer and a commercial concentrate, were exposed to thermoneutral (20 degrees C) and hot (30 degrees C) environments. Glucose, arginine and butyrate (each injection at 0.625 mmol/kg) and insulin (0.2 U/kg) were injected intravenously, and then blood samples were collected at regular intervals through jugular vein catheters. Insulin secretion in response to glucose and arginine injection was not affected by heat exposure. However, the insulin response following butyrate injection was inhibited in heifers exposed to heat. In the hot environment, glucagon responses following the arginine and butyrate injections were augmented significantly, however glucagon levels were inhibited following the glucose injection. It is concluded that heat stress causes an inhibition of the insulin response to butyrate injection, and an increase in the glucagon response following arginine and butyrate injection. Plasma metabolite concentrations altered in accordance with the changes in the concentration of pancreatic hormones.

Non-insulin- and insulin-mediated glucose uptake in dairy cows.

Four mid-lactation Holstein dairy cows (mean milk yield on day of experiments 26.1 kg/d) were used in a series of experiments to establish the contribution of non-insulin-mediated glucose uptake to total glucose uptake at basal insulin concentrations. A secondary objective was to determine whether somatostatin affects the action of infused insulin. In part I of the experiment a primed continuous infusion [6,6-2H]glucose (45.2 micrograms/kg per min) was begun at time 0 and continued for 5 h. After 3 h of [6,6-2H]glucose infusion (basal period) a primed continuous infusion of insulin (0.001 i.u./kg per min) was administered for 2 h. Coincidental with the insulin infusion, normal glucose was also infused in order to maintain the plasma glucose concentration at euglycaemia. Part II of the experiment was the same as part I except that somatostatin was infused for 2 h (0.333 micrograms/kg per min) instead of insulin. In part III of the experiment both insulin and somatostatin were infused for the final 2 h. Plasma insulin levels were increased by insulin infusion (to 0.1476 to 0.1290 i.u./l for parts I and III respectively) and were reduced by somatostatin infusion in part II (to 0.006 i.u./l) relative to the basal periods (mean 0.021 i.u./l). Glucose uptake during somatostatin infusion (2.50 mg/kg per min; part II) was 92.0% of that observed in the respective basal period (2.72 mg/kg per min). Circulating insulin levels were much lower than the dose of insulin that causes a half maximal effect on glucose uptake (0.06-0.10 i.u./l for ruminants); consequently insulin-mediated glucose uptake was probably absent in part II. Secondly, glucose uptake following insulin only infusion (4.05 mg/kg per min) was significantly lower than that observed when insulin plus somatostatin was infused (4.69 mg/kg per min), indicating that somatostatin either directly or indirectly enhanced the action of insulin on glucose uptake.

Growth hormone does not affect non-insulin-mediated glucose uptake in sheep.

Four adult Merino sheep were used in the experiment, which was divided into four parts. For the 5 days before parts 1 and 3 saline was injected and for the 5 days before parts 2 and 4 growth hormone (GH; 4 mg day-1 subcutaneously) was injected. In parts 1 and 2 a primed continuous infusion of [6,6-2H2]glucose and either saline or GH, respectively, were infused for 5 h. The first 3 h was the control period. From 3 to 5 h insulin (0.5 mU kg-1 min-1) was infused. Coincident with the insulin infusion, normal glucose was also infused at a variable rate, dependent on the rapidly determined plasma glucose concentration, in order to keep the plasma glucose concentration constant. Parts 3 and 4 of the experiment were the same as parts 1 and 2, respectively, except for the following: the glucose isotope and saline or GH were infused for 7 h, from 3 to 7 h somatostatin (SRIF; 0.417 microgram kg-1 min-1) was infused, and from 5 to 7 h insulin was infused. Measurements of glucose turnover were made in the last 40 min of the control, insulin-only, SRIF-only and insulin-plus-SRIF infusion periods. Plasma insulin levels were reduced to below the level of detection by the SRIF infusion; under such conditions whole body glucose uptake should be entirely non-insulin mediated (NIMGU). Expressing glucose uptake as glucose metabolic clearance rate revealed that GH had no effect on NIMGU but significantly reduced the level of insulin-mediated glucose uptake (IMGU). Thus a reduction in the rate of NIMGU is probably not part of the mechanism by which GH repartitions glucose to sites of growth and milk production, whilst the present study confirms the antagonistic effect of GH on IMGU.

Effect of growth hormone-releasing factor on the response to insulin of cows during early and late lactation.

The euglycemic clamp technique was used to determine the effect of bovine growth hormone-releasing factor on glucose kinetics and on the response to insulin of 4 dairy cows during early lactation (mean, 35 d postpartum) and of 6 dairy cows during late lactation (mean, 194 d postpartum). Beginning 3 d prior to experiments, cows were injected twice daily with either saline or 2.5 micrograms/kg of growth hormone-releasing factor. On the day of the experiment, saline or the releasing factor (0.0119 microgram/kg per min) was infused into each cow for 5 h. After a basal period, insulin was infused at 1 and then at 6 mU/kg per min; plasma glucose concentrations were maintained at basal concentrations by the infusion of normal glucose. Growth hormone-releasing factor reduced the glucose infusion rate that was required to maintain euglycemia during the insulin infusions during late lactation but had no effect during early lactation. During the insulin infusions of the late lactation experiment only, the rates of glucose appearance, disappearance, and metabolic clearance were lower when plasma growth hormone was elevated. The results demonstrated that elevated concentrations of growth hormone decreased the responsiveness of peripheral tissues to high concentrations of insulin during late lactation but apparently had little effect during early lactation.